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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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Journal ArticleDOI

Is It All in the Genes… ? Nitric Oxide Synthase and Coronary Vasospasm

Thomas F. Lüscher, +1 more
- 08 Jun 1999 - 
TL;DR: Almost 100 years after the introduction of nitroglycerin in the treatment of angina pectoris, the endogenous nitrate was discovered, which, like its pharmacological counterpart, stimulated cGMP in vascular smooth muscle to cause vasodilatation.
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CRP and CD14 polymorphisms correlate with coronary plaque volume in patients with coronary artery disease--IVUS substudy of the ENCORE trials.

Matthias Hermann, +7 more
- 01 Jan 2012 - 
TL;DR: In patients with stable coronary artery disease the CRP 1444TT and CD14 260TT variants are associated with larger coronary plaque volume independently of concomitant cardiovascular risk factors.
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Multi-Omics Approaches to Define Calcific Aortic Valve Disease Pathogenesis

Mark C. Blaser, +4 more
- 30 Apr 2021 - 
TL;DR: In this paper, the authors summarize the application of (epi)genomics, transcriptomics, proteomics, and metabolomics to the study of valvular heart disease and discuss systems biology-and network medicine-based strategies to extract meaning, mechanisms, and prioritized drug targets from multiomics datasets.
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Endogenous estrogens increase postischemic hyperemia in the skin microcirculation.

Vesna Stojanovic, +7 more
- 01 May 2005 - 
TL;DR: It is shown that endogenous estrogens enhance the postischemic hyperemic response of the skin microcirculation in women involved in an in-vitro fertilization program.
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High-density lipoprotein from patients with coronary heart disease loses anti-thrombotic effects on endothelial cells: impact on arterial thrombus formation

Erik W. Holy, +8 more
- 24 Jul 2014 - 
TL;DR: High-density lipoprotein from patients with stable coronary heart disease and acute coronary syndrome loses the ability of healthy HDL to suppress TF and to increase TFPI and t-PA and instead enhances PAI-1 and arterial thrombus formation.