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.