Relationship between high sensitivity C-reactive protein and angiographic severity of coronary artery disease

Background Coronary artery disease(CAD)remains a leading cause of morbidity and mortality.Cytokines play a potential role in atherosclerosis pathogenesis and progression.We investigated the association between high sensitive C-reactive protein(hs CRP)and severity of CAD.Methods CAD patients were stratified according to hs CRP cut-off value into high levels hs CRP group(≥8.4 mg/L)and low levels hs CRP group(<8.4 mg/L).Severity of CAD was assessed according to artery stenosis degree and the number of vessel involved.Statistical analysis was performed using Statistical Package for the Social Sciences(SPSS,version 23.0).Results The mean age was 60.3±11.0 years.The level of hs CRP was increased and ranged from 0.2 to 1020.0 mg/L.Biochemical risk factors and severity of CAD didn’t show significant differences between the two groups.In multivariate linear analysis,cardiac troponin I(c Tn I)and serum amyloid A(SAA)were predictors of hs CRP.As shown in receiver operating characteristic(ROC)curve analysis performed in patients with ST-segment elevation myocardial infarction(STEMI)and compared to myonecrosis biomarkers,hs CRP(area under the curve(AUC):0.905;95%CI:0.844-0.966;P<0.001)could be a powerful predictor marker in evaluating the infarct size after myocardial infarction but not better than c Tn I.Conclusions Hs CRP levels were not associated with the severity of CAD but could be useful in the evaluation of myocardial necrosis in patients with STEMI.

Predictive Factors of No Reflow during Primary Angioplasty

Introduction: No reflow during primary angioplasty is associated with a poor prognosis despite the reopening of the culprit coronary. The aim of our work was to determine the predictive factors of no reflow. Methodology: Single-center retrospective analytical study from June 2000 to December 2016 that included patients presenting with STEMI took care of by primary angioplasty. No reflow was defined according to angiographic criteria: a TIMI flow Results: The prevalence of no reflow was 24%. In univariate analysis mean age, diabetes,hypertension, tachycardia, hypotension, killip stage 4 left ventricular failure, hyperglycemia > 11, renal failure, left ventricular dysfunction, tritruncal status, common trunk involvement, initial TIMI flow at 0, significant thrombotic load, delay to angioplasty > 6 hours, and predilation were all correlated with no reflow with a p 75 years [OR = 6.02, 95% CI 1.4 - 27, p = 0.014], tachycardia [OR = 4.3, 95% CI 1.6 - 7.4, p = 0.037], delay to angioplasty > 6 hours [OR = 1.3, 95% CI 1.1 - 2.1, p = 0.003] and high thrombotic load [OR = 1.5, 95% CI 1.3 - 3.2, p = 0.02] were independent predictors of no reflow. Conclusion: No reflow is associated with a poor short-term prognosis. Its care requires knowledge of predictive factors, prevention and treatment.