• 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.
• Division of Cardiology, University of California, San Francisco, CA, USA.
• Stroke. 2005 Jul 1; 36 (7): 1567-9.

Background And PurposeSerum B-type natriuretic peptide (BNP) is elevated after subarachnoid hemorrhage (SAH), as well as in the setting of congestive heart failure and myocardial infarction. The aim of this study was to prospectively quantify the relationship between BNP levels and cardiac outcomes after SAH.MethodsPlasma was collected for BNP measurements as soon as possible after enrollment; a mean of 5+/-4 days after SAH symptom onset. On days 1, 3, and 6 after enrollment, troponin I (cTi) was measured and 2-dimensional echocardiography was performed. The following cardiac variables were collected and treated dichotomously: left ventricular ejection fraction (LVEF), regional wall motion abnormalities (RWMA), diastolic dysfunction, pulmonary edema, and cTi.ResultsThere were 57 subjects. The median BNP level was 141 pg/mL (range, 0.8 to 3330 pg/mL). Higher mean BNP levels were present in those with RWMA (550 versus 261 pg/mL; P=0.012), diastolic dysfunction (360 versus 44; P=0.011), pulmonary edema (719 versus 204; P=0.016), elevated cTi (662 versus 240; P=0.004), and LVEF <50% (644 versus 281; P=0.015).ConclusionsEarly after SAH, elevated BNP levels are associated with myocardial necrosis, pulmonary edema, and both systolic and diastolic dysfunction of the left ventricle. These findings support the hypothesis that the heart releases BNP into the systemic circulation early after SAH.

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