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Background-Previous studies suggested that transplantation of autologous bone marrow-derived mononuclear cells (BMNCs) improves heart function in chronic chagasic cardiomyopathy. We report the results of the first randomized trial of BMNC therapy in chronic chagasic cardiomyopathy. Methods and Results-Patients 18 to 75 years of age with chronic chagasic cardiomyopathy, New York HeartAssociation class II to IV heart failure, left ventricular ejection fraction (LVEF) Ͻ35%, and optimized therapy were randomized to intracoronary injection of autologous BMNCs or placebo. The primary end point was the difference in LVEF from baseline to 6 and 12 months after treatment between groups. Analysis was by intention to treat and powered to detect an absolute between-group difference of 5%.

Introduction: Despite all efforts to restrict its transmission, Chagas' disease remains a severe public health problem in Latin America, affecting 8-12 million individuals. Chronic Chagas' heart disease, the chief factor in the high mortality rate associated with the illness, affects more than half a million Brazilians. Its evolution may result in severe heart failure associated with loss of functional capacity and quality of life, with important social and medical/labor consequences. Many studies have shown the beneficial effect of regular exercise on cardiac patients, but few of them have focused on chronic Chagas' heart disease. Methods: This study evaluated the effects of an exercise program on the functional capacity of patients with chronic Chagas' disease who were treated in outpatient clinics at the Evandro Chagas Institute of Clinical Research and the National Institute of Cardiology, Rio de Janeiro, Brazil. The exercises were performed 3 times a week for 1 h (30 min of aerobic activity and 30 min of resistance exercises and extension) over 6 months in 2010. Functional capacity was evaluated by comparing the direct measurement of the O 2 uptake volume (VO 2 ) obtained by a cardiopulmonary exercise test before and after the program (p < 0.05). Results: Eighteen patients (13 females) were followed, with minimum and maximum ages of 30 and 72 years, respectively. We observed an average increase of VO 2peak > 10% (p = 0.01949). Conclusions: The results suggest a statistically significant improvement in functional capacity with regular exercise of the right intensity.

The occurrence of ventricular hypertrophy undoubtedly represents an important marker of increased risk for cardiovascular events; therefore, the importance of identifying the patterns of hypertrophy in patients with hypertension is widely justified 1,2 . A recent study by Mensah et al 3 reported that measurement of the left ventricular mass on echocardiography proved to be better for predicting the evolutional process of hypertension as compared with other variables, such as systolic blood pressure, diastolic blood pressure, and hypertension staging 4 . Left ventricular hypertrophy is no longer considered an adaptive process that compensates the pressure imposed on the heart and has been identified as an independent and significant risk factor for sudden death, acute myocardial infarction, and congestive heart failure 4,5 . In cardiac hypertrophy, anomalous collagenous proteins and other types of contractile proteins (myosin with different functional properties) are produced. These myosins show a lower activity of the ATPase enzyme and a lower velocity of power generation. Likewise the formation of anomalous collagenous proteins, changes in contractile proteins also occur. Concomitantly, sarcomeres and fibroblasts proliferate and become hyperplastic. These adaptations aim to maintain the cardiac contractile capacity to compensate the pressure load imposed on the heart 6 . The cardiac adaptive process is not always beneficial for functioning of the heart and causes alteration in myocardial fibers, in the cardiac capacity to respond to adrenergic stimuli, in the left ventricular diastolic function, in the coronary artery flow, and finally in the contractile function 6 . Left ventricular hypertrophy causes important derangements in coronary artery flow. If hypertrophy is mild, the increase in coronary circulation may proportionally accompany the increase in left ventricular mass through vascular neoformation or use of mechanisms of flow reserve. In the cases of significant increase in ventricular mass, generation of new vessels and capillaries is disproportional to the