The Safety and Tolerability of Nebivolol in Hypertensive Patients with Coronary Artery Disease and Left Ventricular Ejection Fraction ≥ 40%: A Population-Based Cohort Study (Nebivolol-TR Study).

BACKGROUND: This study aimed to assess the safety and tolerability of nebivolol in hypertensive patients with coronary artery disease and left ventricular ejection fraction ≥ 40% in a Turkish cohort. METHODS: A total of 1015 hypertensive patients and coronary artery disease with left ventricular ejection fraction ≥ 40% were analyzed from 29 different centers in Turkey. Primary outcomes were the mean change in blood pressure and heart rate. Secondary outcomes were to assess the rate of reaching targeted blood pressure (<130/80 mmHg) and heart rate (<60 bpm) and the changes in the clinical symptoms (angina and dyspnea). Adverse clinical events and clinical outcomes including cardiovascular mortality, cardiovascular hospital admissions, or acute cardiac event were recorded. RESULTS: The mean age of the study population was 60.3 ± 11.5 years (male: 54.2%). During a mean follow-up of 6 months, the mean change in blood pressure was -11.2 ± 23.5/-5.1 ± 13.5 mmHg, and the resting heart rate was -12.1 ± 3.5 bpm. Target blood pressure and heart rate were achieved in 76.5% and 37.7% of patients. Angina and functional classifications were improved by at least 1 or more categories in 31% and 23.2% of patients. No serious adverse events related to nebivolol were reported. The most common cardiovascular side effect was symptomatic hypotension (4.2%). The discontinuation rate was 1.7%. Cardiovascular hospital admission rate was 5% and hospitalization due to heart failure was 1.9% during 6 months' follow-up. Cardiovascular mortality rate was 0.1%. CONCLUSION: Nebivolol was well tolerated and safe for achieving blood pressure and heart rate control in hypertensive patients with coronary artery disease and heart failure with preserved or mildly reduced ejection fraction.

Systemic arterial hypertension and flight.

Hypertension is the major preventable cause of cardiovascular disease and all-cause death. Given its overall high prevalence, hypertension would be one of our major concerns in commercial flights. Hence, the management of hypertension is of great importance. Herein, we discuss the pathophysiological factors for elevated blood pressure during flight, and we make recommendations which should be followed by the passengers and the flight crew and the physicians for trouble-free air travel.

[Turkish Cardiology Association Consensus Report: COVID-19 Pandemic and Cardiovascular Diseases (May 13, 2020)]. / Türk Kardiyoloji Dernegi Uzlasi Raporu: COVID-19 Pandemisi ve Kardiyovasküler Hastaliklar Konusunda Bilinmesi Gerekenler (13 Mayis 2020).

In December 2019, in the city of Wuhan, in the Hubei province of China, treatment-resistant cases of pneumonia emerged and spread rapidly for reasons unknown. A new strain of coronavirus (severe acute respiratory syndrome coronavirus-2 [SARS-CoV-2]) was identified and caused the first pandemic of the 21st century. The virus was officially detected in our country on March 11, 2020, and the number of cases increased rapidly; the virus was isolated in 670 patients within 10 days. The rapid increase in the number of patients has required our physicians to learn to protect both the public and themselves when treating patients with this highly infectious disease. The group most affected by the outbreak and with the highest mortality rate is elderly patients with known cardiovascular disease. Therefore, it is necessary for cardiology specialists to take an active role in combating the epidemic. The aim of this article is to make a brief assessment of current information regarding the management of cardiovascular patients affected by COVID-19 and to provide practical suggestions to cardiology specialists about problems and questions they have frequently encountered.

[Consensus Report from Turkish Society of Cardiology: COVID-19 and Cardiovascular Diseases. What cardiologists should know. (25th March 2020)]. / Türk Kardiyoloji Dernegi Uzlasi Raporu: COVID-19 Pandemisi ve Kardiyovasküler Hastaliklar Konusunda Bilinmesi Gerekenler (25 Mart 2020).

In December 2019, in the city of Wuhan, in the Hubei province of China, treatment-resistant cases of pneumonia emerged and spread rapidly for reasons unknown. A new strain of coronavirus (severe acute respiratory syndrome coronavirus-2 [SARS-CoV-2]) was identified and caused the first pandemic of the 21st century. The virus was officially detected in our country on March 11, 2020, and the number of cases increased rapidly; the virus was isolated in 670 patients within 10 days. The rapid increase in the number of patients has required our physicians to learn to protect both the public and themselves when treating patients with this highly infectious disease. The group most affected by the outbreak and with the highest mortality rate is elderly patients with known cardiovascular disease. Therefore, it is necessary for cardiology specialists to take an active role in combating the epidemic. The aim of this article is to make a brief assessment of current information regarding the management of cardiovascular patients affected by COVID-19 and to provide practical suggestions to cardiology specialists about problems and questions they have frequently encountered.

[Cardiac biomarkers in coronary slow flow: Endocan and omentin-1]. / Koroner yavas akimda kardiyak biyobelirteçler: Endokan ve omentin-1.

In the current issue of Archives of Turkish Society of Cardiology Journal, Sigirci et al., have evaluated serum endocan and omentin-1 levels in patients diagnosed with stable angina pectoris who had coronary slow flow phenomenon on angiography. In this editorial comment, the comments on the article are provided.

Is there a relationship between resistin levels and left ventricular end-diastolic pressure?

OBJECTIVE: Resistin, a cysteine-rich peptide, is associated with atherosclerosis and diabetes. Resistin levels increase corresponding to coronary artery disease (CAD) and heart failure severity. Since resistin level tends to elevate with symptomatic heart failure, it is expected to be associated with left ventricular end-diastolic pressure (LVEDP). However, there is no relevant literature on the relationship between resistin levels and LVEDP. We aimed to evaluate the association between resistin levels and LVEDP, severity of CAD, carotid intima-media thickness (CIMT), and echocardiographic diastolic dysfunction parameters. METHODS: For this study, 128 euvolemic patients with creatinine clearance >50 mg/dL and without acute coronary syndrome, who had typical chest pain or were stress test positive, were enrolled. Resistin level was measured by Enzyme-linked immunosorbent assays (ELISA) method. Severe CAD is defined as ≥50% stenosis in one of the major coronary arteries. LVEDP was measured during left heart catheterization. RESULTS: After coronary angiography, 60 patients (46.9%) had severe CAD. The mean LVEDPs were similar for patients with and without severe CAD (p=0.480). The resistin levels did not differ between the groups (p=0.154). The resistin levels did not correlate with LVEDP (r=-0.045, p=0.627), ejection fraction (EF; r=0.110, p=0.228), the Gensini score (r=-0.091, p=0.328), and CIMT (r=0.082, p=0.457). No significant correlation was found between the echocardiographic diastolic dysfunction parameters and resistin levels. CONCLUSION: There was no significant correlation between resistin level and LVEDP, CAD severity, echocardiographic diastolic dysfunction parameters, and CIMT. Further studies are warranted to determine the efficacy of resistin in clinical use.

Plasma osteopontin concentration is elevated in patients with coronary bare metal stent restenosis.

OBJECTIVE: Osteopontin is a component of atherosclerotic lesions, secreted by monocytes, macrophages and endothelial and vascular smooth muscle cells, which together are responsible for neointimal proliferation. We examined whether elevated plasma osteopontin concentration was associated with in-stent restenosis in patients with coronary artery disease. SUBJECTS AND METHODS: We enrolled 91 patients who underwent coronary artery stenting, and 60 control patients with normal findings on coronary angiography, between June 2012 and September 2013. For patients with stents, we measured plasma osteopontin concentration at the first follow-up coronary angiogram. For controls, plasma osteopontin concentration was measured at the time of angiography. RESULTS: Of the 91 patients who had undergone coronary artery stenting, 31 (34.1%) had developed in-stent restenosis and the mean time passed to control coronary angiography was 36.7 months (±SD 35.1 months). Mean plasma osteopontin concentration in this group was 2721.4 ± 1787.8 pg/ml, significantly higher than the 60 patients (65.9%) with no in-stent restenosis (1770.4 ± 1208.2 pg/ml, p = .011) and the 60 patients with a normal coronary angiogram (1572.4 ± 904.8 pg/ml, p = .002). There was no significant difference in mean osteopontin concentration between the patients with no in-stent restenosis and the control group (p = .312). CONCLUSIONS: Elevated plasma osteopontin concentration is associated with in-stent stenosis in patients with coronary artery disease. Further studies will be needed to establish whether osteopontin can predict in-stent restenosis and guide clinical management strategies.

Effects of Carvedilol Compared to Nebivolol on Insulin Resistance and Lipid Profile in Patients With Essential Hypertension.

BACKGROUND AND AIM:: Beta-blockers have unfavorable effects on metabolic parameters in hypertensive treatment. New generation beta-blockers with vasodilatory capabilities are superior to traditional beta-blockers, but studies examining their effects on metabolic parameters are still lacking. This study aimed to compare the effects of 2 new generation beta-blockers, carvedilol and nebivolol, on insulin resistance (IR) and lipid profiles in patients with essential hypertension. METHODS:: This was a prospective, randomized, open-label, single-center clinical trial. A total of 80 patients were randomized into 2 groups: the carvedilol group (n = 40, 25 mg of carvedilol daily) and the nebivolol group (n = 40, 5 mg of nebivolol daily). Follow-up was performed for 4 months. Fasting plasma glucose, insulin levels, and the lipid profile (high-density lipoprotein [HDL], low-density lipoprotein [LDL], total cholesterol, triglyceride, apolipoprotein AI, and apolipoprotein B levels) were measured and IR was calculated by the homeostasis model assessment (HOMA) index. These variables were compared before and 4 months after treatment. RESULTS:: Blood pressure and heart rate were significantly and similarly reduced in the carvedilol and nebivolol groups after treatment compared to those before treatment (both P < .001). Serum glucose ( P < .001), insulin ( P < .01), HOMA-IR (P < .01), HDL ( P < .001), LDL ( P < .001), total cholesterol ( P < .001), and apolipoprotein B ( P < .05) levels decreased in a similar manner in the carvedilol and nebivolol groups after treatment compared to those before treatment. Serum triglyceride and apolipoprotein AI levels did not change after treatment with both drugs. CONCLUSION:: New generation beta-blockers, carvedilol and nebivolol, efficiently and similarly decrease blood pressure. They have similar favorable effects on glucose, insulin, IR, and the lipid profile.

Treatment-associated change in apelin concentration in patients with hypertension and its relationship with left ventricular diastolic function.

OBJECTIVE: We examined the change in apelin concentration and its relationship with left ventricular diastolic function in patients treated for hypertension. METHODS: Ninety treatment-naive patients with newly diagnosed hypertension and 33 age- and sex-matched control subjects were prospectively enrolled. Patients with hypertension were randomized to treatment either with telmisartan 80 mg or amlodipine 10 mg. Apelin concentration was measured and echocardiography was performed at baseline and after 1 month of treatment. RESULTS: The data of 77 patients and 33 controls were analyzed. Mean age, gender, baseline blood pressure, apelin levels, and echocardiographic measurements were similar between the treatment groups (p>0.05 for all). Apelin concentration was significantly lower in patients with hypertension than in controls. There was a significant increase in apelin level after 1 month of treatment in both groups (0.32±0.17 vs. 0.38±0.17 ng/dL in telmisartan group, p=0.009, and 0.27±0.13 vs. 0.34±0.18 ng/dL in amlodipine group, p=0.013). Diastolic function improved significantly in both groups (p<0.05) but was not significantly associated with change in apelin concentration. CONCLUSION: Apelin concentration increased significantly after 1 month of effective treatment with telmisartan or amlodipine to a similar extent. Change in apelin concentration was not associated with improvement in diastolic function.

Association of rs10757274 and rs2383206 Polymorphisms on 9p21 locus with Coronary Artery Disease in Turkish Population.

BACKGROUND AND OBJECTIVES: Genetic predisposition is an important risk factor for coronary artery disease (CAD). In this study, we aimed to evaluate the impact of rs10757274 and rs2383206 polymorphisms in chromosome 9p21 on presence and severity of CAD in a Turkish population. SUBJECTS AND METHODS: A total of 646 patients who underwent coronary angiography were included in this study. Coronary vessel score and Gensini score were calculated to assess the angiographic severity of CAD. Alleles of AA, AG, and GG were determined for rs10757274 (polymorphism-1) and rs2383206 (polymorphism-2) polymorphisms located in chromosome 9p21 from the blood samples. RESULTS: There was a significant difference between the alleles in polymorphism-1 in the presence of coronary artery disease (38.9% in AA, 48.0% in GG and 56.4% in AG, p=0.017). However, there was no difference between the alleles in polymorphism-2. According to vessel scores, there was a significant difference between the alleles in polymorphism-1 (AA 0.71±1.04, GG 0.88±1.07, AG 1.06±1.12, p=0.018). In polymorphism-2, vessel scores did not show a difference between the alleles. In polymorphism-1, there was a significant difference in Gensini score (p=0.041). Gensini scores did not differ between the alleles in polymorphism-2 (p>0.05 for all). In multivariate analyses, none of the alleles was an independent factor for presence of CAD. CONCLUSION: The presence of rs10757274 polymorphism including AG allele in chromosome 9p21 was related to CAD. However, this relationship was not independent of other cardiovascular risk factors.

Serum cystatin C and neutrophil gelatinase-associated lipocalin in predicting the severity of coronary artery disease in diabetic patients.

OBJECTIVE: Cystatin C and neutrophil gelatinase-associated lipocalin (NGAL) are biomarkers of renal functions. We evaluated their roles in predicting the severity of coronary artery disease (CAD). METHODS: Fifty-two consecutive type 2 diabetic patients (32 males, 65.7±8.6 years) who underwent coronary angiography (CAG) for stable CAD were included in this single-center, prospective, cross-sectional study. Patients with an estimated glomerular filtration rate <60 mL/min/1.73 m2 and with a history of by-pass surgery and/or coronary stent implantation were excluded. The vessel score and Gensini score were calculated to assess the presence and severity of CAD. Mann-Whitney U test, Spearman test, and multiple linear regression analysis were used for the main statistical analyses. RESULTS: Serum cystatin C levels were higher in patients with multivessel disease than in those with single vessel disease [1260 ng/mL (953-1640) vs. 977 ng/mL (599-1114), p=0.017]. According to the median Gensini score, the higher score group also had higher cystatin C levels than the lower score group [1114 ng/mL (948-1567) vs. 929 ng/mL (569-1156), p=0.009]. However, serum NGAL levels were similar between these subgroups. There was a positive correlation between cystatin C and Gensini score (r=0.334, p=0.016). Multiple linear regression analysis revealed serum cystatin C as an independent predictor of the Gensini score (ß=0.360, t=2.311, p=0.026). These results may aid in defining cystatin C as a surrogate marker of the extent of CAD in further clinical trials. CONCLUSION: Serum Cystatin C, but not NGAL levels, could predict the severity of CAD in diabetic patients.

The role of oxidative DNA damage and GSTM1, GSTT1, and hOGG1 gene polymorphisms in coronary artery disease risk.

OBJECTIVE: Atherosclerotic coronary artery disease (CAD) appears to be a multifactorial process caused by the interaction of environmental risk factors with multiple predisposing genes. Therefore, in this study we aimed to determine the role of oxidative DNA damage and some variations in glutathione S-transferase (GSTM1 and GSTT1) and DNA repair (hOGG1) genes in CAD risk. METHODS: A case-control study was conducted on 59 individuals who had undergone coronary angiographic evaluation. Of these, 29 were patients diagnosed with CAD (mean age =61.5±10.3) and 30 were controls examined for reasons other than suspected CAD and who had angiographically documented normal coronary arteries (mean age =60.4±11.6). Basal DNA damage as well as pyrimidine and purine base damage were evaluated in peripheral blood lymphocytes using the modified comet assay. Polymerase chain reaction-restriction length polymorphism (PCR-RFLP)-based assay was used for genotyping. RESULTS: Basal DNA damage levels in patients [9.16 (3.26)] were significantly higher than those in controls [7.59 (3.23); p=0.017], and basal DNA and pyrimidine base damage levels were significantly correlated with disease severity based on Gensini scoring (r=0.352, p=0.006; r=0.318, p=0.014, respectively). However, no significant differences were observed in terms of oxidized DNA bases between patients and controls. The frequencies of studied genotypes (GSTM1, GSTT1, and hOGG1) were similar between groups. CONCLUSION: The results of this study pointed out the role of DNA damage in CAD and its severity. However, GSTM1, GSTT1, and hOGG1 gene polymorphisms seemed to have no effect on individual susceptibility for disease progression.

Hematological parameters can predict the extent of coronary artery disease in patients with end-stage renal disease.

PURPOSE: Aside from traditional factors (e.g., diabetes, age, and hypertension), some hematological parameters, such as neutrophil-to-lymphocyte ratio (NLR), red blood cell distribution width (RDW), and mean platelet volume (MPV), have increasingly been reported as measures of systemic inflammation and atherosclerosis in patients with end-stage renal disease (ESRD). This study aimed to determine whether there is an association between these hematological parameters and the extent of coronary artery disease (CAD) in patients with ESRD. METHODS: A total of 149 consecutive ESRD patients (66 % males) without established CAD were studied. NLR, RDW, and MPV values in all patients were calculated from the complete blood count before coronary angiography. Angiographic views were assessed by an experienced interventional cardiologist, and the extent of CAD was evaluated by the Gensini score. The patients were divided into quartiles of the Gensini score. RESULTS: Age, time on dialysis, calcium-phosphorus product, C-reactive protein levels, NLR, and MPV were significantly different among the groups (all p < 0.05). The Gensini score was correlated with age, time on dialysis (both p < 0.001), NLR (p = 0.004), and C-reactive protein levels (p = 0.034) and inversely correlated with left ventricular ejection fraction (p = 0.023). Multivariate regression analysis showed that age (p = 0.001), time on dialysis (p < 0.001), NLR (p = 0.001), and MPV (p = 0.005) were independent predictors of the extent of CAD. CONCLUSIONS: Aside from the well-known traditional factors, NLR and MPV are independent predictors of the extent of CAD in patients with ESRD.

Comparison of Carvedilol and Metoprolol for Preventing Contrast-Induced Nephropathy after Coronary Angiography.

AIMS: Contrast-induced nephropathy (CIN) is one of the most common causes of hospital-acquired acute renal failure. Oxidative stress and vasoconstriction might play key roles in its pathogenesis. In a few experimental models, antioxidant properties of carvedilol have been documented. The aim of this study was to analyze and compare the effects of carvedilol and metoprolol on the development of CIN in patients undergoing coronary angiography. METHODS: One hundred patients currently taking metoprolol and 100 patients currently taking carvedilol were enrolled into the study. Venous blood samples were obtained before and 48 h after contrast administration. Cystatin C and malondialdehyde values were examined and compared. CIN was defined as a creatinine increase of at least 25% or 0.5 mg/dl from the baseline value. RESULTS: Seven patients in the carvedilol group (7%) and 22 patients in the metoprolol group (22%) developed CIN (p = 0.003). In the metoprolol group, the median cystatin C concentration increased significantly from 978 to 1,086 ng/ml (p = 0.001) 48 h after radiocontrast administration. In the carvedilol group, the median cystatin C concentration did not change significantly (1,143 vs. 1,068 ng/ml; p = 0.94). In the metoprolol group, the mean malondialdehyde concentration increased significantly from 7.09 ± 1.48 to 8.38 ± 2.6 nmol/l (p < 0.001). In the carvedilol group, the mean serum malondialdehyde concentration did not change significantly (7.44 ± 1.21 vs. 7.56 ± 1.11 nmol/l; p = 0.59). CONCLUSION: When compared to metoprolol, carvedilol might decrease oxidative stress and subsequent development of CIN.