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Electrocardiographic markers of abnormal left ventricular wall motion in acute subarachnoid hemorrhage
S A Mayer1, G LiMandri, D Sherman
1Department of Neurology Critical Care Neurology, Columbia University, College of Physicians and Surgeons, New York, New York, USA.
Insights
Subarachnoid hemorrhage (SAH) can cause myocardial dysfunction. Symmetrical T wave inversion and prolonged QTc segments on ECGs may indicate this risk in SAH patients.
Area of Science:
- Cardiology
- Neurology
- Critical Care Medicine
Background:
- Subarachnoid hemorrhage (SAH) is associated with neurogenic myocardial dysfunction.
- The link between electrocardiographic (ECG) abnormalities and left ventricular dysfunction post-SAH is not fully understood.
Purpose of the Study:
- To identify specific ECG changes correlating with abnormal left ventricular wall motion in acute SAH patients.
- To assess the diagnostic value of ECG findings for predicting myocardial dysfunction after SAH.
Main Methods:
- Serial ECGs and echocardiograms were performed on 57 SAH patients without prior cardiac disease.
- Correlation analysis was conducted between ECG findings (T wave inversion, QTc prolongation) and echocardiographic wall motion abnormalities.
Main Results:
- Eight percent of SAH patients showed wall motion abnormalities, often accompanied by hypotension and pulmonary edema.
- Symmetrical T wave inversion and severe QTc prolongation on ECGs were significantly associated with abnormal wall motion.
- ECG findings of T wave inversion or QTc prolongation demonstrated high sensitivity for identifying patients at risk.
Conclusions:
- ECG repolarization abnormalities, specifically T wave inversion and QTc prolongation, are linked to myocardial dysfunction in acute SAH.
- These ECG markers can aid in identifying SAH patients requiring further echocardiographic screening for cardiac complications.
Abstract:
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.