Literature DB >> 24077325

Cytochrome c release in acute myocardial infarction predicts poor prognosis and myocardial reperfusion on contrast-enhanced magnetic resonance imaging.

Zhen-Bing Liu1, Xiang-Hua Fu, Geng Wei, Jun-Ling Gao.   

Abstract

BACKGROUND: Myocardial ischemia and reperfusion injury in ST-segment elevation myocardial infarction (STEMI) can trigger no-flow, resulting in myocardial necrosis and apoptosis, even a poor prognosis. Cytochrome c can induce an apoptotic process. The aim of our study was to assess the relationship between systemic cytochrome c levels and the occurrence of no-reflow in STEMI.
METHODS: One hundred and sixty patients with STEMI undergoing a primary percutaneous coronary intervention (PPCI) were randomly chosen. Patients were divided into two groups defined by the mean cytochrome c peak level after PPCI. No-reflow was assessed using three different methods after PPCI: myocardial blush grade, electrocardiographic ST-resolution, and microvascular obstruction (MO) assessed by cardiovascular magnetic resonance imaging. The primary clinical end points were major adverse cardiovascular events (defined as cardiac death, reinfarction, or new congestive heart failure). Clinical follow-up was carried out for 1 year.
RESULTS: Patients with a cytochrome c level of at least the mean peak level had a greater creatine kinase-MB isoenzyme peak level (P=0.044), a lower left ventricular ejection fraction (P=0.029), a significantly higher occurrence of early MO (P=0.008), and a significantly larger extent of early MO (P=0.020). The cytochrome c peak level was elevated in patients with early MO (P=0.025), myocardial blush grade 0-1 (P=0.002), and ST-resolution less than 30% (P=0.003) after PPCI. A higher incidence of cardiac death at the 1-year follow-up was found in the patients with cytochrome c levels of at least the mean peak level (log rank, P=0.029).
CONCLUSION: Cytochrome c levels above the mean peak level were related to no-reflow and mortality in patients with STEMI.

Entities:  

Mesh:

Substances:

Year:  2014        PMID: 24077325     DOI: 10.1097/MCA.0000000000000040

Source DB:  PubMed          Journal:  Coron Artery Dis        ISSN: 0954-6928            Impact factor:   1.439


  5 in total

1.  Inhibition of MiR-92a May Protect Endothelial Cells After Acute Myocardial Infarction in Rats: Role of KLF2/4.

Authors:  Hongxia Liu; Guofen Li; Wenxue Zhao; Yibo Hu
Journal:  Med Sci Monit       Date:  2016-07-14

2.  Diagnostic and Prognostic Utility of Circulating Cytochrome c in Acute Myocardial Infarction.

Authors:  Giancarlo Marenzi; Nicola Cosentino; Jasper Boeddinghaus; Mirella Trinei; Marco Giorgio; Valentina Milazzo; Marco Moltrasio; Daniela Cardinale; Maria Teresa Sandri; Fabrizio Veglia; Alice Bonomi; Max Kaech; Raphael Twerenbold; Thomas Nestelberger; Tobias Reichlin; Karin Wildi; Samyut Shrestha; Nikola Kohzuharov; Zaid Sabti; Carlo M Cipolla; Christian Mueller; Antonio L Bartorelli
Journal:  Circ Res       Date:  2016-10-31       Impact factor: 17.367

3.  Effects of Serum Cytochrome c on Contrast-Induced Nephropathy in Patients with ST-Elevation Myocardial Infarction Undergoing Percutaneous Coronary Intervention.

Authors:  Chengchun Tang; Jiantong Hou; Gaoliang Yan; Yong Qiao; Dong Wang; Boqian Zhu; Bo Liu; Erfei Luo; Abdul Qadir Nawabi; Long Chen
Journal:  Biomed Res Int       Date:  2019-01-23       Impact factor: 3.411

4.  SCD leads to the development and progression of acute myocardial infarction through the AMPK signaling pathway.

Authors:  Lijie Wang; Fengxia Yu
Journal:  BMC Cardiovasc Disord       Date:  2021-04-20       Impact factor: 2.298

5.  Mitochondrial Damage-associated Molecular Patterns as Potential Biomarkers in DCD Heart Transplantation: Lessons From Myocardial Infarction and Cardiac Arrest.

Authors:  Sarah L Longnus; Nina Rutishauser; Mark N Gillespie; Tobias Reichlin; Thierry P Carrel; Maria N Sanz
Journal:  Transplant Direct       Date:  2021-12-16
  5 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.