C2HEST and CHA2DS2-Vasc for predicting recurrence after catheter ablation of paroxysmal atrial fibrillation.

Aim    The C2HEST score was developed mainly for predicting atrial fibrillation (AF) in cryptogenic stroke. This study investigated the performance of the C2HEST score in predicting AF recurrence after radiofrequency catheter ablation (RFCA).Material and Methods    189 patients with paroxysmal AF were included in the study. AF recurrence and AF-free survival during follow-up was analyzed. The Cox proportional-hazards model was used to identify independent predictors of AF recurrence after RFCA. Receiver operating characteristic curve analysis and the Hanley and McNeil method were performed to evaluate the performances of the C2HEST and CHA2DS2-VASc scores in predicting AF. AF-free periods of the with C2HEST<2 and C2HEST >2 were compared using Kaplan-Mayer analysis and a log-rank test.Results    The AF recurrence rate within 3-12 months after RFCA was 17.5%. C2HEST score >2, hypertension, left atrial (LA) diameter, and LA volume were independent predictors for AF recurrence (p<0.05). The C2HEST score had better discriminatory performance in predicting AF recurrence than CHA2DS2-VASc (area under curve: 0.769 vs 0.644; p=0.021). The patients with a C2HEST score >2 had a significantly shorter AF-free period compared those with a C2HEST SCORE <2 (p<0.001).Conclusion    In patients who underwent a RFCA procedure due paroxysmal AF, LA diameter and volume and the C2HEST score were independent predictors of AF recurrence. C2HEST is a simple clinical score, and it can be the readily performed to identify the risk of AF recurrence. The C2HEST score has greater diagnostic power than the CHA2DS2-VASc score.

A New Perspective for Isolated Coronary Artery Ectasia: Cystatin C.

Introduction The pathophysiology of isolated coronary artery ectasia (iCAE) has not been clearly identified, although multiple abnormalities, including arteritis, endothelial dysfunction, and vascular destruction, have been reported. In this study, we aimed to analyze serum cystatin C concentrations in patients with iCAE and controls. Methods Forty-seven patients with iCAE (mean age: 55.9 ± 11.5) and 32 individuals with normal coronary angiography (mean age: 57.8.1 ± 9.6) were included in the study. Plasma cystatin C levels were measured by using the principle of particle-enhanced turbidimetric immunoassay (PETIA). Results Serum cystatin C concentrations were significantly lower in patients with iCAE compared with the control group (0.98 ± 0.17 mg/L versus 1.17 ± 2.6 mg/L, p-value = 0.001). A significantly positive relationship was found between serum cystatin C levels and creatinine and high-sensitivity C-reactive protein (hs-CRP) levels in both groups (r-value = 0.288, p-value = 0.005, r-value = 0.143, p-value = 0.007, respectively). In multivariate logistic regression analysis, serum cystatin C level found to be a significant predictor for the presence of iCAE (OR: 0.837, CI: 95% (0.341 - 1.637), p-value = 0.013). Receiver operating characteristic (ROC) analysis determined that a cystatin C value < 1.02 mg/L had a sensitivity of 56% and a specificity of 78% for the prediction of ectasia. Conclusion We conclude that cystatin C independently can be a useful predictor for the presence of iCAE.

Relationship between vitamin D deficiency and nondipper hypertension.

Nondipper hypertension is associated with increased cardiovascular morbidity and mortality. Vitamin D deficiency is associated with cardiovascular diseases such as coronary artery disease, heart failure, and hypertension. Vitamin D deficiency activates the renin-angiotensin-aldosterone system, which affects the cardiovascular system. For this reason, a relationship between vitamin D deficiency and nondipper hypertension could be suggested. In this study, we compared 25-OH vitamin D levels between dipper and nondipper hypertensive patients. The study included 80 hypertensive patients and they were divided into two groups: 50 dipper patients (29 male, mean age 51.5 ± 8 years) and 30 nondipper patients (17 male, mean age 50.6 ± 5.4 years). All the patients were subjected to transthoracic echocardiography and ambulatory 24-hour blood pressure monitoring. In addition to routine tests, 25-OH vitamin D and parathormone (PTH) levels were analyzed. All the patients received antihypertensive drug therapy for at least 3 months prior to the evaluations. 25-OH vitamin D and PTH levels were compared between the two groups. No statistically significant difference was found between the two groups in terms of basic characteristics. The average PTH level of hypertensive dipper patients was lower than that of nondipper patients (65.3 ± 14.2 vs. 96.9 ± 30.8 pg/mL, P < .001). The average 25-OH vitamin D level of hypertensive dipper patients was higher than that of nondipper patients (21.9 ± 7.4 vs. 12.8 ± 5.9 ng/mL, P = .001). The left ventricular mass and left ventricular mass index were lower in the dipper patients than in the nondipper patients (186.5 ± 62.1 vs. 246.3 ± 85.3 g, P = .022; and 111.6 ± 21.2 vs.147 ± 25.7 g/m(2), P < .001, respectively). Other conventional echocardiographic parameters were similar between the two groups. Daytime systolic and diastolic blood pressure measurements were similar between dippers and nondippers, but there was a significant difference between the two groups with regard to nighttime measurements (nighttime systolic 118.5 ± 5.8 vs.130.2 ± 9.6 mm Hg, P < .001; and nighttime diastolic 69.3 ± 4.8 vs.78.1 ± 7.2 mm Hg, P < .001, respectively). Our results suggest that vitamin D deficiency has a positive correlation with blood pressure and vitamin D deficiency could be related to nondipper hypertension. The measurement of vitamin D may be used to indicate increased risk of hypertension-related adverse cardiovascular events.

Right and left atrial appendage function in patients with atrial septal aneurysm without patent foramen ovale.

AIM: Atrial septal aneurysm (ASA) is a risk factor for arterial embolism. Despite prior reports concerning paradoxical embolism through a patent foramen ovale, atrial dysfunction and atrial arrhythmias might represent an additional mechanism for arterial embolism.The aim of this study was to evaluate right and left atrial appendage contractilty in patients with ASA. METHODS AND RESULTS: A total of 30 patients with ASA (10 males/20 females, mean age 50.2 +/- 15.3 years) and 30 controls (12 males/ 18 females, mean age 47.7 +/- 10 years) were included. Conventional transthoracic and multiplane transoesophageal echocardiography were performed in patient and control groups. Flow and myocardial velocity were measured in both atrial appendages. Baseline characteristics of both groups were comparable. Flow velocity and myocardial contraction velocity in both atrial appendages were significantly lower in ASA patients. Compared to the control group, patients with ASA had a larger length, base and area of both appendages. CONCLUSION: In ASA patients right and left atrial appendage function are impaired. Biatrial dysfunction may cause arrhythmia and thromboembolism.

Evaluation of atrial conduction features with tissue Doppler imaging in patients with chronic obstructive pulmonary disease.

BACKGROUND: The electrical activity of atria can be demonstrated by P waves on surface electrocardiogram (ECG). Atrial electromechanical delay (AEMD) measured with tissue Doppler imaging (TDI) echocardiography can be a useful non-invasive method for evaluating atrial conduction features. We investigated whether AEMD is prolonged in patients with chronic obstructive pulmonary disease (COPD). PATIENTS AND METHODS: Study consisted of 41 (15 female, 26 male, mean age 62 + 12 years) patients with COPD and 41 healthy subjects. Pulmonary function tests,12 lead surface ECG and echocardiographic examination were performed and recorded. P wave changes on surface ECG, minimum (P (min)) and maximum (P (max)) duration of P wave and its difference as P wave dispersion (P (wd)) were measured and recorded. Atrial electromechanic delay (AEMD) was calculated from colored-TDI recordings. RESULTS: Pulmonary functions were significantly lower in COPD group than the control group as expected. Right atrial areas and pulmonary arterial systolic pressures (PAP) were significantly higher in COPD group than the controls (right atrial area: 11.9 ± 3.4 cm(2) and 8.2 ± 2.2 cm(2), p < 0.0001 and PAP: 38.4 ± 12.2 and 19.0 ± 3.2 mmHg p < 0.0001, respectively). P wave intervals on surface ECG were significantly increased in COPD patients than the control group (P (max): 105 ± 11 and 90 ± 12 ms, p < 0.0001; P (min): 60 ± 12 and 51 ± 10 ms, p = 0.003 and P (wd): 39 ± 10 and 31 ± 7 ms, p < 0.0001). According to the AEMD measurements from different sites by TDI, there was a significant delay between the onset of the P wave on surface ECG and the onset of the late diastolic wave in patients with COPD when compared with controls measured from tricuspid lateral septal annulus (TAEMD) (COPD: 41.3 ± 9.8 ms, control: 36 ± 4.5 ms; p = 0.005). There was a positive correlation between TAEMD and right atrial area (r = 0.63, p < 0.0001) and also between TAEMD and PASP (r = 0.43, p < 0.0005) and a negative correlation between TAEMD and forced expiratory volume (FEV1) (r = -0.44, p = 0.04). CONCLUSIONS: Right atrial electromechanical delay is significantly prolonged in patients with COPD. The right atrial area, PAP and FEV1 levels are important factors of this prolonged delay. Also the duration of atrial depolarization is significantly prolonged and propagation of depolarization is inhomogeneous in patients with COPD. These may be the underlying mechanisms to explain the atrial premature beats, multifocal atrial tachycardia, atrial flutter and fibrillation often seen in patients with COPD secondary to these changes.

Relation between serum anti-p53 antibodies and microvessel density in bladder cancer patients.

INTRODUCTION: Etiology of serum anti-p53 antibodies in bladder cancer patients is still unknown. In this study we evaluated the relationship between serum anti-p53 antibodies and microvessel density in bladder cancer patients. MATERIALS AND METHODS: Seventy-six patients with transitional cell carcinoma of the urinary bladder were assessed prospectively (18 Ta, 30 T1, 28 T2>or =). Serum anti-p53 antibodies were detected by enzyme-linked immunosorbent assay. Tumor p53 overexpression was assessed by immunohistochemical staining. Vessels were stained immunohistochemically using an antibody against platelet endothelial cell-adhesion molecule CD31. Spearman correlation test and t test were used for statistical analysis. RESULTS: Serum anti-p53 antibodies were positive in 25 (60%) of 41 tumor p53-positive patients. While the mean (SD, range) microvessel density was found to be 43 (7.59, 8-99) in patients who had positive serum anti-p53 antibodies, it was found to be 23 (4.53, 6-98) in patients who had negative serum anti-p53 antibodies. There was a good correlation between serum anti-p53 antibodies and microvessel density (p<0.05). No correlation was found between tumor p53 expression and microvessel density (p>0.05). CONCLUSIONS: We found that there is a significant correlation between the microvessel density and serum anti-p53 antibodies. This result may show the role of angiogenesis in the etiology of serum anti-p53 antibodies in bladder cancer patients.

Importance of serum p53 antibodies during follow-up after treatment of invasive bladder tumors.

INTRODUCTION: To investigate the prognostic importance of the changes in serum p53 antibody titrations during follow-up of patients who had anti-p53 antibody-positive invasive bladder tumors with transitional epithelial cells. MATERIALS AND METHODS: The study group consisted of 23 clinically T3