Sleeping hearts: 12 years after a follow up study on cardiac findings due to sleeping sickness

Anna Blum; Junior Mudji; Leticia Grize; Christian Burri; Michael J Zellweger; Johannes Blum

doi:10.1016/j.onehlt.2020.100182

Sleeping hearts: 12 years after a follow up study on cardiac findings due to sleeping sickness

One Health. 2020 Oct 13:11:100182. doi: 10.1016/j.onehlt.2020.100182. eCollection 2020 Dec 20.

Authors

Anna Blum¹, Junior Mudji^{2

3}, Leticia Grize^{1

4}, Christian Burri^{1

4}, Michael J Zellweger^{4

5}, Johannes Blum^{1

2

4}

Affiliations

¹ Swiss Tropical and Public Health Institute, Medical Department, 4002 Basel, Switzerland.
² Hôpital Evangélique de Vanga, Vanga Mission, B.P. 4728, Kinshasa 2, Democratic Republic of the Congo.
³ Protestant University of Congo, Department of Family Medicine and Primary Care, B.P. 4745, Kinshasa 2, Democratic Republic of the Congo.
⁴ University of Basel, 4001 Basel, Switzerland.
⁵ Cardiology Department, University Hospital, University of Basel, 4001 Basel, Switzerland.

Abstract

Both American Trypanosomiasis (Chagas disease) and Human African Trypanosomiasis (HAT) are diseases caused by single-celled flagellate protozoan parasites. While cardiac complications such as conduction problems and heart failure are very common in Chagas disease there is little known about the long-term effects of Human African Trypanosomiasis (HAT) on cardiac sequelae in Sub-Saharan Africa, where heart failure has become an increasing problem and growing burden. In the context of clinical trials conducted between 2004 and 2005 in the Democratic Republic of the Congo (DRC), the prevalence of HAT related signs and symptoms and an ECG were evaluated prior to the initiation of treatment. The object of this follow-up study in 2017 was to assess the prevalence of cardiac sequelae in the same 51 first stage and 18 second stage HAT patients 12-13 years after their treatment by conducting a clinical examination and an ECG. A control group matched by age (± 5 years), sex and whenever possible form the same village was enrolled. There were no significant differences in the prevalence of cardiac symptoms and in ECG findings between patients and their controls at the time of the follow-up evaluation. Repolarization changes disappeared or improved in 24.7% of HAT patients and were even less frequent than in the control group. Peripheral low voltage was the only parameter that increased over time in HAT patients and in three patients, new conduction problems in the ECG (ventricular bigeminy, RBBB, and bifascicular block) could be found, although none of these findings was clinically significant. However, the appearance of these conduction problems might represent an early indication of a HAT related cardiomyopathy or ongoing subclinical infection. This hypothesis would be supported by the findings of an older study in which antibodies (IFAT) against trypanosomiasis in 27% of Cameroonian patients with dilated cardiomyopathy compared to 2% in normal controls had been observed.

Keywords: Conduction problem; Follow up; Heart failure; Human African Trypanosomiasis; Myocarditis; Sequelae; Sleeping sickness.