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The possibility that acute stroke produces an increase in sympathetic tone with resultant cardiac abnormalities was examined in 100 stroke patients admitted to a stroke ICU and in 50 controls found to have diagnoses other than stroke or TIA after admission to the Unit. Continuous 24 hour Holter ECG tapings were performed and serum cardiac enzymes and plasma norepinephrine concentrations were measured within 48 hours after admission. Significantly, (p less than .001) more serious arrhythmias were observed during 24 hour Holter ECG monitoring in stroke patients compared with controls and the difference remained (p less than .01) after matching for age and co-existing heart disease. Arrhythmias were more common in older stroke (p less than .001) and older control (p = .05) patients and with infarction of the cerebral hemispheres (p less than .05) as compared to brainstem lesions. Arrhythmia occurrence was independent of the presence of co-existing heart disease and the level of sympathetic activity. However, the 15 stroke patients with abnormally high CK values (mean 34.3 units) had a higher (p less than .02) mean plasma norepinephrine concentration (650.4 pg/ml) than stroke patients with normal CK (427.7 pg/ml). Acute stroke may cause cardiac arrhythmias and myocardial cell damage, the latter through stroke induced increases in sympathetic tone.

Cardiac arrhythmias, myocardial necrosis and ECG abnormalities in stroke may result from abnormally high levels of sympathetic activity. To examine this possibility, plasma norepinephrine, epinephrine and dopamine were measured in 74 patients with cerebral infarction, 18 with transient ischemic attacks and 33 non-stroke controls. Mean norepinephrine, epinephrine and dopamine values (pg/ml) in cerebral infarction (433.2, 81.6, 75.6 were higher (p less than 0.01) than in controls (281.1, 60.1, 40.5, respectively). Transient ischemic attacks produced values intermediate to these two groups (391.3, 80.9, 54.9). The elevated catecholamine concentrations in cerebral infarction could not be explained by differences in age, blood pressure, heart rate, stress, type or severity of stroke. The high plasma norepinephrine in the stroke group is consistent with an increase in peripheral sympathetic activity which could produce the cardiac abnormalities of cerebral infarction.

Serum cardiac enzyme levels (CK, LDH, SGOT) were estimated and the ECG recorded for 4 days following admission of 288 patients (Group I) to a stroke intensive care unit. Sixty-four of these patients, subsequently found not to have strokes, served as controls. Mean serum levels of all 3 cardiac enzymes were elevated in 8% of the 224 patients with stroke. The mean serum enzyme levels in patients with transient ischemic attacks (TIA) did not differ from controls. In a second group of 230 patients with stroke (Group II) serum CK levels were measured and the isoenzyems were fractionated to determine the tissue source of the enzymes. One hundred and one patients had raised total CK values and 25 of these (11%) had raised CK-MB (heart) iso-enzyme, the remainder having CK-MM (skeletal muscle) fraction. No serum CK-BB (brain) iso-enzyme was detected in any patient. Patients with positive serum levels of CK-MB has more evidence of acute myocardial ischemia on ECG (p less than 0.05), and more cardiac arrhythmias (p less than 0.001) than those with normal CK levels. Scattered areas of myocytolysis were found in the myocardium at autopsy in one patient. The acute rise in serum cardiac enzymes which we have recorded in the initial stages of stroke suggest that acute myocardial involvement is a commoner complication than is generally recognized. Also, since the CK-MB rises were modest and progressive, it is more likely that this acute myocardial dysfunction is a consequence, rather than a cause, of the acute cerebrovascular lesion.