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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

Martin Schillinger, MD

Department of Internal Medicine II, Division of Angiology, University of Vienna, Medical School, Vienna, Austria

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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). . . . [Full Text of this Article]

Related Article:

Plasma B-Type Natriuretic Peptide Levels Are Associated With Early Cardiac Dysfunction After Subarachnoid Hemorrhage

Poyee P. Tung, Elise Olmsted, Alexander Kopelnik, Nader M. Banki, Barbara J. Drew, Nerissa Ko, Michael T. Lawton, Wade Smith, Elyse Foster, William L. Young, and Jonathan G. Zaroff
Stroke 2005 36: 1567-1569. [Abstract] [Full Text] [PDF]