Chronic Chagas' Myocardiopathy (CCM)

Clinical Characteristics

The clinical findings in CCM depend on the severity and number of myocardial lesions, and the development of heart failure and various arrhythmias. In varying reports, 10 to 50% of chronically infected patients will develop congestive failure and 50% of these individuals will be dead within 2 years. The immunological tests will be positive in over 90% of patients at this stage. On physical examination, there may be cardiac enlargement, irregularities of rhythm due to premature ventricular contractions or atrioventricular block, gallop rhythm, sinus bradycardia, diminished heart sounds, a widely split second pulmonary sound, and systolic murmurs from functional mitral or tricuspid regurgitation. There may also be an increase in systemic venous pressure and hepatomegaly. The systolic blood pressure is usually normal to moderately lowered, as is the pulse pressure.

Fig. 4.28. EKG in chronic Chagas' myocardiopathy is often diagnostic, showing various conduction disturbances, principally right bundle branch block and left anterior hemiblock. Negative T waves of the primary type and alterations indicative of apical myocardial necrosis are also common. Frequent and multifocal ventricular extrasystoles are characteristic, as is a sinus bradycardia or an abnormally fixed sinus rhythm associated with heart failure. AFIP 69-4025.

The EKG in CCM is often diagnostic (Fig. 4.28). The panmyocarditis almost always causes conduction disturbances, principally right bundle branch block (seen in 30-60% of patients) and left anterior hemiblock.. Negative coronary T waves of the primary type and alterations indicative of apical myocardial necrosis are common. Apical aneurysms diagnosed by EKG or echocardiography are more frequent in enlarged hearts, but about 26% of patients with a normal radiological cardiac series have EKG evidence of apical lesions. Frequent and multifocal ventricular extrasystoles are characteristic of CCM; a sinus bradycardia or abnormally fixed sinus rhythm associated with heart failure is highly specific and probably a consequence of partial or complete block of the autonomic nervous system or damage to the sinus node itself. This may produce a dysautonomic syndrome of postural hypotension, dizziness and arrhythmias. A recent report of symptomatic patients with chronic Chagas' disease in Venezuela showed that almost 40% had a conduction abnormality, over 75% had ventricular arrhythmias, and nearly 33% had abnormal ST segment and T wave inversion.

The prognosis in patients with clinical CCM is grave. Embolic phenomena, particularly cerebral embolism, are a not uncommon way for patients to present and are the most common cause of stroke in young adults in endemic geographic regions. Many patients have syncope and may die suddenly from the effects of the disease on the conduction system, particularly ventricular fibrillation, while others develop progressive cardiac failure. Most patients with chronic Chagasic cardiopathy die between the ages of 20-40 years. Unfortunately, there is as yet no specific drug which is entirely effective against T. cruzi, especially in the chronic stage, when the morphological alterations of cardiopathy, megaesophagus and megacolon are organized and irreversible.