Triflusal and aspirin have similar efficacy in preventing further cardiovascular events after acute myocardial infarction, but triflusal showed a more favourable safety profile. Triflusal significantly reduced the incidence of non-fatal cerebrovascular events compared with aspirin.

Objectives We investigated whether an intervention mainly consisting of a signed agreement between patient and physician on the objectives to be reached, improves reaching these secondary prevention objectives in modifiable cardiovascular risk factors six-months after discharge following an acute coronary syndrome. Background There is room to improve mid-term adherence to clinical guidelines' recommendations in coronary heart disease secondary prevention, specially non-pharmacological ones, often neglected. Methods In CAM-2, patients discharged after an acute coronary syndrome were randomly assigned to the intervention or the usual care group. The primary outcome was reaching therapeutic objectives in various secondary prevention variables: smoking, obesity, blood lipids, blood pressure control, exercise and taking of medication. Results 1757 patients were recruited in 64 hospitals and 1510 (762 in the intervention and 748 in the control group) attended the six-months follow-up visit. After adjustment for potentially important variables, there were, between the intervention and control group, differences in the mean reduction of body mass index (0.5 vs. 0.2; p < 0.001) and waist circumference (1.6 cm vs. 0.6 cm; p = 0.05), proportion of patients who exercise regularly and those with total cholesterol below 175 mg/dl (64.7% vs. 56.5%; p = 0.001). The reported intake of medications was high in both groups for all the drugs considered with no differences except for statins (98.1% vs. 95.9%; p = 0.029). Conclusions At least in the short term, lifestyle changes among coronary heart disease patients are achievable by intensifying the responsibility of the patient himself by means of a simple and feasible intervention.

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This randomised, double-blind, placebo (PBO)-controlled study evaluated the efficacy and safety of ezetimibe (EZE) co-administered with ongoing atorvastatin (ATV) therapy in 450 hypercholesterolemic patients with coronary heart disease (CHD) who had not achieved their low-density lipoprotein cholesterol (LDL-C) goal < or =2.60 mmol/l while on a stable dose of ATV 10 or 20 mg/day for > or =6 weeks. After a 4-week diet/baseline active run-in period, patients with LDL-C >2.60 mmol/l and < or =4.20 mmol/l were stratified by ATV dose and randomised (1 : 1) to EZE 10 mg or PBO for 6 weeks while continuing open-label ATV. Significantly more patients achieved an LDL-C goal < or =2.6 mmol/l with EZE than PBO (81.3 vs. 21.8%; p < or = 0.001). Compared to PBO, co-administration of EZE with ongoing ATV led to significantly (p < or = 0.001) greater reductions in LDL-C, total cholesterol, triglycerides, non-high-density lipoprotein cholesterol (non-HDL-C), and apolipoprotein B; HDL-C was significantly (p < or = 0.05) increased. Co-administration of EZE and ATV was well tolerated, with an overall safety profile similar to ATV alone.

Previous evidence has shown that coronary angioplasty leads to the release of inflammatory mediators. In this study, we sought to characterize the systemic inflammatory response after coronary stent implantation in patients with unstable angina by measuring different protein markers. Peripheral blood samples were taken before and 24 h, 48 h, and 7 days after successful coronary stenting in 58 patients. Several markers of acute-phase response were determined: C-reactive protein (CRP), alpha2-macroglobulin, haptoglobin, acid alpha1-glycoprotein, prealbumin and albumin. Besides, proinflammatory cytokines (tumor necrosis factor-alpha, IL-6, IL-8) and the anti-inflammatory cytokine IL-10 were also measured. We have found that coronary angioplasty with stent implantation produces a systemic inflammatory response with a rise in inflammation markers concentration. CRP plasma levels declined 1 week after the intervention, but the other marker levels were even higher after 7 days. IL-6 was the only cytokine whose plasma levels significantly increased in peripheral blood after stenting, with a rise after 24 h, maintained after 48 h, and decreased to near-basal levels after 1 week. There was a good correlation between CRP and IL-6 plasma levels (r=0.5, p<0.001). IL-10 levels were slightly decreased after 24 h. Although no significant differences in the means at different time points were found, there was a decrease in IL-10 in most patients 24 h after the intervention. These results indicate that coronary stent implantation induces a systemic inflammatory reaction, with a temporal increase in the concentration of the inflammation markers, especially CRP and IL-6. Since these markers had been previously used as prognostic markers, this needs to be taken into account in patients undergoing stent implantation.