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


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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    • "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.
    BioMed Research International 07/2014; 2014:858496. DOI:10.1155/2014/858496 · 1.58 Impact Factor
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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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    ABSTRACT: Cardiac complications are often developed after subarachnoid hemorrhage (SAH) and may cause sudden death of the patient. There are reports in the literature addressing ischemia modified albumin (IMA) as an early and useful marker in the diagnosis of ischemic heart events. The aim of this study is to evaluate serum IMA by using the albumin cobalt binding (ACB) test in the first, second, and seventh days of experimental SAH in rats.Twenty-eight Wistar albino rats were divided into four groups each consisting of seven animals. These were classified as control group, 1st, 2nd and 7th day SAH groups. SAH was done by transclival basilar artery puncture. Blood samples were collected under anesthesia from the left ventricles of the heart using the cardiac puncture method for IMA measurement. Histopathological examinations were performed on the heart and lung tissues. Albumin with by colorimetric, creatine kinase (CK), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) were determined on an automatic analyser using the enzymatic method. IMA using by ACB test was detected with spectrophotometer. Serum IMA (p = 0.044) in seventh day of SAH were higher compared to the control group. Total injury scores of heart and lung tissue, also myocytolysis at day 7 were significantly higher than control group (p = 0.001, p = 0.001, p = 0.001), day 1 (p = 0.001, p = 0.001, p = 0.001) and day 2 (p = 0.001, p = 0.007, p = 0.001). A positive correlation between IMA - myocytolysis (r = 0.48, p = 0.008), and between IMA - heart tissue total injury score (r = 0.41, p = 0.029) was found. The results revealed that increased serum IMA may be related to myocardial stress after SAH.
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    ABSTRACT: M ReviewArticle easurements of cardiac troponin concentrations are at present universally accepted and recom-mended as the ็ gold standard็ biochemical me-thods for diagnosis of acute myocardial infarction (AMI) in patients presenting with chest pain. In addition, levels of cardiac troponin T (cTnT) and troponin I (cTnI) provide useful prognostic information and can help to guide the management of acute coronary syndrome (ACS) patients. 1 Nonetheless, although the currently available troponins have a nearly absolute cardiac specificity, they are not disease specific and cannot be used to distinguish reversible from irreversible myocardial cell injury. According to the new criteria of international car-diology societies, 1,2 the definitive diagnosis of AMI can be made in the presence of a rise and/or fall of cardiac troponins (or CK-MB mass when the troponins are not available) together with ischemic symptoms, electrocar-diographic changes indicative of new ischemia, or imag-ing evidence of new loss of viable myocardium or new regional wall motion abnormality. Thus, the presence of significant changes in troponin levels is essential for the diagnosis of myocardial cell necrosis. There is, however, thus far no consensus about the extent of these changes should be. Some experts have suggested a troponin change of 20% or more, 3,4 but as has recently been reported, the intra-individual biological variability of troponin concen-trations in healthy persons can be higher than 50% and thus, should be considered in the interpretation of tests results. 5,6 Another biochemical characteristic of myocardial cell necrosis due to obstructive coronary artery disease is the prolonged elevation of cardiac troponins beyond 1 week. This pattern of cardiac troponin release can be explained by the initial egress of the free (unbound) troponins from the cytosolic pool (3-7% of the total troponin content), followed by detachment of the bound form of troponins from the myofilament and subsequent release into the circulation. 7 Accordingly, the serum or plasma troponin concentrations found in patients with AMI are distinctively high, with peak levels usually in the range of 10 to more than 100 folds of the upper limit of reference range. Based on the guidelines of the international cardiology societies mentioned above, the pattern of cardiac troponin elevations may represent AMI type 1 (spontaneous MI) which is due to a primary coronary event such as plaque erosion and/or rupture with subsequent thrombotic occlusion of coronary arteries, or AMI type 2 which is secondary to ischemia due either to increased oxygen demand or decreased supply (e.g. coronary spasm, anemia, hyper-or hypotension). In addition, AMI may lead to sudden cardiac death (AMI type 3) or can occur following coro-nary revascularization procedures such as percutaneous coronary intervention as well as coronary artery bypass grafting (AMI type 4 and 5, respectively). Several conditions other than ACS have been reported to be associated with increased cardiac troponin concentrations indicating myocardial damage. These can be divided into 2 groups of cardiac and non-cardiac causes with myocardial involvement (Table 1). As compared with patients with AMI, different patterns of troponin increases have been reported in these patients and can be described as follows: 1. A constant release of cardiac troponins without a significant rise and/or fall of cardiac marker levels, the difference of which in most cases does not exceed 50%, is usually found in congestive heart failure, myopericarditis, sepsis and septic shock, and drug toxicity. 2. The small troponin increases observed in several cases of thermal burns and extreme exertion return to the reference limit within a few days, reflecting a transient reversible injury. 3. A certain number of patients with stress cardio-myopathy, acute neurologic diseases, phaeochromocytoma and drug abuse exhibit a troponin release profile which mimics AMI.
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