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Paulus Kirchhof

Researcher at University of Birmingham

Publications -  659
Citations -  119822

Paulus Kirchhof is an academic researcher from University of Birmingham. The author has contributed to research in topics: Atrial fibrillation & Medicine. The author has an hindex of 100, co-authored 558 publications receiving 106459 citations. Previous affiliations of Paulus Kirchhof include United States Department of Veterans Affairs & Georgetown University Medical Center.

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Detection of unknown atrial fibrillation by prolonged ECG monitoring in an all-comer patient cohort and association with clinical and Holter variables

TL;DR: Open multispeciality access to prolonged ECG monitoring, for example, as part of integrated, cross-sector AF care, can accelerate diagnosis of AF and increase adequate use of oral anticoagulation, especially in older and symptomatic patients with comorbidities.
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Perceived vs. objective frailty in patients with atrial fibrillation and impact on anticoagulant dosing: an ETNA-AF-Europe sub-analysis

TL;DR: Physicians’ perception of frailty in AF patients is variable, mainly driven by age, sex, and weight, and quite different compared with the results of an objective frailty assessment, Whatever the approach, frailty appears to be associated with non-recommended anticoagulant dosages.
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Almanac 2015: atrial fibrillation research in Heart

TL;DR: An overview of articles on atrial fibrillation published in Heart in 2014–2015 is provided, highlighting new developments, emerging concepts and novel approaches to treatment.
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Drugs that interact with cardiac electro-mechanics: Old and new targets for treatment

TL;DR: Several recently identified regulatory mechanisms may provide novel antiarrhythmic targets associated with the "intermediate" response of the myocardium to stretch, which is a continuum from short-term to long-term effects.
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Cytokine-Mediated Alterations of Human Cardiac Fibroblast’s Secretome

TL;DR: In this paper, the secretome and corresponding transcriptome of human cardiac fibroblasts from patients with dilated cardiomyopathy was investigated under normal conditions and after TNF-α or TGF-β stimulation.