Role of cardiac imaging for the diagnosis and prognosis of CCCD [3]
| Cardiac study | Initial indications | Repeated testing | Typical features |
|---|---|---|---|
| 12-lead ECG | Initial diagnostic and prognostic assessment of every individual with positive serology for CD, enabling the clinical classification. | Perform an ECG annually if there are multiple specific changes or every two years if the ECG is normal or has nonspecific (isolated) changes. | Most frequent and defined alterations are atrioventricular conduction blocks, right bundle branch block, left anterior fascicular block, ventricular repolarization alterations, and ventricular ectopic beats. |
| Association of 2 or more abnormalities in the same electrocardiographic tracing, characterizes severe cardiomyopathy. | |||
| Chest X-ray | Initial diagnostic and prognostic assessment of every individual with CCCD. To diagnose cardiovascular impairment. | Perform when there is clinical evidence of pulmonary or systemic congestion. | An enlarged cardiac area with minimally congested pulmonary fields is often present. In addition, right ventricle enlargement signs are common on posteroanterior and lateral views. Signs of right pleural effusion secondary to systemic congestion can also be evidenced. |
| Echocardiography | Initial assessment and follow-up of patients with CD. Assessment of every individual with CCCD. | Reassess periodically: every 3 to 5 years for preserved ejection fraction cases and no previous segmental contractility changes.Reassess every 1 to 2 years for cases with global or segmental left ventricular dysfunction. | Left ventricular enlargement, segmental and/or diffuse hypokinesia, ventricular aneurysms , and left ventricle dysfunction. |
| Suspicion of CCCD arises from history, clinical examination, or electrocardiographic changes. | Alteration in myocardial relaxation is the first change visible, as it progresses, it can worsen to a typical restrictive pattern. | ||
| CMR | When there is suspicion of concurrent CCCD and coronary artery disease or other non-ischemic cardiomyopathy, CMR is utilized to assess the etiology and extent of myocardial fibrosis. | Not established. | Allows for morphological and functional assessment, globally and segmentally, as well as the detection of intracardial thrombi, overcoming technical limitations of echocardiography. |
| In non-endemic areas where initial clinical suspicion of CD is absent, CMR can strongly indicate probable CCCD diagnosis based on LGE patterns, prompting further serological tests for etiological diagnosis confirmation. | Identification of myocardial inflammatory activity (edema and myocardial hyperemia) at an early stage before the development of irreversible lesions, such as necrosis and fibrosis. They can aid in risk stratification and therapeutic decision-making. | ||
| T2-weighted images and T2 mapping should be included for assessment of myocardial edema in addition of LGE to detect gross regional myocardial fibrosis. T1 mapping should be included to calculate the myocardial extracellular volume (interstitial and diffuse fibrosis measure). | |||
| Computed tomography angiography | Non-invasive evaluation of coronary anatomy in patients with CCCD and a high likelihood of obstructive subepicardial coronary artery disease. | Not established. | Characterization of normal myocardial tissue/fibrosis using late enhancement as an alternative to CMR. |
| Assessment of biventricular systolic function, along with echocardiography, for patients with contraindications to CMR. |
CCCD: chronic cardiomyopathy of Chagas disease; ECG: electrocardiogram; CD: Chagas disease; CMR: cardiovascular magnetic resonance; LGE: late gadolinium enhancement
