The effect of bilirubin on long-term mortality in patients with chronic total coronary occlusion.

AIM: We intended to investigate the association of bilirubin with total mortality in patients with chronic total coronary occlusion (CTO). METHODS: We included 172 patients who underwent coronary angiography due to stable angina pectoris and had CTO. We checked the viability of patients after 9 years of follow-up. RESULTS: Direct bilirubin levels were significantly lower in the non-viable group. We revealed age (OR = 1.045, 95% C.I: 1.009‒1.083; p = 0.015) and direct bilirubin concentrations (OR = 0.029, 95% C.I: 0.002‒0.435; p = 0.029) as independent predictors of mortality. Direct bilirubin value of > 0.2 mg/dL was associated with decreased mortality with a sensitivity of 85 %, and a specificity of 46 %. CONCLUSION: Serum direct bilirubin concentrations independently predict total mortality in patients with chronic total occlusion over 9 years of follow-up (Tab. 1, Fig. 2, Ref. 23).

The effect of different ß-blockers on vascular graft nitric oxide levels: comparison of nebivolol versus metoprolol.

OBJECTIVES: The aim of this study was to investigate the effects of the vasodilating ß-blocker nebivolol and the cardioselective ß-blocker metoprolol on nitric oxide (NO) levels at vascular graft endothelium and vasa vasorum compared to controls in patients undergoing coronary artery bypass graft surgery. METHODS: This was a prospective study. Fifty-five patients were divided into three groups: nebivolol group (group N, n = 23), metoprolol group (group M, n = 16), and control group (group A, n = 16). Group N received nebivolol 5 mg once daily, and group M received metoprolol 50 mg once daily for 15 days in the preoperative period. Control patients did not use ß-blocker therapy. Tissue samples of both left internal mammary artery (LIMA) and saphenous vein grafts were investigated for NO activity using immunohistochemical methods. RESULTS: Demographic characteristics and risk factors were similar between groups. We observed the highest NO activity in group N in both endothelial and vasa vasorum samples of LIMA and saphenous veins. NO activity of metoprolol group was similar to controls. CONCLUSIONS: According to our results, we think that nebivolol may be safer and preferable in order to diminish graft spasm in patients undergoing coronary artery bypass graft surgery due to the NO-mediated vasodilating effect.

Cardiac syncope due to pain: report of a case responsive to duloxetine treatment.

Neurocardiogenic syncope comprises situations triggered by neurological reflexes resulting in abnormal responses of the neurocardiovascular system that cause loss of consciousness. A vast number of clinical conditions may cause this disorder including pain, defecation, micturition, swallowing, cough, sudden fear or excitement, exercise, and long-time standing. Treatment options for syncope prevention are not satisfactory. Several agents were used for pharmacological treatment without success. Selective inhibitors of neuronal norepinephrine transporter (NET) like duloxetine may play a role in neurally mediated syncope by increasing synaptic norepinephrine levels. Therefore, we report the effect of duloxetine in a patient with pain-induced syncope resistant to standard regimens.

Relationship between fragmented QRS complexes and left ventricular systolic and diastolic functions.

BACKGROUND: Fragmented QRS complexes (fQRS) have been associated with increased morbidity and mortality, sudden cardiac death, and recurrent cardiovascular events. The association between left ventricular systolic and diastolic functions and presence of fragmented QRS has not been comprehensively studied to date. We tested the hypothesis that the presence of fragmented QRS is associated with left ventricular systolic and diastolic dysfunction. METHODS: The study included 259 patients who were consecutively admitted to our outpatient clinic for cardiovascular risk factor management. Extensive echocardiographic parameters were obtained from all patients and these were compared with the presence and number of fQRS. RESULTS: Patients with fQRS were of older age (58 ± 12 vs. 55 ± 13 years, p = 0.03) and had prolonged QRS time (105 ± 12 vs. 93 ± 10 ms, p < 0.001) and a higher rate of Q waves on ECG (36% vs. 11%, p < 0.001). In addition, they had worse systolic (lower LVEF%, 44 ± 17 vs. 61 ± 12, p < 0.001) and diastolic functions (DT, 177 ± 77 vs. 211 ± 59 ms, p < 0.001; IVRT, 81 ± 27 vs. 92 ± 22 ms, p = 0.001; Em, 9 ± 4 vs. 10 ± 4 cm/s, p = 0.008; E/Em ratio, 11 ± 5 vs. 8 ± 4, p < 0.001) in comparison to patients with nonfragmented QRS. There was a significant negative correlation between the number of fQRS and left ventricle systolic functions (for LVEF%, r = - 0.595, p < 0.001). After adjustment for age and gender, the number of fQRS remained significantly negatively associated with left ventricular systolic and diastolic functions. CONCLUSION: We found that fQRS is related to left ventricular systolic dysfunction and diastolic dysfunction. fQRS, which may be the result of myocardial ischemia or scar on myocardial electrical parameters at the cellular level, may represent inadequate systolic and diastolic functions.

Increased serum resistin levels in patients with coronary slow-flow phenomenon.

BACKGROUND: Slow coronary flow (SCF) is an angiographic finding characterized by delayed opacification of the epicardial coronary arteries without obstructive coronary disease. Resistin, an adipocytokine, plays a major role besides low-grade inflammation in atherosclerotic vascular processes and may be of importance in other coronary pathologies such as SCF. METHODS: The present study was cross-sectional and observational, consisting of 70 individuals who underwent coronary angiography and had angiographically normal coronary arteries of varying coronary flow rates. The study included 50 patients with isolated SCF and 20 control participants with normal coronary flow (NCF). RESULTS: There were no statistically significant differences between the SCF and NCF groups with respect to age, gender, presence of hypertension or diabetes mellitus, and smoking habit, except for increased creatinine levels (p = 0.014). The serum resistin level was significantly higher in the SCF group than in the NCF group (8.4 ± 7.2 vs. 5.4 ± 2.6 ng/ml, p = 0.014). Ln-transformed resistin levels correlated positively with left anterior descending (LAD) coronary artery TIMI frame count (TFC) (r = 0.408, p < 0.001) as well as with glucose (r = 0.340, p = 0.004), creatinine (r = 0.248, p = 0.044), and C-reactive protein (CRP; r = 0.283, p = 0.023) levels, and negatively with LAD coronary flow velocity (r = - 0.314, p = 0.009). When multivariate analyses were performed, in linear regression analysis, ln-resistin was associated with a longer TFC [beta (standardized regression coefficient): 0.404, p = 0.001] and lower coronary flow velocity (beta: - 0.280, p = 0.035); in logistic regression analysis, ln-resistin was an independent predictor of the presence of SCF (OR: 6.692, 65 %CI: 1.117-40.1, p = 0.037). CONCLUSION: We demonstrated, for the first time, a significant increase in serum resistin levels in patients with SCF compared to subjects with NCF. We believe that further studies are needed to clarify the role of resistin in patients with SCF.

Aortic valve sclerosis is a high predictive marker of systemic endothelial dysfunction in hypertensive patients.

BACKGROUND: Aortic valve sclerosis (AVS) is closely related to hypertension and is an important predictor of coronary artery disease as well as cardiovascular morbidity and mortality. However, the mechanisms causing AVS have not yet been clarified. Therefore, we planned to investigate the influence of atherosclerosis-related risk factors including C-reactive protein (CRP), epicardial adipose tissue (EAT), carotid intima-media thickness (CIMT), pulse wave velocity (PWV), left ventricular hypertrophy, and the conventional risk parameters as well as endothelial dysfunction in untreated hypertensive patients. METHODS AND RESULTS: Our study was cross-sectional and observational, and included 107 consecutive untreated hypertensive patients. All patients underwent vascular evaluation by CIMT, PWV, flow-mediated dilation (FMD%), as well as echocardiographic examinations. Age (OR = 1.180, p < 0.001), male sex (OR = 3.056, p = 0.019), waist circumference (OR = 1.082, p = 0.004), EAT (OR = 1.419, p = 0.001), smoking status (OR = 3.161, p = 0.014), FMD% (OR = 0.649, p < 0.001), mean CIMT (OR = 2.481, P < 0.001), and carotid plaque (OR = 4.692, P = 0.001) were associated with AVS in univariate analyses. Multivariate analyses revealed only age (OR = 1.144, P = 0.006) and FMD% (OR = 0.691, 0.001) as independent predictors of AVS. The presence of AVS had a high positive predictive value (100 %) but a low negative predictive value (51 %) for endothelial dysfunction (FMD < 12 %) in hypertensive patients. CONCLUSION: Our study supports the theory that systemic endothelial dysfunction has an initial and independent effect on AVS pathogenesis. Moreover, we demonstrated that the presence of AVS in patients with hypertension predicts endothelial dysfunction, with a high positive predictive value. Thus, AVS in hypertensive patients may urge clinicians toward aggressive risk factor modification and intensive treatment.

Elevated serum YKL-40 level predicts myocardial reperfusion and in-hospital MACE in patients with STEMI.

BACKGROUND: Macrophages in atherosclerotic plaques secrete YKL-40, a new biomarker of acute and chronic inflammation in patients with stable CAD. We hypothesized that YKL-40 may be a specific marker reflecting the burden of localized inflammation in myocardium and a predictor in patients with STEMI. In this study, we investigated the relationship of YKL-40 to in-hospital major adverse cardiac events (MACE), reperfusion parameters and its predictors in patients with STEMI. METHODS: In total, 80 patients with STEMI and no history of prior coronary artery disease (CAD), who underwent primary percutaneous coronary intervention (p-PCI), were enrolled consecutively. In addition, 30 patients with normal coronary arteries (NCA) were enrolled as a control group. Cardiac biomarker levels including creatinine kinase-MB fraction (CK-MB), troponin-I, admission glucose and inflammatory markers including leukocytes and YKL-40 levels were measured as admission values. RESULTS: In our study, YKL-40 levels correlated to high-sensitivity CRP levels (r = 0.333, p = 0.003), TIMI risk score (r = 0.445, p < 0.001), age (r = 0.477, p < 0.001), pain to balloon time (r = 0.432, p < 0.001), leukocyte and neutrophil count (r = 0.386, p < 0.001 and r = 0.430, p < 0.001, respectively), hemoglobin (r = - 0.345, p = 0.002), admission and fasting blood glucose (r = 0.388, p < 0.001 and r = 0.427, p < 0.001), creatinine levels (r = 0.395, p < 0.001) and myocardial blush grade (r = - 0.334, p = 0.004). When the patients were divided into two groups determined by presence or absence of MACE, the patients with MACE had significantly higher levels of YKL-40 in comparison to the patients without MACE and the control group (194 ± 104, 114 ± 61 and 110 ± 53 µg/L, p < 0.001, respectively). In multivariate logistic regression analysis in STEMI patients, only YKL-40 level (OR: 1.011, 95%CI: 1.002-1.019, p = 0.011) and leukocyte count (OR: 1.264, 95%CI: 1.037-1.540, p = 0.020) were the independent predictors for MACE. Sensitivity and specificity of YKL-40 to predict MACE, when 125 µg/l was accepted as a cut-off value, were 84% and 70%, respectively. CONCLUSION: We found that serum YKL-40 is related to older age, increased admission glucose levels, leukocyte counts and decreased hemoglobin levels; YKL-40 level and leukocyte count independently predicted MACE.