320 Rev Esp Cardiol. 2009;62(3):320-2 Angiotensin-Converting Enzyme Insertion/Deletion Gene Polymorphism and Progression of Chagas’ Cardiomyopathy Carmine Pascuzzo-Lima, Juan C. Mendible, and Rafael A. Bonfante-Cabarcas Unidad de Bioquímica Dr. José Antonio Moreno Yanes, Decanato de Ciencias de la Salud Dr. Pablo Acosta Ortiz, Universidad Centroccidental Lisandro Alvarado, Barquisimeto, Lara State, Venezuela BRIEF REPORTS Correspondence: Dr. C. Pascuzzo-Lima. Sección de Farmacología. Decanato de Ciencias de la Salud Dr. Pablo Acosta Ortiz. Universidad Centroccidental Lisandro Alvarado. Avda. Libertador con Avda. Andrés Bello, 3001 Barquisimeto. Lara. Venezuela. E-mail: carminepl@yahoo.com Received March 23, 2008. Accepted for publication May 21, 2008. Chagas’ disease is common in Latin America and is caused by Trypanosoma cruzi. It is usually associated with chronic cardiomyopathy, the progression of which could be related to genetic factors. As alterations in the renin-angiotensin-aldosterone system have been reported in the disease, the aim of this study was to determine whether associated genetic polymorphisms influence the development of myocardial damage. The study involved 125 patients who were divided into 2 groups according to whether they had mild or severe cardiomyopathy. The insertion/deletion polymorphism of the angiotensin- converting enzyme gene was investigated using standard techniques and results were correlated with disease stage. The genotypes were in Hardy-Weinberg equilibrium. After adjusting for demographic variables, no significant relationship was found between the polymorphism and progression of chronic Chagas’ disease. Although our sample was limited, the results suggest that the progression of cardiomyopathy in chronic Chagas’ disease is unrelated to the insertion/deletion polymorphism. Key words: Chagas’ disease. Insertion/deletion polymorphism of the angiotensin-converting enzyme gene. Polimorfismo I/D del gen de la enzima de conversión de angiotensina y progresión de la miocardiopatía chagásica La enfermedad de Chagas es frecuente en Latinoamé- rica y la causa Trypanosoma cruzi. Suele asociarse a miocardiopatía crónica, cuya progresión podría relacio- narse con factores genéticos. Dado que se han publica- do alteraciones del sistema renina-angiotensina-aldoste- rona en esta enfermedad, este trabajo buscó determinar si los polimorfismos genéticos relacionados afectaban a la progresión del daño miocárdico. Se seleccionó a 125 pacientes y se agrupó según presentasen miocardiopa- tía leve o severa. El polimorfismo de inserción/deleción del gen de la enzima de conversión de angiotensina se analizó por pruebas estandarizadas, y los resultados se correlacionaron con el estadio de la enfermedad. Los ge- notipos cumplieron el equilibrio de Hardy-Weinberg. Des- pués de ajustar según variables demográficas, no hubo relación significativa entre el polimorfismo estudiado y la progresión de la enfermedad de Chagas. Pese a que la muestra fue limitada, los resultados indican que la pro- gresión de la miocardiopatía chagásica no está relacio- nada con el polimorfismo de inserción/deleción. Palabras clave: Enfermedad de Chagas. Polimorfismo inserción/deleción del gen de la enzima de conversión de angiotensina. INTRODUCTION Chagas’ disease, caused by Trypanosoma cruzi , affects around 15 million persons, and is associated with 20 000-50 000 deaths annually. 1,2 Although it is native to America, migration has taken the disease to other regions. 1,2 The disease involves an acute phase of fever and adenopathy, followed by a chronic phase, frequently characterized by cardiac lesions (20%-30%), a long time after parasite entry. 1,3 Not all patients develop chagasic cardiomyopathy, and when it does occur it does not follow a definite pattern, even though the environment may be similar; this implies that progression cannot be explained solely by environment. 1,3 Factors contributing to disease progression should be differentiated from those of its contraction, as the latter depend on exposure and the former depend on other variables, including genetic variables. 4 T cruzi itself presents considerable genetic variability 4 related to its pathogenic potential. Thus, its interaction with the human species varies, but it is precisely human susceptibility which is least