Background Left atrial (LA) dilation is associated with increased risk of atrial fibrillation (AF), heart failure and cardiac arrest in patients with hypertrophic cardiomyopathy (HCM). The factors that influence LA remodelling in HCM are not well described. This study was undertaken to identify factors that influence the rate of LA remodelling and subsequent development of atrial fibrillation in HCM.
Methods Baseline and follow-up echocardiograms were analysed by an experienced echocardiographer blinded to clinical factors or outcomes in an HCM patient cohort. Exclusion criteria were <1 year between first and last echocardiogram, AF was present before follow-up echocardiogram, prior myectomy, or poor image quality. Clinical features and associated outcomes were obtained from medical records. The rate of LA remodelling was calculated by dividing the change in size by the time (in years) between studies. Multivariable linear and logistic regression were used to identify factors associated with LA remodelling and incident AF after controlling for age and body surface area (BSA).
Results A total of 205 HCM patients were studied: mean age 44.4±15.8 years, 40% female, 41% had sarcomere mutations, NYHA class I/II/III 61%/30%/9%, septal thickness 17±5 mm, LV ejection fraction (LVEF) 65%±9%, 30% had obstruction (LV outflow tract gradient ≥30 mm Hg at rest or ≥50 mmHg with Valsalva). At baseline, LA diameter was 4.1±0.6 cm (range 2.4–6.2) and LA volume indexed to BSA (LAVi) was 34±12 ml/m2 (range 11–75) with at least mild LA enlargement present in over 50%. Over a median 5.0 years (IQR 2.7–7.8) follow up, LA diameter increased by 0.2±0.4 cm and LAVi by 5±10 ml/m2. The baseline ratio of the peak E-wave velocity to septal TDI e’ velocity (E/e’) and estimated pulmonary artery systolic pressure were significantly associated with LA enlargement (p=0.0007 and 0.049 respectively). The relationship between E/e’ remained significant after controlling for age, BSA, LVOT gradient, LVEF, and mitral regurgitation. In univariate and multivariate analyses, other clinical and echocardiographic variables, including age, genetic status, blood pressure, LVEF, and the presence or degree of LVOT obstruction, were not associated with LA remodelling. Incident AF developed in 35 patients (17%). Baseline LA diameter was larger (4.5 vs. 4.0 cm, p<0.01) in patients who developed AF. In a multivariable model including age, BSA, and baseline E/e, baseline LA size (p=0.007) and rate of LA enlargement (p=0.01) were significantly associated with the development of AF.
Conclusions Remodelling of the LA is a common feature of HCM that is progressive and associated with future development of AF. E/e’, rather than obstruction, was strongly associated with progressive LA remodelling in this cohort. These findings support the importance of altered myocardial function and haemodynamics in LA remodelling in HCM.
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