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Associations between Cardiac Magnetic Resonance T1 Mapping Parameters and Ventricular Arrhythmia in Patients with
Martha Valéria Tavares Pinheiro1, Renata Junqueira Moll-Bernardes1, Gabriel Cordeiro Camargo1,2
11D'Or Institute for Research and Education (IDOR), Rio de Janeiro, Brazil.
Insights
In Chagas disease, increased myocardial fibrosis markers, like extracellular volume (ECV), are linked to ventricular arrhythmias. ECV shows an independent association with non-sustained ventricular tachycardia (NSVT), suggesting it may be an early risk indicator.
Area of Science:
- Cardiology
- Medical Imaging
- Infectious Diseases
Background:
- Chronic Chagas disease can lead to heart damage, characterized by fibrosis and increased risk of sudden cardiac death due to ventricular arrhythmias.
- Cardiac magnetic resonance (CMR) is a key tool for assessing myocardial fibrosis, a significant factor in Chagas cardiomyopathy progression.
Purpose of the Study:
- To evaluate the association between myocardial fibrosis parameters measured by CMR and non-sustained ventricular tachycardia (NSVT) in patients with early-stage Chagas disease.
- To determine if extracellular volume (ECV) is an independent predictor of ventricular arrhythmias in Chagas cardiomyopathy.
Main Methods:
- A cross-sectional study involving 47 patients with early Chagas disease and 15 controls.
- Cardiac evaluation included CMR to assess myocardial fibrosis using late gadolinium enhancement (LGE), native T1, and ECV.
- Logistic regression analysis was used to identify associations between fibrosis markers, arrhythmias, and clinical scores.
Main Results:
- Patients with Chagas disease showed increased myocardial fibrosis markers and ventricular arrhythmias compared to controls.
- Extracellular volume (ECV) demonstrated an independent association with the presence of NSVT, even after adjusting for fibrosis mass and left ventricular ejection fraction (LVEF).
- The area under the receiver-operating characteristic curve for global ECV in predicting NSVT was 0.85.
Conclusions:
- Extracellular volume (ECV) measured by CMR may serve as an early marker for increased risk of ventricular arrhythmia in Chagas disease.
- ECV shows an independent association with NSVT in the initial stages of chronic Chagas cardiomyopathy.
- These findings highlight the potential of ECV as a prognostic indicator in managing Chagas cardiomyopathy.
Abstract:
Chronic Chagas disease can progress to myocardial involvement with intense fibrosis, which may predispose patients to sudden cardiac death through ventricular arrhythmia. The associations of myocardial fibrosis detected by cardiac magnetic resonance (CMR) parameters with non-sustained ventricular tachycardia (NSVT) were evaluated. This cross-sectional study included patients in early stages of Chagas disease (n = 47) and a control group (n = 15). Patients underwent cardiac evaluation, including CMR examination. Myocardial fibrosis assessment by CMR with measurement of late gadolinium enhancement (LGE), native T1, and extracellular volume (ECV) was performed. There was an increase in myocardial fibrosis CMR parameters and ventricular arrhythmias among different stages of Chagas disease, combined with a decrease in the left ventricular ejection fraction (LVEF) by CMR and also in the right ventricular systolic function by S' wave on tissue Doppler. Fibrosis mass and ECV were associated with the Rassi score, ventricular extrasystole, and E/e' ratio in a logistic regression model adjusted for age and gender. The ECV maintained an association with the presence of NSVT, even after adjustments for fibrosis mass and LVEF assessed by CMR. The receiver-operating characteristic area under the curve for global ECV (0.85; 95% CI: 0.71-0.99) and NSVT was greater than that for fibrosis mass (0.75; 95% CI: 0.54-0.96), although this difference was not statistically significant. Extracellular volume could be an early marker of increased risk of ventricular arrhythmia in Chagas disease, presenting an independent association with NSVT in the initial stages of chronic Chagas cardiomyopathy, even after adjustment for fibrosis mass and LVEF.
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