From Parasite to Plaque? Acute Myocardial Infarction in Severe Plasmodium vivax Malaria

Abstract

Background: Although Plasmodium falciparum is classically associated with severe malaria, Plasmodium vivax—once thought to cause only benign disease—is now recognized as capable of producing life-threatening complications, including acute respiratory distress syndrome (ARDS), renal failure, shock, and severe hematological abnormalities. Cardiac involvement in P. vivax infection is extremely uncommon, typically manifesting as myocarditis or conduction abnormalities. Acute ST-elevation myocardial infarction (STEMI) secondary to P. vivax infection is exceedingly rare, with only a few angiographically confirmed cases reported globally. Case Presentation: We describe a 55-year-old female from Mumbai, India, who presented with high-grade fever, dyspnea, and hypotension. Peripheral smear confirmed P. vivax parasitemia. Laboratory evaluation revealed thrombocytopenia (22,000/µL), metabolic acidosis, and acute kidney injury. The patient developed ARDS requiring mechanical ventilation. Six hours after admission, she experienced acute chest pain, and ECG showed anterior wall STEMI with 4 mm ST elevation in leads V1–V5. Echocardiography demonstrated anterior wall hypokinesia with a left ventricular ejection fraction (LVEF) of 30–35%. After high-risk informed consent, intravenous streptokinase was administered, achieving >70% ST-segment resolution. Coronary angiography performed after stabilization showed a recanalized left anterior descending (LAD) artery with TIMI-3 flow and no residual stenosis. She was managed with artesunate, doxycycline, cautious dual antiplatelet therapy, and supportive care. The patient recovered completely and was discharged on day 12 in stable condition. Discussion: This case illustrates a rare but serious cardiovascular manifestation of P. vivax malaria. Potential mechanisms include cytokine-mediated endothelial activation, coronary microvascular obstruction, catecholamine-induced vasospasm, and inflammatory endothelial injury. The concurrence of STEMI in P. vivax infection presents diagnostic and therapeutic challenges, especially in the presence of thrombocytopenia. Despite the bleeding risk, timely reperfusion was lifesaving. Conclusion: P. vivax malaria can no longer be regarded as benign. Clinicians in endemic areas should maintain a high index of suspicion for acute coronary events when ECG changes or chest discomfort occur in malaria patients. Angiographic documentation, early diagnosis, and prompt reperfusion therapy are crucial for improved outcomes.