ArticleCardiovascular diagnosis and therapy2020
Protective effects of recombinant human brain natriuretic peptide on the myocardial injury induced by acute carbon monoxide poisoning.
Article in Cardiovascular diagnosis and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Prognostic value of X-box binding protein 1 and phospholipase A2 in myocardial injury after ST-segment elevation myocardial infarction: a prospective observational study.Journal of cardiothoracic surgery · 2026Observational
- The expression of MALAT1, plasma brain natriuretic peptide, and Tei index in sepsis-induced myocardial injury.Journal of cardiothoracic surgery · 2025Article
- Effect of Recombinant Human Brain Natriuretic Peptide Therapy After PCI in Patients with Acute Myocardial Infarction and Its Impact on Cardiac Function: A Retrospective Controlled Study.International journal of general medicine · 2025Article
- Lyophilized recombinant human brain natriuretic peptide: A promising therapy in patients with chronic heart failure.World journal of clinical cases · 2023Article
- Protective effect of recombinant human brain natriuretic peptide against contrast-induced nephropathy in elderly acute myocardial infarction patients: A randomized controlled trial.World journal of clinical cases · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
backgroundTo investigate the protective effect of recombinant human brain natriuretic peptide (rhBNP) on myocardial injury after acute carbon monoxide poisoning (ACOP).
methodsWe 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.
resultsA 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.
conclusionsFor 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.
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