Clinical correlates of severe Chagas disease: from a Salvadorian cohort

Abstract Introduction Chagas disease (ChD), caused by Trypanosoma cruzi infection, leads to progressive cardiac damage driven by both parasite-induced and host immune-mediated mechanisms, yet contemporary human patient data remain limited in translating these findings into clinical practice. Given the underrepresentation of Central America—particularly El Salvador—in prior ChD human research, we conducted a cross-sectional study to identify clinical and laboratory markers that could guide treatment strategies for ChD patients in this region. Methods Clinical information and biological specimen were collected from Salvadorian patients with suspected Chagas disease. Blood and plasma were tested for parasitemia and laboratory markers, respectively. Chagas cardiomyopathy (CCM) definition was based on age-adjusted NT-proBNP thresholds. Results 191/200 (95.5%) were confirmed Chagas seropositive. 116/191 (61%) reported receipt of trypanocidals. Patients with CCM (35/191 18%) were older (median 57 IQR 45–68 vs 40 33–50, p0.0001), more arrhythmic (37% vs 16%, p=0.009), and showed reduced ejection fraction (n=83) % (55 48–58 vs 63 59–68, p0.001). Patients with CCM more frequently had elevated Troponin I (29% vs 1.3%, p0.0001) and persistent parasitemia (23% vs 7.1%, p=0.010), showed higher anti-trypanosoma IgG S/CO (13 12–15 vs 8.7 5.8–12, p0.0001), and were less likely to have received past trypanocidal therapy (43% vs 65%, p=0.021). After adjusting for age and sex, multivariate logistic regression confirmed the same variables as independent predictors of CCM. Discussions Our results depict significant morbidity among Salvadorian patients with Chagas disease. Clinical correlates of progression to CCM with risk stratification potential were determined.