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Cees A. Visser

Researcher at VU University Medical Center

Publications -  165
Citations -  8213

Cees A. Visser is an academic researcher from VU University Medical Center. The author has contributed to research in topics: Myocardial infarction & Heart failure. The author has an hindex of 47, co-authored 165 publications receiving 7885 citations. Previous affiliations of Cees A. Visser include VU University Amsterdam & National Heart Foundation of Australia.

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C-Reactive Protein as a Cardiovascular Risk Factor More Than an Epiphenomenon?

TL;DR: It is hypothesized that CRP may directly interact with atherosclerotic vessels or ischemic myocardium by activation of the complement system, thereby promoting inflammation and thrombosis and may provide new directions for prevention of cardiovascular events.
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Atrial Septal Aneurysm in Adult Patients A Multicenter Study Using Transthoracic and Transesophageal Echocardiography

TL;DR: In this retrospective study, patients with ASA (especially with shunts) showed a high frequency of previous clinical events compatible with cardiogenic embolism; in a significant subgroup of patients, ASA appears to be the only source of emblism, as judged by TEE.
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Microbubbles and ultrasound: from diagnosis to therapy

TL;DR: The recent advances of microbubbles as a vehicle for delivery of drugs and genes, and possible therapeutic applications in thrombolysis are reviewed and discussed.
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C-Reactive Protein Colocalizes With Complement in Human Hearts During Acute Myocardial Infarction

TL;DR: It is concluded that in humans, CRP may localize in infarcted heart tissue and suggest that this acute-phase protein promotes local complement activation, and hence tissue damage, in acute myocardial infarction.
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Standardizing the Definition of Hyperenhancement in the Quantitative Assessment of Infarct Size and Myocardial Viability Using Delayed Contrast-Enhanced CMR

TL;DR: Analyzing ceCMR with a standardized definition of hyperenhancement related to the signal of remote, nonenhanced myocardium may result in considerable overestimation of infarct size at the usual cut-off of 2 SD.