Why the study?
The study investigated the relationship between increased brain natriuretic peptide levels after aneurysm rupture and the incidence of MACE, perioperative complications, and long-term neurological outcomes.
Does elevated admission BNP predict major adverse cardiac events and adverse neurological outcomes in patients with aneurysmal subarachnoid hemorrhage?
Does elevated admission BNP predict major adverse cardiac events and adverse neurological outcomes in patients with aneurysmal subarachnoid hemorrhage?
Elevated BNP levels after aneurysmal subarachnoid hemorrhage are strongly associated with in-hospital major adverse cardiac events and delayed cerebral ischemia, highlighting its utility as a biomarker for perioperative risk stratification.
May aid in-hospital risk stratification after aSAH but should not yet change practice; leaves open long-term prediction.
This study investigated the relationship between increased brain natriuretic peptide (BNP) levels following aneurysm rupture and the incidence of major adverse cardiac events (MACE), perioperative complications, and long-term neurological outcomes. We included patients with aneurysmal subarachnoid hemorrhage within 72 hours of bleeding, collecting comprehensive clinical data. Participants were divided into 2 groups based on initial serum BNP levels: elevated (>100 pg/mL) and non-elevated (≤100 pg/mL). To mitigate bias, propensity score matching was employed to balance statistically significant variables. Follow-up assessments focused on in-hospital complications, MACE, and neurological outcomes. A total of 213 patients were analyzed, with an average age of 57.4 ± 12.1 years; 61.5% were women. The average follow-up duration was 34.3 months, with hypertension and coronary heart disease as common histories. After propensity score matching, the elevated BNP group showed higher rates of myocardial infarction (13.3% vs 4.0%, P = .001), acute heart failure (25.3% vs 4.0%, P = .042), delayed cerebral ischemia (25.3% vs 10.7%, P = .032), and hydrocephalus (13.3% vs 1.3%, P = .009). However, there was no significant difference in MACE between groups during follow-up. Logistic regression identified admission BNP as an independent risk factor for MACE (OR: 4.029, 95% CI: 1.753-9.262, P = .001), myocardial infarction (OR: 4.405, P = .038), heart failure (OR: 8.420, P = .002), delayed cerebral ischemia (OR: 3.449, P = .013), and hydrocephalus (OR: 13.726, P = .020). Elevated BNP levels after intracranial aneurysm rupture are associated with MACE, delayed cerebral ischemia, and hydrocephalus during hospitalization, but not with neurological status or MACE at discharge and follow-up.
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Guo et al. (2025) studied this question.
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