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Background: Erectile dysfunction (ED) is a multifactorial disease related to age, vascular disease, psychological disorders, or medical treatments. Beta‐blockade agents are the recommended treatment for hypertensive patients with some specific organ damage but have been outlined as one of leading causes of drug‐related ED, although differences between beta‐blockade agents have not been assessed. Methods: Cross‐sectional and observational study of hypertensive male subjects treated with any beta‐blockade agent for at least 6 months. ED dysfunction was assessed by the International Index of Erectile Dysfunction (IIEF). Results: 1.007 patients, mean age 57.9 (10.59) years, were included. The prevalence of any category of ED was 71.0% (38.1% mild ED; 16.8% moderate ED; 16.1% severe ED). Patients with ED had longer time since the diagnosis of hypertension and higher prevalence of risk factors and comorbidities. The prevalence of ED increased linearly with age. ED patients received more medications and were more frequently treated with carvedilol and less frequently with nebivolol. Patients treated with nebivolol obtained higher scores in every parameter of the IIEF questionnaire. The multivariate analysis identified independent associations between ED and coronary heart disease (OR: 1.57), depression (OR: 2.25), diabetes (OR: 2.27), atrial fibrillation (OR: 2.59), and dyhidopiridines calcium channel blockers (OR: 1.76); treatment with nebivolol was associated to lower prevalence of ED (OR: 0.27). Conclusion: ED is highly prevalent in hypertensive patients treated with beta‐blockade agents. The presence of ED is associated with more extended organ damage and not to cardiovascular treatments, except for the lower prevalence in nebivolol‐treated patients.

The CA125 strategy was superior to the SOC in terms of reducing the risk of the composite of 1-year death or AHF readmission. This effect was mainly driven by significantly reducing the rate of rehospitalizations. (Carbohydrate Antigen-125-guided Therapy in Heart Failure [CHANCE-HF]; NCT02008110).

IntroductionThe potential impact of targeting different components of an adverse lipid profile in populations with multiple cardiovascular risk factors is not completely clear. This study aims to assess the association between different components of the standard lipid profile with all-cause mortality and hospitalization due to cardiovascular events in a high-risk population.MethodsThis prospective registry included high risk adults over 30 years old free of cardiovascular disease (2008–2012). Diagnosis of hypertension, dyslipidemia or diabetes mellitus was inclusion criterion. Lipid biomarkers were evaluated. Primary endpoints were all-cause mortality and hospital admission due to coronary heart disease or stroke. We estimated adjusted rate ratios (aRR), absolute risk differences and population attributable risk associated with adverse lipid profiles.Results51,462 subjects were included with a mean age of 62.6 years (47.6% men). During an average follow-up of 3.2 years, 919 deaths, 1666 hospitalizations for coronary heart disease and 1510 hospitalizations for stroke were recorded. The parameters that showed an increased rate for total mortality, coronary heart disease and stroke hospitalization were, respectively, low HDL-Cholesterol: aRR 1.25, 1.29 and 1.23; high Total/HDL-Cholesterol: aRR 1.22, 1.38 and 1.25; and high Triglycerides/HDL-Cholesterol: aRR 1.21, 1.30, 1.09. The parameters that showed highest population attributable risk (%) were, respectively, low HDL-Cholesterol: 7.70, 11.42, 8.40; high Total/HDL-Cholesterol: 6.55, 12.47, 8.73; and high Triglycerides/HDL-Cholesterol: 8.94, 15.09, 6.92.ConclusionsIn a population with cardiovascular risk factors, HDL-cholesterol, Total/HDL-cholesterol and triglycerides/HDL-cholesterol ratios were associated with a higher population attributable risk for cardiovascular disease compared to other common biomarkers.

Background: Vitamin K antagonists (VKA) have a narrow therapeutic range, and literature analysis reveals poor quality of anticoagulation control. We sought to assess the prevalence of poor anticoagulant control in patients under VKA treatment in the prevention of stroke for atrial fibrillation (AF). Hypothesis: Control of anticoagulation with VKA is inadequate in a high percentage of patients with AF. Methods: Patients with AF under VKA treatment were prospectively recruited in this observational registry. The sample comprised 948 patients. The estimated time spent in the therapeutic range (TTR) was calculated, and variables related with a TTR >65% were analyzed. Results: Mean age was 73.8 ± 9.4 years, and 42.5% of the patients were women. Mean TTR was 63.77% ± 23.80% for the direct method and 60.27% ± 24.48% for the Rosendaal method. Prevalence of poor anticoagulation control was 54%. Variables associated with good anticoagulation control were university studies (odds ratio [OR]: 1.99, 95% confidence interval [CI]: 1.08-3.64), chronic hepatic disease (OR: 8.15, 95% CI: 1.57-42.24), low comorbidity expressed as Charlson index (OR: 0.87, 95% CI: 0.76-0.99), no previous cardiac disease (OR: 0.64, 95% CI: 0.41-0.98), lower risk of bleeding assessed as hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile international normalized ratio, elderly age, and use of drugs or alcohol (HAS-BLED; OR: 0.81, 95% CI: 0.69-0.95), and lower heart rate (OR: 0.99, 95% CI: 0.98-0.99). Conclusions: Patients who receive VKA to prevent stroke for AF spend less than half the time within therapeutic range.