Na Li1, Xun Gao1, Weizhan Wang1, Pu Wang1, Baoyue Zhu1. 1. Department of Emergency, Harrison International Peace Hospital Affiliated to Hebei Medical University, Hengshui, China.
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. 2020 Cardiovascular Diagnosis and Therapy. All rights reserved.
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. 2020 Cardiovascular Diagnosis and Therapy. All rights reserved.
Entities:
Keywords:
Acute carbon monoxide poisoning (ACOP); major adverse cardiac events; recombinant human brain natriuretic peptide (rhBNP)
Authors: I C Jeremias; V J Victorino; J L Machado; W A Barroso; S K Ariga; T M Lima; F G Soriano Journal: Mol Neurobiol Date: 2015-06-18 Impact factor: 5.590