Neurogenic cardiac effects of cerebrovascular disease

Abstract

The electrocardiogram changes and cardiac arrhythmias frequently encountered after stroke are not solely explicable by concomitant ischemic cardiac disease. Excessive sympathoadrenal tone is contributory. Specifically, it is now believed that augmentation of intracardiac sympathetic nerve activity occurs, producing cardiac myocyte damage and depolarizing ionic shifts, resulting in electrocardiogram repolarization changes and arrhythmogenesis. Experimental and clinical evidence now implicates the insular cortex and its subcortical connections in the generation of cardiac arrhythmias under stress and following hemispheric stroke. Lateralization studies indicate that destruction of areas adjacent to the right insular cortex, or involving noncardioactive zones within this region have especially marked cardiac effects. This very likely contributes to the cardiac mortality which is the principle long-term cause of death in stroke patients.