Discussion:
In the present study, atrial mechanical dispersion was found to be prolonged in patients who developed atrial fibrillation with HCM. In addition to prolonged mechanical dispersion, increased age was found to be predictive for the development of atrial fibrillation.
Previous studies have shown that annual AF development incidence in HCM patients is 2-4%; this incidence is 20-30% throughout life, and it can increase to rates of up to 40% in patients older than 70 years old.16,17. In our study, this rate was found to be 16.9%. This lower rate might be caused by our relatively younger patient population and the shorter length of the follow-up period.
Compatible with previous studies, age has been found out to be predictive of AF in our study. 18. The occurrence of structural changes in the atrial wall with advancing age and the long duration of untoward effects of HCM acting on the LA wall contribute to the development of AF by inducing fibrosis in the atrial wall. Advanced age is the most important risk factor in the HCM population as it is in the normal population.
In previous studies, the LA strain was found to be an independent predictor of the development of AF in HCM patients19,20. In our study; although LA strain was found to be lower in the group, in which AF developed, a statistically significant difference was not observed between the groups in the regression analysis. This is probably because of the relatively small number of patients participating in our study.
After a short time following the electrical conduction, mechanical contraction occurs enabling the heart to work synchronously. In various disease states that lead to fibrosis in LV, electrical synchronization is disrupted called asynchrony; which may potentially contribute to mechanical dispersion and the occurrence of arrhythmic events. Previous studies have found out that ventricular mechanical dispersion is associated with arrhythmogenic right ventricular dysplasia (ARVD), a long QT interval, and ischemic cardiomyopathy, and, in HCM patients, with ventricular arrhythmic events 11,21-23. Conditions that affect not only LV but also LA (pressure or volume overload) may induce fibrosis in myofibrils in the LA wall, impairing the electrical and mechanical synchronization. Atrial dispersion can be evaluated by STE-based methods since TDI-based methods are angle-dependent and affected by mechanical withdrawals. In the study conducted by Kawakami et al. on community-based participants with a potential to develop heart failure and AF; atrial dispersion was found increased in patients, in whom AF developed, compared to those who did not develop AF and atrial dispersion was found independently predictive of AF development 12. In the study of Zhijuan Shang et al., atrial dispersion was found increased in PAF patients compared to the healthy group and atrial dispersion was found out to be an independent predictor of AF development in patients with a normal left atrium size 24. In another study; a high atrial dispersion before cardioversion was found decreased after cardioversion in patients, who were planned to undergo cardioversion because of AF25,26. In the study by Kupczynska et al., atrial dispersion was found out to be an independent predictor of thrombus formation in the left atrial appendage (LAA) in patients, in whom transesophageal echocardiography (TEE) was performed because of AF27. However, in a study by Rasmussen et al. on PAF patients, atrial dispersion was found not associated with ischemic stroke 28.
In our study, atrial dispersion was found out to be predictive of the development of AF in HCM patients. Elevated LV filling pressures due to left ventricular hypertrophy and SAM-related mitral insufficiency in HCM patients cause structural changes including fibrosis, called atrial remodeling, in the left atrial wall resulting from increased pressure and volume. While structural and electrical remodeling potentially causing electrical heterogeneity cause nonuniform conduction velocities and inhomogenous refractory periods in the atrial myocardium, increased electrical remodeling may contribute to further progression of structural remodeling. The resulting electrical asynchrony or dispersion and electromechanical dysfunction may lead to the development of atrial fibrillation 6.