The American Heart Association (AHA) has released an update of clinical knowledge and management of Chagas cardiomyopathy, which has been endorsed by the Inter-American Society of Cardiology and published in Circulation.
Although Chagas disease is typically regarded as a tropical disease found primarily in Central and South America, it now affects ≥300,000 residents in the United States and its prevalence is growing elsewhere. Chagas disease is an infection caused by the protozoan Trypanosoma cruzi. Without successful treatment, infection can persist for a lifetime and can result in serious cardiovascular conditions including dilated cardiomyopathy with heart failure, ventricular arrhythmias and conduction disturbances, stroke, and other systemic or pulmonary embolisms.
Chagas cardiomyopathy is known as Chagas disease with cardiac involvement, with ≥1 electrocardiographic abnormality in patients who test positive for T cruzi. In addition, “dilated Chagas cardiomyopathy refers to the hemodynamic pattern of the Chagas cardiomyopathy that is characterized by left ventricular enlargement with segmental or global systolic function impairment, regardless of electrocardiographic findings.”
The parasite-driven immune response and autoreactivity that is triggered by the infection are 2 mechanisms that may be responsible for initiating acute and chronic myocarditis in Chagas heart disease. Neurogenic disturbances and coronary microvascular derangements may also be implicated in cardiac alterations.
T cruzi can have an incubation period ranging from 1 to 2 weeks after vector-borne transmission and up to 3 to 4 months after transfusion or transplant transmission. The acute phase of Chagas diseases can last 8 to 12 weeks, but is often not diagnosed because many patients are asymptomatic or only present with mild or nonspecific symptoms (eg, fever, malaise, and splenomegaly).
In the acute phase, mild cardiac abnormalities such as tachycardia have been noted. Electrocardiographic findings may reveal sinus tachycardia and PR/QT prolongation, low-voltage QRS complexes, and repolarization abnormalities. Right bundle-branch block, atrial fibrillation, or ventricular arrhythmias can be indicative of a worse prognosis.
Chronic Chagas heart disease usually develops several decades after the disease first appears, which implies an imbalance between the parasite and the host immune response. Although the reasons behind progression are not well understood, some risk factors may include male sex, exposure to reinfection, African ancestry, age, severity of infection, nutrition, alcoholism, and other concomitant diseases.
“More recently, there is evidence that the persistence of high parasitemia and tissue parasitism, a proinflammatory immunological profile with sustained oxidative stress, and genes related to natural killer/CD8+ T-cell cytotoxicity may be determinant in the development of Chagas cardiomyopathy, although the exact mechanism remains to be elucidated,” the authors wrote.
The most common findings in patients with Chagas cardiomyopathy include cardiac rhythm abnormalities, myocardial abnormalities, aneurysms, and thromboembolism.
Determining which patients will develop Chagas heart disease remains an ongoing challenge and an important area of research. Electrocardiography is a common means of monitoring patients. Changes such as right branch-bundle block (with or without left anterior hemiblock) can signal the transition from the indeterminate form to the chronic cardiac form, and the presence of a typical electrocardiographic abnormality has been associated with an increased risk for progressing to a more severe cardiomyopathy. Cardiac stress testing, Holter monitoring, and echocardiography can also serve to highlight cardiac findings.
Increases in N-terminal pro B-type natriuretic peptide are sometimes seen before advanced heart disease, but those increases can be subtle and have not always been clinically useful, according to the writing group.
The AHA writing group concluded that until accurate disease estimates are known, cost-effective interventions cannot be developed. In addition, diagnostic testing must be improved; particularly, they recommended a rapid test to identify T cruzi genotypes and strains since data acquired in one area may not be sufficient to predict test sensitivity of infections acquired in another.
Finally, treatment options outside of benznidazole and antitrypanosomal therapies must be explored and expanded.
Pereira Nunes MC, Beaton A, Acquatella H, et al; on behalf of the American Heart Association Rheumatic Fever, Endocarditis and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young; Council on Cardiovascular and Stroke Nursing; and Stroke Council. Chagas cardiomyopathy: an update of current clinical knowledge and management: a scientific statement from the American Heart Association [published online August 20, 2018]. Circulation. doi:10.1161/CIR.0000000000000599
This article originally appeared on The Cardiology Advisor