Background: The increase of serum brain natriuretic peptide (sBNP) is well known in patients with severe subarachnoid hemorrhage (SAH). However, the pathophysiology between the clinical severity of SAH and the sBNP secretion is still not clear. The aim of this study is thus to clarify the cardiovascular pathophysiological mechanisms of sBNP secretion in severe SAH patients.
Methods: From the database of multicenter prospective study (SAH PiCCO study), sBNP level was compared among initial Hunt and Kosnik (H-K) gradings on the first day. Receiver operating characteristics (ROC) analysis was applied to decide the threshold existing between severe (H-K grade 4-5) and non-severe (H-K grade 2-3) patients. Cardiopulmonary parameters were also measured with thermodilution techniques and compared between low and high sBNP groups.
Results: sBNP level was significantly higher in severe patients than in non-severe patients (566.5 ± 204.2 vs. 155.7 ± 32.8 pg/ml, p = 0.034). Based on ROC analysis, the threshold value that divides severe and non-severe was 78.6 pg/ml (AUC = 0.79). In the higher sBNP group (≥78.6 pg/ml), global end-diastolic volume index (GEDI) and intrathoracic blood volume index (ITVI), which indicate the cardiac preload, were significantly higher than in the low sBNP group. The systemic vascular resistance index (SVRI), the indicator for sympathetic activation and cardiac afterload, was also higher in the high BNP group.
Conclusions: In severe SAH patients, sBNP elevation was significantly associated with the increase of both cardiac preload and afterload. sBNP may be a good severity biomarker in SAH patients, reflecting the systemic impact it makes on cardiovascular preload and afterload.
© 2014 S. Karger AG, Basel.