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J Invasive Cardiol ; 21(1): 13-9, 2009 Jan.
Article in English | MEDLINE | ID: mdl-19126922

ABSTRACT

BACKGROUND: The positive effect of reperfusion after ST-elevation myocardial infarction (STEMI) can be reduced by ischemic/reperfusion (I/R) injury.Mannose-binding-lectin (MBL) and soluble C5b-9 (membrane-attack-complex) are involved in complement-driven cell lysis and may play a role in human myocardial I/R injury. We evaluated the potential association between MBL and sC5b-9 in plasma and subsequent cardiac dysfunction in patients with STEMI treated with primary percutaneous coronary intervention (pPCI). METHODS: The study included 74 STEMI-patients with acute occlusion of the left anterior descending coronary artery who were successfully treated with pPCI. Cardiac dysfunction was defined as left ventricular ejection fraction LVEF < 35%. RESULTS: Patients with subsequent LVEF < 35% had significantly higher median MBL and lower sC5b-9 compared to patients with LVEF > or = 35%. After adjustment of the multivariate logistic regression analysis, the odds for reduced LVEF was 5.5 (95% CI:1.5-19.3; p = 0.01) for patients with MBL > or = 800 mcg/L, and 5.0 (95% CI 1.4-18.4; p = 0.01) for patients with sC5b-9 < or = 160 mcg/L. CONCLUSION: High plasma MBL and low plasma sC5b-9 are independently associated with increased risk of cardiac dysfunction in STEMI patients treated with pPCI, probably due to increased complement activity during the ischemic and reperfusion process. The predictive value of low peripheral plasma sC5b-9 may be explained by an accumulation and activation of sC5b-9 in the infarcted myocardium.


Subject(s)
Angioplasty, Balloon, Coronary , Complement Membrane Attack Complex/metabolism , Myocardial Infarction/blood , Myocardial Infarction/therapy , Ventricular Dysfunction, Left/epidemiology , Aged , Biomarkers/blood , Case-Control Studies , Female , Humans , Male , Mannose-Binding Lectin/blood , Middle Aged , Predictive Value of Tests , Regression Analysis , Reperfusion Injury/blood , Retrospective Studies , Risk Factors , Signal Transduction , Stroke Volume/physiology , Ventricular Dysfunction, Left/physiopathology
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