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Background: Statins may provide additional benefits in patients with cardiac failure due to their pleiotropic effects besides their cholesterol-lowering actions. In this study, we aimed to evaluate the impact of 12-week fluvastatin therapy on the inflammatory cytokines and the ventricular performance markers in patients with heart failure., Methods and Results: Fourty chronic heart failure patients, twenty with idiopathic dilated cardiomyopathy (DCM group) and 20 with ischemic cardiomyopathy (ICM group), for whom statin treatment was indicated according to Adult Treatment Panel III were included to this open label and prospective study. After a 12-week treatment with fluvastatin 80 mg/day; clinical functional capacity, echocardiographic indices of cardiac performance and inflammatory markers were evaluated. After the treatment, functional capacity (in DCM group: 2.05+/-0.4 versus 1.65+/-0.6, p=0.005; in ICM group: 2.25+/-0.5 versus 1.8+/-0.6, p=0.003), left ventricular ejection fraction, LVEF (from 30+/-5% to 33+/-5%, p=0.001 in DCM and 29+/-4% to 31+/-5%, p=0.001 in ICM group) and tissue Doppler mitral annular systolic velocity, Sm (5.8+/-1 cm/s to 7+/-1 cm/s, p=0.001 in DCM and 5.4+/-0.8 cm/s to 7+/-1 cm/s, p=0.001 in ICM group) improved. Tumor necrosis factor-alpha and interleukin-6 levels decreased, but no significant changes in high sensitive C-reactive protein and brain natriuretic peptide levels were detected with the fluvastatin treatment in both groups., Conclusion: Fluvastatin improved cardiac functions and the clinical symptoms in HF patients with either idiopathic dilated or ischemic etiology. This positive effect of fluvastatin which might be secondary to inflammatory modulation was more marked in patients with ischemic etiology. Statins in HF deserves special attention by means of further large-scale trials.

Objectives: Erectile dysfunction (ED) commonly coexists with coronary artery disease (CAD) and/or risk factors for atherosclerosis. Because the silent or documented atherosclerosis or vascular risk factors are very frequent, the possibility of endothelial dysfunction in ED patients is expected to be increased. Our aim was to evaluate the endothelial functions in patients with vasculogenic ED with vascular risk factors and compare them with age-matched non-ED patients or healthy controls., Design: We studied 36 patients with presumed vasculogenic ED, 39 age-matched patients with similar risk factors without ED and 25 age-matched healthy controls without ED, known cardiovascular disease or risk factors. Erectile function was evaluated by the International Index of Erectile Dysfunction (IIEF) scores. Brachial artery flow-mediated dilatation (FMD) and nitroglycerine-mediated dilatation (NMD) were measured., Results: Baseline demographics were similar except the IIEF score and duration of diabetes in patients with ED. Brachial artery FMD and NMD were significantly reduced in patients with ED (3.2+/-3. vs. 6+/-4, p<0.0001 for FMD, 12.2+/-6 vs. 15.4+/-6 p=0.032 for NMD). In patients with similar risk factors but without ED, FMD was significantly lower but NMD were not different compared with healthy controls (6+/-4 vs. 10.2+/-3, p<0.0001 for FMD and 15.4+/-8 vs. 16.4+/-6, p=0.81). IIEF scores were weakly correlated with FMD (r=0.25, p=0.028) in patients with ED. There were significant correlations between FMD and NMD in patients with ED (r=0.46, p=0.05) and with risk factors (r=0.72, p<0.0001) but not in healthy controls (r=0.54, p=0.792). Vasculogenic ED patients have more markedly impaired endothelial and smooth muscle functions compared with patients with similar risk factors but no ED.

Background: Although reciprocal ST segment depression (RSTD) in patients with acute inferior myocardial infarction is a common electrocardiogram finding, its significance is not yet established. In this prospective study, the relationship between RSTD and the extent of coronary artery disease (CAD) was investigated., Patients and Methods: One hundred eighty-eight patients with acute inferior myocardial infarction who received thrombolytic therapy were enrolled in this study. The magnitude and location of ST segment depression in noninfarcted leads and the maximum ST segment elevation (STEmax) in inferior leads were measured. All patients were divided into two main groups according to the presence of RSTD and five subgroups according to the location of RSTD, the maximum RSTD and the STEmax. The coronary angiography was performed in all patients 28 +/- 4 days after acute myocardial infarction., Results: There were no significant differences in the proportion of coronary disease risk factors in patients with, versus those without, RSTD (P=0.6). Multivessel CAD was present in 63 of the 108 (58%) patients with RSTD and in 32 of the 80 (40%) patients with no RSTD (P=0.02). According to the location of reciprocal changes, multivessel disease was present in significantly more patients with anterior RSTD concomitant with or without lateral ST segment depression (P=0.01 and P=0.03, respectively); the proportion of single vessel disease was greater in patients with only lateral RSTD (P=0.02). In addition, the presence of anterior RSTD to a greater magnitude than the STEmax in inferior myocardial infarction increases the likelihood of multivessel disease (P=0.006)., Conclusions: The presence of RSTD during an acute inferior myocardial infarction correlates with the presence of multivessel CAD and may not be only an electrical phenomenon.

Left ventricular hypertrophy (LVH) increases the risk of ventricular arrhythmias and sudden death and has a significant effect on total cardiovascular mortality. QT dispersion (QTd) is a measure of inhomogeneous repolarization and is used as an indicator of arrhythmogenicity. In this study we detected QTd in patients with different etiologies of left ventricular hypertrophy and the effect of LVH in QTd on endurance athletes. The study group consisted of 147 white male subjects with 3 different etiologies of LVH and 30 healthy male individuals. The underlying etiologies of LVH were essential hypertension, valvular aortic stenosis and long-term training (athletic heart). QTd was measured by surface electrocardiogram and Bazett's formula was used to correct QTd for heart rate (QTcd). Left ventricular mass was determined by transthoracic echocardiography and left ventricular mass index was calculated in relation to body surface area. The QTcd was significantly higher in patients with pathological LVH (due to hypertension and aortic stenosis) than in the athletes' group (physiological LVH) and healthy subjects (P<0.05). The magnitude of QTcd was similar between athletes and the control group (P=0.6). The difference of QTcd between the groups with pathological LVH was not statistically significant (P=0.1). In conclusion; the increasing of QT dispersion is associated with only pathological conditions of LVH. The left ventricular hypertrophy has not a negative effect in QT dispersion on endurance athletes. The measurement of QT dispersion may be a non-invasive useful method for screening additional pathological conditions in endurance athletes.