May cystatin-c be associated with post-myocardial infarction complications?

Abstract

Aim: Decreased cystatin C increases proteolytic effects of cathepsin contributing to plaque rupture. We aimed to investigate the association of cystatin C levels with in-hospital and post-discharge cardiac events in patients with acute myocardial infarction (AMI). Material and Method: We included 85 patients with AMI. Patients with cancer, systemic diseases, increased creatinine, active infection or aortic aneurysm were excluded. Demographic data, laboratory and echocardiographic parameters were analyzed. Serum cystatin C levels were measured in before coronary angiography. Results: Non-ST elevation myocardial infarction was determined in 32.94% of the patients. There were no differences between the normal and high cystatin C groups in terms of gender, diagnosis, obesity, hypertension, hyperlipidemia, cigarette smoking, Killip classification, preference of primary percutaneous coronary intervention or thrombolytic therapy, frequencies of culprit coronary arteries or the number of obstructed arteries. Diabetes mellitus was more frequent in the high cystatin C group. Complication rates after AMI were similar in both the normal and high cystatin C groups on the 5th day and the 12th month. Mean age was higher in the high cystatin C group. ESR, low density lipoprotein (LDL) and total cholesterol were found to be significantly higher in the high cystatin C group. The optimum cut-off values for ESR, LDL and total cholesterol were 11, 88.6, and 161.5, respectively; diagnostic accuracies were adequate. Discussion: The results of the study showed that ESR, LDL and total cholesterol were higher in high cystatin C group, but complications were similar in both groups. We concluded that cystatin C was not a predictor for post-AMI complications at 12th month.

Association between the No-Reflow Phenomenon and Soluble CD40 Ligand Level in Patients with Acute ST-Segment Elevation Myocardial Infarction

“…Acute coronary syndrome begins with platelet activation and thrombus formation after plaque erosion or rupture. Antiplatelet therapy prevents platelet activation; therefore it is the most critical treatment in ACS [13,14,15]. Although the exact mechanism of the NR occurrence has not been completely understood, the primary mechanism is thought to be increased platelet activation.…”