Relationship between serum osteopontin level and atrial fibrillation recurrence in patients undergoing cryoballoon catheter ablation.

OBJECTIVE: Atrial fibrillation (AF) is the most common sustained arrhythmia and is associated with increased morbidity and mortality. Atrial fibrosis augments recurrence rate following AF catheter ablation. Osteopontin is a multifunctional molecule involved in several pathophysiological pathways, including fibrosis. Presently described is investigation of relationship between serum osteopontin level and AF recurrence after AF cryoablation. METHODS: The study was designed to be prospective and observational; 60 patients with paroxysmal (n=47) and persistent (n=13) AF were included. Osteopontin level was measured both before and 6 months after AF ablation with cryoballoon. RESULTS: Preprocedure and postprocedure osteopontin level did not differ between the 2 groups of AF patients (p=0.286, p=0.493, respectively). Postprocedure osteopontin level was significantly higher compared with preprocedure value (32.18 ng/mL vs 15.58 ng/mL; p=<0.001). Left atrial diameter, AF type, and preprocedure osteopontin level were related to AF recurrence (p≤0.05). An age-adjusted multivariate logistic regression analysis was conducted to determine independent predictors of AF recurrence. Among these, AF type (ß=2.211; p=0.004; odds ratio [OR]: 9.124; 95% confidence interval [CI]: 2.026-41.094) was found to be the most important factor related to AF recurrence. Preprocedure osteopontin level also predicted AF recurrence independently (ß=0.059; p=0.048; OR: 1.061; 95% CI 1.001-1.125). CONCLUSION: Study results revealed persistency of AF and high preprocedure osteopontin level independently predicted AF recurrence in patients undergoing cryoballoon AF ablation. Association of a biochemical marker with AF recurrence might be beneficial to selection of appropriate patients for cryoballoon procedure and assessment of long-term procedural success.

Telmisartan decreases atrial electromechanical delay in patients with newly diagnosed essential hypertension.

BACKGROUND: Atrial electromechanical delay (EMD) parameters predict the development of atrial fibrillation. We investigated the effect of telmisartan treatment on atrial EMD parameters in patients with newly diagnosed essential hypertension. METHODS: Thirty-six patients with essential hypertension were treated with telmisartan (80 mg/day) for 6 months. Baseline electrocardiographic P-wave measurements and echocardiographic atrial EMD parameters were compared with the 6-month follow-up. RESULTS: Pmax and Pd were significantly decreased (108.4 ± 6.1 vs 93.9 ± 6.2 milliseconds, 33.4 ± 8.6 vs 19.5 ± 7.0 milliseconds, respectively, P = .0001 for each) after 6-month telmisartan therapy. The atrial EMD parameters were decreased from baseline (mitral EMD, 68.9 ± 4.9 vs 53.8 ± 4.9 milliseconds; septum EMD, 51.6 ± 7.1 vs 42.6 ± 7. milliseconds1; tricuspid EMD, 48 ± 6.9 vs 39 ± 6.9 milliseconds; interatrial EMD, 20.9 ± 5.5 vs 14.8 ± 5.7 milliseconds; P = .0001 for each parameter). The reduction of interatrial EMD was correlated with the reduction in systolic BP nighttime and the increase in mitral E wave velocity/mitral A wave velocity ratio. CONCLUSION: Telmisartan decreased the atrial EMD parameters in patients with newly diagnosed essential hypertension.

Assessment of atrial conduction time in patients with coronary artery ectasia.

BACKGROUND: Coronary artery ectasia (CAE) is associated with increased sympathetic activity, plasma levels of inflammatory markers, and oxidative stress. These factors can also cause arrhythmias such as atrial fibrillation. Atrial conduction abnormalities in patients with CAE have not been investigated in terms of atrial electromechanical delay obtained by tissue Doppler echocardiography. METHODS: Ninety patients with pure CAE (n = 30), nonobstructive coronary artery disease (NO-CAD) (n = 30), and angiographically normal coronary arteries "controls" (n = 30) were compared in terms of electrocardiographic P-wave measurements, echocardiographic atrial electromechanical coupling (AEC) parameters, and interatrial conduction delay. RESULTS: The mean left atrium diameter in the CAE group was similar to the NO-CAD group but significantly greater than the control group (3.62 ± 0.28 vs 3.46 ± 0.32 vs 3.41 ± 0.31 cm, P = 0.021). P maximum and P-wave dispersion were significantly increased in the CAE group compared to the NOCAD group and the control group (108.6 ± 6.6 vs 97.9 ± 6.6 vs 93.5 ± 6.2, P = 0.0001; 34.4 ± 7.6 vs 23.2 ± 7.8 vs 19.4 ± 7.7 ms, P < 0.0001). Mitral AEC, septal AEC, and tricuspid AEC were significantly higher in the CAE group than the NO-CAD group and the control group (68 ± 4.5 vs 57 ± 4.5 vs 53 ± 4.6 ms, P < 0.0001; 50.7 ± 7 vs 42.7 ± 7 vs 41.7 ± 7.2 ms, P = 0.0001; 47 ± 6.7 vs 39.1 ± 6.7 vs 38.1 ± 6.6 ms, P < 0.0001). Interatrial conduction delay was significantly increased in the CAE group compared to the NO-CAD group and the control group (21 ± 5.5 vs 17.8 ± 5.6 vs 15 ± 5.6 ms, P < 0.0001).The correlation analysis demonstrated that the interatrial conduction delay and P-wave dispersion (Pd) were positively correlated with number of ectatic segments (ESN) (r = 0.41, P = 0.024 vs r = 0.49, P = 0.006). Stepwise multiple linear regression analysis revealed that the ESN was the only independent determinants of interatrial conduction delay (P = 0.024). CONCLUSION: Pd and interatrial conduction delay are prolonged in patients with CAE compared to NO-CAD patients and the healthy controls.

A novel method to estimate pulmonary artery wedge pressure using the downslope of the Doppler mitral regurgitant velocity profile.

Continuous-wave (CW) Doppler recording of mitral regurgitation (MR) is a reflection of the left ventriculoatrial pressure gradient. Accordingly, this jet may yield information about pulmonary artery wedge pressure (PAWP). In this study, we derived and then evaluated a novel method for prediction of PAWP. Patients (n=80) with moderate to severe MR and left ventricular dysfunction were included in the study. Transthoracic echocardiography was performed in patients during pulmonary artery pressure monitoring. A satisfactory CW Doppler recording of MR was obtained in 63/80 (78%). On the late descending portion of the CW recording, the time from a velocity of 4 m/sec to the end of the jet was defined as t1, and from 3 m/sec to the end of the jet as t2. Mathematical derivation of t1/t2 as a predictor of PAWP, was performed based on Weiss' derivation. If t1/t2 was <1.30, the PAWP was normal. If t1/t2 > 1.44, the PAWP was > 16 mmHg. With this new mathematical derivation, it appears that the downslope of the CW Doppler MR waveform may be able to distinguish a normal from elevated PAWP.