Therapeutic Attenuation of Cardiac Remodeling After Acute Myocardial Infarction
A Conversation With Marc A. Pfeffer, MD, PhD
This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
Marc Pfeffer, MD, PhD, is the Dzau Professor of Medicine at Harvard Medical School; and Senior Physician, Cardiovascular Division at Brigham and Women’s Hospital. He was born in Brooklyn, NY, and obtained his MD and PhD at the University of Oklahoma. He married his late wife and research collaborator, Janice Pfeffer, PhD, in 1970. He has won numerous awards, including the American Heart Association James B. Herrick Award for Outstanding Achievements in Clinical Cardiology (2013) and the American Heart Association Distinguished Scientist Award (2015), the American College of Cardiology Distinguished Scientist Award (Translational Domain; 2017), and an Honorary Doctoral Degree from Sahlgrenska Academy, University of Gothenburg, Sweden (2014).
Dr Rutherford asks: In the early 1970s, you, and your late wife Janice, studied adrenergic mechanisms and cardiac hypertrophy and ventricular function, as well, in spontaneously hypertensive rats. What led to your initial animal studies on acute myocardial infarction and your interest in the renin-angiotensin-aldosterone system?
Dr Pfeffer replies: As graduate students in the Department of Physiology and Biophysics at the University of Oklahoma, my late wife, Janice, and I had the privilege to work under the tutelage of Edward D. Frohlich, MD, who is a pioneer in the hemodynamics of hypertension with a major emphasis on the response of the heart to the augmented workload imposed by hypertension. He was keenly interested in the functional consequences of developing left ventricular hypertrophy and obtained breeding stock of the newly developed Japanese strain of the SHR. We developed methods to assess hemodynamics and left ventricular function to compare normotensive with hypertensive rats during aging. We found a marked age-associated deterioration in contractile performance in the hypertensive rats that could be prevented by a variety of antihypertensive agents.
Our studies of the longitudinal changes in ventricular structure and function in an animal model of genetic hypertension caught the attention of Eugene Braunwald, MD, who was organizing a Program Project Grant on the Pathophysiology of Left Ventricular Hypertrophy at the then Peter Bent Brigham Hospital. We moved to the Brigham in 1976 as his postdoctoral fellows (me as a medical intern) …