Cardiac β1-adrenoceptor expression in two stress-induced cardiomyopathy-related deaths.

Stress-induced cardiomyopathy (SICM) is characterized by transient systolic dysfunction of the apical and/or midventricular myocardial segments in the absence of obstructive coronary artery disease and is unique in that it can manifest itself after acute emotional stress. Excessive amounts of catecholamines released from sympathetic nerve endings as well as from the adrenal medulla under stressful conditions are considered to produce intracellular Ca(2+) overload and cardiac dysfunction through the β(1)-adrenoceptor signal transduction pathway. We describe the clinical and pathomorphological findings in two stress-induced cardiomyopathy fatal cases. Levels of catecholamines and their metabolites in urine samples were assessed too. Morphological patterns seen in SICM result from the complex interplay between sympathetic innervations, β-receptor density and function and catecholamine sensitivity.