Cardiac remodeling and predictors of ventricular tachycardia in chagas cardiomyopathy
P R Benchimol Barbosa, A C L Benchimol-Barbosa, B K KanthariaAbstract
Introduction
Ventricular tachycardia (VT) is a major cause of sudden death in Chagas cardiomyopathy. Identifying patients at risk requires understanding the structural substrate. We sought to investigate the incidence of VT and its echocardiographic and electrocardiographic predictors.
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). Sustained VT was documented by serial Holter and ECG monitoring. LA volume (from anteroposterior diameter using spherical model), LV mass (Devereux), and LVEF (Teichholz) were derived by echocardiography from the parasternal long-axis view at admission. LV apical aneurysm, inactive area on ECG, and non-sustained VT (NSVT) on Holter were recorded at baseline. Given the limited number of events, predictors were assessed by Firth-penalized Cox proportional hazards regression to reduce bias. Hazard ratios (HR) for continuous variables are expressed per unit increase. Results were validated by bootstrap resampling (2,000 iterations).
Results
VT occurred in 11 patients (22%), with an incidence of 3.16/100 person-years (95%CI 1.58–5.66). The composite of VT or death occurred in 17 patients (34%; 4.89/100 person-years). Among five patients with both VT and atrial fibrillation, VT preceded AF (100%). Patients who developed VT had increased baseline LV mass (199.9±49.3 g vs 156.0±64.6 g; p=0.012) and larger LV end-systolic diameter (4.05±1.18 cm vs 3.14±1.04 cm; p=0.012) (Figures A2 and A3). On Firth-penalized Cox regression (Figure B), VT predictors were baseline NSVT (HR=9.69; 95%CI [2.78–33.7]; p<0.001), LV apical aneurysm (HR=7.48; 95%CI [2.20–25.5]; p=0.001), inactive area on ECG (HR=3.63; 95%CI [1.11–11.9]; p=0.033), driven by anteroseptal location (HR=6.18; 95%CI [1.87–20.4]; p=0.003) rather than inferior (p=0.74), LV end-systolic diameter (HR=1.83/cm; 95%CI [1.22–2.73]; p=0.004), LV end-diastolic diameter (HR=1.89/cm; 95%CI [1.16–3.1]; p=0.011) and LVEF (HR=0.957/%; 95% CI [0.93–1.0]; p=0.008). Anteroseptal inactive area and LV apical aneurysm were strongly associated (OR=11.7; p=0.006), and the presence of both findings was associated with a VT rate of 80% (4/5). In a two-predictor model, both NSVT (HR=7.53; 95%CI [2.03–27.9]; p=0.003) and anteroseptal inactive area (HR=3.83; 95%CI [1.05–13.9]; p=0.042) remained independent predictors of VT. Bootstrap validation confirmed NSVT, LV apical aneurysm, anteroseptal inactive area, LV end-systolic diameter, LV end-diastolic diameter and LVEF as stable predictors (Figure B).
Conclusion
In Chagas cardiomyopathy, a high-risk arrhythmogenic phenotype is driven by structural remodeling and electrical instability. The combined detection of NSVT, anteroseptal scar, and LV apical aneurysm strongly predicts VT, supporting early risk stratification using combined echocardiographic and electrocardiographic assessment.Structural and Electrical Substrates for VT