Oguzhan Yucel

Sleep quality among relatively younger patients with initial diagnosis of hypertension: dippers versus non-dippers.

Background. Sleep is a basic physiological process. Normal sleep yields decrease in sympathetic activity, blood pressure (BP) and heart rate. Those, who do not have expected decrease in their BP are considered “non‐dippers”. We aimed to determine if there was any association between the non‐dipping status and sleep quality, designed a cross‐sectional study, and enrolled and evaluated the sleep quality of relatively young patients with an initial diagnosis of hypertension. Methods. Seventy‐five consecutive patients, diagnosed to have stage 1 hypertension by their primary physicians, were referred to our study. Patients had newly diagnosed with stage 1 hypertension. Patients with a prior use of any anti‐hypertensive medication were not included. Eligible patients underwent the Pittsburgh Sleep Quality Index (PSQI), which has an established role in evaluating sleep disturbances. All patients underwent ambulatory BP monitoring. Results. There were 42 non‐dipper patients (mean age = 47.5±11.9 years, 24 male/18 female), as a definition, 31 dipper hypertensive patients (mean age = 48.5±12.8 years, 21 male/10 female) and two with white coat hypertension. Daytime systolic and diastolic mean BPs were not significantly different between the two groups. Night‐time mean systolic and diastolic BPs were significantly higher in non‐dippers compared with dippers. PSQI scores, globally, were significantly higher in non‐dippers compared with dippers. Total PSQI score was not correlated with body mass index. It was noticed that, individually, sleep quality, sleep efficiency and sleep disturbance scores were significantly higher in non‐dippers. Being a poor sleeper in terms of high PSQI score (total score>5) was associated with 2.955‐fold increased risk of being a non‐dipper (95% confidence interval 1.127–7.747). Conclusion. We showed that the risk of having non‐dipping hypertension, a risk factor for poor cardiovascular outcomes among hypertensive individuals, was tripled (odds ratios) among poor sleepers. We think that evaluating sleeping status and sleep quality among the hypertensive population may help unmask non‐dipper hypertension, enabling physicians to treat appropriately.

Echocardiographic epicardial adipose tissue predicts subclinical atherosclerosis: epicardial adipose tissue and atherosclerosis.

We examined the relationship between coronary flow rate and epicardial adipose tissue (EAT) in patients with slow coronary flow (SCF) and normal coronary arteries. The study included 40 consecutive patients with stable angina pectoris who had normal coronary arteries. All patients underwent echocardiography. To determine the SCF, thrombolysis in myocardial infarction (TIMI) frame count method was used. Half of the patients had SCF at least in 1 coronary artery. Thrombolysis in myocardial infarction frame counts, the mean TIMI frame count, and EAT thickness were significantly higher in patients with SCF. Slow coronary flow showed a significantly positive correlation with EAT thickness. Epicardial adipose tissue thickness was the only independent predictor of SCF. Our findings suggest that there is a significant correlation between the SCF and EAT. Therefore, echocardiographic EAT may become a predictor of subclinical atherosclerosis in patients with stable angina pectoris.

Microalbuminuria is Associated With the Severity of Coronary Artery Disease Independently of Other Cardiovascular Risk Factors

The potential early predictive value of microalbuminuria (MA) in the estimation of atherosclerosis and the relation between the degree of urinary albumin excretion and the extent of coronary artery disease (CAD) were investigated. Patients (n = 159) with stable angina pectoris and angiographically significant stenosis in at least 1 of the major coronary arteries were included. Microalbuminuria was measured by immunoturbidimetry. The extent of coronary artery stenosis was graded using the Gensini score. The Gensini score was significantly greater in patients who had MA. Also, the Gensini increased by 0.15 units with 1 unit increase in MA. In the groups who had diabetes mellitus and hypertension, there was no correlation between MA and Gensini score. The results of the present study suggest that MA is associated with the severity of CAD independent of other cardiovascular risk factors.

Diagnosis and follow up of patients with primary cardiac tumours: a single-centre experience of myxomas.

Objective In this study, 12 patients who were diagnosed as having cardiac tumours and were operated on in the Department of Cardiovascular Surgery following referral from the Department of Cardiology were enrolled between January 1995 and October 2007. Methods The symptoms, clinical findings, diagnostic methods, localisation of masses and surgical applications were recorded retrospectively. Results There were 10 female (83%) and two (17%) male patients; their ages ranged from 35 to 70 years (mean 68.7 years). Twelve patients were diagnosed with myxomas, nine of which were located within the left atrium and three in the right atrium. The most common symptoms at clinical presentation were those associated with heart failure or embolisation. Diagnosis of the tumours was made by echocardiography in all patients. The masses were completely resected in eight patients and the interatrial septae were partially excised with mass resection in two patients. The defect was reconstructed with a pericardial patch in one of the patients, and primarily reconstructed in the other. We carried out debridement with mass resection in another case. Femoro–popliteal aorto–iliac thrombo-endarterectomy was performed with mass resection in a further case. Conclusion Atrial myxomas are the most common primary cardiac tumours. They can cause valvular or inflow–outflow tract obstruction, thrombo-embolism, arrhythmias, or pericardial disorders. Most atrial myxomas are benign but due to non-specific symptoms, early diagnosis may be a challenge and they must be removed by surgical resection. Diagnosis and follow up with the collaboration of cardiology and cardiovascular surgery departments is important for meticulous care of these patients.

Role of mean platelet volume in the diagnosis of acute coronary events

We have read with great interest the recently published paper by Chu et al 1 about the diagnostic performance of mean platelet volume (MPV) for patients with acute coronary syndrome. In this report, similar to the findings of Yilmaz et al ,2 the authors have shown that MPV was an early and independent predictor of acute coronary syndrome in patients with …

Coronary syndrome Y: Should we focus more on extra-cardiac conditions including renal disease and its management?

⁎ Corresponding author. E-mail address: kyalta@gmail.com (K. Yalta). In their recently published article, Muxel S et al. reported amalewith coronary slow flow (CSF) as measured with increased thrombolysis in myocardial infarction (TIMI) frame counts (TFC), and comment on the different clinical presentations and pathophysiological mechanisms of coronary syndromeXandY [1].We agreewith the authors that coronary syndrome X is generally characterized by impaired coronary vasodilation andcoronaryflow reservewhile coronary syndromeYoccurs due to enhanced coronary resistance leading to CSF [1]. Endothelial dysfunction plays the central role in the pathogenesis of coronary syndrome X and Y [1] indicating their potential co-existence in a portion of cases. However, compared to isolated coronary syndrome X, coronary syndrome Y is more likely to accompany and/or be associated with extra-cardiac pathologies potentially associated with endothelial dysfunction and subclinical myocardial fibrosis, etc. The association between renal disease and coronary syndrome Y, as described below, may potentially harbour some diagnostic, therapeutic and prognostic implications, and has recently drawn particular attention in the clinical setting. Chronic renal failure (CRF) is well known to induce endothelial dysfunction and consequent coronary atherosclerosis possibly due to a variety of CRF-induced pathologies including increased levels of asymmetric-dimethylarginine (ADMA) [2], inflammatory response and oxidative stress, accompanying hypertension, etc. Similarly, coronary syndrome Y (characterized by CSF) may be encountered in the setting of CRF, and may be regarded as a marker of coronary microvascular dysfunction that is largely attributable to increased microvascular resistance associated with endothelial dysfunction, subclinical myocardial fibrosis and hypertrophy [2,3], etc. Endothelial dysfunction is alsowell known to contribute to the pathogenesis of CRF. Therefore, coronary syndrome Y, coronary atherosclerosis and CRFmay share the same clinicopathological background, to some extent indicating the complex relationship among these entities. A recently published study demonstrated significant reductions in coronary blood flow in patients with end-stage renal disease (ESRD) regardless of the degree of epicardial coronary artery stenosis [3]. In another previous study by our group including patients with mild to moderate renal dysfunction and angiographically normal coronary arteries, we were able to demonstrate significant reductions in coronary blood flow as measured with increased TFC values compared to the control group with normal coronary arteries and renal functions [2]. It is also of note that in the patient group of our study, the values of TFC and calculated glomerular filtration rate (GFR) were also found to be independently correlated [2] indicating the close link between coronary syndrome Y and renal failure. Therefore, in the clinical setting, renal failure may accompany (as a result of generalized endothelial dysfunction) and/or beassociatedwith coronary syndromeY. Even though the renal statusof the case reported by Muxel S et al. [1] was not reported, the patient might have suffered some kind of subclinical or incipient renal failure (even with normal blood-urea-nitrogen (BUN) and creatinine levels), and hence may need to be thoroughly evaluated via other diagnostic modalities (GFR calculation, renal imaging, etc.) along with subsequent close follow-up for the possible emergence or progression of renal failure. Itmay be suggested that among coronarymicrovascular syndromes, coronary syndrome Y is more likely to accompany and/or be associated with extra-cardiac conditions (renal disease, etc. even in the subclinical stage) indicating the need for thorough evaluation of patients with this syndrome via various diagnostic modalities. In the setting of coronary syndrome Y (isolated or in combination with coronary syndrome X), besides targeting enhancement of coronary bloodflow, earlier diagnosis andmanagementof associated conditions including renal failuremaybe of utmost clinical value in the management of coronary microvascular dysfunction, and may possibly improve clinical outcomes including renal and cardiac adverse events. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [4].

Prognostic role of soluble suppression of tumorigenicity-2 on cardiovascular mortality in outpatients with heart failure

Objective: Soluble suppression of tumorigenicity-2 (sST2), a member of the interleukin 1 receptor family, is increased in mechanical stress conditions and is produced by cardiomyocytes and cardiac fibroblasts. Elevated sST2 level is associated with the prognosis of acute coronary syndrome, pulmonary arterial hypertension, and acute and chronic heart failure (HF). In this study, we aimed to investigate the relationship between sST2 levels and cardiovascular mortality in outpatients with HF. Methods: This study used a prospective observational cohort design. A total of 130 consecutive outpatients with HF were prospectively evaluated. Clinical characteristics, laboratory results, cardiovascular risk factors, comorbidities, and medication use were recorded. The patients were followed up for a mean period of 12±4 months for the development of cardiovascular death. They were classified into two groups: those who survived and those who died. Results: Mean age of patients was 67±11 years (69% males). After follow-up, 23 of 130 patients (18%) experienced cardiovascular death. sST2 levels were higher among those who died compared with among those who survived [51 (21–162) vs. 27 (9–198) ng/mL, p<0.001]. Optimal cut-off sST2 level to predict cardiovascular mortality was found to be >30 ng/mL with a sensitivity of 87% and a specificity of 67% (AUC =0.808, 95% CI=0.730 to 0.872). sST2 levels were negatively correlated with left ventricular ejection fraction and triglyceride, total cholesterol, LDL cholesterol, and hemoglobin levels and were positively correlated with left atrium size and the presence of right ventricular dilatation. In multiple Cox regression analysis, sST2 level of >30 ng/mL (HR=6.756, p=0.002, 95% CI=1.983–23.018), hemoglobin level (HR=0.705, p<0.001, 95% CI=0.587–0.847), age (HR=1.050, p=0.013, 95% CI=1.010–1.091), and HDL cholesterol level (HR=0.936, p=0.010, 95% CI=0.889–0.984) remained to be associated with an increased risk of mortality. Conclusion: sST2 measurement could help risk stratification in outpatients with HF. Moreover, this is the first study describing the impact of sST2 protein in Turkish patients with HF.

Association between multidrug resistance-1 C3435T gene polymorphism and right ventricular dysfunction in patients with chronic obstructive pulmonary disease: cross-sectional study

BACKGROUND Right ventricular (RV) dysfunction may develop over the course of chronic obstructive pulmonary disease (COPD) and is an important predictor of morbidity and mortality. Polymorphism of the multidrug resistance-1 (MDR-1) gene has been correlated with worse clinical findings among patients with COPD. Our aim here was to investigate the relationship between MDR-1 C3435T gene polymorphism and RV dysfunction in COPD patients. DESIGN AND SETTING This was a cross-sectional study investigating the relationship between RV dysfunction and genetic defects in COPD patients. METHODS Forty-one consecutive patients diagnosed with COPD and hospitalized due to acute exacerbation were enrolled. Polymorphism was analyzed using the strip assay technique. RV parameters were evaluated, and RV dysfunction was identified via transthoracic echocardiography. Patients were categorized into three groups according to gene polymorphism: MDR-1 CC (wild type, n = 9), MDR-1 CT (heterozygote mutant, n = 21) or MDR-1 TT (homozygote mutant, n = 11). RESULTS The study included 14 males and 27 females (mean age 65 ± 11 years). The mean systolic pulmonary artery pressure was 31.4 ± 8 mmHg in the wild-type group, 42.2 ± 12 mmHg in the heterozygote mutant group and 46.5±14 mmHg in the homozygote mutant group (P = 0.027). Presence of RV dilatation was significantly different among the three groups (33%, 71%, and 100%, respectively; P = 0.005). In multiple logistic regression analysis, MDR-1 C3435T gene polymorphism (OR = 9.000, P = 0.019) was an independent predictor of RV dysfunction after adjustment for potential confounders. CONCLUSION MDR-1 C3435T gene polymorphism was associated with RV dysfunction in patients with COPD.

Plasma osmolality predicts mortality in patients with heart failure with reduced ejection fraction

BACKGROUND Heart failure (HF) is a fatal disease. Plasma osmolality with individual impacts of sodium, blood urea nitrogen (BUN), and glucose has not been studied prognostically in patients with HF. AIM This study aims to investigate the impact of serum osmolality on clinical endpoints in HF patients. METHODS A total of 509 patients (383 males, 126 females) with HF with reduced ejection fraction in three HF centres were retrospectively analysed between January 2007 and December 2013. Follow-up data were completed for 496 patients. Plasma osmolality was calculated as (2 × Na) + (BUN/2.8) + (Glucose/18). Quartiles of plasma osmolality were produced, and the possible relationship between plasma osmolality and cardiovascular mortality was investigated. RESULTS The mean follow-up was 25 ± 22 months. The mean age was 56.5 ± 17.3 years with a mean EF of 26 ± 8%. The mean levels of plasma osmolality were as follows in the quartiles: 1st % = 280 ± 6, 2nd % = 288 ± 1, 3rd % = 293 ± 2 (95% confidence interval [CI] 292.72-293.3), and 4th % = 301 ± 5 mOsm/kg. The EF and B-type natriuretic peptide levels were similar in the four quartiles. Univariate and multivariate analyses in the Cox proportional hazard model revealed a significantly higher rate of mortality in the patients with hypo-osmolality. The Kaplan-Meier plot showed graded mortality curves with the 1st quartile having the worst prognosis, followed by the 4th quartile and the 2nd quartile, while the 3rd quartile was shown to have the best prognosis. CONCLUSIONS Our study results suggest that normal plasma osmolality is between 275 and 295 mOsm/kg. However, being close to the upper limit of normal range (292-293 mOsm/kg) seems to be the optimal plasma osmolality level in terms of cardiovascular prognosis in patients with HF.

Investigation of anxiety levels of patients with chest pain admitted to emergency department

Introduction We aimed to investigate the demographical features, anxiety levels and clinical findings of the patients admitted to our Emergency department (ED) due to chest pain. Methods Patients with chest pain older than 18 years were included into the study. Demographical features such as age, sex and education level, initial diagnosis in the ED, whether they were hospitalized or coronary intervention performed, were recorded. To determine the anxiety levels of the patients, State-trait Anxiety Inventory (STAI) was performed. Results Two-hundred and eight adult patients with chest pain were included into the study. We could not determine a relationship between STAI levels of patients according to demographical findings, however, STAI scores tended to decrease by age. Considering the education levels of the patients, it was determined that STAI scores of university graduates were higher than others. The STAI scores of patients discharged from the ED were higher than those hospitalized. When patients were compared according to whether coronary intervention (CI) was performed or not, it was determined that patients who did not require CI had higher STAI scores. When coronary lesion localization of the patients hospitalized was investigated, any relationship could not be determined. Conclusion In this study, we determined that anxiety levels of the patients with chest pain do not correlate with the severity of the disease. Higher anxiety levels of patients discharged from ED when compared to those with ACS is a challenging problem for both ED physicians and cardiologists.