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Summary: This study aimed to measure the serum endocan level of patients with erectile dysfunction (ED) and to investigate the possible association between this and vasculogenic severe ED. We performed a prospective analysis of 86 consecutive patients affected by ED. Patients were divided into severe ED (IIEF‐5 score < 7) and mild or moderate ED (IIEF‐5 score > 7). A strong negative correlation was found between serum endocan levels and peak systolic velocity (p < .001 and r = −.665) in men with severe ED. Univariate logistic regression analysis demonstrated that tobacco consumption (p < .05), serum total 25‐hydroxyvitamin D (p < .01), serum endocan levels (p < .01), peak systolic velocity (p < .01), hypertension (p < .001), dyslipidaemia (p < .001), metabolic syndrome (p = .026) and a history of a cardiovascular event (p < .001) significantly increase the risk of severe ED. In the multivariate logistic regression model, we also found that age, hypertension, metabolic syndrome, cardiovascular events and higher serum endocan levels were independently associated with severe ED. Circulating endocan may be used in daily practice as a new marker that correlates with cardiovascular risks and the severity of ED disease. [ABSTRACT FROM AUTHOR]

The differences between long-acting dihydropyridines and angiotensin-converting enzyme inhibitors with regard to their long-term effects on 24-h heart rate variability (HRV) and left ventricular (LV) mass are less clear in mild-to-moderate essential hypertension. We studied the long-term effects of amlodipine and fosinopril on 24-h HRV and LV mass in mild-to-moderate essential hypertension.In this study, 27 patients with never treated mild-to-moderate essential hypertension were randomised to receive either amlodipine or fosinopril once daily as monotherapy. At baseline and at the end of the third and sixth months, each of the patients underwent 24-h HRV and ambulatory systolic (SBP) and diastolic (DBP) blood pressure analysis. LV mass index was calculated from echocardiographic examination at baseline and at the end of the sixth month.In amlodipine group (n = 14), 24-h SBP/DBP (mmHg) decreased from 144 ± 8/94 ± 4 to 128 ± 6/83 ± 3 at the end of the third month and to 125 ± 5/81 ± 2 at the end of the sixth month (p < 0.0001). In fosinopril group (n = 13), the respective changes were 143 ± 9/97 ± 7, 132 ± 6/87 ± 5 and 127 ± 6/82 ± 3 (p < 0.0001). At the end of the sixth month, LV mass index (g/m2) decreased from 122 ± 26 to 105 ± 21 in amlodipine group (p < 0.0001) and from 118 ± 23 to 101 ± 14 in fosinopril group (p < 0.0001). There were no significant changes in HRV parameters in both the groups.It was concluded that both drugs caused significant decrease in SBP and DBP, and LV mass in patients with mild-to-moderate essential hypertension did not have significant long-term effects of either amlodipine or fosinopril on 24-h HRV parameters reflecting sympathetic or parasympathetic activity in these patients. [ABSTRACT FROM AUTHOR]

Background: Growth hormone deficiency (GHD) is known to cause higher rates of cardiovascular mortality. The purpose of the study was to analyze the structural and functional changes in the heart and investigate their relation to autonomic function as assessed with heart rate variability (HRV).Methods: Eleven untreated GHD patients (mean age 50.4 +/- 10.7 years, M/F: 3/8) and 15 age- and sex-matched healthy persons (mean age 45.3 +/- 10.4 years, M/F: 5/10) were compared. Both groups were examined with echocardiography, HRV, and exercise testing and findings were analyzed.Results: The groups were similar in height, weight, body mass index, body surface area, systolic and diastolic blood pressure, heart rate. The GHD patients had lower exercise duration and metabolic equivalent (MET) compared to controls (7.94 +/- 1.26 vs. 9.8 +/- 1.9 min, P < 0.001, for MET 8.85 +/- 0.86 vs. 10.7 +/- 2.23, P = 0.03). On echocardiography, GHD patients had lower interventricular septum diastolic diameter (9 +/- 0.89 vs. 10.7 +/- 0.88 mm, P < 0.001) and posterior wall thickness (8.4 +/- 0.93 vs. 9.8 +/- 0.91 mm, P = 0.002), and lower left ventricle mass index (90.9 +/- 20 vs. 112 +/- 8 g/m2, P = 0.01). Left ventricular ejection fraction was lower in the GHD patients (57.4 +/- 5.12% vs. 65.5 +/- 4.1%, P < 0.001). Time and frequency domain heart rate variability parameters, SDNN, SDANN, VLF, LF ve LF/HF were lower in GHD patients compared to controls. There was a significant correlation between left ventricle diastolic diameter and LF (r = 0.62, P = 0.02).Conclusion: GHD seemed to cause decreased left ventricle mass and decreases in the sympathetic components of HRV that may have a bearing on the increased cardiovascular risk seen in these patients. [ABSTRACT FROM AUTHOR]