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Am Fam Physician. 2010;81(4):407-414

Original Article: Cardiomyopathy: An Overview

Issue Date: May 1, 2009

to the editor: Chagas disease, caused by infection with Trypanosoma cruzi, should have been included in Table 2 of this article as one of the potential secondary causes of inflammatory cardiomyopathy. T. cruzi is transmitted by various species of bloodsucking “kissing bugs” from the Triatominae subfamily, and is present in many animal species spread throughout most of the United States.1 Chagas disease is a significant public health problem, especially in Central and South America where an estimated 10 million people are still infected with T. cruzi.2 Chagas disease reaches North America through immigration,1 and an estimated 14 million people from countries where Chagas disease is endemic are living in non-endemic areas.3

The heart is the organ most commonly affected in chronic Chagas disease4, and up to 30 percent of affected persons develop a chronic inflammatory cardiomyopathy years or even decades after the initial infection.2 It is possible that many cases of Chagas' cardiomyopathy are being misdiagnosed.

Chronic T. cruzi infection is usually detected through various serologic antibody tests.4 Exposure history can usually be identified, typically attributed to current or previous residence in endemic areas or blood transfusions and solid organ transplantation from infected persons.1

As the article points out, treatment for various cardiomyopathies is directed at treating the underlying disease, reducing symptoms and complications of heart failure, and suppressing arrhythmias. Anti-infectives do not appear to be effective in patients with chronic Chagas cardiomyopathy.5 The heart failure associated with Chagas disease is treated as is cardiomyopathy due to other causes, which includes beta blockers, angiotensin-converting enzyme inhibitors, and diuretics. Treatment of chronic Chagas disease includes monitoring for arrhythmias, as there is a role for pacemaker/defibrillator implantation in the primary and secondary prevention of sudden cardiac death.6

IN REPLY: I appreciate Dr. Junnila's commentary regarding Trypanosoma cruzi as a cause of cardiomyopathy. Though an extensive listing of causes of cardiomyopathy was not possible, T. cruzi does warrant special mention.

Transmission of T. cruzi commonly occurs in rural Latin America because of poor housing conditions and close contact with the primary vector, triatomine bugs.1 Most T. cruzi infections in the United States occur in patients who acquired the infection while living in endemic areas, and affects approximately 100,000 persons.2 Because of increased recognition of the T. cruzi infection owing to increased immigration from endemic areas, the U.S. Food and Drug Administration approved an assay for blood donor screening in 2006.3

Most infected persons will remain asymptomatic, but approximately 30 percent will progress clinically to overt disease, which most commonly affects the heart.1,4 Early on, symptoms are mainly related to conduction abnormalities resulting in right bundle branch block, but left ventricular wall motion abnormalities also occur.5 As the disease progresses, sustained ventricular tachycardia, heart block, thromboembolic disease, and dilated cardiomyopathy may occur.1,6 The underlying cause of cardiac dysfunction is believed to be caused by an autoimmune, as well as a parasite-driven immune response, which promotes an increase in cytokine and chemokine activity.4

Increased immigration from endemic areas and screening on the U.S. blood supply makes it increasingly likely that family physicians will encounter such patients in their practice. Patients with newly diagnosed T. cruzi should undergo a complete history and physical examination, and electrocardiogram (ECG) with rhythm strip.1 These patients should be followed with annual ECG to assess for cardiac changes.1 Family physicians should have a high index of suspicion for T. cruzi in cases of idiopathic cardiomyopathy in immigrants and travelers.

Email letter submissions to afplet@aafp.org. Letters should be fewer than 400 words and limited to six references, one table or figure, and three authors. Letters submitted for publication in AFP must not be submitted to any other publication. Letters may be edited to meet style and space requirements.

This series is coordinated by Kenny Lin, MD, MPH, deputy editor.

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