Introduction The association between erectile dysfunction (ED) and coronary artery disease (CAD) has been described in various settings, but it is unclear if there is an independent interaction with age. Aim To investigate the interaction of age in the association between ED and CAD. Methods This case-control study was conducted among 242 patients referred for elective coronary angiography. One hundred fourteen patients with significant CAD were identified as cases and 128 controls without significant CAD. ED was evaluated by the erectile function domain of the International Index of Erectile Function (IIEF) questionnaire, determined by a score ≤25 points. Main Outcome Measures Significant CAD was based on stenosis of 50% or greater in the diameter in at least one of the major epicardial vessels or their branches. The analysis was conducted in the whole sample and according to the age strata, controlling for the effects of cardiovascular risk factors, testosterone, and C-reactive protein. Results Patients had on average 58.3 ± 8.9 years. CAD and ED were associated exclusively in patients younger than 60 years (ED in 68.8% of patients with CAD vs. 46.7% of patients without CAD, P  = 0.009). The association was independent of cardiovascular risk factors, testosterone and C-reactive protein (risk ratio 2.3, 95% confidence interval from 1.04 to 5.19). Severity of CAD was higher in patients younger than 60 years with ED. Conclusions Men with less than 60 years of age who report ED presented a higher risk of having chronic CAD and more severe disease diagnosed by coronary angiography.

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Metabolic syndrome (MS) identifies cardiovascular risk; however, there is little information regarding the evolution of patients with MS after stent implantation. The aim of this single-center study is to evaluate the possible association between MS and clinical restenosis, after adjustment for highsensitivity C-reactive protein (hs-CRP) and angiographic predictors of restenosis. In a longitudinal study, 159 patients (89 with and 70 without MS) were studied. Criteria for MS were: elevated blood pressure (systolic >or=130 mmHg, diastolic >or=85 mmHg or drug treatment for hypertension; elevated fasting glucose (>100 mg/dl) or drug treatment for elevated glucose; reduced HDL-cholesterol (<40 mg/dl in men and <50 mg/dl in women) or drug treatment for reduced HDL-cholesterol; elevated triglycerides (>or=150 mg/dl) or drug treatment for elevated triglycerides; and obesity (body mass index >28.8 kg/m2). The primary end point was the rate of major adverse clinical events (MACE): cardiovascular death, myocardial infarction, or target lesion revascularization (TLR) during the 12-month follow-up period. The secondary end point was the rate of TLR. MS was neither identified as predictor of MACE [hazard ratio (HR): 0.844; 95% CI: 0.41-1.74; p=0.648], nor TLR (HR: 1.05; 95% CI: 0.44-2.50; p=0.91), even when controlled for hs-CRP levels and angiographic predictors of restenosis. Also, no significant interaction between MS and hs-CRP was found (p=0.135 and p=0.194, for MACE and TLR, respectively). This study shows that patients with MS do not have an additional risk of MACE, even when controlled for angiographic predictors of restenosis and hs-CRP.

Introdução: A reestenose intra-stent permanence como um problema a ser resolvido mesmo na era dos stents farmacológicos. Estudos clínicos de reestenose intra-stent são limitados por questões éticas, tornando os modelos experimentais necessários ao estudo da reestenose intra-stent. Objetivos: Desenvolver e aplicar um protocolo experimental de indução de proliferação neointimal significativa intra-stent (reestenose). Delineamento: Estudo experimental longitudinal, prospectivo, comparativo, não-randomizado. População e Métodos: Entre agosto de 2006 e março de 2009, 69 suínos da raça Large White foram submetidos à cinecoronariografia, seguida de protocolo de lesão vascular mediante implante de 77 stents sobredimensionados (grupo A -relação entre os diâmetros do stent e do vaso= 1,2:1), ou seguida de implante de 25 stents que respeitassem o diâmetro do vaso (grupo B -relação entre os diâmetros do stent e do vaso= 1:1). A colocação dos stents ocorreu em seguimentos das artérias circunflexa ou coronária direita que tivessem diâmetro de referência entre 2,5 -3,0 mm e foi guiada por ultrassom intracoronário. Em 28 dias, todos os suínos foram submetidos a reestudo angiográfico e ultrassonográfico. Resultados: A taxa de reestenose binária foi de 89,6% (69/77 stents) no grupo A, enquanto no grupo B foi de apenas 12,0% (3/25 stents), com diferença estatisticamente significativa (p<0,0001). O diâmetro luminal mínimo e a área luminal mínima imediatamente após o implante do stent no grupo A foram significativamente maiores em comparação ao grupo B (3,5 ± 0,3mm e 40,7 ± 0,3mm 2 vs 3,0 ± 0,2mm e 30,2 ± 0,2mm 2 , respectivamente; p<0,0001). O volume de hiperplasia neointimal foi significativamente maior no grupo A em comparação ao grupo B (5,9 ± 0,8mm 3 /mm de stent vs 1,8 ± 0,7mm 3 /mm de stent, respectivamente; p<0,0001). Conclusões: O protocolo experimental de lesão vascular em artérias coronárias de suínos proposto é eficaz em ocasionar indução de proliferação neointimal significativa intra-stent, tornando este modelo experimental utilizável tanto para o estudo dos mecanismos fisiopatológicos desta proliferação quanto para objetivos terapêuticos, como a avaliação de novos fármacos, novos dispositivos e novos stents farmacológicos, os quais visem prevenir e tratar a reestense intra-stent. Além disso, este modelo experimental demonstra que o uso de stents sobredimensionados deve ser evitado em humanos pelo grande potencial de indução de reestenose.

The study suggests a decrease in vascular complications through the transradial access for coronary angiography with the use of diltiazem as an antispasmodic drug, resulting in the significant increase in the diameter of the radial artery and radial artery output.