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Endothelial dysfunction is a major determinant of atherosclerosis and a negative prognostic factor in patients with coronary artery disease and hypertension. Recovery of endothelial dysfunction has been associated with improved prognosis in these patients. The aim of the present study was to verify whether antagonism of angiotensin II AT1 receptors with an angiotensin receptor blocker, candesartan, improved endothelial function in patients with hypertension, stable coronary artery disease, and endothelial dysfunction. We studied 26 patients who were receiving β‐blockers with optimal blood pressure control, in a randomized, double blind study. Patients were randomized to placebo (n=13) or to candesartan 16 mg/d (n=13) for 2 months. Endothelial function was assessed by ultrasound using hyperemic flow‐mediated dilation of the brachial artery. Mean arterial blood pressure was unchanged in both groups (from 93.3±9.2 to 93.2±17.3 mm Hg in the candesartan group and from 101.3±14.2 to 102.3±13.9 mm Hg in the placebo group; both P=ns). Maximal blood flow was similar between placebo and candesartan groups at baseline and at the end of the study, whereas flow‐mediated dilation significantly increased in the candesartan group (from 5.27%±1.69% to 7.15%±2.67%; P=0.01) but remained unchanged in the placebo group (from 4.49%±1.97% to 5.88%±2.30%; P=ns). AT1 receptor antagonism with candesartan, in addition to β‐blocker therapy, improves endothelial function in high‐risk hypertensive patients.

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Background Recently, the COMPASS trial demonstrated that dual therapy reduced cardiovascular outcomes compared with aspirin alone in patients with stable atherosclerotic disease. Methods and Results We sought to assess the proportion of patients eligible for the COMPASS trial and to compare the epidemiology and outcome of these patients with those without COMPASS inclusion or with any exclusion criteria in a contemporary, nationwide cohort of patients with stable coronary artery disease (CAD). Among the 4068 patients with detailed information allowing evaluation of eligibility, 1416 (34.8%) did not fulfill the inclusion criteria (COMPASS-Not-Included), 841 (20.7%) had exclusion criteria (COMPASS-Excluded) and the remaining 1811 (44.5%) were classified as COMPASS-Like. At 1 year, the incidence of major adverse cardiovascular event (MACE), a composite of cardiovascular death, myocardial infarction and stroke, was 0.9% in the COMPASS-Not-Included and 2.0% in the COMPASS-Like (p = 0.01), and 5.0% in the COMPASS-Excluded group (p < 0.0001 for all comparisons). Among the COMPASS-Like population, patients with multiple COMPASS enrichment criteria presented a significant increase in the risk of MACE (from 1.0% to 3.3% in those with 1 and ≥3 criteria, respectively; p = 0.012), and a modest absolute increase in major bleeding risk (from 0.2% to 0.4%, respectively; p = 0.46). Conclusions In a contemporary real-world cohort registry of stable CAD, most patients resulted as eligible for the COMPASS. These patients presented a considerable annual risk of MACE that consistently increases in the presence of multiple risk factors.

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