Protective effects of recombinant human brain natriuretic peptide on the myocardial injury induced by acute carbon monoxide poisoning

Abstract

Background: To investigate the protective effect of recombinant human brain natriuretic peptide (rhBNP) on myocardial injury after acute carbon monoxide poisoning (ACOP).Methods: We retrospectively reviewed medical records of patients with ACOP and high risk of cardiac events admitted to our hospital, and grouped them into rhBNP group and control group according treatments they received. Patients in control group received conventional treatment while those in rhBNP group were treated with rhBNP intravenously for 72 hours on the basis of conventional treatment. Levels of amino-terminal pro-brain natriuretic peptide (NT-proBNP), cardiac troponin I (cTnI), serum creatine kinase MB fraction (CK-MB), aldosterone (ALD), angiotensin II (AT II), and endothelin-1 (ET-1) prior to and after treatment of rhBNP or conventional treatment were collected. Corrected QT dispersion (QTcd) results were calculated based on the electrocardiography data. The left ventricular end diastolic diameter (LVEDD), interventricular septal thickness (IVS), left ventricular ejection fraction (LVEF), and stroke output (SV) were measured using color Doppler echocardiography. Major adverse cardiovascular events (MACEs) that occurred within 1 month after treatment were recorded.Results: A total of 135 patients in the rhBNP group and 136 patients in the control group were enrolled.Baseline characteristics between the two groups were similar at admission. Levels of cTnI, CK-MB, and ET-1 in the rhBNP group were significantly lower than those in the control group at day 1, 2 and 3 after treatment (P<0.05). Compared with the control group, levels of QTcd, ALD and AT II in the rhBNP group were significantly lower at day 3 after treatment (P<0.05). After 7 days of treatment, the reduction of NT-proBNP in the rhBNP group was significantly greater than that in the control group at each day (P<0.05), and LVEF, SV and LVEDD in the rhBNP group were all greater than those in the control group. After 1 month of treatment, the incidence of MACEs in the rhBNP group was significantly lower than that in the control group.Conclusions: For patients with ACOP and high risk of cardiac events, early treatment of rhBNP can protect injured cardiomyocytes, prevent the injury of carbon monoxide on heart, and reduce the incidence of MACE.

Efficacy of recombinant human brain natriuretic peptide as an adjuvant therapy for severe heart failure, and its impact on oxidative stress and quality of life in patients

“…It mainly regulates hemodynamics by activating vascular endothelial protein kinase so as to promote vasodilation. Previous studies have proven that it is effective in treating myocardial infarction and other diseases [19,20].…”

Effects of Levosimendan Preconditioning on Left Ventricular Remodeling after Myocardial Reperfusion in Acute Myocardial Infarction Patients Receiving Percutaneous Coronary Intervention

“…It has been shown that the calcium-sensitizing effect of levosimendan is achieved by direct binding to troponin [Lin 2018]. Recombinant human BNP obviously reduces the levels of blood AST and CK-MB after reperfusion in patients with acute ST segment-elevation MI, indicating that it can protect cardiac function [Li 2020]. Both recombinant human BNP and levosimendan can lower AST levels in AMI patients undergoing emergency PCI, but the effect of the former was greater [Kreusser 2019].…”

A narrative review on sacubitril/valsartan and ventricular arrhythmias

“…[44,45] At the same time, injection of exogenous BNP also showed that recombinant human BNP improved cardiac function, increased ejection fraction, dilated vessels, and had antifibrotic effects. [46] In addition, a meta-analysis defining the predictors of sudden cardiac death and ventricular arrhythmia in patients with ICD found that high baseline BNP or N-terminal pro-BNP levels were independently associated with the occurrence of ventricular tachyarrhythmia. [47] Gene deletion experiments in mice have indicated that BNP preventing cardiac fibrosis.…”