E
Eugene Braunwald
Researcher at Brigham and Women's Hospital
Publications - 1758
Citations - 278949
Eugene Braunwald is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Myocardial infarction & TIMI. The author has an hindex of 230, co-authored 1711 publications receiving 264576 citations. Previous affiliations of Eugene Braunwald include Boston University & University of California, San Francisco.
Papers
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Journal ArticleDOI
Clinical Application of High-Sensitivity Troponin Testing in the Atherosclerotic Cardiovascular Disease Framework of the Current Cholesterol Guidelines.
Nicholas A Marston,Marc P. Bonaca,Petr Jarolim,Erica L. Goodrich,Deepak L. Bhatt,Philippe Gabriel Steg,Marc Cohen,Robert F. Storey,Per Johanson,Stephen D. Wiviott,Eugene Braunwald,Marc S. Sabatine,David A. Morrow +12 more
TL;DR: The findings of this cohort substudy suggest that a strategy incorporating hsTn into a guideline-derived ASCVD risk algorithm provides enhanced risk stratification and reclassifies 11.9% of patients into a more appropriate risk group.
Journal Article
Unstable angina and non-ST-segment elevation myocardial infarction: part I. Initial evaluation and management, and hospital care.
TL;DR: Management of suspected UA/NSTEMI has four components: initial evaluation and management; hospital care; coronary revascularization; and hospital discharge and post-hospital care.
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A new, noninvasive technique for inducing post-extrasystolic potentiation during echocardiography.
Peter F. Cohn,Gerald H. Angoff,Paul M. Zoll,Laurence J. Sloss,John E. Markis,Thomas B. Graboys,L H Green,Eugene Braunwald +7 more
TL;DR: This technique can safely and reliably induce post-extrasystolic potentiation during echocardiography and is a potentially important adjunct to the noninvasive evaluation of left ventricular function.
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Effects of Frequency of Contraction and lonic Environment on the Responses of Heart Muscle to Acetylcholine
TL;DR: A dual action of ACh on the myocardium is interpreted in terms of an action on the muscarinic receptor that reduces contractility and may be blocked with atropine, and a direct effect on cellular membrane permeability to Ca2+ that stimulates contractilityand may be reduced by prior elevation of intracytoplasmic [Ca2+].
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Evidence-Based Coronary Care
TL;DR: Patients enjoyed the benefit of a halving of the in-hospital mortality rate for acute myocardial infarction but remained susceptible to the late consequences of large infarctions: heart failure and malignant ventricular arrhythmias.