Why the study?
Atrial cardiomyopathy is a frequent complication of Chagas disease driven by chronic inflammation and fibrosis, and this study tested whether left atrial remodeling progresses in parallel with left ventricular damage and predicts new-onset AF.
Does left atrial remodeling progress in parallel with left ventricular damage and predict new-onset atrial fibrillation in patients with chronic Chagas cardiomyopathy?
Cohort (n=50)
No
Does left atrial remodeling progress in parallel with left ventricular damage and predict new-onset atrial fibrillation in patients with chronic Chagas cardiomyopathy?
In chronic Chagas cardiomyopathy, progressive left atrial enlargement strongly correlates with left ventricular mass increase and predicts new-onset atrial fibrillation and mortality, highlighting the value of serial left atrial echocardiography for risk stratification.
Serial LA monitoring may aid AF risk stratification in Chagas cardiomyopathy; extends remodeling observations but leaves open prospective validation.
Introduction Atrial cardiomyopathy is a frequent complication of Chagas disease, driven by chronic inflammation and fibrosis. We hypothesized that left atrial (LA) remodeling progresses in parallel with left ventricular (LV) damage and predicts new-onset atrial fibrillation (AF). Methods We studied 50 patients with chronic Chagas cardiomyopathy (age 51±9 years, 70% female), all in sinus rhythm at baseline, followed at a tertiary center (mean 83.5±40.7 months). New-onset AF was assessed by serial Holter and ECG. LA anteroposterior diameter, LV mass (Devereux), and LVEF (Teichholz) were obtained by echocardiography from the parasternal long-axis view at admission and follow-up. Paired echocardiograms were available in 34 patients. LA enlargement was defined as diameter >4.0 cm. Results At baseline, 37 patients (74%) had normal LA diameter. AF incidence was 2.55/100 person-years (95%CI 1.17–4.85) and new LA enlargement 1.73/100 person-years (95%CI 0.56–4.03); 9 patients died. LA diameter increased at 0.6±1.4 mm/year (p<0.001) and LV mass at 6.9±23.6 g/year (p=0.027). Over follow-up, LA diameter increased from 3.55±0.62 cm to 3.90±0.58 cm (p<0.001), LV mass from 153.8±51.7 g to 206.9±73.0 g (p<0.001), and LVEF declined from 69.3±16.3 % to 61.0±18.9% (p<0.001) (Figure 1). Patients who developed AF had larger baseline LA (4.0±0.6 vs 3.5±0.6 cm; p=0.019); and baseline LA > 4.0 cm predicted AF (OR=5.16; p=0.040). Non-survivors had LA larger at admission (4.0±0.7 vs 3.5±0.5 cm; p=0.031) and at follow-up (4.7±0.7 vs 3.8±0.4 cm; p=0.005). The annual rate of LA enlargement strongly correlated with LV mass increase (r=0.84, p<0.001). Conclusion In Chagas cardiomyopathy, progressive LA enlargement mirrors LV remodeling, and predicts new-onset AF, suggesting that atrial cardiomyopathy is not an isolated event but part of a global fibrotic process. Serial LA assessment may identify patients at higher risk of AF and death.
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Barbosa et al. (2026) conducted a cohort in Chronic Chagas cardiomyopathy (n=50). Baseline left atrial enlargement (diameter >4.0 cm) and progressive LA remodeling vs. Normal baseline left atrial diameter (≤4.0 cm) was evaluated on New-onset atrial fibrillation (OR 5.16, p=0.040).
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