The Serum Level of Brain Natriuretic Peptide Increases in Severe Subarachnoid Hemorrhage thereby Reflecting an Increase in Both Cardiac Preload and Afterload

Abstract

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.

Serum glucose/potassium ratio as a clinical risk factor for aneurysmal subarachnoid hemorrhage

“…14,25 Excessive catecholamine secretion, such as epinephrine and norepinephrine, occurs in the majority of aneurysmal SAH cases, causing sympathetic nervous system activation especially in severe cases, 12,19,20 resulting in the occurrence of systemic complications such as pulmonary cardiac lung edema, arrhythmia, or heart failure, 11,21,28 and reflect the primary brain injury itself. Yokobori et al 32 reported that serum BNP was significantly correlated with SAH grading and was a useful biomarker of systemic clinical impact, reflecting increased cardiac preload and afterload in severe aneurysmal SAH. Because of the breakdown of the blood-brain barrier by the ruptured aneurysm, increasing leukocyte trafficking has also been reported.…”

Brain Natriuretic Peptide as a Marker of Adverse Neurological Outcomes Among Survivors of Cardiac Arrest

“…Several studies have demonstrated its prognostic significance in patients with ischemic stroke, [22][23][24][25] traumatic brain injury, 26 intracranial hemorrhage, 27,28 and subarachnoid hemorrhage. 29,30 Emerging preclinical data suggest an adaptive role for BNP in recovery from acute brain injury. 31 Increased cerebral blood flow is seen with an increase in BNP levels.…”

Comparison of Initial Vasopressors Used for Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage

“…Aneurysmal SAH patients are a unique population of patients with a high risk of cardiac complications including stress cardiomyopathy and systolic dysfunction [23]. High-grade patients are also more likely to have abnormal preload and afterload [24]. Choosing a vasopressor with inotropic activity may have a particular importance in these patients.…”