Association among tenascin-C and NT-proBNP levels and arrhythmia prevalence in heart failure.

PURPOSE: Tenascin-C (TN-C) and amino-terminal fragment of the B-type natriuretic peptide (NT-proBNP) are the important predictors in prognosis of heart failure (HF). The aim of this study was to analyze the relationship of TN-C and NT-proBNP levels with the frequency and severity of ventricular arrhythmia. MATERIALS AND METHODS: Our study included 107 HF patients with EF < 45%. According to Holter analysis, the patients were divided into two groups as malignant arrhythmia group (n=29) with Lown Class 4a and 4b arrhythmia and benign arrhythmia group(n=78) with Lown Class 0-3b arrhythmia. The groups were compared with respect to levels of TN-C and NT-proBNP. The relationship of TN-C and NT-proBNP levels with frequency of ventricular premature beat (VPB) was also analyzed. FINDINGS: NT-proBNP (5042.1±1626 versus 1417.1±1711.6 pg/ml) and TN-C (1089±348.6 versus 758.5±423.9 ng/ml) levels were significantly higher in the malignant arrhythmia group than that of the benign arrhythmia group (p.

Assessment of insulin-like growth factor-1 (IGF-I) level in patients with rheumatic mitral stenosis.

OBJECTIVES: Insulin-like growth factor-1 may serve some regulatory function in the immune system. Rheumatic mitral stenosis is related to autoimmune heart valve damage after streptococcal infection. The aim of this study was to assess the level of insulin-like growth factor-1 and its correlation with the Wilkins score in patients with rheumatic mitral stenosis. METHODS: A total of 65 patients with rheumatic mitral stenosis and 62 age- and sex-matched control subjects were enrolled in this study. All subjects underwent transthoracic echocardiography. The mitral valve area and Wilkins score were evaluated for all patients. Biochemical parameters and serum insulin-like growth factor-1 levels were measured. RESULTS: Demographic data were similar in the rheumatic mitral stenosis and control groups. The mean mitral valve area was 1.6±0.4 cm2 in the rheumatic mitral stenosis group. The level of insulin-like growth factor-1 was significantly higher in the rheumatic mitral stenosis group than in the control group (104 (55.6-267) versus 79.1 (23.0-244.0) ng/ml; p=0.039). There was a significant moderate positive correlation between insulin-like growth factor-1 and thickening of leaflets score of Wilkins (r=0.541, p<0.001). CONCLUSIONS: The present study demonstrated that serum insulin-like growth factor-1 levels were significantly higher in the rheumatic mitral stenosis group compared with control subjects and that insulin-like growth factor-1 level was also correlated with the Wilkins score. It can be suggested that there may be a link between insulin-like growth factor-1 level and immune pathogenesis of rheumatic mitral stenosis.

Decreased parasympathetic activity in patients with functional dyspepsia.

OBJECTIVE: Functional dyspepsia (FD) can be described as the presence of symptoms such as bothersome postprandial fullness, early satiation, epigastric pain, and burning without any evidence of structural disease. The aim of this study was to evaluate the autonomic nervous system using heart rate variability (HRV) in patients with postprandial distress syndrome and epigastric pain syndrome. PATIENTS AND METHODS: The study population included 64 consecutive patients with a diagnosis of FD and 62 age-matched and sex-matched healthy control individuals with no clinical evidence of gastrointestinal, systemic, or cardiovascular diseases. All patients underwent upper gastrointestinal endoscopy and 24 h Holter monitoring. RESULTS: There were 30 patients with postprandial distress syndrome and 34 with epigastric pain syndrome. Twenty-four hour square root of the mean squared differences of the successive normal to normal intervals (RMSSD) (30.5 ± 12.4, 35.8 ± 13.9; P=0.047), 24 h proportion derived by dividing the number of interval differences of successive normal to normal intervals greater than 50 ms (PNN50) (9.8 ± 3.9, 14.1 ± 7.3; P=0.017), daytime PNN50 (6.8 ± 1.6, 18.4 ± 13.8; P<0.001), night SD of the normal to normal intervals (SDNN) (111.4 ± 39.9, 133.4 ± 29.8; P=0.001), and night RMSSD (31.7 ± 12.4, 38.2 ± 17.5; P=0.019) were significantly lower in patients with FD than controls. Other HRV parameters were not significantly different between the two groups. Changes in these parameters showed a decreased parasympathetic tone and discordance in sympathovagal activity in FD. CONCLUSION: Our study showed decreased parasympathetic activity in the patients with FD. Further studies are required to evaluate the significance of HRV parameters and to clarify the mechanism of decreased parasympathetic activity in patients with FD.

Evaluation of early atherosclerosis markers in patients with nonalcoholic fatty liver disease.

OBJECTIVES: Nonalcoholic fatty liver disease (NAFLD) is characterized by the excessive accumulation of fat in the liver cells. It is strongly associated with cardiovascular risk factors for atherosclerosis. Flow-mediated dilation (FMD) and carotid intima-media thickness (CIMT) are noninvasive methods for the evaluation of endothelium. They are considered early markers of atherogenesis. The aim of this study was to evaluate early atherosclerosis markers in patients with NAFLD. METHODS: We examined 161 patients. All the patients underwent hepatic ultrasonography, transthoracic echocardiography, and brachial artery and carotid artery imaging. Fasting blood samples were drawn from all patients for the determination of lipids, insulin, C-peptide, and fasting blood glucose. HOMA-IR was calculated. RESULTS: Among the 161 patients, 44 had normal hepatic ultrasonography, 42 had stage 1 hepatosteatosis, 53 had stage 2 hepatosteatosis and 22 had stage 3 hepatosteatosis. FMD was reduced in patients with NAFLD as compared with the healthy controls (5.9 ± 3.1 vs. 9.6 ± 2.7%, P<0.001). There was a significant negative moderate correlation between ultrasonographic hepatosteatosis grade and FMD (r=-0.556, P<0.001). The mean CIMT was significantly increased in patients with NAFLD as compared with the controls (0.40 ± 0.19 vs. 0.27 ± 0.18, P<0.001). There was a significant positive weak correlation between ultrasonographic hepatosteatosis grade and mean CIMT (r=0.376, P<0.001). CONCLUSION: This study showed that NAFLD is associated with impaired CIMT and FMD, which are early markers of atherosclerosis. These findings may play a crucial role in understanding the pathophysiology of the atherosclerotic process in patients with NAFLD.

Elevation of QT dispersion after obesity drug sibutramine.

BACKGROUND: QT dispersion (QTd) is an arrhythmia parameter that can be used to assess homogeneity of cardiac repolarization. An antiobesity drug sibutramine is linked with several cardiovascular adverse events, including arrhythmias. Previous studies showed that sibutramine may prolong the QT interval and may be associated with cardiac arrest. OBJECTIVES: The aim of this study was to evaluate the effect of sibutramine on QTd. METHODS: The study group consisted of 65 consecutive patients with obesity. All patients were to receive 15 mg of sibutramine once a day in addition to standard care for lifestyle change. Twelve-lead ECG was performed before the onset of the medication and after 16 weeks of treatment. QTd was calculated. RESULTS: Three individuals were withdrawn from the study because of the adverse effects of sibutramine. Sixty-two patients with obesity were recruited into the study. All patients were women (62, 100%). Body weight (106.3 ± 15.0 kg vs. 101.6 ± 16.9 kg, P < 0.001) and low-density lipoprotein cholesterol (128.4 ± 29.7 mg/dl vs. 111.6 ± 24.6 mg/dl, P < 0.001) levels were significantly decreased whereas QTd (46.1 ± 22.6 ms vs. 53.7 ± 16.7 ms, P = 0.026) was significantly increased after 16 weeks of sibutramine treatment. The increase in QTd was not correlated with the decrease in body weight. There was no correlation between QTd and any conditions such as diabetes or hypertension. CONCLUSION: This study has shown an elevation in QTd, which may lead to cardiac arrhythmias, after sibutramine treatment. Molecular mechanisms may play role in increasing QTd. Further randomized studies are needed to clarify cardiac adverse events of the sibutramine.