• T Kono, H Morita, T Kuroiwa, H Onaka, H Takatsuka, and A Fujiwara.
• Osaka Mishima Critical Care Medical Center, Japan.
• J. Am. Coll. Cardiol. 1994 Sep 1; 24 (3): 636-40.

ObjectivesThe purpose of this study was to determine whether a relation exists between electrocardiographic (ECG) abnormalities and left ventricular wall motion in patients with subarachnoid hemorrhage.BackgroundAlthough ECG changes simulating acute myocardial infarction are frequently seen in patients with subarachnoid hemorrhage, their relation to left ventricular wall motion has not been established.MethodsTwelve patients with subarachnoid hemorrhage were classified according to the presence of ST segment elevation in at least two consecutive leads on admission: seven patients with ST segment elevation (group I) and five patients without ST segment elevation (group II). No patients had a previous history of heart disease. Left ventricular regional wall motion was evaluated by the centerline method. The mean (+/- SEM) duration from onset of subarachnoid hemorrhage to left ventriculography was 9 +/- 3 h in group I and 10 +/- 1 h in group II. Coronary angiography was performed to rule out wall motion abnormalities due to coronary artery disease while the ST segment was still elevated. Two-dimensional echocardiography was used to evaluate wall motion thereafter.ResultsAll patients in group I showed ST segment elevation in ECG leads V4 to V6. Wall motion of the left ventricular apex was significantly reduced in group I compared with group II (-2.48 +/- 0.41 vs. -0.45 +/- 0.72, p < 0.02). No patients showed organic stenosis or vasospasm, or both, of epicardial coronary arteries. Wall motion abnormalities decreased echocardiographically in all patients, but one patient in group I died in hospital at 2 or 3 weeks after the onset of subarachnoid hemorrhage, when the T wave was inverted in leads V4 to V6.ConclusionsThese findings suggest that patients with subarachnoid hemorrhage and ST segment elevation may demonstrate transient corresponding regional wall motion abnormalities. The mechanism of neurogenic stunned myocardium was not clearly elucidated in the present study.

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