In 1946 Howard Sprague observed that although “malaria is a disease from which no organ or tissue is exempt, this paper is concerned with its influence upon the circulation, and more particularly upon the heart itself.” He then outlined four ways by which this influence happens:
- its chronic and recurrent nature
- the systemic toxemia of the paroxysm
- the profound anemia produced by hemolysis and suppression of hemopoiesis
- the occlusion of capillaries and arterioles of the myocardium
Since that time other researchers have elaborated on malaria and the cardiovascular system.
Mishra et al. raise a concern that, “The role of the heart in severe malaria has not received due attention.” They point out the following:
- hypotension, shock and circulatory collapse observed in severe malaria patients
- raised cardiac enzymes in complicated malaria
- compromised microcirculation and lactic acidosis as well as excessive production of pro-inflammatory cytokines
- Intravascular fluid depletion associated with severe malaria leading to impaired microcirculation … among others
They conclude that “Sudden cardiac deaths can also occur due to cardiac involvement,” but worry that, “It is not feasible to assess the cardiac indices in resource poor settings.”
A study by Ray and co-researchers indicated “involvement of cardiovascular system in severe malaria as evidenced from ECG and echocardiography. The study also revealed that cardiovascular instabilities are common in falciparum malaria, but can also be observed in vivax malaria.” A fatal case of imported malaria where the sole finding revealed at the postmortem evaluation was an acute lymphocytic myocarditis with myocardiolysis was described by Costenaro and colleagues.
In another example, Onwuamaegbu, Henein, and Coats reviewed the potential role of malaria in chronic and severe malaria and the connection to chronic heart failure. They concluded that, “Our review of the literature suggests that there are significant similarities in the cachexia seen in CHF and that of malaria, especially as related to the effects of muscle mass and immunology.” Clinical manifestations in P. falciparum malaria also include reduced cardiac output as was reported in an imported case of malaria by Johanna Herr and co-workers.
Marrelli and Brotto note that, “Sequestration of red blood cells, increased levels of serum creatine kinase and reduced muscle content of essential contractile proteins are some of the potential biomarkers of the damage levels of skeletal and cardiac muscles.” They explain that, “These biomarkers might be useful for prevention of complications and determining the effectiveness of interventions designed to protect cardiac and skeletal muscles from malaria-induced damage.”
Not just malaria as a disease is involved, but also the medicines used to treat it. Ngouesse and colleagues draw attention to antimalarial drugs with cardiovascular side effects. They draw particular attention to the dangers of halofantrine, quinine and quinidine, but also note mild and/or transient effects of other antimalarials.
Guidelines exist for proper and prompt malaria case management, especially protocols for caring for patients with severe malaria. These and the medicines required must be more readily available to front line health staff. And of course is we are more diligent in preventing malaria through long lasting insecticide-treated nets and other measures, our worries about severe malaria and CVD complications will reduce.