doi: 10.1161/CIRCULATIONAHA.106.645572
(Circulation. 2006;114:867-868.)
© 2006 American Heart Association, Inc.
In Memoriam |
Carl S. Apstein, MD
1941–2005
From the University of Cincinnati College of Medicine, Cincinnati, Ohio (L.W.), and Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (J.S.I.).
Correspondence to Laura F. Wexler, Associate Dean, Student Affairs and Admissions, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Medical Science Building, Room E251, Cincinnati, Ohio 45267-0552. E-mail Wexler{at}ucmail.uc.edu
Carl S. Apstein, Professor of Medicine and Physiology and founder of the Cardiac Muscle Research Laboratory at Boston University School of Medicine died November 8, 2005, after a year-long battle with pancreatic cancer. He was 64.
Carl was born in Brooklyn, NY, and did his undergraduate work at Cornell University, where he was a Telluride Scholar. He graduated from New York University School of Medicine in 1967. After his internal medicine residency and cardiology fellowship at New York Hospital–Cornell Medical Center, he received additional research fellowships at Tufts New England Medical Center and the Massachusetts Institute of Technology. He joined the faculty of Boston University School of Medicine in 1973, where he founded the Cardiac Muscle Research Laboratory, a continuously productive laboratory and highly regarded training site for investigators from all over the world. He also served as Chief of Cardiology at Boston City Hospital from 1982 to 1996.
|
Dr Apstein was an outstanding investigator, a great clinician, and a revered teacher and mentor. As a clinician, he was known for his superb physical examination skills, for his astute diagnostic acumen, and particularly for his wonderful ability to teach pathophysiology and mechanisms of disease. His weekly clinical case rounds at Boston City Hospital were eagerly attended by the entire division and serve as models of the kind of cheerfully provocative Socratic teaching and discussion that characterize a true "Master Teacher," one who was able to bring basic mechanisms of disease discovered in the laboratory into exciting clinical reality.
Dr Apstein was a pioneer in what we now recognize as "translational research." In the 1970s, he became interested in diastolic dysfunction as a cause of heart failure and began to define the basic mechanisms by which diastolic function is altered during ischemia and hypoxia. On the basis of his early studies of cardiac metabolism and mechanics and in particular the role of glucose metabolism on diastolic function during and immediately after ischemia, he became an unrelenting champion of the clinical potential of glucose-insulin-potassium (GIK) to preserve ischemic myocardium. To his great satisfaction, Dr Apstein’s early experiments on the effects of GIK on diastolic dysfunction during ischemia and hypoxia in isolated perfused rabbit and rat hearts1–15 were translated into the Immediate Myocardial Metabolic Enhancement During Initial Assessment and Treatment in Emergency care (IMMEDIATE) trial,16 an ongoing National Institutes of Health–funded multicenter clinical trial. Funding for this trial was in jeopardy after the publication of the Clinical Trial of Metabolic Modulation in AMI Treatment Evaluation (CREATE)–Estudos Cardiológicos Latinoamérica (ECLA), 17–18 which reported no benefit for GIK in patients with ST-elevation myocardial infarction. Although gravely ill, Dr Apstein, collaborating with Lionel Opie, used his decades of experimental results and special insight into the critical role of the timing of increased glucose supply to the ischemic myocardium19 to help convince the National Institutes of Health of the value of testing the hypothesis that early supply of GIK can sustain minimally perfused ischemic myocardium until definitive intervention restores blood flow.
One quality that made Carl Apstein so beloved by those who worked with him was his professional generosity. Dr Apstein had many successful collaborations with colleagues from all over the country and from all around the world, many of whom sent fellows and young faculty to train with him. He spent much of his professional career fostering the success of young investigators, helping them refine their experimental design, reviewing their grant proposals, and reading their manuscripts. His pleasure in their many successes, in the absence of any public attribution to himself, was possibly even greater than the satisfaction he got from his own successes in the laboratory. It is a tribute to Dr Apstein that he successfully collaborated with research groups from all of the major medical schools in Boston, a fiercely competitive milieu in which there have been many warring factions. Dr Apstein managed to work with everyone and everyone liked him.
The number of women who worked in his clinical division and in his laboratory who went on to successful careers in academic medicine is particularly noteworthy. It was fitting and well timed that the American Heart Association’s Women in Cardiology Committee awarded Dr Apstein its Mentoring Award in 2004. To quote the award citation, "He fostered a love of cardiovascular science and medicine in several generations of successful women physicians and scientists with a cheerful and unquestioning assumption that of course we could and should pursue excellence in this very competitive and demanding field" (American Heart Association Council Connections, Spring 2005).
What his many friends, colleagues, postdoctoral trainees, and students will perhaps remember most about Carl Apstein is not only his elegant science and devoted mentoring, but how much they loved him and how delightful it was to be with him. He had an infectious "joie de vivre" and always extracted the maximum enjoyment from the "good life," which for Dr Apstein included great food and wine, beautiful music, art and literature, his loving family, and many decades-long friendships. He expended much thought and effort in planning and preparing to savor these aspects of his life. His enduring passion for great science was one part of his passion for the all the good things in his life.
In the last 10 years of his life, even as he continued to be productive and successful in his laboratory, he pursued his great love of music by taking up a serious study of piano and music theory. After a few years, commenting that he could now play "like a competent 8-year-old," he began advanced study with Emily Corbato, who remained his devoted teacher until shortly before his death. His compact disc of short pieces by Bach, Chopin, Schumann, and Schubert was completed the day before he was admitted to the hospital for the last time. The music reminds one of Carl Apstein’s approach to his life and work: at times serious and then joyful, always beautiful and elegant and challenging, reflecting his capacity for relentless, dogged hard work, and passionate pleasure in equal measure.
 |
Disclosures |
|---|
 Top Disclosures References |
|---|
None.
|
References |
|---|
|
TopDisclosuresReferences |
|---|
1. Brachfeld N, Apstein CS. The influence of available substrate on contraction of the hypoxic myocardium. Cardiology. 1972; 57: 47–50.[Medline] [Order article via Infotrieve]
2. Gmeiner R, Apstein CS, Brachfeld N. Effect of palmitate on hypoxic cardiac performance. J Mol Cell Cardiol. 1975; 7: 227–235.[CrossRef][Medline] [Order article via Infotrieve]
3. Apstein CS, Bing OH, Levine HJ. Cardiac muscle function during and after hypoxia: effects of glucose concentration, mannitol and isoproterenol. J Mol Cell Cardiol. 1976; 8: 627–640.[CrossRef][Medline] [Order article via Infotrieve]
4. Apstein CS, Deckelbaum L, Hagopian L, Hood WB Jr. Acute cardiac ischemia and reperfusion: contractility, relaxation and glycolysis. Am J Physiol. 1978; 235: H637–H648.[Medline] [Order article via Infotrieve]
5. Cunningham MJ, Apstein CS, Weinberg EO, Vogel WM, Lorell BH. Influence of glucose and insulin on the exaggerated diastolic and systolic dysfunction of hypertrophied rats during hypoxia. Circ Res. 1990; 66: 406–415.
6. Eberli FR, Weinberg EO, Grice WM, Horowitz GL, Apstein CS. Protective effect of increased glycolytic substrate against systolic and diastolic dysfunction and increased coronary resistance from prolonged global underperfusion and reperfusion in isolated rabbit hearts perfused with erythrocyte suspensions. Circ Res. 1991; 68: 466–481.
7. Apstein CS, Eberli FR. Critical role of energy supply and glycolysis during short-term hibernation. Basic Res Cardiol. 1995; 90: 2–4.[Medline] [Order article via Infotrieve]
8. Lazar HL, Philippides G, Fitzgerald C, Lancaster D, Shemin RJ, Apstein C. Glucose-insulin-potassium solutions enhance recovery after urgent coronary artery bypass grafting. J Thorac Cardiovasc Surg. 1997; 113: 354–362.
9. Apstein CS, Taegtmeyer H. Glucose-insulin-potassium in acute myocardial infarction: the time has come for a large, prospective trial. Circulation. 1997; 96: 1074–1077.
10. Apstein CS. Glucose-insulin-potassium for acute myocardial infarction: remarkable results from a new prospective, randomized trial. Circulation. 1998; 98: 2223–2226.
11. Apstein CS, Opie LH. Glucose-insulin-potassium (GIK) for acute myocardial infarction: a negative study with a positive value. Cardiovasc Drugs Ther. 1999; 13: 185–189.[CrossRef][Medline] [Order article via Infotrieve]
12. Cave AC, Ingwall JS, Friedrich J, Liao R, Saupe KW, Apstein CS. ATP synthesis during low-flow ischemia: influence of increased glycolytic substrate. Circulation. 2000; 101: 2090–2096.
13. Lazar HL, Chipkin S, Philippides G, Bao Y, Apstein CS. Glucose-insulin-potassium solutions improve outcomes in diabetics who have coronary artery operations. Ann Thorac Surg. 2000; 70: 145–150.
14. Saupe KW, Eberli FR, Ingwall JS, Apstein CS. Metabolic support as an adjunct to inotropic support in the hypoperfused heart. J Mol Cell Cardiol. 2001; 33: 261–269.[CrossRef][Medline] [Order article via Infotrieve]
15. Varma N, Eberli FR, Apstein CS. Left ventricular diastolic dysfunction during demand ischemia: rigor underlies increased stiffness without calcium-mediated tension. Amelioration by glycolytic substrate. J Am Coll Cardiol. 2001; 37: 2144–2153.
16. IMMEDIATE Trial website. Available at: http://www.immediatetrial.com. Accessed July 31, 2006.
17. Apstein CS. The benefits of glucose-insulin-potassium for acute myocardial infarction (and some concerns). J Am Coll Cardiol. 2003; 42: 792–795.
18. Apstein CS. Glucose-insulin-potassium infusion and mortality in the CREATE- ECLA trial. JAMA. 2005; 293: 2596–2597.
19. Apstein CS, Opie LH A challenge to the metabolic approach to myocardial ischaemia. Eur Heart J. 2005; 26: 956–959.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||