Cardiotrophin-1: A new predictor of atrial fibrillation relapses after successful cardioversion.

We aimed to investigate whether or not cardiotrophin-1 (CT-1) can be used as a predictor of sinus rhythm constancy in patients with atrial fibrillation (AF) converted to sinus rhythm. Thirty two patients with AF (48-78 years), without any structural heart disease were enrolled for the study. The control group consisted of 32, age and gender matched healthy persons. Measurements of CT-1 were made after transthoracic and transesophageal echocardiography prior to cardioversion (CV). Relapses of AF were investigated by monthly electrocardiograms (ECGs) and ambulatory ECGs at 1st, 3rd, and 6th month. At the end of 6th month, measurements of CT-1 were repeated. At the beginning patients with AF had increased CT-1 levels when compared to controls (0.94 ± 0.32 pg/mL vs. 0.30 ± 0.12 pg/mL, [p < 0.001]). At the end of follow-up of the 32 patients, 17 (53%) had AF relapse. Age, initial duration of AF, left ventricle diameters, ejection fraction, left atrium appendix flow rates were similar among patients with and without AF relapse. However, basal left atrium diameter (4.24 ± 0.14 cm vs. 4.04 ± 0.22 cm, p = 0.005), pulmonary artery pressure (32.82 ± 5 vs. 28.60 ± 6.23 mmHg, p = 0.004) and CT-1 values (1.08 ± 0.37 vs. 0.82 ± 0.16 pg/mL, p = 0.02) were significantly increased in patients with AF relapse. Furthermore, patients with relapsed AF had higher CT-1 levels at 6th month when compared to those in sinus rhythm (1.00 ± 0.40 vs. 0.71 ± 0.23 pg/mL). We conclude that post-CV, AF relapses are more frequent among patients with increased baseline CT-1 levels, and CT-1 may be a potential predictor of AF relapse.

Effect of statins on endothelial function in patients with acute coronary syndrome: a prospective study using adhesion molecules and flow-mediated dilatation.

BACKGROUND: Accumulating evidence suggests that inflammatory mechanisms play a central role in the development, progression and outcome of atherosclerosis. Recent evidence suggests that statins improve anti-inflammatory, anti-thrombotic and endothelial functions, along with their lipid-decreasing effects. We examined the effect of statins on endothelial function using biochemical markers of endothelial dysfunction and brachial artery flow-mediated dilatation (FMD). METHODS: Thirty male patients presenting with acute coronary syndrome (ACS) and 26 age-matched healthy control subjects aged 40 - 60 years who were not on any medication were enrolled in the study. The patient group was started on atorvastatin (40 mg/day) without consideration of their low-density lipoprotein (LDL)-cholesterol levels. Endothelin, sICAM and E-selectin from stored serum samples were measured using commercially available enzyme-linked immunosorbant assays (ELISAs). Endothelial function was assessed using brachial artery FMD. RESULTS: Prior to statin treatment, E-selectin, sICAM and endothelin levels, endothelial dysfunction markers, were 99.74 ± 34.67 ng/mL, 568.8 ± 149.0 ng/mL and 0.62 ± 0.33 fmol/mL, respectively in the patient group. E-selectin and sICAM levels were significantly higher in the patients than in the control subjects (P < 0.001); however, endothelin levels were not significantly different between groups. Statin treatment significantly reduced E-selectin and sICAM levels (P < 0.001); however, the decrease in endothelin levels was not statistically significant. %FMD values were significantly increased after statin treatment (P = 0.005), and levels of C-reactive protein (CRP), an inflammation marker, were significantly reduced. CONCLUSION: Our results indicate that statins play an important role in treatment endothelial dysfunction by reducing adhesion of inflammatory cells.

Evaluation of adrenomedullary function in patients with congenital adrenal hyperplasia.

BACKGROUND/AIMS: Congenital adrenal hyperplasia (CAH) is characterized by adrenal insufficiency with or without salt wasting. It is also accompanied by adrenomedullary hypofunction. The aim of the present study was to investigate adrenomedullary function in patients with CAH due to 21-hydroxylase and 11beta-hydroxylase deficiencies and in age-matched normal subjects. METHODS: We measured plasma catecholamines (epinephrine and norepinephrine) and urine metanephrine in 44 patients with CAH, 32 due to 21-hydroxylase deficiency (17 patients with the salt-wasting form and 15 patients with the simple virilizing form), and 12 due to 11beta-hydroxylase deficiency, and in 25 healthy controls. RESULTS: Plasma epinephrine and urine metanephrine levels were significantly higher in the controls than in patients with CAH (p = 0.02 and p < 0.001, respectively). Plasma norepinephrine levels were significantly lower in the controls than in patients with CAH (p < 0.001). Interestingly, patients with the salt-wasting form had lower norepinephrine levels in comparison to the other subgroups of CAH. CONCLUSION: Despite the fact that CAH patients have insufficient epinephrine secretion, these patients have the ability to increase compensatory norepinephrine. However, this increase is much lower in patients with the salt-wasting form. These findings need to be confirmed by other studies.