Case Presentation: A 66-year-old male presented to the emergency department with complaints of intermittent high-grade fever of 38℃ for five days and non-specific chest pain for the past 6 hours. The pain was gradual in onset and was a dull nagging type of pain radiating to his left shoulder. He was tachycardic and had shortness of breath on examination. On palpation, a moderately enlarged spleen was felt. The patient’s ECG showed ST-segment elevations, and therefore, the patient was brought in for a cardiac catheterization. The catheterization, however, did not reveal any blockages. His negative catheterization, coupled with his lack of risk factors, allowed us to rule out myocardial infarction. On further questioning, the patient reported that he had just come back from an area with a malaria-endemic, which prompted us to do a blood smear for the parasite. On the second day of admission, his fever spiked to 39℃ with chills, rigors; he also had a severe headache and continued chest pain. A diagnosis of Falciparum Malaria was made due to the blood smear being positive. Echocardiography showed a reduction in the ejection fraction and cardiac index as compared to expected. This, coupled with a rise in NT-ProBNP/BNP, myoglobin, and H-FABP, led the authors to believe that Falciparium Malaria caused myocarditis.
Discussion: The pathophysiology behind the involvement of the myocardium is not well known or documented; however, the best theory is the direct cytotoxic effects of proteins released by the parasites and the production of inflammatory cytokines. Interleukin 17-A is present in complicated malaria, and other proinflammatory cytokines like tumor necrosis factor-alpha can impair function due to the adverse inotropic effects. Another possible mechanism is the mechanical blockage of capillaries by malarial parasites and parasitized red blood cells. Several reports on the autopsy of patients suffering from myocarditis due to malaria have mechanical blockage by both parasites and parasitized red blood cells. Other theories are the damage of the myocardium from tumor necrosis factor, damage from pigment-laden macrophages, hypoglycemia, and acidosis caused by severe malaria, fatty change in the myocardium, and capillary fibrin thrombi. There may also be increased thrombospondin secretion, enhancing the sequestration of knobbed parasites containing red blood cells. The plasmodial glycosylphosphatidylinositol (GPI) was proven by Schofield et al. in a murine model to affect cardiac myocytes directly. Wennickie et al. suggested that GPI might include myocyte apoptosis and lead to an upregulation of NT-proBNP and apoptotic genes. A study by Janka et al. showed increased myocardial wall stress in children with severe malaria due to nitric oxide depletion from intravascular hemolysis. Myocardial damage is implicated by multifactorial pathogenesis, microcirculatory obstruction, systemic acidosis, and humoral mechanisms.
Conclusions: The authors believe that keeping suspicion high for myocardial damage is crucial when the patient presents with chest pain in severe Falciparum malaria. The frequency of primary cardiac complications may be underestimated or unrecognized due to the severity of Falciparum infections. Clinical correlation along with echocardiography and cardiac biomarkers is what the authors found to be most beneficial in the diagnosis of myocarditis in cases of malaria. We believe there should be large-scale studies on the cardiac involvement of Falciparum Malaria as current knowledge is limited.