Electrocardiographic markers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage.
A reversible and presumably neurogenic form of myocardial dysfunction may occur following subarachnoid hemorrhage (SAH), but the relationship of this finding to electrocardiographic abnormalities remains unclear. To clarify this issue, serial electrocardiograms (ECGs, mean 6.2 per patient) and echocardiograms (mean 3.4 days after SAH) were obtained in 57 SAH patients without preexisting cardiac disease. The goal was to determine which specific electrocardiographic changes, if any, reflect abnormal left ventricular wall motion in acute SAH. Wall motion abnormalities were identified in five (8%) of 57 patients. Four of these affected patients experienced hypotension (systolic blood pressure < 100 mm Hg) and three exhibited pulmonary edema within 6 hours of SAH, compared to none of the 52 patients with normal wall motion (p < 0.0001). Patients with abnormal wall motion were more likely than patients with normal echocardiograms to have symmetrical T wave inversion (five of five vs. seven of 52, p < 0.001) and severe (> or = 500 msec) QTc segment prolongation (five of five vs. three of 52, p < 0.001) on serial ECGs. These associations maintained their significance with analysis limited to single ECGs performed on or near the day of echocardiography. Abnormal wall motion was also associated with borderline (2% to 5%) creatine kinase MB elevation (five of five vs. three of 52, p < 0.001) and poor neurological grade (p < 0.0001). Although no combination of findings on a single ECG resulted in 100% sensitivity for abnormal wall motion, the presence of either inverted T waves or severe QTc segment prolongation on serial ECGs was associated with 100% sensitivity and 81% specificity. These results demonstrate an association between reduced left ventricular systolic function, mild creatine kinase MB elevation, and electrocardiographic repolarization abnormalities in acute SAH. Symmetrical T wave inversion and severe QTc segment prolongation best identified patients at risk for myocardial dysfunction and may serve as useful criteria for echocardiographic screening following SAH.
D000208:Acute Disease; D000328:Adult; D003402:Creatine Kinase / Q000378:metabolism; D004452:Echocardiography; D004562:Electrocardiography; D005260:Female; D006801:Humans; D007022:Hypotension / Q000209:etiology; D007527:Isoenzymes; D008875:Middle Aged; D009200:Myocardial Contraction; D011237:Predictive Value of Tests; D011654:Pulmonary Edema / Q000209:etiology; D012680:Sensitivity and Specificity; D013345:Subarachnoid Hemorrhage / Q000150:complications*; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis* / Q000201:enzymology / Q000209:etiology
D007527:Isoenzymes; D003402:Creatine Kinase