DISTINGUISHED ACHIEVEMENT AWARD WINNERS
SCVP is proud to honor these pioneers and leaders of our field.
2024 - E. Rene Rodriguez
E. Rene Rodriguez
Dr. E Rene Rodriguez’s journey into cardiovascular pathology began during his time in medical school, where a stint as a visiting student and later an assistant physician in Anatomic Pathology at the National Institute of Cardiology in Mexico City ignited his passion for the field. This early experience served as the foundation for his future endeavors after he obtained his medical degree from the Universidad Autónoma Metropolitana – Xochimilco in January 1982.
In August 1982, Rene embarked on a four-year fellowship at the Ultrastructure Section, Pathology Branch of the National Heart, Lung, and Blood Institute in Bethesda, MD, under the mentorship of leading experts in the field of cardiovascular pathology. Rene then transitioned into Anatomic and Clinical Pathology residency training at The George Washington University Medical Center in Washington, DC.
In 1990, Rene assumed the directorship of the Cardiovascular Pathology Unit at Rush Heart Institute in Chicago, IL. During his tenure at Rush University, he also undertook the responsibility of directing Autopsy Pathology services. In 2000, Rene took on the role of Director of Clinical Services in Cardiovascular Pathology at The Johns Hopkins Hospital in Baltimore, MD. His leadership and contributions solidified his reputation as a respected figure in cardiovascular pathology.
Since 2004, Rene has served as the Director of Cardiovascular Pathology and Director of Autopsy Pathology at The Cleveland Clinic in Cleveland, OH. In addition to his extensive professional experience, he is a Professor of Pathology at the Cleveland Clinic College of Medicine of Case Western Reserve University. His outstanding contributions to the education of cardiovascular medicine fellows was duly recognized with a teaching award in 2015.
His academic impact include more than 200 manuscripts and book chapters covering his multidimensional expertise in the field from basic science to clinical cardiology. He played a pivotal role in revising the criteria for antibody-mediated rejection in cardiac transplantation during his tenure as Chair of heart sessions at the Banff Conference in Allograft Pathology and later of the Pathology Council of the International Society for Heart and Lung Transplantation.
Throughout his career, Rene has been dedicated to advancing the field of cardiovascular pathology through his clinical expertise, leadership, and scholarly contributions. His commitment to nurturing the next generation of cardiovascular pathologists truly exemplifies the spirit of the 2024 SCVP Distinguished Achievement Award.
2023 - John Veinot
John P. Veinot
Dr. John Veinot is an exemplary physician, educator, investigator, and administrator who has made significant contributions to the field of cardiovascular pathology and to the SCVP over many years.
John received his M.D. from Dalhousie University in Halifax, N.S., in 1988, followed by residency in Anatomical Pathology at Queen’s University in Kingston, ON, and Cardiovascular Pathology fellowship at the Mayo Clinic in Rochester, MN. In 1994, he joined The Ottawa Hospital and the University of Ottawa, where he remained until his recent retirement from anatomical pathology practice.
Along the way, he became Full Professor in the Faculty of Medicine and served many administrative roles, including eleven years as the Chair of the Department of Pathology and Laboratory Medicine at the University of Ottawa, Head of the Departments of Pathology and Laboratory Medicine at The Ottawa Hospital and the Children’s Hospital of Eastern Ontario, and Chief of Medical Staff for the Eastern Ontario Regional Laboratory Association, where he emphasized the need for quality and patient-centered care.
His passion for teaching led to several teaching awards, including the uOttawa Excellence in Education Prize, the Faculty of Medicine Award for Excellence in Medical Education, the Pathology and Laboratory Medicine Best Teacher Award (twice), and the Faculty of Medicine Educator Award for Communicator Competence. He recognized the importance of teaching pathology beyond medicine and is proud of the achievements of those he has mentored.
As a Clinical Investigator at the Ottawa Hospital Research Institute, John made numerous research contributions in cardiovascular pathology, running the gamut from basic science to clinicopathologic correlations, leading to more than 200 manuscripts, multiple book chapters, and a book on echocardiography-pathology correlations.
John has been an integral part of the SCVP, serving on multiple committees and as its past president, and was instrumental in the publication of multiple consensus documents. He promoted the use of new and different modes of education, stressed the importance of diversity, and fostered collaboration with the AECVP – these efforts expanded the reach of our Society.
Most of all, John has always been approachable, dependable, and willing to help promote the discipline of cardiovascular pathology. We are proud to honor him with the 2023 SCVP Distinguished Achievement Award.
2022 - Richard Mitchell
Richard N. Mitchell
Dr. Rick Mitchell is an exemplary physician-scientist-educator who has made broad and impactful contributions to the field of cardiovascular pathology over many years.
Rick received his Ph.D. in Cell Biology/Immunology from The Rockefeller University in 1980 and his M.D. from Harvard Medical School in 1984. Following an internship in internal medicine at the Beth Israel Deaconess Medical Center, he completed pathology residency, cardiac pathology fellowship, and post-doctoral fellowship at the Brigham and Women’s Hospital. He joined Harvard Medical School and BWH as Assistant Professor in 1992 and ascended the academic ranks, culminating in his appointment as the Lawrence J. Henderson Professor of Pathology and Health Sciences and Technology in 2011.
Rick is a leading expert in the discipline and practice of cardiovascular pathology. He serves as a Senior Pathologist in the cardiac pathology and autopsy divisions in the Department of Pathology at BWH. He has made numerous research contributions in work conducted at the interface of immunology and vascular cell biology, including the mechanisms underlying acute and chronic rejection following heart transplantation, the role of specific cytokines and chemokine pathways in allograft vasculopathy, the source of recruited intimal smooth muscle cells in atherosclerosis, the nature of inflammatory cell populations involved in the pathogenesis of abdominal aortic aneurysm, and the immunology of cardiac valve disease. Moreover, he has been and continues to be a highly valued collaborator in studies focused on stem cell biology and the cardiovascular system, amyloidosis, gender differences in gene expression profiles, cardiac electrophysiology, and AI applications to cardiovascular pathology.
Rick also possesses a genuine, strong dedication to and aptitude for teaching and educational leadership, and serves as an important role model to medical students, pathology residents, and faculty colleagues. His teaching of residents on the autopsy and cardiac pathology services at BWH is well known and admired. He is passionate about conveying the scientific basis of medicine in both the pre-clinical and clinical segments of the undergraduate medical curriculum, and has been Director of the HST-030 Human Pathology course for over two decades (notably, this course is ranked by the HST MD students as the most effective and enjoyable course in their entire four-year curriculum). He also actively teaches or has taught in other HST courses in Cardiovascular Pathophysiology, Immunology, and Biomaterials and Tissue Engineering, as well as in the Harvard Medical School New Integrated Curriculum’s Immunology, Microbiology and Pathology course. Rick has demonstrated long-term and highly effective leadership as Associate Director of the HST Division for over two decades, during which he has directly mentored over 500 students. His teaching commitment and prowess have been recognized with seven teaching awards at Harvard Medical School and, nationally, he has received the Robbins Distinguished Educator Award from the American Society of Investigative Pathology (ASIP) and the Michele Raible Distinguished Teaching Award in Undergraduate Medical Education from the Association of Pathology Chairs.
Rick’s educational contributions have had a wide international reach. For many years he has been active in writing and editing the most widely used textbooks that educate most medical students around the world, including Robbins Basic Pathology, Robbins and Cotran Pathologic Basis of Disease, the Pocket Companion to Robbins and Cotran Pathologic Basis of Disease, and Biomaterials Science: An Introduction to Materials in Medicine. He also co-authored Robbins and Cotran Pathology Flash Cards, with an innovative design format, and co-edited a novel online book, Pathobiology of Human Disease.
Rick has given extraordinary service to the SCVP and other leading organizations in pathology. He is a past-Programming Chair and a past-President of the SCVP. He is also past-Chair of the Education Programming Committee and past-President of the American Society for Investigative Pathology, and developed and directed the annual ASIP Summer Academy, during which he taught fundamentals of acute and chronic inflammation and wound healing to graduate students, fellows, junior and senior faculty, and scientists in industry. He is one of the original organizers of the annual ASIP stand-alone meeting Pathobiology for Investigators, Students, and Academicians (PISA). Rick is also a Senior Associate Editor of the American Journal of Pathology, and Associate Editor of both Laboratory Investigation and SCVP’s official journal, Cardiovascular Pathology.
2021 - Not given
2020 - Allen Burke
Allen P. Burke
Dr. Burke is a current member of the Society of Cardiovascular Pathology and an Editorial Board Member of the Society’s Journal since 2002. He has made substantial contributions to the field in the peer-reviewed literature as well as innumerable lectures and workshops for more than 25 years.
His body of work includes more than 260 peer-reviewed journal article publications including a disproportionate number of first and last author publications, 6 complete books, and more than 70 book chapters. He was the senior editor of the 2015 WHO Classification of Heart Tumors.
He has been involved in teaching a large number of medical students, pathology residents, pathologist’s assistants, clinicians and scientists during the past decades, several of whom are active members of the Society and the cardiology community, at-large.
Moreover, his work has been recognized by others in the field, receiving over 21,000 citations, making him among the most cited pathologists in the world.
2019 - Gayle Winters
Gayle Winters
Gayle Winters is a distinguished member of the global cardiovascular pathology and transplantation communities. She received her BS in Biology (with Distinction) from Purdue University, and her MD in 1979 from the Loyola Stritch School of Medicine, followed by a year of general surgery residency, residency in anatomic and clinical pathology, and fellowship in surgical pathology at Loyola University Medical Center. After joining the Loyola faculty and rising to Associate Professor of Pathology, she was recruited to the Brigham and Women’s Hospital (BWH) in 1992, where she is Senior Pathologist and Associate Professor of Pathology at Harvard Medical School.
Dr. Winters has a national and international reputation as a heart transplant pathologist and serves or has served on the Editorial Boards of Circulation, Cardiovascular Pathology, Journal of Heart and Lung Transplantation, and Advances in Anatomic Pathology. Within the Society for Cardiovascular Pathology, Dr. Winters has held important leadership positions as Cor Notes Editor, Secretary, Acting Treasurer, Vice-Present/President Elect, and President.
Among sentinel contributions to her field, Dr. Winters was a member of the working group and co-author on the original 1990 grading system for cardiac transplant biopsies, its revision in 2005, and the grading system for antibody-mediated rejection in 2011. These grading schemas are considered the foundational guidance for all of heart transplant practice to the current time. Her work demonstrated the lack of progression of untreated Grade 2 rejection, and was instrumental in prompting the revision of the grading system in 2005. Other important work within the area of cardiac transplantation includes defining perioperative ischemic injury on post-transplant endomyocardial biopsies, studying the pathologic composition and clinical significance of Quilty effect, and defining the composition of allograft coronary disease and the use of myocyte vacuolization on post-transplant endomyocardial biopsies as a predictor of allograft coronary disease.
Dr. Winters has been actively involved in resident and medical student education throughout her career. In fact, she is a major educational leader in her home institution. She was the Director of the BWH Autopsy Service for over 20 years, Director of the BWH Residency Program in Pathology from 2001-2015, and served as Director of the BWH Harvard Medical School elective clerkship in Pathology. She has taught at Harvard Medical School in the Human Pathology and Cardiovascular Pathophysiology courses. Of perhaps the greatest significance in terms of the continued expertise in cardiovascular pathology as a discipline, Dr. Winters and her colleagues at BWH have trained 12 Cardiovascular Pathology Fellows. Of these Fellows, 7 have pursued a career in cardiovascular pathology and are current members of the Society for Cardiovascular Pathology. At the national level, she has been an active member of the Program Directors for Pathology (PRODS), and served as Member-at-Large of PRODS Council, Co-Chair of the PRODS Outcomes Committee, Secretary-Elect, Secretary, Chair-Elect, and was elected Chair in 2014-15. She received the Graduate Medical Education Distinguished Teaching Award from the Association of Pathology Chairs in 2016.
In summary, Dr Winters exemplifies the professional skills and leadership qualities that the SCVP Distinguished Achievement Award was established to honor. She has been and is a recognized scholar in her field, she is widely known as an educator in cardiovascular and transplant pathology, and she has served in many leadership roles for the SCVP and other related organizations. She certainly is an expert in the field of cardiovascular pathology.
Finally, Dr Winters is an absolutely lovely human being. She is a person of great character and great courage.
2018 - Kricket and Jon Seidman
Kricket and Jon Seidman
Dr. Kricket Seidman is the T.W. Smith Professor of Medicine & Genetics in the Department of Genetics at Harvard Medical School, is a Howard Hughes Investigator, and is a cardiologist at Brigham and Women’s Hospital, where she is also the Director of the Cardiovascular Genetics Center. She has received the American Heart Association Basic Science Prize, the American Society for Clinical Investigation Award, the Glorney-Raisbeck Prize, and the Schottenstein Prize.
Dr. Jon Seidman is the Bugher Foundation Professor of Cardiovascular Genetics, and a former Howard Hughes Investigator. Together they co-direct a lab in cardiovascular genetics that focuses on understanding the causes of hereditary heart disease and have been jointly recognized as recipients of the Pasarow Foundation Award in Cardiovascular Research, the Bristol-Myers Squibb Award for Distinguished Achievement in Cardiovascular Research, and the Institut de France Fondation Lefoulon-Delalande Grand Prix for Science Award.
The Seidmans numerous discoveries have elucidated the role of sarcomeric and other proteins in hypertrophic cardiomyopathy but have also contributed substantially to understanding the role of several genes (such as lamin A/C, eyes-absent-4, phospholamban, myosin heavy chain, troponin T, and titin) in dilated cardiomyopathy. Their recent work in cardiac transcription factor mutations in congenital heart defects has also been groundbreaking. These efforts have enabled improvements in precision diagnostics and therapeutic interventions for these conditions.
By developing and applying advanced sequencing strategies and correlating cardiomyopathy mutations with functional myocyte biology, the Cardiovascular Genetics Center labs have uncovered new and important insights into pathogenic pathways. Using these insights, they (and others) can now target linchpin molecules to develop novel therapeutic strategies to arrest the progression of cardiomyopathies. This is taking us beyond gross and microscopic pathology into the very “heart” of the pathologies of myocardial disease.
2017 - John (Jay) T. Fallon III
John (Jay) T. Fallon III
John T. Fallon III MD, PhD received his BA from Providence College and his MD and PhD from Albany Medical College. Even during medical school he was interested in cardiovascular pathology, as his PhD thesis was entitled Hemodynamics and atherosclerosis: Endothelial damage and ultrasonic arterial lesions. Dr. Fallon then went on to pursue pathology training at Massachusetts General Hospital, Harvard Medical School. He was recipient of an NIH public health service training grant to continue fellowship training Massachusetts General Hospital, Harvard Medical School. He remained at Massachusetts General Hospital as an Assistant then Associate Professor of Pathology both at Harvard Medical School and Massachusetts Institute of Technology, Division of Health Sciences and Technology. Dr. Fallon joined Mount Sinai School of Medicine in 1994 as a Professor of Pathology. He became Chairman and Professor of Pathology at New York Medical College in 2009.
Dr. Fallon has a strong history of research with over 290 original reports, overwhelmingly related to cardiovascular pathology and his major research interests in pathophysiology of ischemic heart disease, experimental vascular injury, and the immunopathology of human myocarditis and allograft rejection. His research in the field of atherosclerosis has helped to delineate the pathogenesis of thrombogenicity of atherosclerotic plaques, the role of inflammation in plaque rupture, and the mechanisms of intimal hyperplasia and restenosis after vascular interventions, to name but a few areas of his investigations. Dr. Fallon is a former member of the NIH Scientific Review Group of the Cardiovascular and Renal Study Section and he has also been the PI on NIH SCOR and training grants, most recently PI for NIH Thrombosis SCOR – Pathology Core and Co-Investigator in vulnerable Plaque Studies. He also served as a member of the NIH Myocarditis Study Group.
Dr. Fallon is a Founding- Member, Past- President, Past Awards Chairman and Past Councilor of the Society for Cardiovascular Pathology and is on the editorial board of Cardiovascular Pathology.
2016 - Jeffrey E. Saffitz
Jeffrey E. Saffitz
Dr. Saffitz received his M.D. and Ph.D. degrees from Case Western Reserve University in 1978. He completed both a Residency in Anatomic Pathology and a Cardiovascular Research Fellowship at Washington University School of Medicine in St. Louis. From 1982-1983 he was Visiting Fellow in Cardiac Pathology at the National Heart, Lung and Blood Institute with Dr. William Roberts. He then returned to Washington University on the faculty in the Departments of Pathology and Medicine (Cardiovascular Division) and rose through the ranks to become Paul and Ellen Lacy Professor of Pathology in 1999. In 2005 he was recruited to his current position in Boston.
Dr. Saffitz is a leading basic and translational investigator in the area of sudden cardiac death, arrhythmia mechanisms in arrhythmogenic cardiomyopathies, and cardiac myocyte electrical communication. His several decades of independent, federally funded research have yielded over 260 original contributions to the literature. His research has elucidated molecular and structural determinants of normal and abnormal intercellular coupling and defined the role of altered expression of connexins (gap junction channel proteins) and remodeling of gap junctions in the pathogenesis of lethal ventricular arrhythmias. He has characterized the molecular pathology of human cardiomyopathies with the clinical phenotypes of arrhythmogenic right ventricular cardiomyopathy (ARVC), such as Naxos disease, Carvajal syndrome, ARVC Type 8 and plakophilin-related cardiomyopathies, which are caused by mutations in genes encoding proteins at cell-cell mechanical junctions. He described a new endomyocardial biopsy test that looks for abnormally low levels of plakoglobin, an essential component of cardiac myocyte junctions, and identified low levels of plakoglobin as a possible marker for ARVC (NEJM, 2009).
Dr. Saffitz has served as President of the Society for Cardiovascular Pathology, and in leadership roles in the American Heart Association and the Heart Rhythm Society. He has been a member of the Editorial Boards of 10 journals of pathology and cardiovascular medicine and is currently an Associate Editor of Cardiovascular Pathology, Circulation, and the American Journal of Pathology, and he is on the Editorial Board of the American Journal of Cardiology. He authored the chapter on The Heart in the 6th and several prior editions of Rubin’s Pathology. He is also a national leader in genomic pathology in personalized medicine, and has spearheaded efforts to use next generation sequencing and other high-throughput technologies in routine clinical laboratory diagnostics. He is an accomplished teacher and academic leader, and a prototypical role-model for the cardiovascular pathologist-scientist.
2015 - Michael C. Fishbein
Michael C. Fishbein
Dr. Michael Fishbein was born May 25, 1946 in Brussels, to holocaust survivors, who with the help of the Belgian people, survived in hiding in the Belgian countryside for all of WWII. In 1949, the family emigrated to Chicago where Michael’s mother had relatives. When Michael was 12, and his father was 51, his father had his first myocardial infarction. From then on, cardiovascular disease, in one way or another, has played a major role in Michael’s life.
With the help of State of Illinois Scholarships, Michael received his undergraduate and medical school education at the University of Illinois. In medical school, his teacher of congenital heart disease was Dr. Maurice Lev. Michael used one medical school elective to go to the Bispebjerg Hospital in Copenhagen where he participated in a busy autopsy service, and one elective in cardiology at the Mayo Clinic where he had the opportunity to spend time with Dr. Jack Titus on the autopsy service. In part, to escape Chicago winters, he did an internship and residency in pathology at UCLA/Harbor General Hospital (HGH) in Torrance, CA. Because he had an interest in cardiovascular pathology not shared by any of the faculty, Michael inherited most cardiac autopsies and collaborative research projects with the active adult and pediatric cardiologists at HGH. These individuals were very enthusiastic and supportive and urged him to get additional training. Michael was fortunate to be able to secure an elective with Dr. William C. Roberts at the NIH. While at the NIH, he was again fortunate to know and work with outstanding individuals in the field of cardiovascular pathology, namely, Dr. Victor Ferrans, Dr. Max Buja, Dr. Bernadine Bulkley/Healy, and Dr. Barry Maron. He also spent time with Dr. Hugh McAllister at the AFIP where he reviewed the vast collection of congenital hearts, and an elephant’s heart as well.
In addition to being a great teacher, mentor, and friend, Dr. Roberts, through his association with Dr. Eugene Braunwald, was instrumental in recruiting Michael to the then Peter Bent Brigham Hospital. In fact, he was the first appointee of the new Pathology Chairman, Dr. Ramzi Cotran, who took a big chance hiring Michael since he was straight out of residency, very inexperienced, and had not even taken pathology board exams when appointed. After 3 exciting, productive years at the Brigham, and the blizzard of ’77, Michael and his family returned to Los Angeles. He spent 19 very productive years at Cedars-Sinai Medical Center where he was a general anatomic pathologist with a subspecialty interest in cardiovascular pathology. While challenging, practising general pathology exposed him to the full gamut of human disease and a wide array of tools in pathology, such as EM, histochemistry, and immunohistochemistry, that have played a major role in his study of cardiovascular diseases.
In 1997, Michael had the opportunity to move to UCLA, where the anatomic pathology service was more subspecialized. The greater subspecialization, and funding from the Piansky Endowment he received, allowed him more opportunities to pursue research interests in heart disease. From the individuals named above, and brilliant and generous collaborators that are too numerous to name, Michael had exceptional exposure to giants in cardiovascular disease. In his opinion, good fortune, and the generosity of time and effort on the part of his mentors, allowed him to have a fulfilling career in medicine and cardiovascular pathology particularly. Working hard also helped.
Of course, none of his “success” would have been possible without the help of family: devoted parents who sacrificed whatever necessary so he could be educated; his loving and supportive wife of 40 years, Astrid, who took care of most matters while Michael was busy with his career; and two wonderful and accomplished now-grown and married children, Danielle and Gregory, who have been a source of great pleasure and pride. While no one knows what the future holds, Michael’s short-term plans are to continue his current activities at UCLA on a part-time basis, and to spend his “free-time” with his new granddaughter, Maxine, as well as to improve his golf game.
2014 - Jagdish Butany
Jagdish Butany
Jagdish Butany is Professor in the Department of Laboratory Medicine and Pathobiology at the University of Toronto, Canada and Director of the Division of Pathology in the Department. He is a Staff Cardiovascular Pathologist at the University Health Network (Toronto General Hospital Site), and Director of Autopsy Services. Dr. Butany works in an interdisciplinary setting with colleagues from related specialities and other health professions. Dr. Butany’s investigative work has primarily been based on clinical investigations and outcomes and collaboration with clinical colleagues in basic and applied research. His major interest has been prosthetic heart valves, an interest nurtured by contact with (late) Dr. Victor Ferrans, and with Dr. Malcolm Silver and Dr. Frederick Schoen.
He trained in India (MBBS), at the Kasturba Medical College in Mysore (Manipal and Mangalore) and had his Post-Graduate training at the All India Institute of Medical Sciences, New Delhi. Dr. Butany moved to Toronto in 1975 and started his pathology training at the University of Toronto (U of T), which he completed in 1979. Since then, he has worked at the Toronto General Hospital (now University Health Network) and the University of Toronto, starting as a Lecturer in 1980, with a break of one year when he was a Fellow at the NIH (National Heart Lung and Blood Institute) at Bethesda, Maryland with (late) Dr. Victor J. Ferrans. During this time, he had the pleasure of working with/meeting a number of pathologists who were fellows there, and Dr. William C. Roberts, then head of the Pathology branch. On his return from the NIH, Dr. Butany joined the Pathology Department of the Women’s College Hospital and six months later started at the Toronto General Hospital as a cardiovascular pathologist. He has worked on several committees at the University, at the Toronto General Hospital, and in the Pathology Department.
Dr. Butany has been involved in teaching at the undergraduate and post-graduate levels, including medical students, pathology residents, cardiology residents and cardiac surgery residents and fellows. He has mentored and taught cardiovascular pathology to numerous students from their second year at university onwards as they went on to become medical students, residents and staff members in diverse disciplines. He is actively involved in undergraduate and graduate teaching at the U of T School of Pharmacy with a focus on cardiovascular pathology. For several years he participated in teaching at the Occupational Therapy/Physiotherapy and nursing schools. One of the interesting aspects of his teaching is the hands on approach to cardiovascular pathology, based significantly on the use of archived cardiac specimens. He has been part of the Laboratory Medicine and Pathobiology Specialist program since its inception, teaching two courses, one on Cardiovascular Pathology and the other on Neoplasms to undergraduate students, using a mix of didactic and “hands on” teaching. These courses have been very well received since their inception. He has been honored by the Toronto General Hospital, the Department of Laboratory Medicine and Pathobiology (University of Toronto) with several teaching awards and by the Faculty of Medicine, University of Toronto with the Aiken’s Award for Individual Undergraduate Medical Student Teaching (1995) and the Colin Wolfe Award for Commitment to Continuing Medical Education (2012).
Dr. Butany has had an abiding interest in Continuing Professional Development for pathologists and was involved with the Royal College of Physicians and Surgeons of Canada, in the setting up of its Maintenance of Certification Program (MOCOMP). He has been involved in continuing medical education programs for many years, and has organized and spoken at two courses on cardiovascular pathology in the late 1980s (in Toronto), courses at the USCAP and at the CAP. He is involved in teaching at courses in India, as well as in other countries. Since its inception, Dr. Butany has been involved in the CME activities of the Association of Indian Pathologists in North America (AIPNA) and often participates in their annual programs in India. He was their Keynote speaker at Vancouver in 2012 and delivered the named Oration (the Nagalotimath Oration) at the Annual CME program at Pondicherry, India, in January of 2013.
Professor Butany played a significant role as the pathologist involved with the SARS pandemic in Toronto (2003). His work on prosthetic mechanical valves was critical in the recall/ taking off the market, of one bileaflet valve (January 2000). He has over 280 peer reviewed publications which cover the gamut of cardiovascular disease with an emphasis on prosthetic heart valves and other cardiovascular devices. Dr. Butany’s publications include many other publications as well as authorship of book chapters and participation as an Editor of other books.
Dr. Butany has been President of the Canadian Association of Pathologists (2006 – 2009), and before that, the Chair of their CME Committee, responsible for organising the educational courses (Short courses) offered at the annual meeting (nine years). Dr. Butany has been honored by the Canadian Association of Pathologists with their Distinguished Service Award (July 2012).
Dr. Butany is a founding member of the Society for Cardiovascular Pathology and has participated in its growth to its present stature as the pre-eminent Society for Cardiovascular Pathologists. He was the President of the Society for Cardiovascular Pathology (2007 – 2009). Dr. Butany has been Co-Editor-in-Chief of Cardiovascular Pathology (with Dr. Avrum Gotlieb), the official journal of the Society of Cardiovascular Pathology and continues to serve on its Editorial Board. Dr. Butany is a member of the Editorial Board of several other journals.
On a more personal note, his personal achievements have made Jagdish realise how blessed and fortunate he has been in his career in Canada and in the colleagues he has worked with. From this has come a deep sense of obligation and the desire to “give back.” He is currently the Secretary-Treasurer of the World Association of Societies of Pathology and Laboratory Medicine (2009 – ) and a member of the Board of the World Pathology Foundation (2009 – ). The primary focus of both of these organisations (WASPaLM and WPF) is improving the quality of pathology and laboratory services worldwide and in helping countries-in-need improve their pathology and laboratory medicine services. Their approach is multifaceted, one facet being the organisation of CME programs for “countries-in-need”. Dr. Butany serves as a Director on the Board of Directors of The Scarborough Hospital (2008- ), the second largest Community/Academic Hospital in the country. Dr. Butany is a member of the Board of Trustees of his community’s Temple and participates actively in the management of the Temple.
Jagdish has had the love and companionship of his charming wife, Vidya Butany (a practising psychiatrist), for over four decades and the pleasure of being involved in the growth of their daughter Indrani, and now their grandchildren Neveah and Riaan and son-in-law Dirk. Amongst the things in his career that Jagdish has found most satisfying is the opportunity to work with his colleagues at the TGH, in the SCVP and his Co-Editor of CVP, Prof (Dr) Avrum Gotlieb.
2013 - Michael A. Gimbrone
Michael Gimbrone
I am so pleased that Michael A. Gimbrone, Jr. is receiving the 2013 Society for Cardiovascular Pathology Distinguished Lifetime Achievement Award. As a long-term colleague and collaborator, I am delighted to introduce him for this lecture. Dr. Gimbrone is a pioneer and leading investigator in vascular biology, who is widely recognized for his immense contributions to the initiation and scientific and conceptual development of the discipline. Moreover, and importantly, he has shown immense leadership throughout his career in fostering a broad multidisciplinary academic environment in our department locally and far beyond, in which the highest academic standards converge with highly talented young people and key opportunities to promote career and personal success.
Dr. Gimbrone received his A.B. degree from Cornell University and his M.D. degree from Harvard Medical School in 1970. During his medical studies he pursued research in the Department of Anatomy at Harvard Medical School, learning ultrastructural anatomy and cell biology with Donald Fawcett. After completing an Internship at the Massachusetts General Hospital, Boston, and a Research Fellowship at the Children’s Hospital Medical Center, Boston, with Dr. Judah Folkman, he served as a Staff Associate at the National Cancer Institute in Bethesda, Maryland. He then returned to the Peter Bent Brigham Hospital in Boston for residency training in Pathology and subsequently rose through the academic ranks from Instructor to Professor of Pathology at Harvard Medical School in 1985. In 1976, he established the Vascular Pathophysiology Research Laboratory. In 1998, he was named the first Director of the Center for Excellence in Vascular Biology at the Brigham and Women’s Hospital/Harvard Medical School.
Dr. Gimbrone’s research has focused on the cellular and molecular mechanisms of vascular disease, in particular the role of the endothelial cell in complex disease processes such as angiogenesis, atherosclerosis, thrombosis and inflammation. Indeed, Michael’s lecture today in honor of his Award is most appropriate to the focus of this session on Angiogenesis. In 1967 he sought out one of his first mentors, the young surgeon, Judah Folkman, and with whom he ultimately developed a rabbit cornea model and confirmed the capacity of tumors to secrete diffusible angiogenic factors that they needed to recruit new blood vessels in order for them to grow wild. With Dr. Folkman and another key mentor, Ramzi Cotran, Dr. Gimbrone was among the first to establish reproducible methods for the in vitro culture of endothelium and smooth muscle from human blood vessels. This platform permitted him to begin his lifelong scientific quest (and the development of an active and worldwhile line of research): to utilize the tools of modern cell biology and molecular biology to dissect the functions of vascular cells, especially endothelium, in health and disease. His laboratory subsequently discovered inducible endothelial-leukocyte adhesion molecules important in inflammation and atherogenesis. Most recently his group has focused on the molecular mechanisms linking biomechanical stimulation and endothelial genetic regulation in atherogenesis. This has led to the discovery of “athero-protective genes” that provide potential therapeutic targets for the prevention of heart attacks and strokes, and dissection of the mechanisms of athero-protective functions is a current major effort in the Gimbrone laboratory.
Dr. Gimbrone has published more than 250 research articles, book chapters and reviews in vascular biology. He was founding President of the North American Vascular Biology Organization (NAVBO). Among many honors and achievements, he has received the Basic Research Prize from the American Heart Association, a MERIT Award from the National Heart Lung and Blood Institute, the Cardiovascular Research Lifetime Achievement Award from the Bristol-Myers Squibb Institute, the Earl Benditt Lifetime Achievement Award in Vascular Biology from NAVBO, the Warner-Lambert Parke Davis Award in Experimental Pathology (FASEB), and the King Faisal International Prize in Medicine. He has been elected to the National Academy of Sciences (USA), the American Academy of Arts and Sciences, and the Institute of Medicine of the National Academy of Sciences.
Michael stepped down one year ago from approximately a decade as Chairman of the Department of Pathology at the Brigham and Women’s Hospital in Boston, Massachusetts (USA) and Ramzi S. Cotran Professor of Pathology at Harvard Medical School. For much of that decade he served as the HMS Academic Dean for Partners Healthcare Systems and a member of the Council of Academic Deans at HMS. He continues to serves as the BWH Director of the Center for Excellence in Vascular Biology.
It is highly appropriate that Michael follows other pioneering Vascular Biologists who previously received the Distinguished Achievement Award of the Society for Cardiovascular Pathology, including Earl Benditt (1989), Guido Majno (1990), Ramzi Cotran (1997) and Russell Ross (1998).
2012 - Avrum Gotlieb
Avrum Gotlieb
Prof. Gotlieb is the Senior Academic Advisor to the Dean (2011-2013), and Acting Vice-Dean, Graduate Affairs (2011-2013) in the Faculty of Medicine, University of Toronto. He obtained his BSc, MDCM and his Anatomic Pathology training at McGill University. He trained in the Department of Biology, University of California, San Diego, with S.J. Singer. Prof. Gotlieb joined the Department of Pathology at the University of Toronto in 1978. He is a cardiovascular pathologist at the University Health Network and a senior scientist at the Toronto General Research Institute. Prof. Gotlieb served as the founding Chair of the Department of Laboratory Medicine and Pathobiology (1997-2008), and as Interim Vice-Dean Research and International Relations (2009-2010) in the Faculty of Medicine, University of Toronto.
Prof. Gotlieb has received teaching awards from the hospital, the department, Faculty of Medicine, including two prestigious Aikins Awards and the Sustained Excellence in Graduate Teaching Award, as well as the Robbins Distringuished Educator Award from the American Society for Investigative Pathology (2011). He initiated an innovative and unique undergraduate arts and science specialist program in pathobiology that is in its 10th year and has seen many of its graduates go on to graduate and medical school. Prof Gotlieb authored the widely-disseminated informative career guide booklet, “The Road to Becoming a Biomedical Physician Scientist in Pathology and Laboratory Medicine,” sponsored by the American Society of Investigative Pathology and the Department of Laboratory Medicine & Pathobiology, University of Toronto, and in 2009 co-authored (with Dr. Tara Sander) a second career guide booklet for ASIP, “Journey to Success: Career Pathways for Biomedical Scientists in Pathology and Laboratory Medicine.”
Prof. Gotlieb’s research includes atherosclerosis and valvular heart disease. Studies on the cell biology of cardiac valves focus on the role of interstitial valvular cells in maintaining the structure and function of heart valves, and interstitial cell function related to repair and cell heterogeneity. In vitro studies on endothelial injury and repair directed at understanding how the cell cytoskeleton regulates cell migration, and how various growth factors and cytokines modulate both migration and proliferation related to repair. Earlier studies include the pathogenesis of intimal hyperplasia, a lesion that predisposes to fibrofatty plaque formation; and the role of growth factors, cytokines, and proteinases on intimal hyperplasia. He has published over 100 peer-reviewed papers, and 37 reviews and book chapters. He has edited three books, including the comprehensive textbook Cardiovascular Pathology, edited with colleagues Malcolm D. Silver of the University of Toronto, and Frederick J. Schoen of Harvard Medical School. He has been an invited visiting professor and keynote speaker at national and international universities and research institutes. He is co-editor of the journal Cardiovascular Pathology (2001-2011) and serves on the editorial board of several leading journals in pathology, the American Journal of Pathology and Laboratory Investigation.
Prof. Gotlieb has been an innovative leader in academic medicine creating national and international infrastructures to promote research and education. His focus has been on Pathology and Laboratory Medicine and Cardiovascular Pathology. He has provided guidance through carrying out external academic reviews, leading grant review panels and lecturing on the academic missions of Pathology and Laboratory Medicine. He is a past-president of the Canadian Society of Atherosclerosis, Thrombosis and Vascular Biology, the Society for Cardiovascular Pathology and the American Society for Investigative Pathology. He is past vice-president for science policy of the Federation of American Societies for Experimental Biology, Bethesda, MD. In 2006, Prof. Gotlieb was elected as a fellow of the Canadian Academy of Health Sciences, and will be awarded the Distinguished Achievement Award from the Society for Cardiovascular Pathology (2012).
2011 - Gaetano Thiene
Gaetano Thiene
Gaetano Thiene M.D. is Professor of Pathology and Consultant of Cardiovascular Pathology, Department of Medical Diagnostic Sciences and Special Therapies at the University of Padua Medical School, Padua, Italy. He was Director of the Institute of Pathological Anatomy at the University of Padua from 1998-2006.
Following graduation from the Medical School at the University of Padua, Dr. Thiene trained as both a Cardiologist (University of Padua) and a Pathologist (University of Trieste). He is Honorary Fellow of the Royal College of Physicians in London, U.K., Foreign Member of the Serbian Academy of Science and Arts in Beograd, Serbia, Corresponding Member of the Galileian Academy in Padua and Vice-President of the Olympic Academy in Vicenza, Italy.
His research interests have been across the broad fields of Cardiovascular Medicine and Pathology, particularly directed to clinicopathologic studies and clinical translation of basic research. Dr Thiene first reported Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) as a major cause of sudden death in the young and in athletes (NEJM 1988) and has contributed to the elucidation of the genetic basis for ARVC. He is a principal architect of the Italian program in which all young individuals who participate in sports activities are screened for potential cardiovascular problems and in which all sudden unexpected deaths in the young are formally investigated by expert cardiovascular pathologists. This is the most successful such screening program in the world and it has led to major advances in understanding the causes of sudden death in the young. It resulted in a sharp decline (by 90%) of sudden death in the athletes of the Veneto Region, Italy, thanks to identification and disqualification of young people affected by cardiomyopathies. Dr. Thiene has been and continues to be a true visionary in this field.
Dr. Thiene has been the leader of the group in Padua which has worked at the interface between pathology and genetics in the cardiomyopathies and has identified several disease-causing mutations, correlating them with the clinical and pathological features of the disease. He has given important contributions to defining clinicopathologic correlations in heart valve disease and in the pathology of tissue valve substitutes, including the initial observation that calcification in human bioprostheses was initiated in cells. Dr. Thiene has made other contributions to congenital heart disease, molecular genetics and pathology of myocarditis, coronary artery disease, arrhythmias and conduction system disease, cardiac tumors, the use of the endomyocardial biopsy and cardiac transplantation.
Up to October 31st 2010, he has published nearly 700 reports of original investigations and reviews in Index leading journals of pathology and cardiovascular medicine, and additionally is co-author and/or co-editor of 15 monographs. His papers collected an overall Impact Factor of 2826 and 14083 quotations, with an Hirch index of 52 from 1996.
Dr. Thiene is Associate Editor of Cardiovascular Pathology and of the Journal of Heart Valve Disease, and serves on the Editorial Board and/or acts as reviewer of other prestigious journals in cardiology, medicine and pathology.
Moreover, Dr. Thiene has been a tireless champion of and participant in the Society for Cardiovascular Pathology (SCVP), of Cardiovascular Pathology as a subspecialty as well as of international cooperation. He has been a major driver of the Association for European CardioVascular Pathology (AECVP) and has motivated young people in Europe to enter the field of Cardiovascular Pathology, training several as a direct mentor.
More generally he has led the definition of educational and training requirements for Cardiovascular Pathology. He is Past-President of the SCVP (2003-05) and of the AECVP (2004-06). As immediate past SCVP Program Chair, he “revitalized” the Sunday Companion Society meetings in conjunction with the USCAP and he initiated a topical Saturday afternoon session of specific interest to Cardiovascular Pathologists.
2010 - Bruce McManus
Bruce McManus
Dr. Bruce McManus earned his BA and MD from the University of Saskatchewan, an MSc from Pennsylvania State University, and a PhD from the University of Toledo. He pursued post-doctoral fellowships at the University of California, Santa Barbara (Environmental Physiology) and the National Heart, Lung, and Blood Institute in Bethesda, MD (Cardiovascular & Pulmonary Pathology), and completed residency training in Internal Medicine and Pathology at the Peter Bent Brigham Hospital, Harvard University.
Dr. McManus’s research is centered on understanding the mechanisms, consequences, detection, and prevention of injury and abnormal repair processes in inflammatory diseases of the heart and blood vessels. He has a particular interest in the diagnosis and management of acute viral myocarditis. Throughout his career, he has authored over 400 peer-reviewed publications, contributed to more than 60 book chapters, and written several books. Renowned as an extraordinary mentor, Dr. McManus has been widely recognized for his leadership and contributions to both research and education in the health sciences.
Among his many accolades, Dr. McManus received the prestigious Max Planck Research Award in 1991, and was elected as a Fellow of the Royal Society of Canada in 2002. He is currently a Professor Emeritus in the Department of Pathology and Laboratory Medicine at the University of British Columbia, and CEO of the Centre of Excellence for Prevention of Organ Failure (PROOF Centre).
Dr. McManus’s leadership extends beyond his research, as he has co-founded the Personalized Medicine Initiative of British Columbia and participated in several life sciences and technology start-ups. His work in advancing trans-omic biosignatures has been instrumental in moving cardiovascular research forward. For his exceptional contributions to the field, Dr. McManus is receiving the SCVP Distinguished Achievement Award, celebrating his pioneering research, mentorship, and profound impact on heart and vascular health.
2009 - L. Maximilian Buja
L. Maximilian Buja
Dr. L. Maximilian Buja is a distinguished physician-scientist and cardiovascular pathologist whose exceptional contributions to medical education, research, and leadership have had a profound impact on the field of cardiovascular pathology. With over 35 years of service at UTHealth Houston, Dr. Buja’s legacy reflects his unwavering commitment to advancing scientific knowledge, fostering educational excellence, and improving patient care.
Dr. Buja earned his medical degree with honors from Tulane University School of Medicine in 1967, where he also completed a Master of Science in Anatomy. He launched his medical career with an internship at Charity Hospital in New Orleans, followed by a staff associate position at the National Heart and Lung Institute in Bethesda, Maryland. His training continued at the National Cancer Institute as a pathology resident, later serving as a Senior Investigator in Cardiovascular Pathology at the National Heart and Lung Institute. Before joining McGovern Medical School at UTHealth in 1989, Dr. Buja was on the faculty at the University of Texas Southwestern Medical Center.
At UTHealth, Dr. Buja made significant strides in advancing medical education and research. He was appointed Chair of the Department of Pathology and Laboratory Medicine in 1989 and served as Dean of McGovern Medical School from 1996 to 2003, leading the institution through important growth and innovation. His leadership expanded beyond the medical school as he also held the roles of Executive Vice President for Academic Affairs at UTHealth and Chief of Cardiovascular Pathology at the Texas Heart Institute.
Dr. Buja’s research has been instrumental in advancing the understanding of myocardial ischemic and hypoxic injury. Supported by funding from the NIH and other agencies, his work has resulted in over 500 publications, including original research articles, reviews, book chapters, and two atlases of pathology, alongside a comprehensive textbook on cardiovascular pathology. His pioneering work has greatly influenced both the scientific community and clinical practice, deepening our understanding of cardiovascular diseases.
A passionate educator, Dr. Buja founded the Shine Academy to promote excellence in health sciences education. He continues to serve as a Distinguished Teaching Professor at McGovern Medical School, shaping the careers of numerous students, residents, and fellows through his mentorship.
Dr. Buja’s many accolades include the Caldwell Award from the Texas Society of Pathologists, the Haran J. Spjut Award from the Houston Society of Clinical Pathologists, and election as a Fellow of the American Association for the Advancement of Science. He was also named a Chancellor’s Health Fellow in Education by The University of Texas System.
Dr. Buja’s remarkable career in cardiovascular pathology and education, marked by innovation, leadership, and a dedication to scientific advancement, serves as an inspiration to all in the medical and academic fields. It is with great honor that the Society for Cardiovascular Pathology presents him with the Distinguished Achievement Award, recognizing his outstanding contributions to cardiovascular pathology and his enduring commitment to advancing the field of cardiovascular pathology.
2008 - William D. Edwards
William D. Edwards
2007 - Renu Virmani
Renu Virmani
Dr. Renu Virmani earned her medical degree at Lady Hardinge Medical College in New Delhi, India. After moving to the U.S., she worked with Dr. William C. Roberts, a prominent cardiac pathologist, who became her mentor. Following her residency at George Washington University Medical Center, she completed a fellowship at the National Heart, Lung, and Blood Institute. Dr. Virmani went on to become the Chair of the Department of Cardiovascular Pathology at the Armed Forces Institute of Pathology (AFIP), a role she held from 1984 to 2004.
In the 1980s, she also served as an associate professor at Vanderbilt University and as director of autopsy services at the Veterans Administration Medical Center in Nashville. Today, Dr. Virmani is a Clinical Professor at multiple universities, including Georgetown University, George Washington University, and Vanderbilt University.
In 2005, Dr. Virmani founded CVPath Institute, an independent nonprofit organization focused on cardiovascular disease research. The institute has been pivotal in advancing understanding of vulnerable plaque, stents, and transplanted transaortic valves. Dr. Virmani is also recognized for her early warnings regarding the potential risks of brachytherapy and drug-eluting stents, which have had a profound impact on the field.
A prolific researcher and educator, Dr. Virmani has delivered over 800 presentations worldwide, published more than 600 articles, and written numerous book chapters and books. She has received multiple research grants and has contributed significantly to the fields of atherosclerosis, plaque progression, and cardiovascular diseases.
For her pioneering work and substantial contributions to cardiovascular pathology, Dr. Virmani is receiving the SCVP Distinguished Achievement Award.
2006 - Frederick J. Schoen
Frederick J. Schoen
Dr. Schoen is a distinguished Professor of Pathology and Health Sciences and Technology at Harvard Medical School (HMS) and the Executive Vice-Chairman of the Department of Pathology at Brigham and Women’s Hospital (BWH). He holds a B.S.E. in Materials and Metallurgical Engineering from the University of Michigan, a Ph.D. in Materials Science from Cornell University, and an M.D. from the University of Miami School of Medicine. Dr. Schoen completed his medical training with a residency in Anatomic Pathology and a fellowship in Thoracic and Cardiovascular Pathology at the University of Florida before joining BWH in 1980 as Director of Cardiovascular Pathology.
In his leadership roles, Dr. Schoen has significantly contributed to fostering multidisciplinary collaboration and innovation in healthcare technology. He actively mentors students and professionals in fields such as Cardiovascular Pathology, Biomaterials, Tissue Engineering, and Medical Device Development. He is a renowned researcher in the development of heart valve substitutes, cardiovascular prostheses, and cardiovascular tissue engineering, having published over 470 manuscripts and authored/co-authored several influential books in these areas.
Dr. Schoen has held prominent roles in professional organizations, including past President of the Society for Biomaterials (SFB), the Society for Cardiovascular Pathology (SCVP), and the International Society for Applied Cardiovascular Biology (ISACB). He has received numerous accolades, including the SFB Clemson Award for Applied Biomaterials Research (1990), and the SFB Founders Award for Lifetime Achievement in Biomaterials (1999), among others.
In recognition of his outstanding contributions to cardiovascular pathology, biomaterials, and healthcare innovation, Dr. Schoen received the SCVP Distinguished Achievement Award for his groundbreaking work in cardiovascular prostheses and tissue engineering.
2005 - Thomas N. James
Thomas N. James
Dr. Thomas N. James, MD, MACP, is an internationally recognized cardiologist, pathologist, and scientific investigator renowned for his groundbreaking research on cardiovascular pathology, particularly the cardiac conduction system. His pioneering work began in 1961 with the publication of a seminal textbook on the anatomy of the coronary arteries. Over the years, his focus shifted to the conduction system of the heart, where his discoveries on the electrical pathways, especially the James fibers, gained international prominence. These fibers, which bypass the atrioventricular node, contributed to the understanding of cardiac pacing and led to advancements in pacemaker design.
Dr. James’s contributions to the field of cardiovascular science have had far-reaching effects, particularly his research on long-QT syndrome and sudden cardiac death. His work in this area has influenced not only cardiology but also sports medicine and primary care, helping to shape the understanding and management of sudden cardiac death and related conditions. In addition to his research, Dr. James’s leadership was evident in his roles as president of the American Heart Association (1979), president of the International Society and Federation of Cardiology (1982), and as director of the Cardiovascular Center of the World Health Organization from 1988 to 1998.
Throughout his career, Dr. James made significant contributions to the anatomic-pathologic and genetic research of sudden cardiac death, with his findings continuing to stimulate global interest in the field. His recent work on crib death and the ongoing genetic research into long-QT syndrome have further solidified his legacy as a leader in the field of cardiovascular pathology.
In recognition of his groundbreaking contributions to the study of the cardiac conduction system, long-QT syndrome, and sudden cardiac death, Dr. James received the SCVP Distinguished Achievement Award for his lifelong impact on cardiovascular science and pathology.
2004 - Anton E. Becker

2003 - Keith A. Reimer
Keith A. Reimer
Keith A. Reimer, MD, PhD, is a distinguished experimental cardiologist and cardiac pathologist, best known for his pioneering research in cardioprotection and ischemic injury. Born in Beatrice, Nebraska, in 1945, Keith displayed exceptional academic promise early in life. He earned his MD and PhD in experimental pathology from Northwestern University, where he embarked on a career that would have a lasting impact on both cardiovascular science and medical education.
Dr. Reimer’s most notable contributions to cardiovascular research were in the areas of myocardial ischemia, reperfusion injury, and cardioprotection. His work in creating the AMPIM (Animal Models for Protecting Ischemic Myocardium) study provided an important framework for evaluating therapies aimed at protecting the ischemic heart. Additionally, his concept of the “wavefront of ischemic cell death” has significantly advanced the understanding of ischemic injury in the heart. One of his most important discoveries was the identification of ischemic preconditioning, a phenomenon where brief episodes of ischemia can protect the heart from more severe ischemic injury, a finding that has influenced subsequent research in the field and led to significant advances in the treatment of heart disease.
Throughout his career, Dr. Reimer held influential academic and leadership roles. He was appointed Chief of Cardiovascular Pathology at Duke University, where he became a leading figure in the study of cardiovascular disease. His lab attracted talented postdoctoral fellows and medical students, many of whom went on to have successful careers of their own in cardiovascular research. Dr. Reimer’s ability to combine rigorous scientific inquiry with mentorship was one of his greatest strengths, and he is remembered for his exceptional teaching and commitment to the next generation of scientists.
In addition to his work at Duke, Dr. Reimer was actively involved in the International Society for Heart Research (ISHR), where he held several leadership positions, including Secretary and President of the American Section. His contributions to the ISHR helped shape the direction of cardiovascular research and fostered international collaboration in the field.
Dr. Reimer’s research continues to be recognized for its transformative impact on the understanding of ischemic heart disease and cardioprotection. In recognition of his extraordinary contributions to the field, Dr. Reimer received the SCVP Distinguished Achievement Award for his pioneering work in cardiovascular pathology, particularly in the areas of ischemia, reperfusion injury, and cardioprotective strategies.
2002 - Ariela Pomerance
2001 - Hugh A. McAllister, Jr.
Hugh A. McAllister, Jr.
Dr. Hugh Alexander “Chip” McAllister, Jr., a distinguished cardiovascular pathologist, was born in Washington, DC, and raised in Lumberton, North Carolina. After earning his MD from the University of North Carolina (UNC) in 1966, Dr. McAllister embarked on a remarkable military career, training in pathology and cardiac pathology at Walter Reed Army Medical Center and the Armed Forces Institute of Pathology (AFIP). Upon retiring from the U.S. Army in 1984, he joined the Texas Heart Institute (THI) in Houston, where he became the founding chairman of the Department of Cardiovascular Pathology and made significant contributions to the fields of heart transplantation, cardiac tumors, and coronary artery diseases.
Dr. McAllister’s collaborative work at AFIP and THI led to key publications, including the seminal Tumors of the Cardiovascular System (1978) with Dr. John J. Fenoglio, a classic reference in the field. He also developed a widely recognized system for grading cardiac allograft rejection, which became the foundation for heart transplant management and was adopted internationally.
In addition to his research, Dr. McAllister made notable contributions to cardiovascular education and served in leadership roles at institutions such as the University of North Carolina and the Texas Heart Institute. He received multiple prestigious awards, including the Legion of Merit Award.
Outside of medicine, Dr. McAllister IS a passionate supporter of art and nature, with an extensive Southwestern art collection donated to the Ackland Art Museum and involvement in the World Wildlife Fund. His legacy is marked by his groundbreaking research, dedication to education, and philanthropic contributions.
In recognition of his outstanding achievements, Dr. McAllister is being honored with the Distinguished Achievement Award from the Society for Cardiovascular Pathology.
2000 - Giorgio Baroldi
Giorgio Baroldi
Giorgio Baroldi, born in Piacenza, Italy, in 1925, earned his medical degree from the University of Milan in 1949. He developed a keen interest in coronary arteries and pioneered the method of casting the coronary artery tree in both normal and pathological hearts. His early research, conducted with Giuseppe Scomazzoni, was published in Circulation Research and awarded the prestigious Ganassini Prize in 1955.
In 1960, Baroldi moved to the United States to join the Armed Forces Institute of Pathology (AFIP) in Washington, DC. There, he worked with Dr. William Manion and published his seminal monograph Coronary Circulation in the Normal and the Pathologic Heart, which became a crucial reference in the field. Baroldi’s research challenged the conventional view that coronary thrombosis caused myocardial infarction, proposing instead that it was a result of hemodynamic changes, a theory that influenced the delay in the use of thrombolysis for treating myocardial infarction.
In collaboration with Malcolm Silver at the University of Toronto, Baroldi conducted a landmark study on myocardial infarction, finding that coronary thrombosis was present in only 34% of cases, which stirred debate in the cardiovascular pathology community.
Giorgio Baroldi returned to Italy in the 1970s, where he contributed to the development of cardiovascular pathology and helped establish a pathology laboratory in Pisa and Milan. He played a pivotal role in the National Program of Cardiac Transplantation, coordinating the pathology program and monitoring organ rejection.
In 1989, Baroldi helped found the Italian Group of Cardiovascular Pathology, becoming its first president. His career, marked by over 350 publications on ischemic heart disease, myocarditis, and cardiac transplantation, has left a lasting impact on the field.
The Society for Cardiovascular Pathology (SCVP) recognizes his lifetime achievements and honors him with the Distinguished Achievement Award.
1999 - Richard and Stella van Praagh
Richard and Stella van Praagh
Richard van Praagh was born in April 1930 in London, Ontario, Canada, to a family originally from Moravia and the Netherlands. Along with his brother Ian, who would later become a gynecologist, Richard financed his medical studies at the University of Toronto through various jobs, including working as a gravedigger. He completed his medical degree in 1954. His postgraduate training in pediatrics, cardiology, and pathology spanned ten years, taking him from Toronto to Boston, the Mayo Clinic, and finally to Baltimore. It was there, after one of his lectures, that he met a young assistant who captivated him with her “great brown eyes” and intelligent questions. This encounter marked the beginning of a 44-year romance, culminating in their marriage in 1962.
Stella Zacharioudaki, born in 1927 in Crete, Greece, came from a family of winemakers. She graduated at the top of her class from medical school in Athens in 1952. Later that year, she emigrated alone to the United States. In the U.S., she pursued her interest in congenital heart defects, training in New Jersey, Buffalo, and Baltimore, where she worked as a fellow with Helen Taussig. At the time of her marriage to Richard in 1962, Stella was working as a cardiology staff member in Buffalo, NY, while Richard was focused on pathology in Toronto and later in Chicago.
During the rapid development of pediatric cardiology in the early 1960s, one significant issue was the absence of a standardized nomenclature and classification system for congenital heart defects, which hindered communication and scientific progress. Richard had already begun developing a system for his own use, and Stella applied it to her own work, demonstrating that tetralogy of Fallot (TOF) was not a random occurrence of four separate defects, but rather a single, developmentally related malformation of the heart.
In 1965, they were both recruited to Children’s Hospital at Harvard University in Boston to help establish the new pediatric cardiology program, where they were appointed to lead the “cardiac registry.” Their collaboration was exceptionally successful, and their work continues to have a lasting impact on the field today.
Richard van Praagh introduced his “segmental situs” system in 1964 to describe the morphology of complex congenital heart defects, such as dextrocardia, and published his foundational work, The Segmental Approach to Diagnosis of Congenital Heart Disease, in 1972. This system divides the heart into three segments—the atria, ventricles, and great vessels—and later extended it to apply to all congenital heart defects.
For their extraordinary contributions to the field of pediatric cardiology and pathology, Richard and Stella van Praagh are being honored with the Distinguished Achievement Award from the Society for Cardiovascular Pathology.
1998 - Russell Ross
Russell Ross
1997 - Michael J. Davies
Michael J. Davies
Professor Michael J. Davies is a leading figure in cardiovascular medicine, best known for his groundbreaking work on plaque rupture and its role in acute myocardial infarction. His career began at the Middlesex Hospital Medical School, followed by significant contributions to cardiovascular pathology during his time at St George’s Hospital. In 1981, he became the first British Heart Foundation Chair of Cardiovascular Pathology, where his research revolutionized the understanding of atherosclerosis, cardiac valve disease, and cardiomyopathies. He authored over 200 articles and chapters, as well as key reference books and atlases, with his photography of atherosclerotic plaques being particularly renowned. His work was marked by collaborations across disciplines, advancing not only pathology but also mechanics, genetics, and cell biology.
Professor Davies’ achievements earned him numerous honors, including fellowships with prestigious medical societies, and he played a key role in shaping cardiovascular pathology education. He was known for his meticulous attention to detail, enthusiasm, and dedication to mentoring future researchers. His personal warmth and generosity made a lasting impact on his colleagues and students. Professor Davies’ contributions to cardiovascular science and education continue to resonate worldwide, ensuring that his legacy endures.
In recognition of his immense contributions to the field of cardiovascular pathology, Professor Davies is receiving the Distinguished Achievement Award from the Society for Cardiovascular Pathology (SCVP). This award honors his pioneering research, leadership, and enduring influence on the discipline, which continues to inspire generations of scientists and clinicians alike.
1997 - Ramzi S. Cotran
Ramzi S. Cotran
Dr. Ramzi S. Cotran is a distinguished figure in the field of pathology, known for his groundbreaking contributions and transformative leadership. He currently serves as the F. B. Mallory Professor of Pathology at Harvard Medical School and Chair of Pathology at Brigham and Women’s Hospital, where he has been instrumental in shaping the department into one of the leading academic pathology centers in the world. In addition, Dr. Cotran serves as the interim Chair of the Pathology Department at Children’s Hospital Medical Center in Boston, a position he took on in 1990 and continues to excel in today.
Dr. Cotran’s journey began in Haifa, Palestine, where he was born, and he graduated from the American University of Beirut in 1956. He went on to receive his medical degree there before pursuing postgraduate training in Pathology at Boston City Hospital’s Mallory Institute and Memorial Sloan-Kettering Cancer Center in New York City. Returning to the Mallory Institute in 1960 as a Harvard faculty member, he soon became a driving force in the academic and scientific community.
Over the past three decades, Dr. Cotran has built an exceptionally successful and influential academic department at Brigham, earning recognition as both a dedicated educator and a pioneering scientist. He has served as the primary author of Robbins’ Pathological Basis of Disease since 1979, and his research has been instrumental in the advancement of modern vascular biology. His leadership extends beyond Brigham, with Dr. Cotran serving as a Trustee of the American Board of Pathology, Past President of the American Society of Investigative Pathology, and a key figure in numerous other governing bodies within the field.
In recognition of his immense impact, Dr. Cotran was elected to the Institute of Medicine of the National Academy of Sciences, and he recently received the Lifetime Achievement Award in Mentoring from Harvard Medical School. His contributions have had a lasting influence, both locally and nationally, shaping the careers of numerous senior members of the pathology community.
It is for these remarkable contributions to the field of pathology—his groundbreaking research, visionary leadership, and unwavering commitment to mentorship—that Dr. Cotran is receiving the Distinguished Achievement Award from the Society for Cardiovascular Pathology. This prestigious recognition honors his profound impact on the field and the countless individuals who have been inspired by his work and leadership.
1996 - Robert B. Jennings
Robert B. Jennings
Robert Burgess Jennings, MD, is a distinguished figure in cardiovascular research whose groundbreaking work and leadership have had a profound impact on Duke University and the broader field of pathology. He has dedicated nearly five decades to Duke Pathology, where he began his pioneering work in the 1950s. His research focused on understanding the molecular events underlying ischemic myocardium, leading to significant discoveries, including the identification of sarcolemma disruption as a critical factor in heart muscle cell death during ischemia.
In 1986, Dr. Jennings made a pivotal contribution to cardiovascular science with his discovery of ischemic preconditioning, a phenomenon in which brief episodes of ischemia help protect the heart from subsequent, prolonged ischemic events. This discovery has since become a cornerstone in the field of cardiovascular health.
Dr. Jennings also played a crucial role in shaping Duke’s Pathology department, serving as chair from 1975 to 1989. Under his leadership, the department became a hub for innovative cardiovascular research, attracting top talent and fostering a collaborative research environment. His visionary contributions to both research and education continue to inspire the field.
Throughout his career, Dr. Jennings has received numerous prestigious awards, including the Gold-Headed Cane of the American Society for Investigative Pathology in 1996. However, he remains humble, always emphasizing the importance of collective work and collaboration over personal recognition. His legacy is carried on through the many students, colleagues, and researchers who continue to be inspired by his work and leadership.
Dr. Jennings is being honored with the Distinguished Achievement Award from the Society for Cardiovascular Pathology in recognition of his exceptional contributions to the field of cardiovascular research and pathology. His leadership in developing a collaborative research environment at Duke, along with his mentorship of countless students and colleagues, has left an enduring legacy.
1995 - Malcolm D. Silver
Malcom D. Silver
Dr. Malcolm D. Silver currently holds the title of Professor Emeritus at the University of Toronto, where he served as professor and chairman of the Department of Pathology for several years. In addition to this role, he excels as chief of pathology at Toronto General Hospital (affiliated with the University Health Network) and as chairman of the Department of Pathology at Western University. Specializing in pathology, Dr. Silver has co-authored more than 200 scientific publications.
Dr. Silver earned an MBBS from the University of Adelaide in 1957, followed by an MS in 1963 and a PhD in 1965, both from McGill University. In 1970, he was also honored with an MD from the University of Adelaide for his published work. He holds a diploma from the American Board of Pathology and has been elected a fellow of the Royal College of Pathologists of Australasia, the Royal College of Physicians and Surgeons, and the Canadian Cardiovascular Society. Notably, Dr. Silver and his late wife endowed the Meredith and Malcolm Silver Scholarship in Cardiovascular Studies at the University of Toronto.
1994 - William C. Roberts
William C. Roberts
Dr. William Clifford Roberts, born in 1932 in Atlanta, Georgia, earned his MD from Emory University in 1958. After completing his medical degree, he undertook a residency in internal medicine at Boston City Hospital before beginning a 3-year residency in anatomic pathology at the NIH.
From 1964 to 1993, Dr. Roberts served as Chief of the Pathology Section at the National Heart, Lung, and Blood Institute (NHLBI) of the NIH. During this time, he mentored 51 fellows, many of whom went on to become leaders in cardiovascular pathology. His research was instrumental in advancing the understanding of cardiovascular disease, particularly through his work on heart disease lesions. By mid-September 1993, he had published 993 papers.
Dr. Roberts is currently the Executive Director of the Baylor Cardiovascular Institute at Baylor University Medical Center in Dallas, Texas, where he continues his influential work in cardiac pathology. He also serves as Editor-in-Chief of the American Journal of Cardiology and is a member of the editorial boards of several prestigious journals. His leadership in both research and editorial roles has left a lasting impact on the field of cardiology.
In recognition of his distinguished career, Dr. Roberts received the 1994 Distinguished Achievement Award from the Society for Cardiovascular Pathology. This honor reflects his significant contributions to cardiovascular medicine through his extensive research, publications, and mentorship, solidifying his legacy as a pioneer in the field.
1993 - Jack L. Titus
Jack L. Titus
Dr. Jack L. Titus, MD, PhD, is an internationally renowned cardiovascular pathologist known for his leadership, mentorship, and significant contributions to the field of cardiovascular pathology. He was born in South Bend, Indiana, and began his education at Notre Dame University at just 16. After serving as a sergeant in World War II, he returned to Notre Dame, earning his degree in 1948, before attending medical school at Washington University in St. Louis, where he graduated in 1952. Dr. Titus initially worked as a “country doc” in Rensselaer, Indiana, before pursuing postgraduate training in pathology at the Mayo Graduate School of Medicine, where he earned his PhD in Pathology under Jesse E. Edwards, MD.
In 1961, Dr. Titus joined the Mayo Graduate School faculty, eventually rising to Full Professor in 1972. That year, he was recruited to Baylor College of Medicine as Chair of Pathology, where he served until 1987. During his time at Baylor, Dr. Titus made lasting impacts on the department, focusing on advancing cardiovascular pathology, fostering patient-oriented pathology, and growing the faculty. He also played a critical role in the formation of the Gulf Coast Regional Blood Center, and mentored numerous young pathologists who went on to become experts and leaders in the field.
After retiring from Baylor, Dr. Titus returned to Minnesota, where he served as medical director for the Jesse E. Edwards Registry of Cardiovascular Disease at United Hospital in St. Paul, and continued his academic work at the University of Minnesota and Baylor College of Medicine. Throughout his career, he published 229 peer-reviewed articles and remained academically active into his 80s.
Dr. Titus’s contributions are recognized with the Distinguished Achievement Award from the Society for Cardiovascular Pathology. He is remembered by colleagues and mentees as a brilliant, compassionate leader and mentor. His legacy continues to inspire those who have had the privilege of working with him.
1992 - Victor J. Ferrans
Victor J. Ferrans
1991 - Margaret E. Billingham
Margaret E. Billingham
Margaret E. Billingham is a pioneering pathologist at Stanford University Medical Center, known for her groundbreaking work in cardiac transplantation. Born in Tanzania in 1930 and educated at the Royal Free Hospital in London, she moved to the United States in 1963 with her husband, Dr. John Billingham, and their two children. Since joining Stanford in 1966, she has focused her research on detecting and managing heart transplant rejection, becoming a key figure in the field of cardiac pathology.
Billingham works closely with the cardiac transplant team at Stanford, developing techniques to use endomyocardial biopsies to monitor transplant rejection. Her “Billingham’s Criteria” for grading rejection has become the international standard, significantly improving patient care and outcomes in heart transplantation. She also conducts research on chronic rejection, further enhancing long-term survival rates for transplant recipients.
In 1990, Billingham became the first female president of the International Society for Heart and Lung Transplantation (ISHLT), a testament to her leadership and influence in the field. She has published 220 scientific papers and is widely recognized as an expert in cardiac pathology, frequently invited to lecture at medical institutions across the country.
1990 - Guido Majno
Guido Majno
Dr. Guido Majno, born in Milan, Italy, in 1922, is a world-renowned pathologist known for his groundbreaking work in inflammation and wound healing. After earning his medical degree from the University of Milan in 1947, Dr. Majno initially pursued a career in surgery. However, a temporary placement in the pathology department at the University of Geneva changed the course of his career. After completing his pathology training, he moved to the United States in 1952, joining the faculty at Tufts University and later Harvard Medical School, where he became an associate professor of pathology.
During his time at Harvard, Dr. Majno made significant contributions to the field of pathology, particularly in understanding the vascular and cellular mechanisms of inflammation. His work at the Rockefeller Institute, alongside Nobel Laureate Dr. George Palade, laid the foundation for much of our modern understanding of inflammatory processes and wound healing. In the late 1960s, he returned to Geneva, where he led the Department of Pathology and made key discoveries, including the identification of myofibroblasts.
In 1973, Dr. Majno became the Chair of the Department of Pathology at the University of Massachusetts Medical School, a position he continues to hold. His work during this time has been pivotal in shaping the modern understanding of pathology. He is widely respected for his research on cell death, including apoptosis, and for his numerous influential papers on the biology of inflammation. Dr. Majno is also the author of the classic medical history book The Healing Hand, which explores ancient wound treatment and reflects his passion for connecting historical perspectives with modern medicine.
In recognition of his lifelong contributions to pathology, Dr. Majno is awarded with the Distinguished Achievement Award from the Society for Pathology Cardiovascular Pathology, a testament to his enduring impact on the field. His profound influence on pathology, both as a researcher and educator, makes him a deserving recipient of this distinguished award.
1989 - Earl P. Benditt
Earl P. Benditt
Dr. Earl Philip Benditt is a prominent experimental pathologist and Professor Emeritus in the Department of Pathology at the University of Washington School of Medicine. Benditt’s career is deeply rooted in histochemistry, and his early work in the 1950s, including studies on phosphatase localization and histochemical reagents for connective tissue, laid the foundation for much of his later research. His collaboration with George Gomori and others led to significant discoveries, including identifying serotonin as a mast cell-derived mediator and contributing to the understanding of amyloid proteins. His work also includes explaining the optical properties of amyloid proteins stained with Congo Red.
He began his experimental pathology career at the University of Chicago, focusing on amino acid deficiencies, and his interest in serotonin later led to groundbreaking work on amyloid and atherosclerosis. In the 1970s, he hypothesized that atherosclerotic plaques might be similar to benign tumors, which was a novel concept that influenced later research. Benditt’s work on endothelial cell proliferation and the role of platelet-derived growth factor (PDGF) in atherosclerosis was foundational.
Benditt served as Chair of the Department of Pathology at the University of Washington from 1957 to 1981, fostering a thriving academic environment that led to the creation of multiple pathology chairs and supported the success of many faculty members. His scientific contributions earned him membership in the National Academy of Sciences and several prestigious awards, including the Rous–Whipple and Gold Headed Cane Awards from the American Association of Pathologists.
1988 - Donald B. Hackel
Donald B. Hackel
Dr. Donald Benjamin Hackel, born on July 7, 1921, in Boston, Massachusetts, has made significant contributions to the field of pathology throughout his illustrious career. He earned both his A.B. in Biology (Magna Cum Laude) in 1943 and his M.D. in 1946 from Harvard. Following his internship at Beth Israel Hospital, he entered the Army Medical Corps, where his research in pathophysiology began to flourish. After his military service, he pursued pathology training at Cleveland City Hospital, Western Reserve School of Medicine, under the mentorship of Dr. Thomas D. Kinney. It was during this time that Dr. Hackel cultivated his interest in cardiovascular research, leading to his distinguished career.
Dr. Hackel’s early work at Western Reserve focused on the heart’s reaction to injury, particularly thiamine deficiency and hemorrhagic shock. His innovative research, combining physiological, biochemical, and morphological techniques, earned him the Parke-Davis Research Award in experimental pathology in 1961. His dedication to research and education paved the way for his lifelong interest in medical curriculum reform and teaching.
In 1961, Dr. Hackel joined the Duke University faculty as a professor of pathology, following Dr. Kinney. At Duke, he continued to pursue groundbreaking research in cardiovascular pathology, particularly focusing on cardiac failure in hemorrhagic shock. His work identified the key role of catecholamines in cardiac malfunction, and he mentored numerous students and fellows who went on to distinguished careers. Dr. Hackel also served as editor-in-chief of the American Journal of Pathology from 1977 to 1982, where he upheld the journal’s high standards and fostered innovative editorial practices.
Known for his dedication to medical education, Dr. Hackel was a beloved teacher at Duke, where he taught the introductory pathology course for two decades. His students honored him with the prestigious “Golden Apple Award” for excellence in teaching on three separate occasions, culminating in a Lifetime Golden Apple Award in 1988. His influence extended beyond the classroom as his work in cardiovascular pathology helped shape modern understanding of ischemic heart disease.
In recognition of his outstanding achievements in the field of cardiovascular pathology, it is an honor to present Dr. Donald Benjamin Hackel with the Distinguished Achievement Award from the Society for Cardiovascular Pathology in 1988. His unwavering commitment to research, teaching, and service continues to inspire the next generation of pathologists.
1987 - Robert W. Wissler
Robert W. Wissler
Dr. Robert W. Wissler, born in Richmond, Indiana, is a leading figure in pathology and cardiovascular research. After earning his Ph.D. in 1946 and M.D. in 1948 from the University of Chicago, he quickly rose to prominence in the field. From 1957 to 1972, he chaired the Department of Pathology at the University of Chicago, where he played a transformative role in advancing both research and education within the department.
Dr. Wissler’s research is renowned for its focus on atherosclerosis. He was one of the first to demonstrate the development of atheromatous lesions in animal models, particularly in rats, laying the foundation for future studies on diet and gene manipulation in atherogenesis. His work in nonhuman primates provided critical insights into the regression of atherosclerosis, influencing cardiovascular research worldwide.
One of his most significant contributions is the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study, which examined the early onset of atherosclerosis in young people. Using autopsy samples from over 3,000 individuals, the PDAY study showed the effects of elevated cholesterol and smoking in teenagers and young adults, shaping modern preventive strategies for coronary heart disease.
In addition to his research, Dr. Wissler made significant educational contributions, revitalizing the pathology graduate program at the University of Chicago and mentoring many pathologists who went on to have distinguished careers. His leadership extended to several major pathology organizations, including serving as President of the American Society for Experimental Pathology and the American Association of Pathologists and Bacteriologists.
Dr. Wissler’s dedication to pathology and his mentorship have left a lasting impact on the field. It is with great honor that the Society for Cardiovascular Pathology presents him with the Distinguished Achievement Award, recognizing his remarkable contributions to cardiovascular research and pathology.
1987 - Maurice Lev
Maurice Lev
1987 - Reginald E. B. Hudson
Reginald E. B. Hudson
Reginald E. B. Hudson is widely regarded as the father of cardiovascular pathology in Britain. Appointed to the National Heart Hospital in 1948, he took on all aspects of pathology and, under his guidance, the department rapidly expanded. Within a short time, it grew to include three medical and 15 technical staff, covering all disciplines in pathology. He developed a unique stereographic-photographic technique and designed state-of-the-art laboratories at the National Heart Hospital, which remained cutting-edge for many years.
Hudson has gained an international reputation and built strong ties with Emory University and Grady Hospital in Atlanta, Georgia. A member of many prestigious societies, he became an honorary fellow of the Council of Clinical Pathology of the American Heart Foundation in 1972. Known for his excellent teaching, both at the undergraduate and postgraduate levels, his dry humor made his lectures enjoyable.
His contributions to medical literature are vast, with numerous classic papers on congenital and acquired heart disease, particularly studies on the conductive system and human aortic valve homografts. His three-volume monograph Cardiovascular Pathology, totaling 3300 pages, is the most comprehensive work on the subject ever published.
To honor his exceptional career, Dr. Hudson is being awarded the Distinguished Award by the Society for Cardiovascular Pathology. Despite his many achievements, he remains a modest and caring educator and colleague, respected for his commitment to both his work and his family. His influence continues to impact the field of cardiovascular pathology, leaving a legacy that will guide future generations of pathologists.
1987 - Jesse E. Edwards
Jesse E. Edwards
YOUNG INVESTIGATOR AWARD WINNER
SCVP celebrates the future leaders of our discipline.
Scoring criteria for our young investigator talks can be found here.
2024 - Michael Kritselis
2024 AWARD WINNING ABSTRACT
Michael Kritselis
The Application of Proposed Criteria for the Diagnosis and Classification of Lymphocytic Myocarditis to Autopsy Specimens
Michael Kritselis, Joseph J. Maleszewski, Melanie C. Bois, Andrew Layman.
Background: Historically, no diagnostic criteria were available for lymphocytic myocarditis in autopsy specimens. In the absence of such, the Dallas criteria has been adapted to postmortem specimens in a non-validated manner. Recently, the Society for Cardiovascular Pathology and Association for European Cardiovascular Pathology (SCVP and AECVP, respectively) are working to rectify this, bringing autopsy into alignment with endomyocardial biopsies. The aim of this study is to evaluate the provisional criteria comparing it with the adapted Dallas criteria.
Design: Institutional autopsy records were queried for cases containing a diagnosis of “lymphocytic myocarditis” (1999-2022). Existing H&E-stained slides were reviewed (by consensus of 3 cardiovascular pathologists) and assigned one of the following classifications based on the proposed criteria (Figure 1): Lymphocytic Infiltrate of Undetermined Significance (LIUS), Focal, Multifocal, Diffuse. Cause and manner of death and demographic information were abstracted.
Results: 25 cases (12 women) were available to review. The average decedent age was 58 yrs (range: 14– 86 yrs). The manner of death was natural in 22 cases; 3 were accidents. Of 8 cases that had originally been called “borderline,” five were re-classified as focal or multifocal myocarditis (Table 1). Of 17 cases originally called ‘active,” three were re-classified as LIUS. Both cases with diffuse patterns of myocarditis had been adjudicated to have infectious/inflammatory causes of death (Table 2). 7 cases had multifocal patterns, 4 (57%) of which had been adjudicated to have infectious/inflammatory causes of death, compared to 3 (30%) focal cases and 2 (33%) LIUS cases.
Conclusion: Herein, we present a direct head-to-head comparison of adapted Dallas criteria and the recently proposed draft criteria set forth by the SCVP/AECVP for the diagnosis of myocarditis in non-biopsy specimens. This early data shows correlation between the multifocal and the diffuse patterns with previously adjudicated cause of death in our institution. More than half of the cases previously regarded as active myocarditis were “downgraded” to focal or LIUS. This better definition may help practicing pathologist better put into context myocardial inflammation that they encounter in non-biopsy samples.
2023 - Liang Lu
2023 AWARD WINNING ABSTRACT
Liang Lu, MD, PhD
Correlation of ISHLT Grading for Cellular and Antibody Mediated Rejection with Heart Allograft Survival: a Retrospective Observational Study
Liang Lu, Kelly Smith. University of Washington, Seattle, WA
Background: The International Society for Heart and Lung Transplantation (ISHLT) has developed standardized grading systems for the evaluation of allograft biopsies for cellular and antibody-mediated rejection. Controversy still exists concerning how these scores should be used to guide patient care. To better understand the significance of biopsy findings for patient allograft outcomes we analyzed the association between ISHLT grading and allograft survival.
Design: Clinical information was collected on 204 patients who received first heart transplants and no other solid organ or stem cell/bone marrow transplants between 1/1/2013 and 3/29/2021. Cellular rejection (pCMR) was graded using both ISHLT 1990 and 2004 criteria. Patients who had immunostaining for C4d +/- C3d were assigned pathologic antibody-mediated rejection (pAMR) scores. CD68 staining was not used to assess immunopathologic pAMR, since this is considered to be a redundant measure of histologic AMR. Statistical analyses were performed to evaluate the influence of histopathologic scores on allograft survival. Seven patients (3.5%) lost their graft between 13 and 86 days post-transplant due to primary graft dysfunction. For the remaining 197 patients (3243 biopsies, mean 16 and range 4 – 29 biopsies per patient) we evaluated associations between histopathologic parameters and graft outcomes (mean follow-up 5 years, range 256 – 3351 days). 165 patients (81%) had staining for C4d +/- C3d (753 biopsies) and were assigned pAMR scores. Factors that significantly associated with allograft survival include: pCMR greater than 1R by ISHLT 2004 (p=0.005), pCMR greater than 1B by ISHLT 1990 criteria (p=0.0013), histologic AMR (pAMR1(H+), p=0.0098), immunopathologic AMR (pAMR1(I+), p=0.0032) and combined histologic and immunopathologic pAMR (pAMR2, p <0.0001, median survival 4.6 years) (Figure 1.A-D).
Conclusion: Our results support ongoing use of the 1990 scoring system for cellular rejection to identify ISHLT 1990 grade 2 rejection in patients, who may benefit from closer follow-up or increased immunosuppression. Our results also demonstrate that pAMR1(H+), pAMR1(I+) and pAMR2 are associated with poor graft survival, supporting intervention for all grades of pAMR.
2022 - Monica De Gaspari
2022 AWARD WINNING ABSTRACT
Monica De Gaspari, MD
Diagnosing Myocarditis in Endomyocardial Biopsies: Survey of Current Practice
Monica De Gaspari, Brandon Larsen, Giulia d’Amati, Kasey Kreutz, Cristina Basso, Chieh-Yu Lin
Background: Dallas criteria (DC) and European Society of Cardiology (ESC) criteria have provided valuable frameworks for the histologic diagnosis and classification of myocarditis in endomyocardial biopsy (EMB) specimens. However, the adaptation and usage of these criteria is variable and depends on local practice settings. Moreover, several ancillary tests that are not included in the current criteria such as immunohistochemistry (IHC) or viral PCR, have proven useful for the diagnosis of myocarditis.
Design: As a joint effort from the Association for European Cardiovascular Pathology (AECVP) and the Society for Cardiovascular Pathology (SCVP), we conducted an online survey to understand the
current practice of diagnosing myocarditis.
Results: A total of 100 pathologists from 23 countries responded to the survey with the majority practicing in North America (46%) and Europe (43%). Most of the pathologists (85%) examined less than 200 native heart biopsies per year, and rendered diagnosis of myocarditis less than 30 cases per year (92%). Most of the pathology labs (89%) routinely receive 3-5 fragments of tissue per case. The
number of hematoxylin-eosin stained levels for each case varies from 1 to more than 9 levels, with 20% of pathologists routinely asking for more than 9 levels per case. Among the 100 pathologists, 80 use DC and 41 the ESC criteria. Breaking down by regions, DC is more commonly used than bESC criteria in North America (80% versus 19.6%) while both criteria are commonly used in Europe (79.1% and 62.8%). IHC is utilized in either every case or selected cases for 79% of participants, and viral PCR is performed by 32% of participants. Variable terminologies are used in EMB
myocarditis reporting, some as histological diagnoses and others as clinical diagnoses (e.g. fulminant myocarditis), and 34 pathologists do no use the term “borderline myocarditis”. The majority of the participants think it is time to update the current criteria (83%).
Conclusion: The survey data demonstrated that pathologists who diagnose myocarditis practice with variable tissue preparation, ancillary studies, guideline usage and reporting. These results highlight the clinically unmet need and desire to update and standardize the current diagnostic criteria for myocarditis on EMB. Additional studies are warranted to establish standard of practice.
The abstract later became a publication in the Journal of Cardiovascular Pathology.
2021 - Phillip Hurst
2021 AWARD WINNING ABSTRACT
Phillip Hurst, MD
Amyloid deposition in surgically resected aortic valves
PD Hurst MD, JJ Maleszewski MD, ED McPhail MD, MC Aubry MD, PT Lin MD, YC Lo MD PhD, S Mansour MBBS, M Grogan MD, O AbouEzzeddine, MC Bois MD
Background: Amyloid deposition is variably reported in aortic valves (AVs), with a frequency between 15% and 82% in published series. However, its true incidence, proteomic characteristics, and clinical significance remain unclear. A detailed assessment of surgically resected aortic valves was undertaken with the following aims: 1) employ robust methodology to further characterize AV amyloid incidence, 2) determine the proteomic signature of such deposits, and 3) investigate clinical importance of this finding.
Methods: 100 consecutive surgically resected AVs (11/2018-2/2019) were identified through institutional records. Clinical material was semiquantitatively scored for the degree of calcium and inflammation present. Congo red (CR) histochemistry was performed to determine the presence and morphology of CR+ deposits. A subset of cases with adequate CR+ deposits underwent liquid chromatography-tandem mass spectrometry (LC-MS/MS) and electron microscopy. Relevant clinical information was abstracted from the medical record. Echocardiograms, including pre-operative and most recent (if different) were reviewed for features indicative of cardiac amyloidosis.
Results: Patient characteristics are presented in Table 1. Half (52%) of the resected AVs contained CR+ deposits. Patients with CR+ deposits were older (p=0.003), and more commonly men (p=0.047). Though nonspecific sequelae of systemic amyloidosis were more common in this population (erectile dysfunction, p=0.029; carpal tunnel syndrome, p<0.0001), no significant difference was apparent on echocardiography and no patients were diagnosed with cardiac amyloid during the follow-up period. CR+ deposits were directly associated with calcium deposition (p<0.0001) and usually adjacent to it (65%), with 5 (10%) valves containing exclusively nodular deposits away from calcium, and 13 (25%) showing both morphologies. Proteomic analysis was performed on microdissected CR+ deposits from 9 cases, all revealing a universal amyloid protein signature. Pericalcific deposits show a non-specific proteome, while nodular deposits have a profile more typical of ATTR (transthyretin) amyloidosis. Ultrastructural and additional LC-MS/MS analysis is ongoing.
Conclusions: CR+ deposits are relatively common in AVs, specifically those in which there is concomitant fibrocalcific degeneration, and are associated with degree of calcification, older age, and male sex, in keeping with prior literature. However, morphologic differences are present, requiring correlation with proteomic and ultrastructural studies, as well as clinical outcome, to further characterize the nature of these deposits.
2020 - Joseph Westaby
2020 AWARD WINNING ABSTRACT
Joseph Westaby, MBBS, PhD
Sudden Cardiac Death in Hypertensive Heart Disease
Joseph Westaby and Mary N. Sheppard, St George’s, University of London
Background: Hypertensive heart disease refers to changes in myocardial structure and function that result from sustained hypertension. The relationship between hypertensive heart disease and sudden cardiac death is well established but there are few pathological studies. We examined the clinical and pathological features of hypertensive heart disease in sudden cardiac death victims.
Design: We investigated 5239 consecutive cases of sudden cardiac death referred to our national cardiovascular pathology center between 1994 and 2018. Hearts were examined by an expert cardiac pathologist. Diagnostic criteria included increased heart weight and left ventricular wall thickness in the absence of other causes. Exclusion criteria were significant coronary artery disease and no premorbid diagnosis of hypertension.
Results: Of 75 sudden cardiac death cases due to hypertensive heart disease (age at death: 54±16years; 56% male), 56 (75%) reported no prior cardiac symptoms. Thirty-four (45%) recorded a BMI≥30.
Four (5%) were labelled with hypertrophic cardiomyopathy in life, but lacked the diagnostic feature of myocyte disarray at autopsy. The mean heart weight was 563±153grams (males 636±140, females 470±114), with a maximal left ventricular wall thickness of 17.5±3.5mm. All hearts showed concentric hypertrophy. Fibrosis was present in 59 cases (81%) and was not associated with sex (p=0.31), BMI (p=0.17), or heart weight (p=0.48).
Conclusion: Most sudden deaths due to hypertensive heart disease occurred without prior cardiac symptoms so risk stratification is challenging. All cases exhibited concentric hypertrophy and myocardial fibrosis was frequently reported. Hypertensive heart disease should be excluded in those with left ventricular hypertrophy and hypertension prior to consideration of hypertrophic cardiomyopathy.
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2019 - Paul Hanson
2019 AWARD WINNING ABSTRACT
Paul Hanson, MD, PhD
Differential Expression of NUP98‐ERBB4‐PSEN1‐NRG1 (NEPN) Signaling Axis as Potential Blood‐Based Biomarker for Viral Myocarditis
Paul Hanson, Veena Lin, Bruce McManus, University of British Columbia and St. Paul’s Hospital, Vancouver, BC
Background: Myocarditis, inflammation of the myocardium, is a leading cause of unexpected heart failure in young adults, commonly attributable to viral infections. Myocarditis manifests in a wide range of clinical presentations, from asymptomatic to acute heart failure. The current gold standard for diagnosis relies upon invasive endomyocardial biopsy, requiring histopathological demonstration of inflammation with/without associated myocyte damage. Under these guidelines, diagnostic sensitivity in independent published studies is
Design: HeLa cells and human induced pluripotent stem cell (iPSC)‐derived cardiomyocytes (CM) were CVB3‐ or sham‐infected. Western blot analysis and confocal microscopy were performed to determine the expression and subcellular localization of NEPN signaling axis proteins in tissue culture. In addition, tissue and blood from murine models of viral myocarditis (A/J and C57BL/6 mice) were collected at 4 dpi (viremic phase) and5 to 8 dpi (acute phase), and were analyzed by Western blot analysis, IHC and IF to detect protein expression.
Results: NEPN proteins all show changes in expression and subcellular localization throughout the infection time course. NUP98 is upregulated and cleaved during infection. NRG1 is upregulated in both lysates and supernatants. ERBB4 co‐localizes at the cell membrane with the protease PSEN1. ERBB4 and NRG1 cleavage fragments are secreted and detected in both tissue culture supernatant and mouse plasma. In the plasma of the less susceptible C57BL/6 mice, ERBB4 and NRG1 cleavage fragments increase throughout the viremic and acute phases. However, in the highly susceptible A/J mice, ERBB4 and NRG1 cleavage fragments were not detected in the plasma until 6 dpi (acute phase), when they are highly upregulated as compared to C57BL/6 mice (p=0.001).
Conclusion: Differential expression, subcellular localization and cleavage fragments of NEPN signaling axis proteins were detected during the pathogenesis of viral myocarditis. These composite changes may be useful in the development of a blood‐based diagnostics.
The abstract later became a publication in The FASEB Journal.
2018 - Carolyn Glass
2018 AWARD WINNING ABSTRACT
Carolyn Glass, MD, PhD
CD68/CD31 Immunohistochemistry Double Stain Demonstrates Increased Accuracy in Diagnosing Antibody‐Mediated Rejection in Cardiac Transplant Patients
Carolyn Glass, Yasmeen Butt, Tunc Gokaslan, Jose Torrealba, UT Southwestern Medical Center
Background: Antibody mediated rejection (AMR) occurs in 10%‐20% of cardiac transplant patients and is associated with increased mortality. The endomyocardial biopsy, used to identify microvascular injury with intravascular macrophages, activated endothelial cells, immunohistochemical (IHC) evidence of complement deposition, and/or > 10% intravascular macrophages within capillaries, remains the primary diagnostic tool for AMR. However, as recently addressed at the XIIIth Banff Allograft Pathology Conference, identifying the intravascular location of macrophages by routine histology can present diagnostic challenges. This prompted us to perform a screen of cardiac transplant cases to determine if double labeling with an endothelial and histiocytic marker could improve diagnostic accuracy.
Design: Twenty‐two cardiac transplant endomyocardial biopsies previously diagnosed at a high‐volume transplant center as pAMR‐2 based on histologic evidence of endothelial activation, endothelial
deposition with C3d or C4d or >10% intravascular macrophages, were screened using a CD68/CD31 IHC double stain. To determine whether the diagnosis of pAMR‐2 would be altered using the double
stain, CD68 positive intravascular macrophage percentages were calculated and retrospectively compared in the same cases diagnosed using CD68 IHC alone.
Results: The CD68/CD31 double stain showed 13 of 22 (59%) cases which had been previously been diagnosed as >10% intravascular macrophages using a CD68 IHC stain alone, had 30%, >20% and >10% in 26%, 12% and 23% of cases, respectively. The mean C4d positivity by immunofluorescence was 75% (N=12), 37% for C3d by IHC (N=8), and 30% for >10% CD68 by IHC (N=22). The patients (mean age 51 years, 27% female) had 45 months post‐transplant follow up, and one third of patients had pre‐ transplant left ventricular assist devices.
Conclusions: Based on our institution’s experience at a high cardiac transplant volume center, over a third of patients were over‐diagnosed as pAMR‐2 using CD68 by IHC alone. We demonstrate here the value of using a CD68/CD31 double stain to accurately determine the percent of intravascular macrophages to diagnose the “I” component of pAMR‐2.
The abstract later became a publication in the American Journal of Transplantation.
2017 - Melanie Bois
2017 AWARD WINNING ABSTRACT
Melanie Bois, MD
The Pathology of Subaortic Membranes: An Analysis of 83 Surgically Resected Cases with Molecular Genetic Correlation
Melanie Bois, Linnea M Baudhuin, Michelle L Kluge, Katrina E Kotzer, Laura J Train, Michael J Ackerman, Joseph J Maleszewski. Mayo Clinic, Rochester, MN
Background: Subaortic membranes (SAM) are subvalvular collections of fibro(muscular) tissue that result in fixed obstruction. The pathogenesis of subaortic membranes (SAM) remains obscure and while both congenital and acquired forms have been identified, the latter is thought to be more common. Phenotypic overlap exists with other forms of outflow obstruction, such as hypertrophic
cardiomyopathy (HCM) and differentiating between them is important given the heritable implications of cardiomyopathic states. Herein, histopathologic and molecular genetic features of a population of 83 surgically resected cases of SAM are evaluated.
Design: Formalin‐fixed paraffin embedded (FFPE) tissue was obtained on 83 patients having undergone surgical resection of a discrete or tunnel SAM (2009‐2015). Clinical information and hemodynamic data was abstracted from the medical record. Light microscopic features, including myocyte disarray, myocyte hypertrophy, and interstitial fibrosis were semiquantitatively scored. Extracted genomic DNA underwent Agilent SureSelect targeted capture of 54 genes associated with cardiomyopathies, followed by sequencing on the Illumina MiSeq platform. Variants were classified according to established guidelines.
Results: 83 patients (54 women) were included in the study, with a mean age of 49.8 years (range, 4‐80). 77 cases of SAM were discrete membranous, while 6 were tunnel‐type. Myocyte hypertrophy was absent or mild in 6 cases, moderate in 53 and severe in 23 cases. Interstitial fibrosis was absent or mild in 56 cases, moderate in 25, and severe in 1. Myocyte disarray was absent or mild in 75 cases and moderate in 7. The majority of genetic variants identified were benign polymorphisms; however, 4 pathogenic/likely pathogenic and 77 variants of unknown significance were identified (average, 1.7/case). Of the pathogenic/likely pathogenic variants, mutations in PTPN11 were present in 2 cases, MYH7 mutation in 1, and SOS1 in 1 case. 25 cases were believed clinically to have concomitant HCM, though none of those carried a molecular genetic mutation compatible with such. No histopathologic or clinical parameter appeared to correlate with identified pathogenic mutations.
Conclusions: Hitherto, this is the first systematic survey of SAMs to evaluate their histopathologic features. Additionally, it is the largest series of cases of SAMs to undergo molecular genetic
interrogation to evaluate for concomitant cardiomyopathy or syndrome. Histologic findings alone did not appear to be a predictor of underlying genetic variation to help in evaluation for a cardiomyopathic or syndromic state.
2016 - Charles LeDuc
2016 AWARD WINNING ABSTRACT
Charles LeDuc, MD
Evaluation for Heritable Cardiovascular Disorders using Targeted Next-Generation Sequencing on Formalin-Fixed Paraffin Embedded Tissue
Charles Leduc, Laura J. Train, Rajeswari Avula, Katrina E. Kotzer, Michelle L. Kluge, Michael J. Ackerman, Linnea M. Baudhuin, Joseph J. Maleszewski. Mayo Clinic, Rochester, MN
Background: Heritable cardiovascular (CV) disorders are diverse and include channelopathies (CP), cardiomyopathies (CM) and connective tissue disorders (CTD). Because they are associated with catastrophic CV events, identification of those at-risk is paramount. While a strong family history can prompt screening, postmortem genetic testing is often lacking. Furthermore, ideal specimens (i.e. whole blood (WB)) often are note retained at autopsy. Ubiquitous use of formalin-fixed paraffin embedded tissue (FFPET) in autopsy makes it an ideal source for interrogation; however its use in traditional sequencing is limited owing to genomic integrity. Targeted next generation sequencing (NGS) technology offers the ability to circumvent such limitations. The primary aim was to evaluate the efficacy of testing FFPET for heritable CV disorders using NGS.
Methods: Paired FFPET (heart) and blood (WB or dried blood spot (DBS)) samples were obtained from 13 patients. 7 were random autopsy samples, 3 were autopsies with clinical phenotype of a heritable CV disorder butunknown genotype, and 3 were surgical samples from patients with genotype-confirmed hypertrophic cardiomyopathy (HCM) on blood. Extracted genomic DNA underwent Agilent SureSelect targeted capture of 101 genes associated with CP, CM, and CTD, followed by sequencing on the Illumina MiSeq. Quality metrics were compared. Variants were classified by consensus.
Results: In quality comparisons of 10 cases using the CM discovery panel (63 genes), there were no significant differences between FFPET, WB and DBS in average percent mapped reads (60 vs 55 vs 60%), average depth of coverage (1259 vs 1425 vs 1490X), and Phred quality scores (all >30). Analysis of surgically derived FFPET from HCM patients, confirmed pathogenic mutations in TPM1, MYH7, and MYBC3, previously detected on WB. In the 3 autopsy cases with unknown genotype, testing on FFPET identified pathogenic mutations in FBN1, RAF1, and MYBC3, consistent with the clinical phenotype of Marfan syndrome, Noonan syndrome, and HCM, respectively. There was 100% concordance for all genotype calls, with no false positives or false negatives.
Conclusions: The results of this validation study show similar performance characteristics for NGS of DNA derived from FFPET (less than 15 years old), WB, and DBS, in the evaluation of inherited CV disorders. Such has important implications for molecular genetic testing when only FFPET is available. Additionally, interrogation of such tissues has important implications for extensive genotype-phenotype correlation in archival tissue, which is currently ongoing.
2015 - George Eng
2015 AWARD WINNING ABSTRACT
George Eng, MD, PhD
Optimization of serum free light chain analysis for rapid and reliable subclassification of cardiac amyloidosis
George Eng, Marc K. Halushka, Daniel P. Judge, Marc J. Semigran, James R. Stone
Background: Accurate classification of cardiac amyloidosis, between transthyretin and light chain kappa or lambda, is paramount for optimal patient management. However, direct subtyping of amyloid deposits has significant drawbacks such as long turnaround time, high cost, and in some cases, the need to send the material to an outside reference laboratory. Potential differences in serum free light chain kappa/lambda ratios may provide a method to distinguish between different forms of cardiac amyloidosis. However, the standard upper and lower limits of normal for the assay are not optimized for cardiac amyloidosis classification. Therefore we investigated if optimization of the kappa/lambda serum free light ratios could allow for a novel method to accurately and rapidly subclassify cardiac amyloidosis.
Design: We investigated 78 cases of tissue proven cardiac amyloidosis (endomyocardial biopsy: n=65, ventricular septal myectomy: n=1, ventricular apical core: n=1, explanted heart: n=9, and autopsy heart: n=2) at two separate medical centers. All patients had serum free light chain analysis obtained prior to plasma cell neoplasm treatment in conjunction with routine classification of cardiac amyloidosis (mass spectrometry n=51, or immunofluorescence n=27). We then stratified the cases based on the ratio of kappa to lambda serum free light chains and correlated that value to their classification of cardiac amyloidosis.
Results: The serum free light chain kappa/lambda ratios were non-overlapping for the three types of amyloid identified: AL-lambda (0.01-0.41, n=29), ATTR (0.63-2.7, n=38), and AL-kappa (6.7-970, n=11). Using optimized cut-off values for the kappa to lambda serum free light chain ratio, we were able to accurately distinguish between the three common forms of ventricular cardiac amyloidosis within this cohort of patients. A kappa to lambda ratio value between 0.5 and 5.0 had 100% sensitivity and 100% specificity for distinguishing transthyretin from amyloid light-chain amyloidosis (n=78, 95% confidence interval: 89%-100% for both sensitivity and specificity). The capacity of this test to distinguish between forms of amyloidosis was equivalent for cases subtyped by either mass spectrometry or immunofluorescence.
Conclusions: Optimized ranges for serum light chain kappa/lambda ratio can provide extremely robust classification of cardiac amyloidosis. The assay is widely available, relatively inexpensive and can deliver accurate, rapid results. Cases of cardiac amyloidosis in which the kappa/lambda free light chain ratio falls close to these new cut-off values would likely benefit most from direct amyloid subtyping.
2014 - Kamran M. Mirza
2014 AWARD WINNING ABSTRACT
Kamran M. Mirza, MD, PhD
C4d Immunoreactivity in Endomyocardial Biopsies after Heart Transplantation: A 10-Year Prospective Analysis
M Kamran Mirza, Savitri Fedson, Aliya N Husain.
Background: In the past decade C4d has emerged as a potential marker for AMR, however, literature regarding its use as a prognostic tool has been controversial. Currently, the ISHLT recommends C4d staining only in the first 90 days post-transplant. Our aim was to prospectively determine the prognostic value of C4d positivity in post-transplant endomyocardial biopsies (EMBs) by correlating with clinical cardiac dysfunction, cellular rejection, HLA status, death, and cardiac allograft vasculopathy (CAV) at autopsy.
Design: All 5862 endomyocardial surveillance biopsies from 241 consectuvie heart transplant recipients (transplant date 1/2002 – 12/2012) were stained prospectively for C4d from 2004. Immunohistochemical stains were performed on paraffin-embedded tissue using an anti-human C4d polyclonal antibody. Only strong diffuse endothelial staining was considered positive. All patients had at least 1 year of follow-up. Cardiac dysfunction at the time of positive biopsy was evaluated by hemodynamics and echocardiography. Cellular rejection was graded per ISHLT 1990 criteria.
Results: Positive C4d staining was present in 64 biopsies from 34 (14%) patients, 9 of whom (26%) had clinically significant cardiac dysfunction. 22/34 (65%) of C4d positive patients died. Autopsy was performed on 19 (8 C4d negative and 11 C4d positive patients) of the 58 deaths. 11/11 C4d positive patients had histologic evidence of CAV. Six of 8 C4d negative patients (75%) had no CAV, while 2 of 8 did. Time to first episode of C4d positivity was 406+383 (7-1302) days. Time to C4d positivity in 12 surviving patients was 224+191 days and in the 22 expired patients was 505 + 427 days.
Conclusions: In this study, C4d positive patients were younger (by a decade), had higher PRAs and higher mortality (65% vs. 17%) as compared to C4d negative patients. Later C4d positivity is not benign; warranting long-term surveillance. All 11 C4d positive autopsies revealed CAV as the cause of death. Even 1 episode of C4d positivity correlated with a poorer outcome. These findings show a positive association of C4d with CAV and death. Our results indicate a prognostic role for C4d in heart transplantation warranting routine detection (including long-term surveillance) of this marker in the pathologic evaluation of cardiac AMR.
2013 - Stefania Rizzo
2013 AWARD WINNING ABSTRACT
Stefania Rizzo
Intercalated Disc Ultrastructural Abnormalities Precede Histopathologic Changes in Desmoglein 2 Transgenic Mice and Are Associated with Conduction Slowing and Inducible Arrhythmias.
Stefania Rizzo, Elisabeth M Lodder, Arie O Verkerk, Rianne Wolswinkel, Leander Beekman, Kalliopi Pilichou, Cristina Basso, Carol A Remme, Gaetano Thiene and Connie R Bezzina
Background: We sought to evaluate the pathological substrate of electrical instability in the pre- phenotypic stage of arrhythmogenic cardiomyopathy (AC), before myocardial cell death and fibro- fatty replacement onset.
Design: We studied transgenic mice carrying mutation of desmoglein2 (dsg2) in the adhesive extracellular domain (Tg-NS). Gross, histological and ultrastructural analyses were used in the pre- phenotypic stage of the diseases, i.e., between 2 and 6 weeks. The structure and molecular composition of the ID was assessed by electron microscopy (EM) and by immunofluorescence. Mice with cardiac over expression of wild-type dsg2 (Tg-WT) and wild-type mice served as controls. Surface ECGs, electrical epicardial mapping and patch-clamp experiments were performed to determine ventricular conduction and arrhythmia susceptibility.
Results: At gross and histologic examination, Tg-NS hearts appeared normal, with no evidence of replacement-type fibrosis. Immunofluorescence uncovered no differences in the level and localization of junctional proteins between Tg-NS/L mice and controls. Ultrastructural examination of the myocardium ruled out cardiomyopathic changes, including cell necrosis, focal myofibrillar lysis, dilated sarcoplasmatic reticulum and T-tubules, and mitochondrial clustering at this age. Widening of the intercellular spaces at the level of desmosomes/adherens junctions was seen in otherwise morphologically normal cardiomyocytes in 25% of TgNS at 2 weeks and in 100% at 6 weeks and the percentage of widened cellular junctions increased with age (from about 10% at an age of 2 weeks to 60% at 6 weeks). Morphometric analysis showed that the intercellular space was significantly widened in Tg-NS/L mice (149 +/- 80 nm) compared with controls (32 3.5nm), p<0.05. None of the control mice (Tg-WT, WT) displayed any intercellular space widening. QRS- prolongation and inducible ventricular arrhythmias were observed in mutant mice. A reduced action potential (AP) upstroke velocity due to a lower Na(+) current density was also observed at this stage of the disease
Conclusions: Dsg-2 mutant mice display ultrastructural evidence of desmosomes /adherens junctions widening, before development of cardiomyopathic changes. This coincided with conduction slowing and inducible ventricular arrhythmias thus emphasizing the importance of ID integrity for proper electrical conduction.
The abstract later became a publication in Cardiovascular Research.
2012 - Sean Hynes
2012 AWARD WINNING ABSTRACT
Sean Hynes, MD, PhD
Investigations into eNOS and Phosphomimetic eNOS Gene Delivery to the Vasculature
SO Hynes, S Ganly, F Sharif, L Smith, K McCullagh, U Greiser, Z Katusic, T O’Brien. University Hospital Galway, Galway, Ireland; National University of Ireland, Galway, Galway, Ireland; Mayo Clinic, Rochester, MN.
Background: Endovascular procedures including stenting, denudes endothelium. Removal of this layer, decreases the levels of active endoethelial nitric oxide synthase(eNOS) and bioavailability of NO. Gene delivery of eNOS or an engineered phosphomimetic constitutively active eNOS may prove of benefit to the vasculature.
Design: Two principles are critical to improving outcomes from endovascular procedures. First, to accelerate re-ednothelialisation and second, to prevent neointimal proliferation. We have examined gene therapy approaches to produce beneficial effects in the vasculature. We compared eNOS and phosphomimetic eNOS for their effects on vasomotor activity. Thereafter, we examined the usefulness of eNOS delivery from a stent platform in preventing in-stent restenosis and promoting re-endothelialisation. Two rabbit models of vascular injury were used. The fi rst was a physiological model where we overexpressed our two candidate transgenes. The second was an injury model where a stent carrying the lead gene was delivered following inflation/deflation injury of the external iliac artery.
Results: Overexpression of phosphomimetic and wild type eNOS both improved vasomotor activity in a rabbit carotid artery model. However, there was no difference between either enzyme. Therefore, wild type eNOS was examined for its beneficial effects following delivery from a stent platform. We then compared viral (adenovirus) versus non-viral (liposome) delivery of wild type eNOS, head-to-head. Both vectors resulted in improved re-endothelialisation, however, only the use of viral vectors decreased neointimal formation.
Conclusions: Our study found that overexpression of an engineered constitutively active form of eNOS is not superior to wild type delivery. This may be due to suboptimal mimicking of pophosphorylation. Interestingly, the vector is critical for delivery of eNOS. When compared head-to-head only the viral vector improved both neointimal and re-endothelialisation results. We speculate that this may be due to the expression of non-viral vectors by macrophages which also express inducible nitric oxide synthase. The direct competition for substrates may be the reason for less effective eNOS function. Whereas, eNOS delivered by virus is expressed in smooth muscle cells and these have no native NOS to compete with the transgene.
2011 - Xuchen Zhang
2011 AWARD WINNING ABSTRACT
Xuchen Zhang
Oxidative Stress and ERK1/2 MAP Kinase Mediate Cardiomyocyte Injury in Transthyretin Cardiac Amyloidosis
Xuchen Zhang, Qiang Xie, Duanjun Tan, Patty J Lee, Felicitas L Lacbawan, Jenny Libian. State University of New York, Downstate Medical Center, Brooklyn; Yale University School of Medicine, New Haven, CT
Background: Transthyretin (TTR) is associated with two forms of cardiac amyloidosis: familial (mutant TTR) and systemic senile amyloidosis (wildtype TTR). Approximately 4% of African Americans are heterozygous for V122I variant TTR, a mutation associated with familial amyloidotic cardiomyopathy. The mechanisms of TTR-induced cardiac injury remain elusive. Markers of oxidative stress have been associated with TTR amyloid deposits in peripheral nerve and we previously reported that oxidative stress and ERK1/2 activation mediate cell death in lung epithelium. We investigated the potential role of oxidative stress and ERK1/2 activation in mediating TTR-induced cardiomyocyte injury.
Design: Cases of TTR cardiac amyloidosis and age-matched controls were identified from 2007-2010 autopsy records. TUNEL and 8-OH-dG staining was performed on formalin-fixed paraffin-embedded sections from left ventricle. The TTR gene was sequenced using genomic DNA extracted from the paraffin blocks. Cultured rat cardiomyocytes were exposed to TTR fibrils formed by incubating wildtype TTR under acidic conditions. Apoptosis was assessed by TUNEL staining and Annexin V flow cytometry. Oxidative stress was examined by Western blot for heme oxygenase-1 (HO-1), reactive oxygen species (ROS) production, and 8-OH-dG staining. ERK1/2 activation was measured by Western blot of phospho-ERK1/2.
Results: Four cases of TTR cardiac amyloidosis (average age 82.8 years; range 80 to 87 years) were identified. All patients had presented with chronic heart failure and arrhythmia. TTR gene sequencing identified mutant TTR (V122I) in 3 cases and wildtype TTR in 1 case of cardiac amyloidosis. Positive staining of TUNEL and 8-OH-dG was more prominent in cases of cardiac amyloidosis than in control heart tissue. Rat cardiomyocytes treated with TTR fibrils showed more ROS production, HO-1 expression, phospho-ERK1/2, and apoptosis than untreated cardiomyocytes. Inhibition of ERK1/2 activation by PD98059 or ROS production by diphenylene iodonium ameliorated TTR fibril-induced oxidative injury and apoptosis.
Conclusions: Apoptosis and oxidative injury are increased in hearts of patients with cardiac amyloidosis compared with age-matched controls. Oxidative stress, ERK1/2 activation, and apoptosis are involved in TTR-induced injury of cultured rat cardiomyocytes. Inhibition of oxidative stress and ERK1/2 activation may provide a potential mechanism for prevention and treatment of cardiac injury associated with TTR cardiac amyloidosis.
2010 - Vidhya Nair
2010 AWARD WINNING ABSTRACT
Vidhya Nair, MBBS, MD
New Insights into Stentless Porcine Bioprosthesis Failure
V Nair, KB Law, K Phillips, AY Li, TE David, J Butany. Toronto General Hospital/UHN, Toronto, Canada; University of Toronto, Toronto, Canada; Mcmaster University, Hamilton, Canada.
Background: The Medtronic Freestyle valve is a stentless porcine valve fixed in glutaraldehyde at “zero” pressure on the cusps and treated with a-amino oleic acid. This valve reportedly has excellent clinical and hemodynamic results, but has had some failures, however little has been reported about its long-term pathology.
Design: Seventeen Freestyle valves (explanted 2003 to2009) were reviewed to assess reasons for bioprosthesis failure. Clinical data, including implant age, gender, native aortic valve lesion and implant duration were recorded. All valves were examined in detail, using histochemistry and immunohistochemistry to identify morphological changes and cellular and humoral responses.
Results: One Freestyle valve, explanted for mitral valve endocarditis on the fifth postoperative day, was excluded from analysis. The average implant duration was 71±35.2 months (6±2.9 years). Six valves were explanted for infective endocarditis, six for aortic insufficiency, and four for aortic stenosis. Infective endocarditis was seen in six, calcification in eleven, pannus in fifteen, twelve showed thrombus, cusp tears in nine and 10 showed old needle tract like injuries in the porcine aorta. Acute inflammation was seen in one and a chronic inflammatory reaction involving the xenograft arterial wall was seen in fifteen of sixteen valves. The cells were comprised of macrophages and lymphocytes. The lymphocytes were T cells(CD8 positive) and B cells. Significant damage to the porcine aortic wall was seen in fifteen cases and cusp myocardial shelf damage in seven cases. All cases stained positively for IgG and C4d par.
Conclusions: The porcine aortic cusps showed no significant cellular reaction. The porcine aortic tissue showed multifocal T cell mediated rejection associated with significant porcine aortic medial damage, consistent with dilatation of the porcine aortic root. This likely lead to porcine valvular incompetence. The demonstration of IgG and C4d staining suggests the likelihood of humoral rejection, in addition to the cellular. One possibility underlying this is, that the porcine aortic tissues are inadequately fixed and hence the retained antigenicity. This is one of the few demonstrations of a rejection reaction to porcine bioprosthetic tissues, associated with bioprosthesis failure, and needs further studies.
2009 - Huifang Zhang
2009 AWARD WINNING ABSTRACT
Huifang Zhang
Cardiac Overexpression of CXCL10 Causes Spontaneous Leukocyte Infiltration but Not Cardiac Dysfunction
J Yuan, T Lim, JQ He, YJ Wang, HF Zhang, A Sall, Z Liu, B McManus, DC Yang. Medical College of Georgia, Augusta, GA; The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, Vancouver, BC, Canada.
Background: The essential role of chemokines in dilated cardiomyopathy (DCM) has been demonstrated by recent studies. We previously showed the upregulation of cysteinx-cystein (CXC) chemokine ligand 10 (CXCL10) in Coxsackievirus B3 (CVB3)-induced myocarditis, a major cause of DCM.
Design: To explore the contribution of CXCL10 to CVB3-induced myocarditis and associated DCM, we performed functional analyses using newly generated transgenic mice (Tg) that cardiac-specifically overexpress CXCL10.
Results: A transgenic mouse model with cardiac-specific overexpression of CXCL10 was generated. The cardiac specific upregulation of CXCL10 was confirmed by PCR, RT-PCR, in situ hybridization, and Western blot analyses. Cardiac-specific expression of CXCL10 resulted in spontaneous infiltration of CD4+ T cell, CD8+ T cell, and NK cell in perivascular and interstitial regions of the myocardium as compared to control wild type littermates by both real time qRT-PCR and immunohistochemical staining. The number of infiltrations was age-dependent, with the greatest number in older Tg mice, but barely any in four-week-old mice. Further, the expression levels of IFN-γ, and counterinflammatory IL-10 cytokine in Tg hearts were significantly elevated as compared to that in wild type mouse hearts, but the expression levels of the proinflammatory cytokines (TNF-α, IL-4, IL-5, IL-6, IL-12) were unchanged. Despite the presence of mononuclear cell infiltrations and limited mRNA upregulation of IFN-γ and IL-10 in the myocardium, there were no discernible pathological alterations in the hearts of Tg mice, as revealed by (i) cardiac troponin I levels, a serum marker of myocyte injury; (ii) echocardiography, a measure of heart ejection fraction; and (iii) heart mass/body weight.
Conclusions: These findings indicate that CXCL10 primarily directs T cells and NK cells to the myocardium, and is associated with minor defense immunity but is insufficient to cause cardiac dysfunction.
The abstract later became a publication in Circulation Research.
2008 - Elisa Carturan
2008 AWARD WINNING ABSTRACT
Elisa Carturan, BSc, PhD
Myocarditis in Arrhythmogenic Right Ventricular Cardiomyopathy Due to Desmosomal Gene Mutations: Is There an Infective Etiopathogenesis?
E Carturan, B Bauce, N Protonotarios, A Rampazzo, A Tsatsopoulou, A Nava, M Valente, G Thiene, C Basso. University of Padua, Padua, Italy; Yannis Protonotarios Center, Naxos, Greece.
Background: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited disease characterized by a gradual loss of myocytes and fibro-fatty replacement. Recently, mutations of gene encoding desmosomal proteins have been demonstrated in up to 50% of probands. Inflammatory infiltrates are identified in two-thirds of cases as to support an infective etiopathogenesis. The aim of this study was to assess the presence of viral genomes in the myocardium by molecular pathology investigation on hearts of genotyped ARVC patients.
Design: Ten ARVC hearts (8 male, 2 female, mean age 28 yrs), coming from either sudden death (7) or cardiac transplantation (3) were investigated. Genetic screening identified pathogenetic mutations in plakophilin-2 (5 cases), desmoplakin (3), desmoglein-2 (1) and plakoglobin (1). After gross examination, extensive sampling of both ventricles and septum was performed for histology and immunohistochemistry. Paraffin-embedded or formalin fixed myocardial samples were analysed by polymerase chain reaction for the presence of cardiotropic viruses, including adenovirus, herpes virus, influenza virus A and B, hepatitis C, enterovirus and parvovirus.
Results: At macroscopic examination, there was biventricular involvement in all (predominantly right in 3 and left in 1). At histology, fibro-fatty replacement with inflammatory infiltration were evident in all (100%). The latter was either diffuse (3, 30%) or focal (7, 70%), and mostly consisted of T-lymphocytes in 8 (80%) and was polymorphous in 2 (20%). Clear-cut evidence of myocyte necrosis was present in 3 (33%). Nucleic acids extraction was adequate in 9 (90%). Molecular investigation was negative in all but 1 case in which HCV was identified (10%)
Conclusions: Myocarditis is a usual feature in genotyped ARVC hearts, which are characterized also by biventricular involvement and fibrofatty replacement. On the opposite, viral genome is a exceptionally detected in the myocardium as to question a causative role of viruses and to support the view of myocarditis as a reactive phenomenon accompanying the injury and repair process of ARVC.
2006 - Husain Sattar
2006 AWARD WINNING ABSTRACT
Husain Sattar, MD
Presence of a CD21+ Follicular Dendritic Cell (FDC) Network Distinguishes Invasive Quilty Lesions from Acute Cellular Rejection
HA Sattar, AN Husain, T Krausz. University of Chicago Hospitals, Chicago, IL.
Background: First described by Billingham, Quilty lesions arise in the majority of cardiac transplant patients. Neither the etiology nor the importance of these endomyocardial infiltrates has been fully elucidated. What is clear, however, is that invasive Quilty lesions are diagnostic challenges that mimic acute cellular rejection resulting in inter-observer variability and over-diagnosis of rejection. To date, there exists no definite means of distinguishing these lesions from rejection. Quilty lesions are characterized by capillary-sized blood vessels and a central aggregate of B-cells with a rim of T-cells, an organization similar to the primary follicle of a lymph node. We hypothesized that the organization of invasive Quilty lesions is dependent upon an
underlying FDC network, and that the presence of such a network is useful in distinguishing it from cellular rejection.
Design: Consecutive cases of acute cellular rejection (n=25) and invasive Quilty (n=23) for which adequate tissue was available were collected from the pathology archives. The specimens consisted of endomyocardial biopsies taken from transplant recipients over a one-year period (2004-2005). Hematoxylin and eosin staining was used to establish the diagnoses. A single unstained section was immunostained for CD21 to investigate the presence of a FDC network.
Results: A compact CD21+ FDC network was present in 15 of the 17 invasive Quilty lesions that were 0.3mm or larger in greatest dimension (p<0.00001), and was completely absent in all 25 lesions of acute cellular rejection (G1A/1B, n=7; G2, n=13; G3A/3B,
n=4; G4, n=1). Of the 8 invasive Quilty lesions that lacked an FDC network, 6 measured less than 0.3mm (n=6) and the remaining 2 were between 0.3 and 0.4mm. When present, the follicular dendritic cells were in the center of the lesion and the number of positive cells was proportional to the size of the lesion, likely explaining the lack of staining for the FDC-network in some of the smaller lesions.
Conclusions: The presence of a CD21+ FDC network reliably distinguishes invasive Quilty lesions from acute cellular rejection, especially in those lesions (>0.3mm) that are most likely to be over-diagnosed as moderate or severe acute cellular rejection (sensitivity 88%, specificity 100%, positive predictive value 100%). Use of CD21 immunoreactivity to highlight this network would be of benefit in reducing the rate of over-diagnosis known to be associated with invasive Quilty lesions, alleviating unnecessary immunosuppression and its associated risks.
The abstract later became a publication in the American Journal of Surgical Pathology.
2004 - Dylan V. Miller
2004 AWARD WINNING ABSTRACT
Dylan Miller , MD
Surgical pathology of noninfectious ascending aortitis: a study of 45 cases with emphasis on an isolated variant
Division of Anatomic Pathology, Mayo Clinic, Rochester, Minnesota, USA
Background: Aortitis is emerging as an important cause of ascending aortic aneurysm in the elderly. Its features have not been described in a surgical population.
Design: Retrospective clinicopathologic review of 45 cases of active noninfectious aortitis among 513 consecutive ascending aortic resections (1985 to 1999).
Methods: Clinical data were collected from medical records. Histopathologic features were recorded during review of slides stained with hematoxylin-eosin and Verhoeff-van Gieson. Cases were categorized by predefined clinical criteria. Clinicopathologic features were compared among groups, with emphasis on unsuspected aortitis without systemic arteritis.
Results: The 2 largest groups were isolated aortitis (47%) and giant cell arteritis (31%). Other aortitis groups included Takayasu (14%), rheumatoid (4%), and unclassified (4%). Patients with isolated aortitis and giant cell arteritis were generally women (80%; mean age 73 y). All 6 with Takayasu arteritis were women (mean age 26). Although giant cell arteritis and isolated aortitis were histologically indistinguishable, their clinical courses differed substantially. Among 21 patients with isolated aortitis (2 treated with corticosteroids), only 10% later developed aortic aneurysms. In contrast, of 14 patients with giant cell arteritis (11 treated with corticosteroids), 21% subsequently developed aneurysms (P=0.09).
Conclusions: Aortitis primarily affected women. Patients with isolated aortitis and giant cell arteritis were generally older than 50 years and, by definition, those with Takayasu arteritis were younger. In patients with isolated aortitis, outcomes were generally good, despite the absence of anti-inflammatory therapy. Accordingly, a conservative approach may be warranted for managing this subset of patients with aortitis.
The abstract later became a publication in the American Journal of Surgical Pathology.

2003 - Michael A. Laflamme
2003 AWARD WINNING ABSTRACT
Michael A. Laflamme, BS, PhD, MD
Extracardiac Progenitor Cells Repopulate Most Major Cell Types in the Transplanted Human Heart
Elina Minami, MD, Michael A. Laflamme, MD, PhD, Jeffrey E. Saffitz, MD, PhD, and Charles E. Murry, MD, PhD. Department of Pathology (M.A.L., C.E.M.), University of Washington School of Medicine, Seattle, WA
Background: Extracardiac progenitor cells are capable of repopulating cardiomyocytes at very low levels in the human heart after injury. Here, we explored the extent of endothelial, smooth muscle, and Schwann cell chimerism in patients with sex-mismatched (female-to-male) heart transplants.
Design: Autopsy specimens from 5 patients and endomyocardial biopsies from 7 patients were used for this study. Endothelial, vascular smooth muscle, and Schwann cells were stained with antibodies against CD31 or Ulex europaeus lectin, smooth muscle α-actin, and S-100, respectively, and the Y chromosome was identified with in situ hybridization. Biopsy specimens from 1, 4, 6, and 12 months and 5 and 10 years after heart transplantation were evaluated. Y-positive cells were counted by conventional bright-field microscopy and confirmed by confocal microscopy.
Results: Endothelial cells showed the highest degree of chimerism, averaging 24.3±8.2% from extracardiac sources. Schwann cells showed the next highest chimerism, averaging 11.2±2.1%; vascular smooth muscle cells averaged 3.4±1.8%. All 3 cell types showed substantially higher chimerism than we previously observed for cardiomyocytes (0.04±0.05%). Endothelial chimerism was much higher in the microcirculation than in larger vessels. Analysis of serial endomyocardial biopsies revealed that high levels of endothelial chimerism occurred as early as 1 month after transplantation (22±6.6%) with no significant increases even up to 10 years after cardiac transplantation.
Conclusions: Extracardiac progenitor cells are capable of repopulating most major cell types in the heart, but they do so with varying frequency. The signals for endothelial progenitor recruitment occur early and could relate to injury during allograft harvest or transplantation. The high degree of endothelial chimerism may have immune implications such as for myocardial rejection or graft vasculopathy.
The abstract later became a publication in Circulation.
2001 - C. Basso
2001 - B. Thurberg
1999 - J. Ford
1998 - B. Sampson
1996 - C. Tan
1994 - C. Phillips
1993 - Billie Fyfe-Kirschner
1993 AWARD WINNING ABSTRACT
Billie Fyfe-Kirschner, MD
Heart transplantation-associated perioperative ischemic myocardial injury. Morphological features and clinical significance
Fyfe B, Loh E, Winters GL, Couper GS, Kartashov AI, Schoen FJ. Department of Pathology, Mt. Sinai College of Medicine, New York, NY, USA.
Background: The frequency and clinical significance of perioperative ischemic myocardial injury (PIMI) after heart transplantation and the diagnostic features distinguishing PIMI from rejection are not well defined.
Design: We evaluated PIMI in the first four weekly endomyocardial biopsies and/or autopsy myocardium from 140 consecutive orthotopic heart transplantation recipients (1984 to 1991) by grading the severity of coagulative myocyte necrosis (CMN) as absent, 0; mild-focal, 1; moderate-multifocal, 2; or severe-confluent, 3, and determining the evolution of morphological features of its healing.
Results: CMN (often with contraction bands) was noted in 124 patients (89%); 24 patients (17%) had grade 3 CMN, of which 4 died within 30 days of transplantation. Nevertheless, at 1 year after surgery, survival was similar in patients with and without severe injury. Increased cold ischemic time but neither donor age nor intensity of inotropic support correlated with more severe early ischemic injury. PIMI inflammation was characterized by a predominantly polymorphonuclear/histiocytic infiltrate that contained lymphocytes and plasma cells, expanding the interstitium but not encroaching upon and separable from adjacent viable myocytes. Histological features of PIMI developed and resolved more slowly than those of typical myocardial infarct necrosis in nonimmunosuppressed patients; at 4 weeks, CMN persisted in 20% of patients and residual healing in nearly half. Diagnostic rejection was observed concurrently with PIMI in 54 of 533 biopsies (10%).
Conclusions: Diagnosed by conventional histological criteria, PIMI is prevalent early after heart transplantation and has a protracted healing phase that can mimic or coexist with rejection. Extensive PIMI has deleterious impact on short-term survival, but the long-term impact of PIMI remains to be established.
The abstract later became a publication in Circulation.
1993 - A. Joshi
1990 - G. Leclerc
1989 - Kandice Kottke-Marchant
1989 AWARD WINNING ABSTRACT
Kandice Kottke-Marchant, MD, PhD
Cardiac transplant-associated vascular disease: Evolution, immunophenotype, and evidence of endothelial activation
Kandice Kottke-Marchant, Walter E. Newman, Norman Ratliff. The Cleveland Clinic Foundation, Cleveland, Ohio, USA
Background: Transplant-associated vascular disease (TAVD) is a major cause of late mortality after cardiac transplantation.
Design: To elucidate the evolution of TAVD, the autopsy histopathology of five cardiac allograft recipients who died ≥12 months post-transplantation was studied semi-quantitatively. Vessel cross sections were analyzed for size, proliferative lesions, inflammation, lipid, and thrombi. The type of inflammatory cells in the vessels were characterized by immunohistochemistry, and the activation state of the vessel endothelium was characterized by immunohistochemistry for HLA-DR and inducible endothelial leukocyte adhesion proteins [endothelial leukocyte adhesion molecule-1 (SLAM-1) and vascular cell adhesion molecule-1 (VCAM-1)].
Results: The mean post-transplantation interval was 27.2 months (range 12–40). TAVD was present in all five patients and was the cause of death in four of five. The percentage of vessels with proliferative lesions increased progressively with the duration of survival after transplantation. Both arteries and veins contained proliferative lesions, but more arteries than veins were involved at all time points. Large veins and large arteries had a significantly higher proportion of proliferative lesions than small veins (p < 0.04) and small arteries (p < 0.06), respectively. Inflammatory lesions were more prevalent in arteries than veins, 55.7% versus 10.9% (p < 0.001). The inflammatory vascular lesions were comprised principally of T lymphocytes, with smaller numbers of B lymphocytes and macrophages. The endothelium of arteries and veins expressed HLA-DR as well as VCAM-1, but stains for ELAM-1 showed only focal expression. By linear regression, intimal/medial inflammation decreased with time (r = −0.81, p < 0.06) and adventitial inflammation increased with time (r = +0.98, p < 0.001). Lipid-containing lesions were observed in 13.0% of arterial cross sections and were not seen in veins. Lipid containing arterial lesions increased progressively with both time and vessel size, but, in contrast to proliferative and inflammatory lesions, were not seen at any time interval in veins or small arteries.
Conclusion: In summary, TAVD is an inflammatory and proliferative process that involves arteries more than veins, and is more prevalent in large vessels and at greater post-transplantation intervals. Vascular T cell inflammation, intimal proliferation, and an activated endothelial cell phenotype appear to be closely related in the development of TAVD.
The abstract later became a publication in the Journal of Cardiovascular Pathology.

MARGARET BILLINGHAM AWARD WINNERS
SCVP celebrates the top publications in Cardiovascular Pathology.
In 2021, the SCVP began awarding yearly recognition for the top article and top review paper in Cardiovascular Pathology, our journal. The award is named after the legendary cardiovascular pathologist, Margaret Billingham, whose career included the publication of many seminal studies.
2023 - Top Article The spectrum of macrophage-predominant inflammatory myocardial disease presenting as fulminant heart failure
2023 - Top Review Myocardial fibrosis: morphologic patterns and role of imaging in diagnosis and prognostication
2022 - Top Article COVID-19 myocarditis: quantitative analysis of the inflammatory infiltrate and a proposed mechanism
2022 - Top Review Current state of vaccine development and targeted therapies for COVID-19: impact of basic science discoveries
2021 - Top Article Myocarditis: something old and something new
2021 - Top Review The emerging spectrum of cardiopulmonary pathology of the coronavirus disease 2019 (COVID-19): Report of 3 autopsies from Houston, Texas, and review of autopsy findings from other United States cities
2020 - Top Article Thrombus on the inflow cannula of the HeartWare LVAD: an update
2020 - Top Review Lysosomal storage disorders affecting the heart: a review
HONORS FOR SCVP MEMBERS
The Society for Cardiovascular Pathology is proud of the honors our members have receive]d through their contributions to pathology and education.
Dr. Alison Krywanczyk
A 2022 top five winner of the ASCP 40 under Forty honor.
Dr. Yasmeen Butt
Dr. Peter Anderson
Dr. Melanie Bois
Dr. Barbara Sampson
Dr. Gayle Winters
Dr. Richard N. Mitchell
Dr. Peter Anderson
Dr. Peter Anderson
2011 Association of Pathology Chairs Michele Raible Distinguished Teaching Award in Undergraduate Medical Education
Dr. Avrum Gotlieb
2011 ASIP Robbins Distinguished Educator Award
Dr. L. Maximilian Buja
2009 Executive director of the Houston Academy of Medicine – Texas Medical Center Library
Know of an SCVP member who has received a big honor? Let us know.