Malaria remains a long-standing
and leading cause of morbidity
and mortality worldwide. In the
20th century, malaria accounted
for between 150-300 million
deaths(1). In 2022, according to
the WHO malaria report (2), there
were an estimated 249 million
cases of malaria and around
600,000 deaths in 85 countries (majority being low and middle income countries), highlighting
the significant burden of the disease.
Malaria is caused by protozoan Plasmodium species typically transmitted by marsh mosquitoes
and is endemic to Asia, Oceania, South and Central America. However, the highest burden of
disease is in Sub-Saharan Africa (3). Severe and fatal malaria is generally caused by Plasmodium
falciparum which is responsible for more than 90% of the world’s malaria mortality (4).
While the malarial parasite can affect all organs, cardiovascular (CV) sequalae of malaria are
poorly understood due to the paucity of published research on the area. A small prospective
study has suggested that in patients with severe malaria (clinical or laboratory evidence of vital
organ dysfunction including reduced conscious levels, severe anaemia and renal impairment), the
incidence of CV involvement can be as high as 26% (5). In this editorial we explore the
prevalence of CV compromise, the theories related to the pathophysiology of CV complications
in malaria and the management of such patients.