Metabolic syndrome is associated with atrial electrical and mechanical dysfunction.

OBJECTIVE: In this study, we aimed to investigate the left atrial (LA) electrical and mechanical functions in patients with metabolic syndrome (MetS). SUBJECTS AND METHODS: The study population consisted of 87 patients with MetS and 67 controls. Intra-atrial and interatrial electromechanical delays (EDs) were measured with tissue Doppler imaging. P-wave dispersion (Pd) was calculated from the 12-lead electrocardiograms. LA volumes were measured echocardiographically by the biplane area-length method. RESULTS: Intra-atrial and interatrial EDs and Pd were significantly higher in patients with MetS (10.3 ± 6.3, 21.0 ± 11.5 and 41.7 ± 10.8) than in controls (7.4 ± 5.5, 12.3 ± 10.4 and 29.2 ± 7.4; p = 0.003, p < 0.001 and p < 0.001, respectively). The LA preatrial contraction volume and active emptying volumes were higher in this population, but the LA passive emptying fraction was lower. In the multivariate linear regression analysis, the presence of MetS, LA active emptying volume and left ventricular early diastolic (E) wave velocity/late diastolic (A) wave velocity (E/A) ratios were independent correlates of interatrial ED (p = 0.002, p = 0.001 and p = 0.025, respectively). CONCLUSIONS: This study showed that intra-atrial and interatrial EDs and Pd were prolonged and LA mechanical functions were impaired in patients with MetS.

A Rare Case of Acute Coronary Syndrome in a Patient With Turner Syndrome.

INTRODUCTION: In Turner syndrome, cardiovascular complications are the most important causes of early mortality. Congenital cardiovascular abnormalities are found in approximately one third of Turner syndrome patients. Developments in diagnosis and treatment have decreased the rate of mortality related to these abnormalities. In recent years, many papers have mentioned that coronary artery disease developing at early ages in patients with Turner syndrome causes sudden deaths. CASE PRESENTATION: The patient, a 27-year-old female was admitted to the emergency room with chest pain at rest. She was diagnosed with Turner Syndrome in her teenage years due to amenorrhea. Patients with ECG changes and cardiac enzyme elevations were treated with acute coronary syndrome. CONCLUSIONS: The young woman with Turner Syndrome have several risk factors for early Coronary Artery Disease development. In such cases, dramatic results like sudden death or heart attack at an early age may occur in cases of insufficient follow-up and treatment.

The presence of fragmented QRS on 12-lead ECG in patients with coronary slow flow.

BACKGROUND: Coronary slow flow (CSF) is characterised by delayed opacification of coronary arteries in the absence of epicardial occlusive disease. It has been reported that CSF may cause angina, myocardial ischaemia, and infarction. Fragmentation of QRS complex (fQRS) is an easily evaluated non-invasive electrocardiographic parameter. It has been associated with alternation of myocardial activation due to myocardial scar and/or ischaemia. Whether CSF is associated with fQRS is unknown. The presence of fQRS on ECG may be an indicator of myocardial damage in patients with CSF. AIM: To investigate the presence of fQRS in patients with CSF. METHODS: Sixty patients (mean age 55.5 ± 10.5 years) with CSF and 44 patients with normal coronary arteries without associated CSF (mean age 53 ± 8.4 years) were included in this study. The fQRS was defined as the presence of an additional R wave or notching of R or S wave or the presence of fragmentation in two contiguous leads corresponding to a major coronary artery territory. RESULTS: The presence of fQRS was higher in the CSF group than in the controls (p = 0.005). Hypertension was significantly more common in the CSF group (p < 0.001). There was no significant association between the presence of fQRS and an increasing number of vessel involvements. Logistic regression analysis demonstrated that the presence of CSF was the independent determinant of fQRS (OR = 10.848; 95% CI 2.385-49.347; p = 0.002). CONCLUSIONS: Fragmented QRS, indicating increased risk for arrhythmias and cardiovascular mortality, was found to be significantly higher in patients with CSF. We have not found an association between the presence of fragmented QRS and the degree of CSF. Further prospective studies are needed to establish the significance as a possible new risk factor in patients with CSF.

Increased level of resistin predicts development of atrial fibrillation.

BACKGROUND: Resistin is a peptide hormone that is secreted from lipid cells and is linked to type-2 diabetes, obesity, and inflammation. Being an important adipocytokine, resistin was proven to play an important role in cardiovascular disease. We compared resistin levels in patients with and without atrial fibrillation (AF) to demonstrate the relationship between plasma resistin levels and AF. METHOD: One hundred patients with AF and 58 control patients who were matched in terms of age, gender, and risk factors were included in the trial. Their clinical risk factors, biometric measurements, echocardiographic work up, biochemical parameters including resistin and high-sensitivity C-reactive protein (hs-CRP) levels were compared. RESULTS: In patients with AF, plasma resistin levels (7.34±1.63ng/mL vs 6.67±1.14ng/mL; p=0.003) and hs-CRP levels (3.01±1.54mg/L vs 2.16±1.28mg/L; p=0.001) were higher than control group. In subgroup analysis, resistin levels were significantly higher in patients with paroxysmal (7.59±1.57ng/mL; p=0.032) and persistent AF (7.73±1.60ng/mL; p=0.006), but not in patients with permanent AF subgroups (6.86±1.61ng/mL; p=0.92) compared to controls. However, hs-CRP levels were significantly higher only in permanent AF patients compared to control group (3.26±1.46mg/L vs 2.16±1.28mg/L; p=0.02). In multivariate regression analysis using model adjusted for age, gender, body mas index, hypertension, diabetes mellitus, and creatinine levels, plasma resistin levels [odds ratio (OR): 1.30; 95% confidence interval (CI): 1.01-1.70; p=0.04] and hs-CRP levels (OR: 1.44; 95% CI: 1.12-1.86; p=0.004) were the only independent predictors of AF. CONCLUSION: The elevated levels of plasma resistin were related to paroxysmal AF group and persistent AF group, but not to permanent AF group.

Evaluation of coronary microvascular function and nitric oxide synthase intron 4a/b polymorphism in patients with coronary slow flow.

OBJECTIVE: Slow coronary flow (SCF) is reported to be associated with increased risk of cardiovascular disease. We have used coronary flow reserve measurement by transthoracic Doppler echocardiography to determine coronary microvascular function in patients with SCF and to determine whether the intron 4a/b polymorphism of the eNOS gene influences coronary endothelial function. METHODS: Overall, 96 patients with SCF and 79 controls were enrolled in the study. Coronary flow was quantified according to the thrombolysis in myocardial infarction (TIMI) frame count (TFC) on angiogram. Coronary diastolic peak flow velocities (DPFV) were measured with color Doppler flow mapping at baseline and after dipyridamole infusion. Coronary flow reserve was calculated as the ratio of hyperemic to baseline DPFV. The eNOS 4a/b polymorphism was detected by PCR. Patients with diabetes were excluded from the study. RESULTS: The SCF group was comparable to the control group in terms of demographic and clinical characteristics, except for hemoglobin and HDL-cholesterol levels, TFC of the left anterior descending artery, the circumflex artery, and the right coronary artery; the mean TFC was higher in the SCF group. Hyperemic DPFV and the hyperemic/baseline DPFV ratio were significantly lower in the SCF group when compared with the control group. However, baseline DPFV were similar in both groups. The number of patients with eNOS4 a/a and eNOS4 a/b phenotypes was statistically higher in SCF groups. The frequency of allele 'a' of the eNOS4 gene was also statistically higher in the SCF group. When patients were grouped according to the presence or absence of allele 'a' of the eNOS4 gene, statistically significant differences were found in the TFC of the left anterior descending artery, the circumflex artery; mean TFC; baseline DPFV; and hyperemic/baseline DPFV. Univariate analysis in which eNOS4 b/b was used as the referent group showed that the presence of allele 'a' of the eNOS4 gene significantly predicted SCF (odds ratio: 2.79, 95% confidence interval: 1.32-5.89; P=0.007). In multivariate analysis using a model adjusted for variables with a P value lower than 0.10 in univariate analyses, the presence of allele 'a' of the eNOS4 gene was found to be an independent predictor of SCF (odds ratio: 3.22, 95% confidence interval: 1.28-8.82; P=0.013). CONCLUSION: The presence of allele 'a' may be a risk factor for microvascular endothelial dysfunction and higher TFCs in SCF patients.