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From the Departments of Cardiology (I.A.C.v.d.B., A.A.M.W.) and Neurosurgery (W.P.V.), Academic Medical Center, Amsterdam; Department of Intensive Care (D.H.), Viecuri, Venlo; Department of Neurology (A.A., G.J.E.R.) and Julius Centre for Patient Oriented Research (A.A.), University Medical Center Utrecht; and Department of Cardiology (F.C.V.), Erasmus Medical Center Rotterdam, The Netherlands.
Address correspondence and reprint requests to Dr. Ivo A.C. van der Bilt, Academic Medical Centre, Department of Cardiology, PO Box 22660, 1100 DD Amsterdam, The Netherlands i.a.vanderbilt{at}amc.uva.nl
Impact of cardiac complications after aneurysmal subarachnoid hemorrhage (SAH) remains controversial. We performed a meta-analysis to assess whether EKG changes, myocardial damage, or echocardiographic wall motion abnormalities (WMAs) are related to death, poor outcome (death or dependency), or delayed cerebral ischemia (DCI) after SAH.
Methods: Articles on cardiac abnormalities after aneurysmal SAH that met predefined criteria and were published between 1960 and 2007 were retrieved. We assessed the quality of reports and extracted data on patient characteristics, cardiac abnormalities, and outcome measurements. Poor outcome was defined as death or dependence by the Glasgow Outcome Scale (dichotomized at 
3) or the modified Rankin scale (dichotomized at >3). If studies used another dichotomy or another outcome scale, we used the numbers of patients with poor outcome provided by the authors. We calculated pooled relative risks (RRs) with corresponding 95% confidence intervals for the relation between cardiac abnormalities and outcome measurements.
Results: We included 25 studies (16 prospective) with a total of 2,690 patients (mean age 53 years; 35% men). Mortality was associated with WMAs (RR 1.9), elevated troponin (RR 2.0) and brain natriuretic peptide (BNP) levels (RR 11.1), tachycardia (RR 3.9), Q waves (RR 2.9), ST-segment depression (RR 2.1), T-wave abnormalities (RR 1.8), and bradycardia (RR 0.6). Poor outcome was associated with elevated troponin (RR 2.3) and creatine kinase MB (CK-MB) levels (RR 2.3) and ST-segment depression (RR 2.4). Occurrence of DCI was associated with WMAs (RR 2.1), elevated troponin (RR 3.2), CK-MB (RR 2.9), and BNP levels (RR 4.5), and ST-segment depression (RR 2.4). All RRs were significant.
Conclusion: Markers for cardiac damage and dysfunction are associated with an increased risk of death, poor outcome, and delayed cerebral ischemia after subarachnoid hemorrhage. Future research should establish whether these cardiac abnormalities are independent prognosticators and should be directed toward pathophysiologic mechanisms and potential treatment options.
Abbreviations: AF = atrial fibrillation; BBB = bundle branch block; BNP = brain natriuretic peptide; CI = confidence interval; CK-MB = creatine kinase MB; DCI = delayed cerebral ischemia; GCS = Glasgow Coma Scale; HR = hazard ratio; LVH = left ventricular hypertrophy; NT-proBNP = N-terminal prohormone brain natriuretic peptide; pt = patient; RR = relative risk; SAH = subarachnoid hemorrhage; STROBE = Strengthening the Reporting of Observational Studies in Epidemiology; WFNS = World Federation of Neurosurgical Societies; WMA = echocardiographic wall motion abnormality.
Supplemental data at www.neurology.org
Disclosure: The authors report no disclosures.
Received July 28, 2008. Accepted in final form November 17, 2008.
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