Cardiomyopathies in Tropical Countries: Causes and Nosological Perspective


Background: Cardiomyopathy is the main cause of heart failure in developing countries, mainly in Africa. In those areas the concept of “tropical cardiomyopathy” is still used to design all unexplained cardiomyopathy. The primary aim of this review is first to review the main etiologies of cardiomyopathies observed in tropical countries and second to gain a better understanding of the nosological place of the so-called “tropical cardiomyopathies” in the current framework of cardiomyopathies. Methods and Results: We reviewed relevant references over the last forty years (June, 1976 to May 2012). Given literature data, endomyocardial fibrosis (EMF) is mainly diagnosed in sub-Saharan countries, as well as Brazil and India. Peripartum cardiomyopathy (PPCM) is observed with a higher prevalence than in temperate countries. Sickle cell anemia does not induce specific cardiomyopathy in all echocardiographic studies. Malnutrition and chronic anemia can induce reversible cardiac dysfunction. Myocardial involvement in parasitic infections is restricted to Chagas disease and probably to human African trypanosomiasis. Helminthiasis is not involved in the pathogenesis of cardiomyopathy except for the deleterious effect of high eosinophilia induced by some endemic diseases (filariasis, schistosomiasis). Primary cardiomyopathies (dilated, hypertrophic, and restrictive cardiomyopathy) have no specificity. Arrhythmogenic right ventricular dysplasia and left ventricular noncompaction are also reported and do not differ from elsewhere. Conclusions: The concept of tropical cardiomyopathy is no longer relevant as most of the cardiomyopathies observed in tropical countries have no specificity, with few exceptions (PPCM, EMF, Chagas disease). In this context, the European Society of Cardiology classification offers a simpler clinical approach and allows the inclusion of the rare tropical specificities.

Share and Cite:

Touze, J. and Fourcade, L. (2013) Cardiomyopathies in Tropical Countries: Causes and Nosological Perspective. World Journal of Cardiovascular Surgery, 3, 201-208. doi: 10.4236/wjcs.2013.37040.

Conflicts of Interest

The authors declare no conflicts of interest.


[1] J. E. Touze, J. P. Bounhoure, L. Fourcade, C. Jaffiol and D. Thomas, “Les Facteurs de Risque Cardiovasculaire dans les Pays en Développement: Evolution et Enjeux,” Bulletin de L’Académie Nationale de Médecine, Vol. 195, 2011, pp. 1285-1288.
[2] E. Bertrand, “Les Cardiomyopathies en Zone Tropicale,” Annales de Cardiologie et d Angéiologie, Vol. 35, 1986, pp. 305-310.
[3] A. G. Shaper, “On the Nature of Some Tropical Cardiomyopathies,” Transactions of the Royal Society of Tropical Medicine and Hygiene, Vol. 61, No. 4, 1967, pp. 458-481.
[4] WHO, “Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task force on the Definition and Classification of Cardiomyopathies,” Circulation. Vol. 93, 1996, pp. 841-842.
[5] B. J. Maron, J. A. Towbin, G. Thiene, C. Antzelevitch, D. Corrado, D. Arnett, A. J. Moss, C. E. Seidman and J. B. Young, “Contemporary Definitions and Classification of the Cardiomyopathies: An American Heart Association Scientific Statement From the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention,” Circulation. Vol. 113, 2006, pp. 1807-1816.
[6] A. O. Falase, “Endomyocardial Fibrosis in Africa,” Postgraduate Medical Journal, Vol. 59, No. 689, 1983, pp. 170-177.
[7] J. Freers, J. Amandua, R. Mugerwa and C. Sezi, “Endomyocardial Fibrosis and Eosinophilia,” Lancet, Vol. 342, No. 8881, 1993, pp. 1233-1234.
[8] J. J. Andy, P. O. Ogunowo, N. A. Akpan, C. O. Odigwe, I. A. Ekanem and R. A. Esin, “Helminth Associated Hypereosinophilia and Tropical Endomyocardial Fibrosis (EMF) in Nigeria,” Acta Tropica, Vol. 69, No. 2, 1998, pp. 127-140.
[9] C. L. Sezi, “Effect of Protein Deficient Cassava Diet on Cercopithecus Aethiops Hearts and Its Possible Role in the Aetiology and Pathogenesis of Endomyocardial Fibrosis in Man,” East African Medical Journal, Vol. 73, Suppl. 5, 1996, pp. S11-16.
[10] D. Metras, A. O. Coulibaly and K. Ouattara, “The Surgical Treatment of Endomyocardial Fibrosis: Results in 55 Patients,” Circulation, Vol. 72, 1985, pp. 274-279.
[11] D. Metras, A. Q. Coulibaly and K. Ouattara, “Recent Trends in the Surgical Treatment of Endomyocardial Fibrosis,” The Journal of Cardiovascular Surgery, Vol. 28, 1987, pp. 607-613.
[12] K. Tibazarwa and K. Sliwa, “Peripartum Cardiomyopathy in Africa: Challenges in Diagnosis, Prognosis, and Therapy,” Progress in Cardiovascular Diseases, Vol. 52, No. 4, 2010, pp. 317-325.
[13] H. Yamac, I. Bultmann, K. Sliwa and D. Hilfiker-Kleiner “Prolactin: A New Therapeutic Target in Peripartum Cardiomyopathy,” Heart, Vol. 96, No. 17, 2010, pp. 1352-1357.
[14] K. Sliwa, D. Hilfiker-Kleiner, M. C. Petrie, A. Mebazaa, B. Pieske, E. Buchmann, V. Regitz-Zagrosek, M. Schaufelberger, L. Tavazzi, D. J. van Veldhuisen, H. Watkins, A. J. Shah, P. M. Seferovic, U. Elkayam, S. Pankuweit, Z. Papp, F. Mouquet and J. J. McMurray, “Current State of Knowledge on Aetiology, Diagnosis, Management, and Therapy of Peripartum Cardiomyopathy: A Position Statement from the Heart Failure Association of the European Society of Cardiology Working Group on peripartum cardiomyopathy,” European Journal of Heart Failure, Vol. 12, No. 8, 2010, pp. 767-778.
[15] W. Covitz, M. Espeland, D. Gallagher, W. Hellenbrand, S. Leff and N. Talner, “The Heart in Sickle Cell Anemia: The Cooperative Study of Sickle Cell Disease (CSSCD),” Chest, Vol. 108, No. 5, 1995, pp. 1214-1219.
[16] P. Acar, C. Maunoury, M. de Montalembert and Y. Dulac, “Anomalies de la Perfusion Myocardique dans la Drépanocytose de L’enfant: étude par la Tomoscintigraphie Myocardique,” Archives des Maladies du Coeur et des Vaisseaux, Vol. 96, 2003, pp. 507-510.
[17] T. Mardelle, A. Ekra and E. Bertrand, “LV Function in Sickle Cell Anemia,” American Heart Journal, Vol. 12, No. 6, 1986, pp. 1356-1357.
[18] A. C. Eddine, O. Alvarez, S. E. Lipshultz, R. Kardon, K. Arheart and S. Swaminathan, “Ventricular Structure and Function in Children with Sickle Cell Disease Using Conventional and Tissue Doppler Echocardiography,” American Journal of Cardiology, Vol. 109, No. 9, 2012, pp. 1358-1364.
[19] T. L. Miller, D. Neri, J. Extein, G. Somarriba and N. Strickman-Stein, “Nutrition in Pediatric Cardiomyopasthy,” Progress in Pediatric Cardiology, Vol. 24, No. 1, 2007, pp. 59-71.
[20] S. L. Tobias, J. van der Westhuyzen, R. E. Davis, G. C. Icke and P. M. Atkinson, “Alcohol Intakes and Deficiencies in Thiamine and Vitamin B6 in Black Patients with Cardiac Failure,” South African Medical Journal, Vol. 76, 1989, pp. 299-302.
[21] M. H. Roehrl, M. P. Alexander, S. B. Hammond, M. Ruzinova, J. Y. Wang and C. J. O’Hara, “Eosinophilic Myocarditis in Hypereosinophilic Syndrome. American Journal of Hematology, Vol. 86, No. 7, 2011, pp. 607-608.
[22] P. U. Ogbogu, D. R. Rosing and M. K. Horne, “Cardiovascular Manifestations of Hypereosinophilic Syndromes,” Immunology And Allergy Clinics of North America, Vol. 27, No. 3, 2007, pp. 457-475.
[23] B. L. Wright, K. M. Leiferman and G. J. Gleich, “Eosinophil Granule Protein Localization in Eosinophilic Endomyocardial Disease,” The New England Journal of Medicine, Vol. 365, 2011, pp. 187-188.
[24] S. Yacoub, H. J. Lang, M. Shebbe, et al., “Cardiac Function and Hemodynamics in Kenyan Children with Severe Malaria,” Critical Care Medicine, Vol. 38, No. 3, 2010, pp. 940-945.
[25] WHO, “Severe and Complicated Falciparum Malaria,” Transactions of the Royal Society of Tropical Medicine and Hygiene, Vol. 94, Suppl. 1, 2000, pp. 1-90.
[26] H. Acquatella, “Echocardiography in Chagas Disease,” Circulation, Vol. 115, 2007, pp. 1124-1131.
[27] S. Yacoub, A. O. Mocumbi and M. H. Yacoub, “Neglected Tropical Cardiomyopathies (I): Chagas Disease,” Heart, Vol. 94, No. 2, 2008, pp. 244-248.
[28] F. J. Carod-Artal, “’Trypanosomiasis, Cardiomyopathy and the Risk of Ischemic Stroke,” Expert Review of Cardiovascular Therapy, Vol. 8, No. 5, 2010, pp. 717-728.
[29] J. A. Blum, M. J. Zellweger, C. Burri and C. Hatz, “Cardiac Involvement in African and American Trypanosomiasis,” The Lancet Infectious Diseases, Vol. 8, No. 10, 2008, pp. 631-641.
[30] E. Bertrand, “L’atteinte Cardiaque dans la Trypanosomiase Africaine,” Médecine Tropicale, Vol. 47, 1987, pp. 91-93.
[31] K. Blackett and J. L. Ngu, “Immunological Studies in Congestive Cardiomyopathy in Cameroon,” British Heart Journal, Vol. 38, 1976, pp. 605-611.
[32] K. Sliwa, A. Damasceno and B. M. Mayosi, “Epidemiology and Etiology of Cardiomyopathy in Africa,” Circulation, Vol. 112, 2005, pp. 3577-3583.
[33] B. Maharaj, “Causes of Congestive Heart Failure in Black Patients at King Edward VIII Hospital, Durban,” Cardiovascular Journal of South Africa, Vol. 2, 1991, pp. 31-32.
[34] A. G. Amoah, C. Kallen, “Aetiology of Heart Failure as Seen from a National Cardiac Referral Centre in Africa,” Cardiology, Vol. 93, 2000, pp. 11-18.
[35] B. Maharaj, M. G. Hammond, “HLA-A, B, DR, and DQ Antigens in Black Patients with Idiopathic Dilated Cardiomyopathy,” American Journal of Cardiology, Vol. 65, No. 20, 1990, pp. 1402-1403.
[36] B. Abegaz, “The Impact of Echocardiography in the Diagnosis of Hypertrophic Cardiomyopathy,” East African Medical Journal, Vol. 67, 1990, pp. 556-567.
[37] J. C. Moolman-Smook, B. M. Mayosi, P. A. Brink and V. A. Corfield, “Molecular Genetics of Cardiomyopathy: Changing Times, Shifting Paradigms,” Cardiovascular Journal of South Africa, Vol. 14, 2003, pp. 145-155.
[38] M. J. Munclinger, J. J. Patel and A. S. Mitha, “Follow-Up of Patients with Arrhythmogenic Right Ventricular Cardiomyopathy Displasia,” South African Medical Journal, Vol. 90, 2000, pp. 61-68.
[39] D. A. Watkins, N. Hendricks, G. Shaboodien, M. Mbele, M. Parker, B. Z. Vezi, A. Latib, A. Chin, F. Little, M. Badri, J. C. Moolman-Smook, A. Okreglicki and B. M. Mayosi, “Clinical Features, Survival Experience, and Profile of Plakophylin-2 Gene Mutations in Participants of the Arrhythmogenic Right Ventricular Cardiomyopathy Registry of South Africa,” Heart Rhythm, Vol. 6, 2009, pp. S10-17.
[40] P. Paule, L. Braem, D. Mioulet, B. Jop, A. Théron, J. M. Gil, P. Héno and L. Fourcade, “La non Compaction du Ventricule Gauche, une Cardiomyopathie du Sujet Jeune: Premières Observations Africaines,” Médecine Tropicale, Vol. 67, 2007, pp. 587-593.
[41] A. Qaqa, J. Daoko, N. Jallad, O. Aburomeh, I. Goldfarb and F. Shamoon, “Takotsubo Syndrome in African American vs. Non-African American Women,” Western Journal of Emergency Medicine, Vol. 12, 2011, pp. 218-223.
[42] H. M. Patel, B. K. Kantharia, D. L. Morris and S. Yaz-danfar, “Takotsubo Syndrome in African-American Women with Atypical Presentations: A Single Center Experience,” Clinical Cardiology, Vol. 30, No. 1, 2007, pp. 14-18.
[43] P. Elliott, B. Andersson, E. Arbustini, Z. Bilinska, F. Cecchi, P. Charron, O. Dubourg, U. Kühl, B. Maisch, W. J. McKenna, L. Monserrat, S. Pankuweit, C. Rapezzi, P. Seferovic, L. Tavazzi and A. Keren, “Classification of the Cardiomyopathies: A Position Statement from the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases,” European Heart Journal, Vol. 29, No. 2, 2008, pp. 270-276.
[44] R. N. Millar and B. M. Mayosi, “Utilization of Implantable Defibrillators in Africa,” Cardiac Electrophysiology Review, Vol. 7, No. 1, 2003, pp. 14-16.

Copyright © 2024 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.