Cardiac effects of stroke

Opinion statement

Our brain regulates all bodily functions either directly or indirectly, and cardiovascular control is no exception. There is strong clinical evidence of cerebrogenic cardiac arrhythmias and myocardial changes during ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage. Alternative scenarios include cardioembolic stroke, multisystem diseases with stroke-like and cardiac features, and coincidental detection of cardiac disorders in a stroke patient. Cardiac effects of stroke may be severe or even fatal and worsen the prognosis. Clinical and experimental studies suggest that cortical and subcortical structures such as the insular cortex and amygdala play a pathogenic role. The peripheral mechanisms involve abnormal sympathetic activity, altered parasympathetic activity, and raised levels of circulating catecholamines, whereas the central mechanisms are largely unknown. Because stroke patients are best managed in an acute stroke unit during their initial presentation, a cardiocerebral approach is desirable with close cardiovascular and neurologic monitoring. Prolonged and intensive cardiovascular monitoring is recommended in patients manifesting cerebrogenic cardiovascular disturbances and in high-risk patients with insular involvement, rightsided stroke, advancing age, coexisting hypertensive or coronary artery disease, or intense emotional stress. Although the best management is largely unknown, treatment of cardiac effects of stroke is largely supportive according to the type of disturbance. Severely affected patients should be evaluated by a cardiologist prior to the initiation of appropriate therapy. Much more clinical and basic research is needed to allow a full understanding of the brain-heart control, the consequences of disruption of this control, the true incidence of cardiac effects of stroke, and the evidence-based treatment options.