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.

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

ABSTRACT 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.

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.

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.

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.

Familial genetic risk factors in premature cardiovascular disease: a family study.

Cardiovascular disease (CVD) is closely associated with familial predisposition. The aim of the present study was to investigate predisposing risk factors in the family of a young patient who underwent coronary artery bypass graft surgery due to CVD. The father and uncle of the patient died at an early age due to myocardial infarction. Various stages of CVD were identified in both of the patient's brothers (28 and 32 years of age). Biochemical tests (fasting blood glucose, lipid profile, urea, creatinine and liver enzymes) and a complete blood count (haemoglobin, haematocrit, white blood cell count, and platelet count) were performed. Physiological coagulation inhibitory factors (protein C, protein S, and antithrombin III), prothrombotic genetic risk factors (factor V Leiden, plasminogen activator inhibitor-1, methylenetetrahydrofolate reductase A1C and C6T, angiotensin-converting enzyme, ß-fibrinogen, glycoprotein IIIa and factor XIII) and homocysteine levels were evaluated in all cases. Defects were observed in many genetic factors and in the systems regulated by these factors. The results were compatible with those reported in the literature. In conclusion, it is possible to determine a specific family history in young adults with CVD. From this perspective, the emergence of more serious CVD may be prevented by providing disease-related information to the other family members and implementing preventive measures.

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.