Working Group Heinzel
Cellular Mechanisms and Clinical Early Detection of Heart Failure and Arrhythmias
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Heart failure is a common disease with high morbidity and mortality and severe impact on quality of life in affected patients. Heart failure is also associated with an increased incidence of relevant arrhythmias predisposing to stroke and sudden cardiac death. The prevalence of heart failure is steadily increasing. Heart failure is preceded by functional and structural changes in the heart ("remodeling") which are driven by common co-morbidities, such as hypertension, diabetes or renal dysfunction. Despite advances in symptomatic treatment there is currently no causal medical therapy for this progressive disease.
Our goals are to explore underlying pathomechanisms in order to identify and manage patients at risk and establish potential new therapeutic targets for optimal medical therapy (OMT). Our research work relates to myocardial remodeling, contractile dysfunction and associated arrhythmias.
In experimental studies, we investigate pathomechanisms that promote contractile dysfunction, cellular arrhythmias and (hypertrophic) remodeling of ventricular and atrial cardiomyocytes. In particular, we focus on Ca2+- and Na+-mediated signaling pathways and their diversification through functional and structural cellular compartmentation. Using clinically relevant models as well as functional measurements in human myocardial samples we aim at early translation of potential new targets. [more]
In the clinical setting, our group aims to implement new strategies to identify patients at risk for developing incidental heart failure and arrhythmias, i.e. at an early stage. We combine clinical risk scores, imaging and biomarkers to improve risk assessment and management. We investigate how co-morbidites such as renal impairment influence cardiac remodeling and vice versa, also guided by insights from our experimental work.[more]