Atrial Electromechanical Coupling in Patients with Lichen Planus

BACKGROUND AND OBJECTIVES: A chronic inflammatory disease, lichen planus may cause disturbance of atrial electromechanical coupling and increase the risk of atrial fibrillation. The aim of this study was to evaluate atrial electromechanical delay with both electrocardiography (ECG) and echocardiography in patients with lichen planus (LP). SUBJECTS AND METHODS: Seventy-two LP patients (43 males [59.7%], mean age: 44.0±16.7 years) were enrolled in this cross-sectional case-control study. The control group was selected in a 1:1 ratio from 70 patients in an age and sex matched manner. P wave dispersion was measured by ECG to show atrial electromechanical delay. All of the patients underwent transthoracic echocardiography for measuring inter- and intra-atrial electromechanical delays. RESULTS: The baseline characteristics of the patients and the control group were similar except for the presence of LP. P-wave dispersion measured by ECG was significantly higher in patients with LP (p<0.001). Patients with LP had significantly prolonged intra- and interatrial electromechanical delays when compared to the control group (p<0.001). In addition, all of these variables were significantly correlated with high sensitive C-reactive protein (hsCRP) levels. CONCLUSION: Atrial electromechanical coupling, which is significantly correlated with increased hsCRP levels, is impaired in patients with LP.

investigation of tenascin-c levels in rheumatic mitral stenosis and their response to percutaneous mitral balloon valvuloplasty

The purpose of this study was to evaluate the tenascin-C levels in severe rheumatic mitral stenosis before and after percutaneous mitral balloon valvuloplasty [PMBV]. Forty patients with severe mitral stenosis requiring PMBV and 20 age-matched healthy subjects were included in the study. The mitral valve areas, mitral gradients and systolic pulmonary artery pressure [sPAP] were measured by echocardiography. The sPAP values and mitral gradients were also measured by catheterization before and after PMBV. The blood tenascin-C levels were measured before PMBV and 1 month after the procedure. The echocardiographic mean mitral gradients had a significant decrease after PMBV [11.7 +/- 2.8 vs. 5.6 +/- 1.7 mm Hg; p < 0.001] and also those of catheterization [13.9 +/- 4.4 vs. 4.0 +/- 2.4 mm Hg; p < 0.001]. Mitral valve areas increased significantly after PMBV [from 1.1 +/- 0.1 to 1.8 +/- 0.2 cm[2], p < 0.001]. Tenascin-C levels decreased significantly in patients after PMBV [from 15.0 +/- 3.8 to 10.9 +/- 3.1 ng/ml; p < 0.001]. Tenascin-C levels were higher in patients with mitral stenosis before PMBV than in healthy subjects [15.0 +/- 3.8 and 9.4 +/- 2.9 ng/ml; p < 0.001, respectively]. There were no significant differences between patients with mitral stenosis after PMBV and healthy subjects [10.9 +/- 3.1 and 9.4 +/- 2.9 ng/ml; p = 0.09, respectively]. There was a significant positive correlation between tenascin-C levels and sPAP [r = 0.508, p < 0.001]. In multivariant analysis, tenascin-C predicted mitral stenosis [p = 0.004, OR: 2.31]. Tenascin-C was an independent predictor for rheumatic mitral stenosis