Yusuf Izzettin Alihanoglu

Intravenous N-acetylcysteine plus high-dose hydration versus high-dose hydration and standard hydration for the prevention of contrast-induced nephropathy: CASIS—A multicenter prospective controlled trial

BACKGROUND Contrast-induced nephropathy (CIN) is a leading cause of acute renal failure and affects mortality and morbidity. We investigated the efficacy of prophylactic intravenous (IV) N-acetylcysteine (NAC) and hydration for the prevention of CIN in patients with mild to moderate renal dysfunction who are undergoing coronary angiography and/or percutaneous coronary intervention (PCI). METHODS A total of 220 patients who had mild to moderate renal dysfunction with serum creatinine (SCr) ≥ 1.1mg/dL or creatinine clearance ≤ 60 mL/min were randomized in 3 groups: 80 patients were assigned to IV NAC plus high-dose hydration with normal saline, 80 patients to only high-dose hydration with normal saline and 60 patients to standard hydration with normal saline (control group). The primary end point was the alteration of SCr level. The secondary end point was the development of CIN after the procedure. RESULTS SCr levels changed the least in the NAC plus high-hydration group (P=0.004). The rate of the CIN in the NAC plus high-dose hydration group was also lower than the high-dose hydration group (P=0.006). No significant differences in the primary and secondary end points were found between high-dose hydration and control group. CONCLUSION The results of this study suggest that NAC plus high-dose hydration was superior to high-dose hydration alone as well as standard hydration for the protection of renal functions in patients with mild to moderate renal dysfunction who are undergoing coronary angiography and/or PCI. High-dose hydration without NAC was not better than standard hydration alone.

microRNA -143 and -223 in obesity

BACKGROUND Obesity alters endocrine and metabolic functions of adipose tissue and has been recognized as a chronic inflammatory disease, which in turn may contribute to the development of insulin resistance, type 2 diabetes, obesity-associated vasculopathy and cardiovascular disease. The pathogenesis of obesity involves many regulatory pathways including transcriptional regulatory networks, including microRNAs. METHODS A total of 83 patients were included in the study. Patients were recruited from a cardiology outpatient clinic and were allocated into 3 age- and sex-matched groups according to their body mass index. Group 1 included 23 morbidly obese, group 2 30 obese, and group 3 30 normal or overweight subjects. RESULTS In our study, we showed that miR-143 and miR-223 levels were significantly lower in groups 1 and 2 than the control group (normal BMI or overweight). CONCLUSIONS Obesity leads to alterations in miRNA expressions and miRNA-143 and -223s can be used as biomarkers for the metabolic changes in obesity.

Atorvastatin given prior to electrical cardioversion does not affect the recurrence of atrial fibrillation in patients with persistent atrial fibrillation who are on antiarrhythmic therapy.

Objective: In this study, our aim was to evaluate the effect of a higher dose of atorvastatin on the recurrence rate of atrial fibrillation (AF) after electrical cardioversion (EC) in addition to antiarrhythmic therapy. Subjects and Methods: 48 patients with persistent AF were included in this study. The patients were randomized to an atorvastatin 40-mg treatment group and a control group. Atorvastatin was started 3 weeks before EC and was continued for 2 months after EC. EC was performed using biphasic shocks after 3 weeks of treatment with the orally administered anticoagulant warfarin. Lipid and inflammatory parameters (high-sensitivity C-reactive protein, white blood cell count and fibrinogen level) were evaluated at the baseline and before EC. The endpoint of this study was electrocardiographically confirmed recurrence of AF of >10 min. Results: There were no significant differences in baseline characteristics and lipid and inflammatory marker levels between the treatment and control groups. Total cholesterol and low-density lipoprotein levels were significantly decreased in patients taking atorvastatin for 2 months compared with baseline values (174 ± 31 vs. 129 ± 25 mg/dl, p = 0.001, and 112 ± 23 vs. 62 ± 20 mg/dl, p = 0.001, respectively), while no significant change occurred in control patients (168 ± 26 vs. 182 ± 29 mg/dl, p = 0.07, and 99 ± 18 vs. 108 ± 26 mg/dl, p = 0.1, respectively). At the end of the 2-month follow-up period, 9 patients (20.5%) experienced AF recurrence, and there was no significant difference in AF recurrence rate between the treatment and control groups (26 vs. 13%; p = 0.2). Conclusion: Atorvastatin therapy prior to EC does not prevent the recurrence of arrhythmia in patients with persistent AF who are receiving antiarrhythmic therapy.

A comparison of blood pressure and pulse pressure values obtained by oscillometric and central measurements in hypertensive patients

Abstract Objective. Wide pulse pressure (PP) affects the accuracy of oscillometric blood pressure measurements (OBPM): however, the degree of this impact on different patient groups with wide PPs is unclear. This study will investigate the accuracy of OBPM in achieving target BP and PP in isolated systolic hypertension (ISH) group compared with mixed hypertension (MHT) group. Method. A total of 115 patients (70 with ISH and 45 with MHT) were enrolled in the study. Upper arm and wrist OBPM, obtained by OmronM3 and OmronR6 devices respectively, were compared with the simultaneously measured values from the ascending aorta. The ISH was defined as a systolic blood pressure (SBP) ≥140 mmHg and a diastolic blood pressure (DBP) <90 mmHg. MHT was defined as a SBP≥140 mmHg and a DBP≥90 mmHg. Results. The mean central arterial blood pressure (BP) and central PP were higher in the ISH group than those in the MHT group. The upper arm OBPM underestimated the central SBP in two groups (−5 mmHg, −3 mmHg, p=0.5, respectively), but overestimated DBP in the ISH group compared with MHT patients (6.8 mmHg, 1 mmHg, p=0.04, respectively). Wrist OBPM similarly underestimated to the central SBP in each group (−16 mmHg, −19 mmHg, p=0.15), whereas the sum of overestimation of DBP was significantly higher in the ISH than in the MHT group (+6 mmHg, − 1 mmHg, p=0.001, respectively). Also, each of the devices underestimated the central PP in the ISH group (about 10 mmHg) as being higher than that of the MHT group. Conclusion. Oscillometric devices may be used for self-BP measurement in patients with ISH without clinically important disadvantages compared with the patients with MHT. For PP measurement in patients with ISH, there were substantial differences between intra-arterial and indirect arm BP measurements.

Circadian Rhythm of Infarct Size and Left Ventricular Function Evaluated with Tissue Doppler Echocardiography in ST Elevation Myocardial Infarction.

BACKGROUND We aimed to investigate the circadian rhythm on left ventricular (LV) function and infarct size, according to the onset of ST elevation myocardial infarction (STEMI), with echocardiography in patients with first STEMI successfully revascularised with primary percutaneous coronary intervention (PCI). METHODS We conducted a retrospective analysis of 252 STEMI patients. Patients were divided into the four, six-hour periods of the day. Conventional and tissue Doppler imaging (TDI) echocardiography were performed within 48hours after onset of chest pain. The average of peak systolic myocardial velocities (Sm) in each of the four myocardial segments and LV ejection fraction (LVEF) were calculated. RESULTS A negative linear correlation was shown between CK-MB levels and Sm (r= -0.209, p=0.001). There was an oscillation between time of day and average of Sm. The lowest Sm and largest infarct size were in the period of 06:00-noon compared with period of noon-18:00 and 18:00-midnight (p=0.029 and p=0.031, respectively). A secondary analysis showed that both LVEF and Sm were lower in the midnight-noon group compared with the noon-midnight group (44.9±7.3% versus 47.3±7.9%, p=0.018, and 7.6±1.4cm/s versus 8.2±1.6cm/s, p=0.003, respectively). CONCLUSIONS This study has shown that there was a circadian rhythm of infarct size and LV function evaluated by echocardiography according to time of STEMI onset. The largest infarct size and poor LV function occurred in the midnight-noon period, in particular in the 06:00-noon period.

Effects of ivabradine therapy on heart failure biomarkers

BACKGROUND Heart rate (HR) reduction is associated with improved outcomes in patients with heart failure (HF) and biomarkers can be a valuable diagnostic tool in HF management. The primary aim of our study was to evaluate the short-term (6 months) effect of ivabradine on N-terminal pro B-type natriuretic peptide (NT-proBNP), CA-125, and cystatin-C values in systolic HF outpatients, and secondary aim was to determine the relationship between baseline HR and the NT-proBNP, CA-125, cystatin-C, and clinical status variation with ivabradine therapy. METHODS Ninety-eight patients (mean age: 65.81 ± 10.20 years; 33 men), left ventricular ejection fraction < 35% with Simpson method, New York Heart Association (NYHA) class II-III, sinus rhythm and resting HR > 70/min, optimally treated before the study were included. Among them, two matched groups were formed: the ivabradine group and the control group. Patients received ivabradine with an average (range of 10-15) mg/day during 6 months of follow-up. Blood samples for NT-proBNP, CA-125, and cystatin-C were taken at baseline and at the end of a 6-month follow-up in both groups. RESULTS There was a significant decrease in NYHA class in the ivabradine group (2.67 ± ± 0.47 vs. 1.85 ± 0.61, p < 0.001). When ivabradine and control groups were compared, a significant difference was also found in NHYA class 6 months later (p = 0.013). A significant decrease was found in HR in the ivabradine and control groups (84.10 ± 8.76 vs. 68.36 ± ± 8.32 bpm, p = 0.001; 84.51 ± 10 vs. 80.40 ± 8.3 bpm, p = 0.001). When both groups were compared, a significant difference was also found in HR after 6 months (p = 0.001). A significant decrease was found in cystatin-C (2.10 ± 0.73 vs. 1.50 ± 0.44 mg/L, p < 0.001), CA-125 (30.09 ± 21.08 vs. 13.22 ± 8.51 U/mL, p < 0.001), and NT-proBNP (1,353.02 ± 1,453.77 vs. 717.81 ± 834.76 pg/mL, p < 0.001) in the ivabradine group. When ivabradine and control groups were compared after 6 months, a significant decrease was found in all HF parameters (respectively; cystatin-C: p = 0.001, CA-125: p = 0.001, NT-proBNP: p = 0.001). Creatinine level was significantly decreased and glomerular filtration rate (GFR) was significantly increased in the ivabradine group (1.02 ± 0.26 vs. 0.86 ± 0.17, creatinine: p = 0.001; 79.26 ± 18.58 vs. 92.48 ± 19.88, GFR: p = 0.001). There was no significant correlation between NYHA classes (before and after ivabradine therapy) and biochemical markers, or HR. CONCLUSIONS In the outpatients with systolic HF, persistent resting HF > 70/min with optimal medical therapy, the NT-proBNP, CA-125, and cystatin-C reductions were obtained with ivabradine treatment. Measurement of NT-proBNP, CA-125, and cystatin-C may prove to be useful in biomarker panels evaluating ivabradine therapy response in HF patients.

Does Spironolactone Have a Dose‐Dependent Effect on Left Ventricular Remodeling in Patients with Preserved Left Ventricular Function After an Acute Myocardial Infarction?

AIMS The aim of this study was to investigate the effects of spironolactone on left ventricular (LV) remodeling in patients with preserved LV function following acute myocardial infarction (AMI). METHODS AND RESULTS Successfully revascularized patients (n = 186) with acute ST elevation MI (STEMI) were included in the study. Patients were randomly divided into three groups, each of which was administered a different dose of spironolactone (12.5, 25 mg, or none). Echocardiography was performed within the first 3 days and at 6 months after MI. Echocardiography control was performed on 160 patients at a 6-month follow-up. The median left ventricular ejection fraction (LVEF) increased significantly in all groups, but no significant difference was observed between groups (P = 0.13). At the end of the sixth month, the myocardial performance index (MPI) had improved in each of the three groups, but no significant difference was found between groups (F = 2.00, P = 0.15). The mean LV peak systolic velocities (Sm ) increased only in the control group during the follow-up period, but there is no significant difference between groups (F = 1.79, P = 0.18). The left ventricular end-systolic volume index (LVESVI) and the left ventricular end-diastolic volume index (LVEDVI) did not change significantly compared with the basal values between groups (F = 0.05, P = 0.81 and F = 1.03, P = 0.31, respectively). CONCLUSION In conclusion, spironolactone dosages of up to 25 mg do not augment optimal medical treatment for LV remodeling in patients with preserved cardiac functions after AMI.

Circulating adhesion molecules and arterial stiffness.

Summary Aim VCAM-1 and ICAM-1 are two important members of the immunoglobulin gene superfamily of adhesion molecules, and their potential role as biomarkers of diagnosis, severity and prognosis of cardiovascular disease has been investigated in a number of clinical studies. The aim of the present study was to determine the relationship between circulating ICAM-1 and VCAM-1 levels and aortic stiffness in patients referred for echocardiographic examination. Methods Aortic distensibility was determined by echocardiography using systolic and diastolic aortic diameters in 63 consecutive patients referred for echocardiography. Venous samples were collected in the morning after a 12-hour overnight fast, and serum concentrations of ICAM-1 and VCAM-1 were measured using commercial enzyme immunoassay kits. Results Data of a total of 63 participants (mean age 55.6 ± 10.5 years, 31 male) were included in the study. Circulating levels of adhesion molecules were VCAM-1: 12.604 ± 3.904 ng/ml and ICAM-1: 45.417 ± 31.429 ng/ml. We were unable to demonstrate any correlation between indices of aortic stiffness and VCAM-1 and ICAM-1 levels. Conclusion The role of soluble adhesion molecules in cardiovascular disease has not been fully established and clinical studies show inconsistent results. Our results indicate that levels of circulating adhesion molecules cannot be used as markers of aortic stiffness in patients.

Choroidal changes after cardiopulmonary bypass.

Aim: Choroid, which is the vascular tissue responsible for blood supply to the outer parts of the retina, might be affected by hemodynamic events. We aimed to reveal choroidal thickness and ocular pulse amplitude changes after cardiopulmonary bypass in which gross hemodynamic alterations occur. Methods: Forty-two eyes of 42 patients who underwent heart surgery with cardiopulmonary bypass were examined in this prospective, cross-sectional case series. The spectral domain optical coherence tomography (Spectralis, Heidelberg, Germany) was used to analyze sub-foveal choroidal thickness. The ocular pulse amplitude, the surrogate of gross choroidal blood flow, was measured with the Pascal dynamic contour tonometer (Pascal DCT, Swiss Microtechnology AG, Port, Switzerland).. The intraocular pressure was also measured with this tonometer. The examinations were performed pre-operatively and post-operatively at the first week and first month. Results: The mean age of the patients was 58.8 ± 12.4 years. The mean sub-foveal choroidal thickness and ocular pulse amplitude values did not change statistically significantly after the operations at the follow-up visits (p>0.05). Also, there were no important correlations between cardiopulmonary bypass time and mean sub-foveal choroidal thickness and ocular pulse amplitude changes at the post-operative first week (p>0.05). The intraocular pressure values were decreased markedly at the control visits (p<0.05). Conclusions: Sub-foveal choroidal thickness and ocular pulse amplitude are unchanged, while intraocular pressure decreases one week and one month after cardiopulmonary bypass.

Impaired systolic blood pressure recovery and heart rate recovery after graded exercise in patients with metabolic syndrome.

Abstract The aim of this study was to evaluate and compare systolic blood pressure recovery and heart rate recovery (HRR) values obtained at various time intervals after maximal graded exercise treadmill testing between patients with metabolic syndrome (MS) and the controls without MS. To our knowledge, this is the first study indicating systolic blood pressure recovery (SBPR) impairment and its relations to HRR and other variables in this group of patients. The study population included 110 patients with MS (67 men, 43 women; mean age: 46 ± 9 years) and 110 control subjects who did not meet the criteria for MS (58 men, 52 women; mean age: 44 ± 10 years). All patients were selected from nonobese, apparently healthy sedentary individuals who had the ability to perform maximum exercise testing. SBPR was assessed by calculating the ratio of systolic blood pressure (SBP) obtained in the third minute of the recovery period to either the peak-exercise SBP or the SBP in the first minute of the recovery period after graded exercise testing. HRR values were calculated by subtracting the HR at the first, second, third, fourth, and fifth minutes of the recovery period from the HR reached at peak exercise. There was no significant difference found between the 2 groups with respect to age and sex distribution. As expected, patients with MS had higher waist circumference, fasting plasma glucose and serum triglyceride, and lower high-density lipoprotein cholesterol compared with control subjects. All HRR values calculated in the first, second, third, fourth, and fifth minutes were significantly detected lower in the MS group compared with the control group (HRR 1st: 32 ± 10 vs 36 ± 11; P = 0.009; HRR 2nd: 47 ± 10 vs 51 ± 11; P = 0.02; HRR 3rd: 53 ± 11 vs 58 ± 12; P = 0.001; HRR 4th: 57 ± 11 vs 64 ± 12; P < 0.001; HRR 5th: 60 ± 16 vs 69 ± 15; P < 0.001). In addition, calculated mean values for SBPR1 and SBPR2 were >1 in patients with MS (1.01 ± 0.2 vs 0.91 ± 0.1 and 1.01 ± 0.1 vs 0.94 ± 0.1) and these were statistically significant compared with the control group (P < 0.001 and P = 0.002, respectively). The existence of MS was found to be the only parameter that was independently and positively related to SBPR values in the study population. Our findings suggest that only the existence of MS itself, not the presence of any MS components, is independently associated with SBPRs. We are of the opinion that significantly impaired SBPR values, in addition to the decreased HRR values observed in this group of patients, such as those with MS, may especially help identify patients with potentially increased cardiovascular risk despite normal exercise stress testing findings.