Chagas disease (CD) is caused by the protozoan Trypanosoma cruzi and is transmitted by triatomine insects in endemic areas such as Mexico, Central America, and South America. In 2023, Peru was considered a high-prevalence country, with 19 confirmed cases of CD reported [1, 2]. The infection leads to an acute phase lasting 4–8 weeks, with 20–30% of cases progressing to chronic CD, characterized by cardiomyopathy and megaviscera, ultimately leading to heart failure (HF) [3].

Recently, cardiovascular magnetic resonance (CMR) has gained significance as a noninvasive tool for identifying myocardial inflammatory activity (edema and myocardial hyperemia) at an early stage. These changes are identifiable before irreversible lesions such as necrosis and fibrosis develop. However, other tools have also emerged, such as computed tomography (CT), for the early recognition of tissue characterization. The combined use of these modalities can further enhance our ability to assess myocardial inflammation and guide therapeutic interventions [3].

A 58-year-old male from San Martín, Peru, with a history of valvular disease diagnosed in 2020 and HF (NYHA functional class II), sought medical care after two years of persistent and worsening respiratory symptoms. He has worked in the agriculture field over the past decades. A transthoracic echocardiogram revealed severe symptomatic mitral valve insufficiency. He was evaluated at a tertiary care hospital due to exacerbated dyspnea (NYHA functional class IV), orthopnea, prominent edema, chest pain, and syncope. Cardiovascular examination revealed jugular distension, hepatojugular reflux, and a holosystolic murmur at the mitral and tricuspid foci.

As part of the medical evaluation, an electrocardiogram revealed sinus rhythm with left anterior fascicular block and low QRS voltage (Figure 1); a chest X-ray showed moderate to severe cardiomegaly. Subsequently, transthoracic echocardiography revealed a significant reduction in left ventricular systolic function with a reduced left ventricular ejection fraction (LVEF 24%), global hypokinesia associated with a suggestive image of an interatrial aneurysm, four-chamber dilation, and severe mitral and tricuspid insufficiency (Figure 2). Mortality risk stratification was performed using the Rassi score, which yielded a high-risk score of 17/20, considering the NYHA functional class IV, cardiomegaly, global wall-motion abnormality, male sex, and low QRS voltage [4].

Due to suspicion of chronic ischemia, patient age, and findings of mitral insufficiency on echocardiography, a coronary computed tomography angiography (CTA) was conducted, along with high-sensitivity cardiac troponin T test (hs-cTnT) and C-reactive protein (CRP) levels. The imaging test did not reveal abnormalities, and the hs-cTnT level upon admission was 6 ng/L, with no significant changes during hospitalization, ruling out the probability of obstructive subepicardial coronary artery disease (Figure 3). Additionally, the CRP levels were within the normal range at 0.55 mg/dL. Iodine contrast enhancement confirmed inferolateral and apical aneurysmatic images, revealing transmural enhancement patterns in aneurysmatic segments (Figure 4).

Systematically, the most common causes of non-ischemic dilated cardiomyopathy were excluded, including toxic, endocrinological, nutritional, and autoimmune factors. Notably, given the endemic nature of CD vectors in Peru, suspicion was raised, prompting the performance of an indirect chemiluminescent immunoassay to detect specific IgG antibodies against excretory-secretory antigens of T. cruzi, as well as an enzyme-linked immunosorbent assay for IgG, both of which returned positive results.

CMR was performed to quantify myocardial fibrosis and assess disease severity. T1 mapping revealed prolonged global relaxation times (1,100 ms), indicating diffuse myocardial fibrosis (Figure 5). The examination also revealed a 32% extracellular volume (ECV) fraction in post-contrast-enhanced T1 mapping, suggesting edema (Figure 6). Furthermore, contrast-enhanced gadolinium images confirmed a transmural pattern of late gadolinium enhancement (LGE), revealing 16 grams of fibrosis mass in aneurysmal segments (Figure 7).

A 24-hour Holter study revealed sinus rhythm with a mean heart rate of 65 bpm. Additionally, it showed isolated supraventricular extrasystoles, including bigeminy and trigeminy patterns, without supraventricular tachycardia. Due to the high mortality risk associated with chronic cardiomyopathy of Chagas disease (CCCD), an implantable cardioverter-defibrillator (ICD) was recommended for the prevention of sudden cardiac death (SCD). The patient was discharged without complications following the placement of the ICD.

The diagnosis of CD involves conventional and non-conventional serological tests. According to the World Health Organization, confirmation requires two positive results. Common electrocardiographic abnormalities include complete right bundle branch block and left anterior fascicular block [3, 5].

Echocardiography plays a crucial role in assessing CCCD, enabling the prediction of mortality from early changes to advanced stages with left ventricular enlargement and impaired systolic function. CCCD patients presenting with atypical pain may undergo CTA to rule out obstructive subepicardial coronary artery disease. Additionally, CT can be used for the early characterization of myocardial fibrosis through late enhancement assessment and evaluate biventricular systolic function, complementing echocardiography [6].

Holter monitoring aids in detecting cardiac arrhythmias for routine CCCD assessment, facilitating the diagnosis of conditions such as sinus node dysfunction and supraventricular tachyarrhythmias [3].

Long-term mortality risk stratification using the Rassi score aids in directing therapy based on individual survival probabilities determined by the existence of six clinical features: NYHA class III or IV, cardiomegaly on chest radiography, segmental or global wall-motion abnormalities on echocardiography, non-sustained ventricular tachycardia on Holter monitoring, low QRS voltage on electrocardiography, and male sex. Patients at high risk of mortality may benefit the most from aggressive therapeutic interventions, including ICD, heart transplantation, and cardiac resynchronization [4].

Comprehensive evaluation of CCCD also involves CMR, which correlates myocardial fibrosis with disease severity, ventricular arrhythmias, and cardiovascular events. CMR assesses biventricular systolic function, T2 mapping for edema, and LGE for regional fibrosis detection. Myocardial T1 mapping measures ECV for interstitial fibrosis assessment, and global T1-weighted enhancement aids in detecting hyperemia and inflammation. ECV fraction has a prognostic role in early-stage cardiomyopathy. The late enhancement technique in CMR serves as a crucial predictor for severe cardiovascular events, independently forecasting total death, cardiovascular death, and sustained ventricular tachyarrhythmias. The European Association of Cardiovascular Imaging and the SBC Cardiovascular Imaging Department recommend CMR for quantifying myocardial fibrosis extension, assessing SCD risk, and potentially influencing implantable ICD indications [3, 7].

With a confirmed diagnosis of non-ischemic HF, a LVEF of 24%, and NYHA class IV, the individual met class I Level B evidence criteria for an ICD according to the 2012 American Heart Association guidelines. The ICD effectively addresses potential ventricular arrhythmias, preventing SCD, and offers a promising approach to enhancing overall survival [8, 9].

The clinical case presented demonstrates how patients can benefit from a multimodality-based strategy in CCCD, aiding in the selection of the most appropriate therapeutic management based on specific findings (Table 1). While iodine late enhancement is an innovative technique that can assist in guiding management, it does not replace gadolinium late enhancement for the determination of fibrosis and disease severity.