Page 50 - Cardiac abnormalities after aneurysmal subarachnoid hemorrhage

Chapter 3
NT-proBNP is therefore probably explained by the secretion of NT-proBNP by the cardiac ventricles in response to increased wall stress of the myocardium when WMAs occur after aSAH. This is supported by the finding that NT-proBNP levels in stress cardiomyopathy or TTC are elevated and correlate with catecholamine increase and severity of LV dysfunction.16 Other studies also found an elevated NT-proBNP in patients with SAH.17-20 However, these studies had relatively small sample size, used different cut-off values for elevated NT-proBNP, or had not defined outcome. The cause of cardiac abnormalities after SAH cannot be answered by the present study. The generally accepted pathway is that due to massive sympathetic activation a catecholamine burst causes myocardial dysfunction by epicardial spasm, microvascular dysfunction, hyperdynamic contractility with midventricular or outflow tract obstruction, or that it is caused by direct effects of catecholamines on cardiomyocytes.21 Myocardial ischemia is an unlikely cause of the dysfunction as myocardial perfusion was reported to be normal.22
Although in the univariable analysis several ST-segment changes were associated with outcome, none of the ECG parameters predicted outcome in the multivariable analyses. Possibly, ST-segment changes in aSAH are caused by changes in wall stress due to catecholaminergic stress after the aSAH. Another likely explanation is that ECG abnormalities, Troponin and NT-proBNP elevation, together with WMAs represent the same phenomenon; cardiac dysfunction after aSAH. Furthermore, we considered only the admission ECG whereas we know from earlier studies that serial ECG changes after SAH occur frequently, and have been linked to outcome.23-25 Earlier studies found similar proportions of patients with WMAs as the present study.26-29 However, these studies did not find a relation between WMAs and outcome, although an association with elevated troponin and outcome was reported.30 In our study all examinations were performed within 96 hours of the aSAH, which was usually not the case in other studies. Also, our study was appropriately powered and had considerable follow-up duration.
We found that the distribution of the WMAs did not correspond with the territory of a single coronary artery, which has been described before in aSAH.31 Some patients showed a diffusely disturbed systolic function and of the patients who had apical wall motion abnormalities, almost all also showed basal hyperdynamic contractility, consistent with a TTC. Although it has widely been accepted that TTC is a benign condition which carries an excellent prognosis32, in our secondary analysis the patients with apical WMAs had more risk of DCI whereas midventricular WMAs were associated with death. This finding might be explained by an impaired cardiac
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