Assessment of atrial conduction time in patients with coronary artery ectasia

Abstract

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.