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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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Is takotsubo syndrome a microvascular acute coronary syndrome? Towards of a new definition

TL;DR: The diagnosis of ACS relies on typical symptoms of ischaemia (chest pain) and typical ECG changes and/or elevated levels of cardiac troponins or other biomarkers of myocardial necrosis.
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Thrombin-induced endothelium-dependent inhibition and direct activation of platelet-vessel wall interaction. Role of prostacyclin, nitric oxide, and thromboxane A2.

TL;DR: In arteries devoid of functional endothelial cells, as occurs in patients with coronary artery disease, a combined inhibition of thromboxane production and action provides a potent therapeutic tool to interfere with the thrombin-induced activation of platelet-vessel wall interaction.
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Endothelium-independent relaxation and hyperpolarization to C-type natriuretic peptide in porcine coronary arteries.

TL;DR: In conclusion, in contrast to bradykinin, CNP induces endothelium-independent and weaker relaxation and hyperpolarization of coronary artery vascular smooth muscle, suggesting that CNP is an unlikely mediator of endothelia-dependent hyperpolarsization of porcine coronary arteries.
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Cardiac CT and echocardiographic evaluation of peri‐device flow after percutaneous left atrial appendage closure using the AMPLATZER cardiac plug device

TL;DR: The aim of the study was to examine frequency, size, and localization of peri‐device leaks after percutaneous left atrial appendage‐closure with the AMPLATZER‐Cardiac‐Plug by using a multimodal imaging approach, i.e. combined cardiac‐CT and TEE follow‐up.
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Pharmacological Mechanisms of Clinically Favorable Properties of a Selective β1‐Adrenoceptor Antagonist, Nebivolol

TL;DR: The antioxidant property of nebivolol can at least in part explain why treatment with this drug enhances eNOS activity and minimizes the reperfusion-induced myocardial injury and make nebivlol a promising therapeutic tool for the treatment of arterial hypertension and chronic heart failure.