Electrocardiographic changes associated with acute cerebrovascular disease: a clinical review.

Patients with acute vascular disorders of the CNS demonstrate an abundance of both rhythm and morphologic changes in their ECG. Of these a few will demonstrate myocardial dysfunction and or damage. The value of the ECG in evaluating and predicting which patients will have myocardial dysfunction or damage is questionable. One would assume the echocardiogram would be of more help than the ECG in identifying patients with myocardial damage; however, little data are available. The reason for the poor correlation between ECG findings and clinical correlates has not been explained to date, but it is possible to postulate a theory. There are two mechanisms that might mediate ECG changes in these patients, ie, autonomic neural stimulation from the hypothalamus or elevated circulating catecholamines. Hypothalamic stimulation may cause ECG changes without associated myocardial damage whereas elevated catecholamines may result in myocardial damage. This might explain why so many patients have ECG changes and very few have demonstrable myocardial damage in general, or ischemic damage in particular. That cardiac antiischemic therapy does not change mortality may relate to the fact that treatment has been directed towards patients with ECG changes, which in turn do not correlate with myocardial damage. Better patient selection for such therapy might rest upon demonstration of wall motion abnormalities on echocardiogram. The weakness of this strategy is that many patients with stroke have preexisting coronary disease and wall motion abnormalities and thus echo findings may only document remote infarction rather than acute ischemia.