T
Thomas F. Lüscher
Researcher at University of Zurich
Publications - 1613
Citations - 88517
Thomas F. Lüscher is an academic researcher from University of Zurich. The author has contributed to research in topics: Endothelium & Myocardial infarction. The author has an hindex of 134, co-authored 1560 publications receiving 79034 citations. Previous affiliations of Thomas F. Lüscher include University of Texas Southwestern Medical Center & Durham University.
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The classification of calcium antagonists and their selection in the treatment of hypertension. A reappraisal.
TL;DR: This article reviews and updates a 3-generation classification of calcium antagonists currently, or soon to be, marketed in several counties, based on chemical structure, tissue selectivity, administration frequency and duration of action, and concludes that third generation calcium antagonists possess distinct advantages.
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I1-Imidazoline Agonist Moxonidine Decreases Sympathetic Nerve Activity and Blood Pressure in Hypertensives
TL;DR: Moxonidine decreases systolic and diastolic blood pressure by inhibiting central nervous sympathetic activity, which makes this new drug suitable for the treatment of human hypertension and possibly for other cardiovascular diseases with increased sympathetic nerve activity, ie, ischemic heart disease and heart failure.
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Vascular protective effects of angiotensin converting enzyme inhibitors and their relation to clinical events.
TL;DR: ACE inhibitors are an important class of drugs providing cardiovascular protection in patients with increased cardiovascular risk, as they inhibit the circulating and local renin angiotensin system.
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PARP1 is required for adhesion molecule expression in atherogenesis
Tobias von Lukowicz,Paul O. Hassa,Christine Lohmann,Jan Borén,Vincent Braunersreuther,François Mach,Bernhard Odermatt,Monika Gersbach,Giovanni G. Camici,Barbara E. Stähli,Felix C. Tanner,Michael O. Hottiger,Thomas F. Lüscher,Christian M. Matter +13 more
TL;DR: Evidence is provided that endogenous PARP1 is required for atherogenesis in vivo by increasing adhesion molecules with endothelial activation, enhancing inflammation, and inducing features of plaque vulnerability, and inhibition of PARP 1 may represent a promising therapeutic target in atherosclerosis.
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Age-related changes in vascular smooth muscle and endothelium.
TL;DR: The alterations of vascular smooth muscle and endothelial cells occurring with age may have important clinical implications for the pathogenesis of cardiovascular disease.