Published online before print June 9, 2005, doi: 10.1161/01.STR.0000170716.51658.a7
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(Stroke. 2005;36:1570.)
© 2005 American Heart Association, Inc.
Research Reports |
Editorial Comment—Brain Natriuretic Peptide and Early Cardiac Dysfunction After Subarachnoid Hemorrhage
Department of Internal Medicine II, Division of Angiology, University of Vienna, Medical School, Vienna, Austria
Subarachnoid hemorrhage (SAH) can be a catastrophic event for the brain and patients’ neurocognitive function; however, SAH also exerts cardiac adverse effects causing rhythm disturbances or myocardial necrosis in up to 40% of the patients.1–3 Evidence suggests that an increased sympathetic nervous activity and excessive catecholamine release during and after the event may cause deterioration of cardiac function.4 In this context, Tung et al demonstrated previously that the degree of neurological injury correlates with the extent of cardiac damage.5 Cardiac dysfunction after SAH adversely affects patients’ overall prognosis3 and, more specifically, the clinical sequelae of heart failure, namely low-output and hypotension, negatively influence neurological outcome after hemorrhagic brain injury. Early identification and monitoring of cardiac dysfunction thus is becoming increasingly recognized as a critical issue in patients with SAH.6
A variety of laboratory parameters may yield prognostic information on cardiac function in SAH patients. Among the panel of promising biomarkers, mainly parameters indicative for myocardial necrosis like cardiac troponins or creatine kinase MB fraction have been studied,7 and, particularly, troponin I seems to be useful in predicting ischemia-related myocardial dysfunction.7 During the past decade, natriuretic peptides emerged as novel and potentially powerful cardiovascular risk predictors and unequivocally have been shown to predict outcome of patients with heart failure and coronary artery and valvular heart disease.8–11 Brain natriuretic peptide (BNP) is synthesized as a pro-hormone in ventricular cardiocytes in response to cardiac wall stress and pressure overload, and is cleaved into the active BNP and inactive N-terminal pro-brain natriuretic peptide (NT-proBNP). Levels of BNP correlate with left ventricular dilatation and dysfunction12 and were initially recognized mainly as markers of chronic heart failure.13 More recently, BNP was established also as a sensitive prognostic parameter in patients with myocardial ischemia.8,9 It has been shown that even transient myocardial ischemia results in an immediate increase of BNP, with the magnitude of the increase proportional to the severity of ischemia.14 It is well-recognized, that BNP is elevated after SAH, but the source of its release and its prognostic impact remained to be determined.
In this issue of Stroke, Tung et al15 report the association between serum BNP levels measured in 57 patients after SAH and occurrence of cardiac dysfunction by echocardiography and cardiac troponin I elevation. BNP was significantly associated with all measures of cardiac dysfunction: higher BNP values were observed in patients with regional wall motion abnormalities, reduced left ventricular function, diastolic dysfunction, pulmonary edema, and cardiac troponin I elevation. Furthermore, BNP levels were associated with in-hospital mortality. The authors concluded that cardiac injury occurring early after SAH is associated with BNP elevation, supporting the hypothesis that the increase of BNP levels frequently observed after SAH is caused by BNP release from the heart. Importantly, elevated BNP was also identified as a prognostic marker with respect to early mortality in these patients.
Discussing the implications of this report several interesting issues arise. The data from Tung et al15 seem to support the notion that the heart is the source of BNP release after SAH rather than being derived from the brain. However, BNP elevation after SAH seems to directly reflect the extent of cardiac deterioration in these patients, which may be useful for routine clinical applications. BNP is a global indicator of cardiac dysfunction,13 sensitive both for systolic and diastolic cardiac deterioration.12,16 After SAH, electrocardiogram has its limitations in detecting myocardial necrosis as changes in waveforms are largely neurally mediated and myocardial lesions tend to be small and patchy.1 Currently, echocardiography therefore is considered the golden standard to detect cardiac dysfunction after SAH, but daily investigations and close monitoring of SAH patients by echocardiography does not seem feasible on a routine basis, and many SAH patients will undergo echocardiography only in cases of clinical evidence for heart failure. Routine measurements of BNP thus may provide a tool to monitor cardiac function and enable early identification of patients with incipient heart failure after SAH. Importantly, patients with higher BNP levels had an increased risk for in-hospital mortality, but the question whether therapeutic interventions may improve the prognosis of patients with BNP elevation after SAH remains unresolved and needs further evaluation. In the context of coronary artery disease, controversial data exist. A substudy of FRISC II indicated a survival benefit from early revascularization of patients with elevated levels of NT-proBNP,17 TACTICS-TIMI-18,18 in contrast, suggested that revascularization did not benefit patients with elevated BNP levels.
Some limitations of the study by Tung et al15 seem worth further consideration. First, although "prospective," the analytic character of this study remains cross-sectional. Blood samples for BNP measurements were obtained on average 5 days after onset of SAH symptoms and BNP was correlated with abnormal cardiac results "on any of the 3 study days." Without knowing the baseline levels of BNP before the event (which rarely can be obtained) or at least very early BNP measurements, it is virtually impossible to differentiate between BNP elevation caused by preexistent chronic cardiac pathologies and BNP increase in parallel with acute cardiac dysfunction caused by SAH. Second, only a subset of 57 of 174 patients was available to study BNP levels and clinical follow-up was limited to hospital discharge. Confirmation of these data in larger patient series and prolonged neurological and cardiovascular follow-up seems important before considering BNP measurements after SAH in clinical routine.
In conclusion, the findings by Tung et al suggest that patients with cardiac injury and dysfunction early after SAH can be identified by measurement of BNP levels and that elevation of BNP may be of immediate prognostic importance.
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