Duration of migraine is associated with cardiac diastolic dysfunction.

OBJECTIVE: Migraine is a common type of headache accompanied or preceded by signs of central and autonomic nervous system dysfunction. Autonomic dysfunction has been suggested to be a potential contributor to impaired cardiac diastolic function. Cardiac diastolic dysfunction is characterized by normal left ventricular contractility but impaired ventricular relaxation. It is a growing clinical entity implicated in morbidity and mortality due to heart failure. The aim of this study was to determine if any relationship exists between migraine and diastolic dysfunction. METHODS: Migraineurs (N = 55), and age- and sex-matched healthy controls (N = 52) were evaluated by conventional and tissue Doppler echocardiography. Migraine-related disability in the previous 3 months was assessed by the Migraine Disability Assessment questionnaire. Baseline characteristics were recorded, and blood samples were collected. RESULTS: The groups did not differ in terms of sex or age. The migraine group had higher lipid levels compared with the control group. Diastolic dysfunction was significantly higher among the 30 migraineurs with a history of migraine of 10 years or more compared with the 25 migraineurs with a history of less than 10 years, (P = 0.003). In logistic regression analysis, migraine duration was shown to be an independent predictor of diastolic dysfunction (odds ratio 1.130, 95% confidence interval, P = 0.044). CONCLUSIONS: Cardiac diastolic dysfunction is associated with migraine. A long history of migraine is an independent predictor of diastolic dysfunction.

Investigation of miR-26a-5p and miR-19a-3p expression levels in angiographically confirmed coronary artery disease.

BACKGROUND: MicroRNAs have been found to have an essential role in cardiovascular diseases. In previous experiments, the changed expressions of miR-26a-5p and miR-19a-3p were confirmed in patients with severe coronary atherosclerosis by miRNA microarrays. However, the role of two miRNAs in coronary artery diseases (CAD) still needs to be investigated further. Our current study aimed to analyse two miRNAs in angiographically confirmed CAD and non-CAD with insignificant coronary stenosis. This study aimed to identify the potential diagnostic value of circulating miRNA with CAD. METHODS: The CAD patients (n = 50) and non-CAD controls (n = 43) were studied. miRNAs (miR-26a-5p and miR-19a-3p) were quantified by TaqMan miRNA assays using real-time PCR. We subsequently assessed the diagnostic value of the miRNAs and correlations of miRNA with clinical parameters. Target prediction tools were utilised to identify miRNA target genes. RESULTS: The expression of miR-26a-5p was significantly increased in CAD compared to non-CAD controls (p < 0.05). Tertile groups were formed according to the expression levels of miRNAs, and high expression tertile (T3) was compared with low expression tertile (T1). It was found that CAD presence was more prevalent in T3 of miR-26a-5p, and the frequency of diabetes was higher in T3 of miR-19a-3p. There were significant correlations between miRNAs and diabetes risk factors such as HbA1c, glucose levels, and BMI (p < 0.05). CONCLUSIONS: Our findings show that miR-26a-5p expression is altered in CAD presence while miR-19a-3p expression is different in diabetes. Both miRNAs are closely related to risk factors of CAD, therefore, could be therapeutic targets for CAD treatment.

The relationship of the ESR1 gene polymorphisms with the presence of coronary artery disease determined by coronary angiography.

Effects of estrogen on the cardiovascular system, mediated mainly by estrogen receptor type alpha (ER alpha), have been well-defined and specific polymorphisms in the ER alpha gene (ESR1) have been associated with several coronary heart diseases including coronary artery disease (CAD) in studies covering different populations. In the present study, we aimed to investigate whether there is an association between two of the known polymorphisms in the ESR1, named c.454-397T>C and c.454-351A>G, and CAD in a Turkish population. One hundred sixty eight patients with CAD and 99 patients without CAD were included in the study. The ESR1 c.454-397T>C and c.454-351A>G polymorphisms were studied by the conventional polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. While no association was found between the c.454-351A>G polymorphism and CAD, the c.454-397T>C genotype distributions were statistically significant independent of known risk factors between CAD-positive (CAD+) and CAD-negative (CAD-) groups (p = 0.001). TT genotype was more frequent in CAD- group than in CAD+ group, 22.2% and 4.8%, respectively. CC genotype was associated with increased risk of CAD (p = 0.001) compared to the TT genotype. When comparing the distribution of CC + TC genotypes to that of TT genotype in CAD+ and CAD- groups, the frequency of CC + TC genotypes showed a significant increase independent of known CAD risk factors in CAD+ subjects (p = 0.001). As a conclusion, a statistically significant relationship between the ESR1 c.454-397T>C polymorphism and CAD were found independent of known CAD risk factors in a Turkish population.

Epicardial adipose tissue thickness can be used to predict major adverse cardiac events.

OBJECTIVE: Increase in epicardial adipose tissue (EAT) thickness is associated with subclinical and manifest coronary artery disease. In addition, it is associated with the severity and extent of coronary atherosclerosis. We aimed to investigate whether increased EAT thickness is associated with adverse cardiovascular outcomes. PATIENTS AND METHODS: Two hundred consecutive patients who were admitted with stable angina pectoris, unstable angina pectoris or acute myocardial infarction (MI), and had undergone coronary angiography were included and followed for revascularization, nonfatal MI, hospitalization for heart failure and cardiovascular death for 26 (5-30) months. RESULTS: There were significantly more revascularizations, nonfatal MI and cardiovascular death in patients with an initial EAT thickness more than 7 mm (P<0.001 for all). Significant predictors of cardiovascular death were identified as an EAT thickness more than 7 mm [hazard ratio (HR) 1.9, 95% confidence interval (CI) 0.4-8.3, P=0.039] and diabetes (HR 3.42, 95% CI 0.7-17.5, P=0.014) in the multivariate Cox regression analysis. Event-free survival for cardiovascular death in the EAT up to 7 mm group was 97.9%, whereas it was 90.7% in the EAT more than 7 mm group (P=0.021). In addition, significant predictors of MI were identified as an EAT thickness more than 7 mm (HR 2.4, 95% CI 0.6-10.0, P=0.021) and diabetes (HR 3.4, 95% CI 1.0-11.2, P=0.04). Event-free survival for MI in the EAT up to 7 mm group was 96.4%, whereas it was 68.2% in the EAT more than 7 mm group (P=0.001). CONCLUSION: Increase in EAT thickness independently predicts adverse cardiac events including MI and cardiovascular death.

Lack of association between matrix metalloproteinase-9 and endothelial nitric oxide synthase gene polymorphisms and coronary artery disease in Turkish population.

Polymorphic variants of genes encoding proteins involved in vascular remodeling may genetically diverge among different populations and play a role in the susceptibility to the coronary artery disease (CAD). MMP-9-1562 C/T (rs3918242), eNOS T-786C (rs2070744), and Glu298Asp (rs1799983) are among the most studied of these polymorphisms. The aim of this study was to determine the relationship between CAD and these polymorphisms in the Turkish population. The analysis included 146 CAD+ and 122 CAD- individuals. Genomic DNA was isolated from whole blood and genotyping was performed by the PCR-RFLP method. No significant associations were found between -1562 C/T (p = 0.557), Glu298Asp (p = 0.432), and -786 T/C (p = 0.055) polymorphisms and CAD. The distribution of each haplotype also did not differ between CAD+ and the CAD- samples (p > 0.05). The present investigation is the first to study an association between -1562 C/T polymorphism and CAD in the Turkish population. In conclusion, no appreciable differences between CAD+ and CAD- samples were found in terms of polymorphisms mentioned above.