Key result
Antimalarial, HF, and anticoagulant therapy improves LVEF to ~30% and resolves LV thrombi.
Why the study?
Cardiac involvement in Plasmodium falciparum malaria is uncommon, and the combination of severe LV systolic dysfunction and LV apical thrombus formation is rarely reported.
Case Report (n=1)
No
This case report highlights that Plasmodium falciparum malaria can be complicated by severe left ventricular systolic dysfunction and multiple apical thrombi, which may partially recover with antimalarial, heart failure, and anticoagulation therapies.
Partial LV recovery in malaria cardiomyopathy warrants cardiac surveillance; leaves open reversibility with antimalarial therapy.
Background Cardiac involvement in Plasmodium falciparum malaria is uncommon, and the combination of severe left ventricular (LV) systolic dysfunction and LV apical thrombus formation is rarely reported. We describe a young man with confirmed falciparum malaria who developed severe LV systolic dysfunction and two LV apical thrombi in a resource-limited setting. Case summary A previously healthy 23-year-old man from a malaria-endemic rural coastal region presented with febrile illness and subsequently developed progressive dyspnoea and acute decompensated heart failure. Peripheral blood smears repeatedly demonstrated P. falciparum ring forms. Echocardiography showed severe global LV systolic dysfunction, with an estimated LVEF of 16.9–19%, LV dilatation, and two mobile LV apical thrombi. Intravenous artesunate followed by oral artemether–lumefantrine was administered, together with diuretic therapy, guideline-directed heart failure treatment, and therapeutic anticoagulation. At 1-month follow-up, LVEF had increased to approximately 30%, and the previously visualised thrombi were no longer detected, although complete resolution could not be confirmed because contrast-enhanced echocardiography and cardiac magnetic resonance imaging were unavailable. During later follow-up, a small popliteal arterial thrombus was identified, and rivaroxaban was increased to 20 mg once daily. Discussion Severe LV systolic dysfunction and intracardiac thrombus formation may occur during falciparum malaria. In resource-limited settings, delayed antimalarial treatment and limited access to advanced cardiac imaging may complicate diagnosis, management, and assessment of causality.
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Almammari et al. (2026) conducted a case report in Plasmodium falciparum malaria with severe left ventricular systolic dysfunction and apical thrombi (n=1). Antimalarial therapy (IV artesunate followed by oral artemether-lumefantrine), guideline-directed heart failure treatment, and therapeutic anticoagulation (including rivaroxaban) was evaluated on Left ventricular ejection fraction (LVEF) and resolution of LV apical thrombi at 1-month follow-up. Antimalarial, heart failure, and anticoagulant therapy increased LVEF from 16.9-19% to ~30% with non-detection of two LV apical thrombi at 1 month in a 23-year-old man with falciparum malaria.
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