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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.

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Haemodynamic alterations induced by isoprenaline in patients with obstruction to right ventricular outflow.

TL;DR: The infusion of isoprenaline (isoproterenol), a drug that exerts a powerful stimulating action on the contractile state of the myocardium, either intensifies or provokes obstruction to left ventricular outflow in patients with IHSS, and measurement of the heemodynamic response to this drug provides a useful test for detecting dynamic obstruction.
Journal Article

Rivaroxaban in Patients Stabilized after a ST-Elevation Myocardial Infarction: Results from the ATLAS ACS 2-TIMI 51 Trial.

TL;DR: In patients with a recent STEMI, rivaroxaban reduced cardiovascular events early and persisted during continued treatment with background antiplatelet therapies, as well as in analyses that included events while on background anti Platelet therapies.
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Role of reflex sympathetic withdrawal in the hemodynamic response to an increased inotropic state in patients with severe heart failure.

TL;DR: In 16 patients with severe heart failure, a 48 hour intravenous infusion of milrinone, a positive inotropic vasodilator drug, resulted in an increase in stroke volume index, which was associated with a reduction in plasma norepinephrine, and a withdrawal of sympathetic tone contributed to this vasodilation.
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Recent trials of lipid lowering

TL;DR: A narrative review summarises the key recent clinical trials of lipid lowering since 2004 and their implications for future patient care.
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Mechanochemistry of cardiac muscle. IV. Utilization of high-energy phosphates in experimental heart failure in cats.

TL;DR: It is concluded that in this form of experimentally produced heart failure the utilization of ∼P is reduced but only in relation to the reduction in contractile element work and that the direct conversion of chemical energy to mechanical work is not an inefficient process in this state.