OMEGA-3-FORUM

The major pathophysiological cause of SCD is seen in the electrical instability of the infarct zone and the non infarcted muscle. Because of the loss of contractile tissue, the surviving hypertrophied myocardium is subjected to various adverse neuroendocrine influences. A consequence is an unfavorable cellular and molecular restructuring of the extracellular matrix and the cardiomyocyte. The fibrosis also worsens coronary blood supply and thus amplifies the risk of reinfarction. In approximately one third of post-MI patients, dilatation of the left ventricle occurs. Since dilated hearts exhibit an increased wall stress favouring also the opening of stretch-activated ion channels (1), the resulting electrical instability contributes to the increased risk of ventricular tachyarrhythmias. All these adverse processes contribute to worsening of pump function which is reflected in a reduced EF which is the most often used predictor of malignant arrhythmias. Conventional therapy is, however,..

Primary location: Marburg Germany