Article

Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage: A meta-analysis

Academic Medical Centre, Department of Cardiology, PO Box 22660, 1100 DD Amsterdam, The Netherlands.
Neurology (Impact Factor: 8.29). 02/2009; 72(7):635-42. DOI: 10.1212/01.wnl.0000342471.07290.07
Source: PubMed

ABSTRACT

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.
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 < or = 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.
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.
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.

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    • "Specific cardiopulmonary complications associated with mortality included hypotension of less than 90 mm Hg treated with pressors (which affected 24 % overall), congestive heart failure (8 %), and nonneurogenic myocardial ischemia (7 %), which was defined as acute or delayed troponin elevation possibly or probably due to coronary ischemia. The association of troponin elevation with stunned myocardium, hypotension, pulmonary edema, and poor outcome after SAH is well described [11, 33, 34] and supports multimodality monitoring data implicating hypoxia and hypotension as important causes of secondary brain injury [35]. A robust association between vasospasm and in-hospital mortality is notably absent in the present study. "

    Full-text · Dataset · Feb 2016
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    • "Elevations in serum cardiac enzymes, including creatine kinase, MB isoenzyme (CK-MB), and cTnI, were elevated following SAH [79, 80]. Previous studies have shown that 17 to 28% of SAH patients develop elevated serum levels of cTnI [81, 82]. "
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    ABSTRACT: Subarachnoid hemorrhage (SAH) is a devastating neurological disorder. Patients with aneurysmal SAH develop secondary complications that are important causes of morbidity and mortality. Aside from secondary neurological injuries, SAH has been associated with nonneurologic medical complications, such as neurocardiogenic injury, neurogenic pulmonary edema, hyperglycemia, and electrolyte imbalance, of which cardiac and pulmonary complications are most common. The related mechanisms include activation of the sympathetic nervous system, release of catecholamines and other hormones, and inflammatory responses. Extracerebral complications are directly related to the severity of SAH-induced brain injury and indicate the clinical outcome in patients. This review provides an overview of the extracerebral complications after SAH. We also aim to describe the manifestations, underlying mechanisms, and the effects of those extracerebral complications on outcome following SAH.
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    • "In clinical studies, in SAH patients, chances of ECG, high cardiac markers [1,7,15,25], wall motion abnormalities [7,25] were noted. Szabo et al. investigated myocardial perfusion with myocardial scintigraphy. "
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