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Guillermo Torre-Amione

Researcher at Baylor College of Medicine

Publications -  121
Citations -  8177

Guillermo Torre-Amione is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Heart failure & Transplantation. The author has an hindex of 41, co-authored 110 publications receiving 7843 citations. Previous affiliations of Guillermo Torre-Amione include Houston Methodist Hospital.

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New therapeutics for chronic heart failure.

TL;DR: The rationale for existing heart failure therapies is reviewed and the reasoning behind the development of some emerging therapies is discussed, in which heart failure progresses because of the toxic effects of endogenous biological systems that become activated in heart failure.
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Decreased Expression of Tumor Necrosis Factor-α and Regression of Hypertrophy After Nonsurgical Septal Reduction Therapy for Patients With Hypertrophic Obstructive Cardiomyopathy

TL;DR: The initial experimental evidence is provided to suggest that TNF-&agr; may play a pathogenetic role in the hypertrophy of pressure overload in HOCM patients.
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The implications for cardiac recovery of left ventricular assist device support on myocardial collagen content

TL;DR: It is demonstrated that chronic mechanical circulatory support significantly reduces fibrosis in the failing myocardium and regional collagen expression of an explanted heart.
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The hemodynamic and neurohormonal effects of low doses of tezosentan (an endothelin A/B receptor antagonist) in patients with acute heart failure

TL;DR: In previous studies, tezosentan, an intravenous (i.v.)‐balanced dual endothelin (ET‐A/B) antagonist, in doses of 50 and 100 mg/h, improved the hemodynamics but not the clinical outcome of patients with acute heart failure (AHF).
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Cardiac Hypertrophy After Transplantation Is Associated With Persistent Expression of Tumor Necrosis Factor-α

TL;DR: It is suggested that the contribution of hypertension to cardiac allograft hypertrophy is minimal and that persistent intracardiac expression of TNF-α may contribute to the development of cardiacAllografthypertrophy.