Prevalence and correlates of non-optimal secondary medical prevention in patients with stable coronary artery disease.

BACKGROUND: In patients with coronary artery disease (CAD), non-optimal use of evidence-based medications is associated with an increased risk of adverse outcome. AIMS: To assess the prevalence and correlates of non-optimal secondary medical prevention in patients with stable CAD. METHODS: We included 4184 consecutive outpatients with stable CAD. Treatment at inclusion was classified as optimal/non-optimal regarding the four major classes of secondary prevention drugs: antithrombotics; statins; angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs); and beta-blockers. For each treatment, the prescription was considered non-optimal if the drug was missing despite a class IA indication according to international guidelines. To assess the information globally, non-optimal secondary prevention was defined as at least one major treatment missing. RESULTS: The proportions of patients with non-optimal treatment were 0.7%, 7.8%, 12.9% and 10.3% for antithrombotics, statins, ACE inhibitors/ARBs and beta-blockers, respectively. Non-optimal secondary medical prevention was observed in 16.8% of cases. By multivariable analysis, the correlates of non-optimal secondary medical prevention were long time interval since last coronary event (P<0.0001), older age (P<0.0001), diabetes mellitus (P<0.0001), hypertension (P<0.0001), no history of myocardial infarction (P=0.001), no history of coronary revascularization (P=0.013) and low glomerular filtration rate (P=0.042). CONCLUSIONS: Although most patients with stable CAD are receiving evidence-based medications according to guidelines, there remain subgroups at higher risk of non-optimal treatment. In particular, it might be feasible to improve prevention by focusing on patients in whom a long time has elapsed since the last coronary event.

Left ventricular remodeling after anterior wall acute myocardial infarction in modern clinical practice (from the REmodelage VEntriculaire [REVE] study group).

Left ventricular (LV) remodeling after acute myocardial infarction (AMI) has been well described in previous studies. However, there is a paucity of data on the incidence of and risk factors for LV remodeling in modern clinical practice that incorporates widespread use of acute reperfusion strategies and almost systematic use of "antiremodeling" medications, such as angiotensin-converting enzyme inhibitors and beta blockers. We enrolled 266 patients with anterior wall Q-wave AMI who had >or=3 segments of the infarct zone that were akinetic on echocardiography before discharge. Echocardiographic follow-up was performed 3 months and 1 year after AMI. LV volumes, ejection fraction, wall motion score index, and mitral flow velocities were determined in a blinded analysis at a core echocardiographic laboratory. Acute reperfusion was attempted in 220 patients (83%; primary angioplasty in 29% and thrombolysis in 54%). During hospitalization, 99% of patients underwent coronary angiography and 87% underwent coronary stenting of the infarct-related lesion. At 1 year, 95% of patients received an antiplatelet agent, 89% a beta blocker, 93% an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker, and 93% a statin. Echocardiographic follow-up was obtained in 215 patients. There was recovery in LV systolic function as shown by a decrease in wall motion score index and an increase in ejection fraction. There was a significant increase in end-diastolic volume (EDV; 56.4 +/- 14.7 ml/m2 at baseline, 59.3 +/- 15.7 ml/m2 at 3 months, 62.8 +/- 18.7 ml/m2 at 1 year, p <0.0001). LV remodeling (>20% increase in EDV) was observed in 67 patients (31%). Peak creatine kinase level, systolic blood pressure, and wall motion score index were independently associated with changes in EDV. In conclusion, recent improvements in AMI management do not abolish LV remodeling, which remains a relatively frequent event after an initial anterior wall AMI.