%A Guski, Hans %A Kogan, Evgenya A. %A Shvalev, Vadim N. %D 2019 %T Etiology and Pathogenesis of Sudden Cardiac Death %K %X Background and definition : This article contributes to the current state of knowledge in etiology and pathogenesis of sudden cardiac death (SCD). SCD is a well - defined disease entity which recently approved international guidelines address (cardiac death within 1 hour). Etiology: The condition of coronary arteries contributes to common causes of SCD. Stenotic coronary artery sclerosis (80%) has been reported in most cases. In non-coronary causes (15%), cardiomyopathies (CMP) are frequently found, and alcoholic CMP dominates the CMP cohort. Genetically related causes are comparatively rare (5%). Pathogenesis: In pathogenesis, only the consecutives of coronary ischemia have been extensively studied, in contrast to non-coronary causes. Herein, only some (mostly infectious) forms of myocarditis have been investigated in detail. The pathogenesis of different causes of SCD is less well studied. These include pathologic changes of adrenergic and cholinergic heart nerves, of intra- and extra-cardiac ganglia and of the conduction system. Morphological changes that clearly explain SCD are still difficult to reproducibly detect in clinical-pathologic and forensic autopsy diagnosis because these lesions might morphologically at first manifest after 1 hour or even later. This statement holds particularly true for detecting early ischemic heart muscle cell deaths being the most common cause of SCD Conclusions: The reported methods and special staining have proven to be less suitable for routine diagnostics. Attempts are now undergoing to solve the problem by the use of specific antibodies. They provide evidence of immunoreactivity of ischemic damaged cardiomyocytes which can be detected even after prolonged postmortem lay times. %U https://www.diagnosticpathology.eu/content/index.php/dpath/article/view/275 %J Diagnostic Pathology %0 Journal Article %R 10.17629/www.diagnosticpathology.eu-2019-5:275 %V 5 %N 1 %@ 2364-4893 %8 2019-07-04