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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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Differential effects of endothelin-1 on normal and postischemic reperfused myocardium.

TL;DR: The effects of ET-1 but not of U-46619 are enhanced in reperfused hearts, which may contribute to the delayed recovery of the postischemic reperfusion myocardium.
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Captopril in various forms of severe therapy-resistant hypertension

TL;DR: The results show that captopril is a potent blood pressure lowering agent in severe and therapy resistant hypertension and the vast majority of patients required concomitant therapy with a diuretic and/or a betablocker.
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Beyond Traditional Risk Factors: Homocysteine and Atherosclerosis

TL;DR: In patients with hyperhomocysteinemia and a high risk for cardiovascular events (i.e. patients with multiple risk factors or established atherosclerotic vascular disease), the dietary intake of folic acid and vitamins B6 and B12 should be optimized.
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Impact of arterial injury on neointimal hyperplasia after implantation of drug-eluting stents in coronary arteries: an intravascular ultrasound study.

TL;DR: Arterial injury does not correlate with the amount of neointimal hyperplasia following DES implantation, and conventionally aggressive DES implantations techniques do not adversely affect long-term outcome with respect to restenosis.
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Lifelong dietary omega-3 fatty acid suppresses thrombotic potential through gut microbiota alteration in aged mice

TL;DR: In this paper, the authors demonstrate that lifelong dietary ALA decreases platelet hyperresponsiveness and thrombus formation in aged mice, which can be attributed to alteration of microbial composition and reduction of its metabolite trimethylamine N-oxide and inflammatory mediators including TNF-α, as well as upregulated production of short-chain fatty acid acetate.