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


CONCLUSIONS
Cytochrome c levels above the mean peak level were related to no-reflow and mortality in patients with STEMI.
aDepartment of Cardiology, Second Hospital of Hebei Medical University, Shijiazhuang bSchool of Public Health Fudan University, Shanghai, China.
Zhen-Bing
ZB
Liu
Xiang-Hua
XH
Fu
Geng
G
Wei
Jun-Ling
JL
Gao
D000368:Aged; D015415:Biomarkers / Q000097:blood; D003287:Contrast Media; D017023:Coronary Angiography; D003326:Coronary Circulation; D052279:Creatine Kinase, MB Form / Q000097:blood; D045304:Cytochromes c / Q000097:blood*; D004562:Electrocardiography; D005260:Female; D006801:Humans; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000175:diagnosis / Q000201:enzymology / Q000401:mortality / Q000503:physiopathology / Q000628:therapy*; D055414:Myocardial Perfusion Imaging / Q000379:methods*; D054318:No-Reflow Phenomenon / Q000097:blood / Q000175:diagnosis / Q000201:enzymology / Q000209:etiology* / Q000401:mortality / Q000503:physiopathology; D009942:Organometallic Compounds; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects / Q000401:mortality; D011237:Predictive Value of Tests; D012307:Risk Factors; D013318:Stroke Volume; D013997:Time Factors; D016896:Treatment Outcome; D016277:Ventricular Function, Left
D015415:Biomarkers; D003287:Contrast Media; D009942:Organometallic Compounds; C090600:gadobutrol; D045304:Cytochromes c; D052279:Creatine Kinase, MB Form