Assessment of the relationship between endocan and obstructive sleep apnea severity.

INTRODUCTION: Obstructive sleep apnea (OSA) and endothelial dysfunction are associated with cardiovascular risk factors and the development of atherosclerosis. Endocan is a marker of endothelial dysfunction, while obstructive sleep apnea is one of the causes of endothelial dysfunction. In this study, we investigated the relationship between endocan and obstructive sleep apnea severity. MATERIAL AND METHODS: A total of 179 patients with snoring complaints were included. All patients underwent polysomnography, and based on the results, the participations were allocated to the control group (n = 39) or to the obstructive sleep apnea group (n = 140). The OSA group was classified as having mild (apnea-hypopnea index (AHI) = 5-15; n = 43), moderate (AHI = 15-30; n = 42), or severe OSA (AHI > 30; n = 55). All participations had their endocan levels measured. RESULTS: Endocan levels in OSA patients were significantly higher than in the control group (11.8 (3.13-200) vs 3.13 (3.13-23) ng/ml, p < 0.001). Also, endocan levels were significantly higher in the severe OSA group than moderate and mild obstructive OSA (13.2 (3.13-200), 12.6 (3.13-200) and 8.44 (3.13-50.5) ng/ml, p = 0.015, respectively). Multiple logistic regression analysis showed that smoking, age and endocan levels were independent predictors of OSA severity (p = 0.024, p = 0.037, p = 0.004, respectively). CONCLUSIONS: Endocan seems to be a potential risk stratification marker in this patient population.

Decreased neurotensin levels as a biomarker in resistant hypertension.

Objective: Although neurotensin is found throughout the body including cardiovascular structures, the correlation of plasma neurotensin levels with resistant hypertension (RH) has never been examined. Therefore, we aimed to compare plasma neurotensin concentration, between patients with RH and those with controlled hypertension (CH).Methods: Forty-one patients with RH and 45 patients with CH who had undergone outpatient ambulatory blood pressure measurements were prospectively recruited. RH was defined as uncontrolled blood pressure despite using three antihypertensive agents including a diuretic or need of four or more drugs to control blood pressure. The demographic properties, medications, laboratory parameters including neurotensin levels, and echocardiographic parameters were recorded.Results: There was no significant difference among groups in terms of age, sex, smoking or body mass index. Office and ambulatory blood pressures and mean number of antihypertensive drugs used were significantly higher in patients with RH compared to patients with CH. Plasma neurotensin levels were significantly lower in patients with RH (median: 0.380 ng/ml; interquartile range: 0.292-0.471) than in the patients with controlled blood pressure (median: 0.638 ng/ml; interquartile range: 0.483-0.783). Multivariate and receiver-operating characteristics curve analyses showed that neurotensin is an independent predictor for RH and the optimal cut-off value of neurotensin for RH was lower than 0.509 ng/ml, with a sensitivity of 85.4% and a specificity of 73.3% (area under the curve = 0.793, 95% CI: 0.691-0.894, p < .001)Conclusion: This study is the first to show a correlation between lower neurotensin levels and RH.

Galectin-3 is associated with coronary plaque burden and obstructive sleep apnoea syndrome severity.

BACKGROUND: Obstructive sleep apnoea syndrome (OSAS) is reported to be associated with hypertension, coronary artery disease, atrial fibrillation, and heart failure. Galectin-3 plays an important role in the regulation of inflammation, development of cardiac fibrosis, and remodelling. A significant relationship between galectin-3 and the total number of coronary plaques and the macrocalcified plaque structures of patients with type 2 diabetes mellitus has been reported. AIM: The aim of this study was to investigate the association between galectin-3 level and coronary plaque burden as well as OSAS severity in patients with OSAS. METHODS: A total of 87 consecutive patients with a diagnosis of OSAS and 21 age- and gender-matched control subjects were recruited for the present study. The patients with OSAS were also categorised according to their apnoea hypopnoea index (AHI) as follows: mild (AHI = 5-15), moderate (AHI = 15-30), and severe (AHI > 30). All study subjects underwent coronary computed tomography angiography to detect coronary atherosclerosis. Also, all participants of serum galectin-3 concentrations were measured. RESULTS: Mean galectin-3 level was significantly higher in patients with OSAS compared to control subjects (p < 0.001) and in the severe OSAS group, compared to the moderate and mild OSAS groups (p < 0.001). Correlation analysis indicated significant positive relationships between galectin-3 concentrations and the total number of coronary plaques (p < 0.001), high-sensitivity C-reactive protein (p = 0.001), and severity of OSAS (p < 0.001). In multivariate analysis, galectin-3 (p = 0.01) and age (p = 0.025) were significant independent predictors of coronary atherosclerosis, after adjusting for other risk factors. Also, it has been found that galectin-3 concentration is a predictor of OSAS severity (p = 0.001). CONCLUSIONS: Galectin-3 is associated with coronary atherosclerosis and OSAS severity in OSAS patients.

Visfatin levels are increased in patients with resistant hypertension and are correlated with left ventricular hypertrophy.

OBJECTIVE: The aim of this study was to investigate the possible correlation of serum visfatin levels with resistant hypertension (RHT). PATIENTS AND METHODS: Patients who had undergone ambulatory blood pressure measurements (ABPM) during the outpatient controls were prospectively recruited. Seventy-one patients with RHT and 94 patients with controlled hypertension (CHT) were included in the study. RHT was defined as 'uncontrolled blood pressure (BP) despite using three antihypertensive agents including a diuretic or need of four or more drugs to control BP'. The demographic properties, medications used, and laboratory parameters including visfatin levels were recorded. RESULTS: In the RHT group, left ventricular mass index was significantly higher compared with the CHT group (108.13±26.86 vs. 89.46±24.09 g/m, P<0.01). High-sensitivity C-reactive protein and visfatin levels were significantly higher in the RHT group [4.0 (5.2) vs. 2.3 (3.0) mg/l, P<0.01, and 12.87±4.98 vs. 9.46±4.69 ng/ml, P<0.01, respectively] compared with the CHT group. In the multivariate linear regression model, visfatin level remained as an independent predictor for office systolic BP [B: 2.07, 95% confidence interval (CI): 1.17-2.98, P<0.01]; office diastolic BP (B: 0.71, 95% CI: 0.27-1.16, P<0.01); mean 24-h systolic ABPM (B: 1.46, 95% CI: 0.79-2.13, P<0.01); and mean 24-h diastolic ABPM (B: 0.88, 95% CI: 0.42-1.34, P<0.01) and was also correlated independently with left ventricular mass index (B: 3.13, 95% CI: 2.58-3.99, P<0.01). CONCLUSION: In this cohort of RHT patients diagnosed with ABPM, we have found an independent correlation between higher visfatin levels and the presence of RHT and left ventricular hypertrophy.

Assessment of relationship between galectin-3 and ambulatory ECG-based microvolt T-wave alternans in sustained systolic-diastolic hypertension patients.

OBJECTIVES: Galectin-3 is a marker associated with myocardial fibrosis and left ventricular myocardial index (LVMI). Myocardial fibrosis and LVMI have been reported in many studies to be associated with microvolt T-wave alternans (MTWA) positivity. In this study, galectin-3 levels of normotensive individuals and sustained systolic-diastolic hypertensive patients were compared and the association between galectin-3 levels and ambulatory ECG-based MTWA was investigated. METHODS: A total of 184 individuals were included in the study, among whom, 43 were normotensive and 141 had sustained systolic-diastolic hypertension without cardiovascular or chronic renal failure. Galectin-3, MTWA, and LVMI were evaluated in all participants. Galectin-3 levels of hypertensive and normotensive participants were compared. The association between galectin-3, MTWA, LVMI, and estimated glomerular filtration rate (eGFR) was investigated in hypertensive patients. RESULTS: LVMI and galectin-3 levels were higher among hypertensive patients compared with normotensives (94.9±26.8 vs. 76.4±22.9 g/m, 7.325±2.123 vs. 5.233±1.506 ng/ml; P<0.001, P<0.001). Correlation analysis carried out among the hypertensive patients showed that the galectin-3 level was correlated positively to LVMI, age, and MTWA positivity (r=0.396, P<0.001; r=0.358, P<0.001; r=0.361, P<0.001, respectively), whereas it was correlated negatively to eGFR and male sex (r=-0.364, P<0.001; r=-0.280, P=0.001, respectively). Multiple logistic regression analysis indicated that LVMI and galectin-3 showed an independent association with MTWA positivity in hypertensive patients (P=0.003 and 0.005, respectively). CONCLUSION: Increased galectin-3 levels are associated with ambulatory ECG-based MTWA positivity, decreased eGFR, and increased LVMI in hypertensive patients. This association may be used for risk classification in this patient group.

The prognostic value of admission mean platelet volume to platelet count ratio in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

BACKGROUND: Mean platelet volume to platelet count (MPV/Plt) ratio has been demonstrated to be a good indicator of long-term mortality in patients with non-ST-segment elevation myocardial infarction (NSTEMI). However, the prognostic value of MPV/Plt in ST-elevation myocardial infarction (STEMI) is not reported. AIM: To determine whether the MPV/Plt ratio on admission has any predictive value for major adverse cardiac events including short- and long-term mortality in STEMI. METHODS: In this prospective study, 470 STEMI patients who underwent primary percutaneous coronary intervention (PCI) were enrolled. The patients were divided into three tertiles based on the MPV/Plt ratio on admission. The first tertile (n = 149) was defined as MPV/Plt ratio ≤ 0.029, second tertile (n = 154) 0.029-0.038, and third tertile (n = 159) ≥ 0.038. Primary clinical outcomes consisted of the sum of cardiovascular (CV) mortality, non-fatal re-infarction, and stroke. Secondary clinical outcomes were CV mortality, non-fatal re-infarction, target-vessel revascularisation, stroke, and advanced heart failure. RESULTS: There was no difference between study groups regarding the primary (p > 0.05) and the secondary outcomes (p > 0.05) except for one-year non-fatal re-infarction rate, which was found to be significantly higher in the highest MPV/Plt ratio group (p = 0.045). Age, Killip class > 1, and left ventricular ejection fraction were found to be independent predictors of long-term CV mortality in multivariate analysis (p = 0.009, p = 0.035, and p < 0.001, respectively). CONCLUSIONS: While the MPV/Plt ratio was demonstrated to be associated with one-year non-fatal re-infarction, it was not related to in-hospital, one-month, and one-year CV mortality in patients with STEMI, who underwent primary PCI.

Assessment of the Relationship Between Serum Vascular Adhesion Protein-1 (VAP-1) and Severity of Calcific Aortic Valve Stenosis.

BACKGROUND: Vascular adhesion protein-1 (VAP-1), a dual-function glycoprotein, is secreted by endothelial cells, adipocytes, and kidney and vascular smooth muscle cells. It has been reported to participate in the development of atherosclerosis as an adhesion molecule and a pro-inflammatory enzyme. Increased VAP-1 levels are related to type 2 diabetes mellitus, atherosclerosis, stroke and chronic renal failure. The study aim was to investigate serum VAP-1 levels in patients with calcific aortic stenosis (AS) and the possible relationship between VAP-1 and severity of calcific AS. METHODS: A total of 168 patients was categorized as having mild (n = 54), moderate (n = 58), or severe (n = 56) AS. Serum VAP-1 levels were measured using an enzyme-linked immunosorbent assay. RESULTS: The mean serum VAP-1 level was significantly higher in patients with AS compared to healthy controls (244.3 ± 50.1 ng/ml versus 149.8 ± 27.5 ng/ml, p <0.001), and in the severe AS group compared to the moderate and mild AS groups (288.3 ± 30.1 ng/ml, 243.1 ± 31.8 ng/ml, and 200.8 ± 43.2 ng/ml, respectively, p <0.001). The VAP-1 level was positively related to the maximum aortic gradient, mean aortic gradient, and maximum aortic jet velocity (r = 0.649, p <0.001; r = 0.660, p <0.001; r = 0.655, p <0.001, respectively) and negatively related to the aortic valve area (r = -0.683, p <0.001). CONCLUSIONS: The present study was the first to demonstrate a significant relationship between increased serum VAP-1 levels and the severity of calcific AS. VAP-1 might be a useful biomarker for the evaluation of AS and the follow up of its severity.