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Thomas M. Schiele

Researcher at Ludwig Maximilian University of Munich

Publications -  63
Citations -  1511

Thomas M. Schiele is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Restenosis & Stent. The author has an hindex of 19, co-authored 63 publications receiving 1452 citations.

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NAD(P)H oxidase-dependent platelet superoxide anion release increases platelet recruitment.

TL;DR: It is strongly suggested that collagen activation induces NAD(P)H oxidase-dependent O release in platelets, which in turn enhances availability of released ADP, resulting in increased platelet recruitment.
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Cardiac magnetic resonance perfusion imaging for the functional assessment of coronary artery disease: a comparison with coronary angiography and fractional flow reserve.

TL;DR: This study compared CMRI with CA plus a standard invasive functional assessment (FFR) and demonstrated that CMRI is able to distinguish haemodynamically relevant from non-relevant coronary lesions with a high sensitivity and specificity and may contribute to clinical decision-making.
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Are high doses of intracoronary adenosine an alternative to standard intravenous adenosine for the assessment of fractional flow reserve

TL;DR: This study suggests a dose-response relationship on hyperemia for intracoronary adenosine doses >60 microg and should be the preferred mode of application for the assessment of FFR.
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Diagnostic accuracy of optical coherence tomography and intravascular ultrasound for the detection and characterization of atherosclerotic plaque composition in ex-vivo coronary specimens: A comparison with histology

TL;DR: Optical coherence tomography is superior to intravascular ultrasound for the detection and characterization of coronary atherosclerotic plaque composition, specifically for the differentiation of noncalcified, lipid-rich, or fibrous plaque.
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Selective COX-2 inhibitors and risk of myocardial infarction.

TL;DR: The rationale for the development of selective COX-2 inhibitors and the pathophysiological consequences of selective inhibition of COx-2 with special regard to vasoactive prostaglandins are outlined and the consequences that should be drawn are critically discussed.