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Introduction: Abuse of anabolic‐androgenic steroids (AAS) has been linked to a variety of different cardiovascular (CV) side effects, but still the clinical effects of AAS abuse on CV risk are not clear. The aim of this study was to assess the CV phenotype of a large cohort of men with long‐term AAS use compared with strength‐trained athletes without AAS use. Methods: Fifty one strength‐trained men with ≥3 years of AAS use was compared with twenty one strength‐trained competing athletes. We verified substance abuse and non‐abuse by blood and urine analyses. The participants underwent comprehensive CV evaluation including laboratory analyses, 12‐lead ECG with measurement of QT dispersion, exercise ECG, 24 h ECG with analyses of heart rate variability, signal averaged ECG, basic transthoracic echocardiography, and coronary computed tomography angiography (CCTA). Results: Hemoglobin levels and hematocrit were higher among the AAS users compared with non‐users (16.8 vs. 15.0 g/dl, and 0.50% vs. 0.44%, respectively, both p < 0.01) and HDL cholesterol significantly lower (0.69 vs. 1.25 mmol/L, p < 0.01). Maximal exercise capacity was 270 and 280 W in the AAS and the non‐user group, respectively (p = 0.04). Echocardiography showed thicker intraventricular septum and left ventricular (LV) posterior wall among AAS users (p < 0.01 for both), while LV ejection fraction was lower (50 vs. 54%, p = 0.02). Seven AAS users (17%) had evidence of coronary artery disease on CCTA. There were no differences in ECG measures between the groups. Conclusions: A divergent CV phenotype dominated by increased CV risk, accelerated coronary artery disease, and concentric myocardial hypertrophy was revealed among the AAS users. [ABSTRACT FROM AUTHOR]

Use of anabolic-androgenic steroids (AAS) is associated with adverse cardiovascular (CV) effects, including potential prothrombotic effects. This study aimed to assess platelet activation and aggregation, coagulation, and fibrinolysis, in long-term AAS users compared to non-using strength-trained athletes. Thirty-seven strength-trained men using AAS were compared to seventeen non-using professional strength-trained athletes at similar age (median 33 years). AAS use was verified by blood and urine analyses. Platelet Function Analyzer 100 (PFA-100) and whole blood impedance aggregometry with thrombin, arachidonic acid, and ADP as agonists, were performed to evaluate platelet aggregation. ELISA methods were used for markers of platelet activation. Fibrinogen, D-dimer, the coagulation inhibitors protein S and C activity, and antithrombin were measured by routine. Fibrinolysis was evaluated by Plasminogen Activator Inhibitor-1 (PAI-1) activity. There were no significant differences in platelet aggregation between the two groups. Von Willebrand factor was lower among the AAS users (p < 0.01), and P-Selectin was slightly higher (p = 0.05), whereas CD40 Ligand, β-thromboglobulin, and thrombospondin did not differ significantly. No differences were found in the assessed coagulation inhibitors. Higher D-dimer levels (p < 0.01) and lower PAI-1 activity (p < 0.01) were found among the AAS users. The investigated long-term users of AAS did not exhibit elevated platelet activity compared to strength-trained non-using athletes. However, AAS use was associated with higher D-dimer levels and lower PAI-1 activity. These findings suggest that any prothrombotic effect of long-term AAS use may predominantly involve other aspects of the hemostatic system than blood platelets. [Display omitted] • Anabolic steroids are associated with an increased risk of cardiovascular diseases. • It has been hypothesized that anabolic steroids might have a prothrombotic effect. • The prothrombotic effects of anabolic androgenic steroids are still unclear. • We found an increased activation of coagulation and fibrinolysis. • No increase of blood platelet activation was observed. [ABSTRACT FROM AUTHOR]

To test the hypothesis that a statin could reduce the recurrence rate of atrial fibrillation after electrical cardioversion (EC), we performed an open, controlled multicenter study. Patients (n = 114) who had atrial fibrillation >48 hours and who were scheduled for EC were randomized to receive 40 mg of pravastatin once daily for 3 weeks before and 6 weeks after EC or no drug in addition to standard therapy. Pravastatin did not reduce the recurrence rate of atrial fibrillation after EC. [Copyright &y& Elsevier]