We thank Günaydın et al . for their interest in our article. We agree that atrial fibrillation (AF) adversely affects atrial as well as ventricular structure and function. However, there are a number of reasons why we did not consider excluding patients with AF. First, the primary objective of our study was to assess serial changes in left ventricular (LV) myocardial mechanics in response to percutaneous balloon mitral valvotomy (BMV) in patients with severe mitral stenosis (MS). Because the follow-up echocardiographic study was performed relatively soon (72 hours) after BMV, it is unlikely that AF per se could have led to a change in LV myocardial mechanics within such a short period of time. Second, AF is an integral feature of the natural history of MS, particularly in patients with severe MS. Therefore, excluding the patients with AF would have resulted in a selection bias and would have rendered our study population not truly representative of what is encountered in clinical practice. Third, there also may have been a small number of patients who had undocumented, intermittent AF in the past but were in sinus rhythm when the present study was conducted. It would have been impossible to identify them and to exclude them from the study to obtain a study population that was truly free of any present or past AF.

Nevertheless, to address these concerns, we reanalyzed the data after excluding patients who were in AF at the time of this study. The repeat analysis revealed the same findings: LV end-diastolic volume was an independent determinant of LV global longitudinal strain on multiple linear regression (standardized coefficient, −0.46; P = .012). Furthermore, the increment in LV end-diastolic volume after BMV was found to be the only parameter that correlated with the increment in LV global longitudinal strain (Pearson’s r = −0.35, P = .03). Third, as already mentioned in our report, we found that 48 of the 57 patients (84.2%) with MS already had significant impairment of LV global longitudinal strain (values lower than the 25th percentile for the controls), although only seven of these 48 patients (14.6%) had AF. This clearly suggests that the impairment of LV systolic function in severe MS is likely to be a direct consequence of the hemodynamic aberrations resulting from LV inflow obstruction. AF, when it develops, may lead to further worsening of the already existing LV systolic dysfunction, but it is not the only pathophysiologic mechanism responsible for the development of LV systolic dysfunction in these patients. In the study by Shikano et al . cited in the letter by Günaydın et al ., a significantly higher prevalence of AF was seen in patients with MS with LV systolic dysfunction; however, the authors did not elaborate whether the high prevalence of AF was a contributory factor responsible for LV systolic dysfunction or was itself a consequence of an adverse hemodynamic milieu characterized by more impaired LV systolic function.

We did not report coronary angiographic findings, because the presence of coronary artery disease was one of the exclusion criteria in our study. However, four of the 57 patients (three women) in our study were >40 years of age and had undergone coronary angiography at the time of BMV. All of them were found to have normal coronary arteries.