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.

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