Association between C-reactive protein and angiographic restenosis after bare metal stents: an updated and comprehensive meta-analysis of 2747 patients

BACKGROUND: Previous studies have shown conflicting results about the relationship between baseline C-reactive protein (CRP) and restenosis after stenting with bare metal stent (BMS). METHODS: We assessed the association between serum CRP and angiographic restenosis after BMS by meta-analysis. Studies that reported basal serum CRP levels, above a prespecified cutoff value, before BMS deployment were included. An inverse random weighted meta-analysis was performed by entering the logarithm of the odds ratio (OR) of angiographic restenosis with its standard error for each study. RESULTS: Nine studies enrolling 2747 patients were selected. CRP threshold value was around 3 mg/l in three studies, 5 mg/l in four studies, and 6.98 and 10 mg/l in one study. Follow-up duration was 6.2+/-3.0 (mean+/-S.D.) months. Higher preprocedural CRP levels were a significant predictor of angiographic restenosis: OR 1.59, 95% confidence interval 1.21-2.07, P=.001. Heterogeneity was found: chi2 14.47, P=.07; I2=44.7%. Publication bias was also detected (P=.01, Egger's test). A sensitivity analysis, after excluding each study in turn, confirmed the predictive value of higher CRP levels, in agreement with the results of the main analysis. CONCLUSIONS: Among patients with coronary artery disease, undergoing percutaneous coronary intervention with BMS, higher baseline CRP levels are associated with higher risk of angiographic restenosis. A targeted therapeutic approach to patients with high baseline CRP, based on statins, oral corticosteroids, or PPAR gamma agonists, or selective use of drug-eluting stents, aiming at abating the higher risk of in-stent restenosis should be considered

Effect of intensive vs standard statin therapy on endothelial progenitor cells and left ventricular function in patients with acute myocardial infarction: Statins for regeneration after acute myocardial infarction and PCI (STRAP) trial

BACKGROUND: Intensive statin therapy can lower the risk of recurrence of major cardiac events in patients with acute coronary syndromes. This could be related to the ability of statins to increase levels of Endothelial Progenitor Cells (EPCs), which were demonstrated to be favorably associated with a better prognosis and post-infarction left ventricular remodeling in patients with ischemic heart disease. AIM OF THE STUDY: First, to evaluate, in a randomized clinical trial, the effect of an intensive vs a standard treatment with statins on EPC mobilization in patients undergoing a successful primary or rescue percutaneous coronary intervention; secondary, to evaluate whether left ventricular remodeling could be influenced by statin therapy through EPC mobilization. METHODS: Forty ST-segment elevation myocardial infarction (STEMI) patients undergoing a successful primary or rescue PCI were randomized to receive atorvastatin 80 mg immediately after the admission (Intensive Treatment, IT) or atorvastatin 20 mg from the day of the discharge (Standard Treatment, ST). CD34+/KDR+ EPC count by flow cytometry and left ventricular function by 2-D Echo were measured on admission, at discharge and at 4 months follow up. RESULTS: We found that EPC count was similar in the two groups of patients both on admission and at discharge. At follow up, however, EPC count was higher in patients randomized to IT compared to patients randomized to ST (7.59+/-7.30 vs 3.04+/-3.93, p=0.04). However, LV volumes, ejection fraction and wall motion score index were similar in both groups. CONCLUSIONS: An intensive statin treatment after primary or rescue PCI is associated with a higher EPC count at follow up as compared to standard treatment. This beneficial effect did not translate in an improvement of LV function

Safety of granulocyte-colony-stimulating factor in acute myocardial infarction (the Rigenera study)

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Investigation of the effect of Interleukin-1 receptor antagonist (IL-1ra) on markers of inflammation in non-ST elevation acute coronary syndromes (The MRC-ILA-HEART Study)

Background: Acute Coronary Syndromes account for 15% of deaths in the UK, and patients remain at significant risk of re-admission for future complications and death. Pathologically the underlying process of atherosclerosis is driven by inflammatory mechanisms, which are activated in ACS patients. Previous studies have investigated the role of inflammatory markers in this process, including interleukin 1 (IL-1) and C Reactive Protein (CRP). Pre-clinical studies indicate that IL-1 may be a primary driver of ACS and that the naturally occurring interleukin-1 receptor antagonist (IL-1ra) may inhibit the atherosclerotic process. This study will investigate the effects of IL-1ra on inflammatory markers in man. Methods/design: Three centres inthe UK are planning to recruit 186 Non-ST elevation myocardial infarction patients to receive either interleukin-1 receptor antagonist (Anakinra) or matching placebo. Patients will receive a daily subcutaneous injection of either study drug or placebo over a 14 day period. The primary outcome is area under the curve of high sensitivity C-Reactive Protein (CRP) over the first 7 days. Discussion: The MRC-ILA-HEART Study is a proof of concept clinical trial investigating the effects of IL-1ra upon markers of inflammation in patients with Non-ST elevation myocardial infarction. It is hoped this will provide new and exciting information in relation to an "anti-inflammatory" strategy for patients with acute coronary syndrom