Acute myocarditis in vivax malaria: an extremely rare complication

Introduction

About 95% of the population in India reside in malaria endemic areas and 80% of malaria cases reported are from the 20% of the population who reside in tribal, hilly, difficult and inaccessible areas. In the hilly northern Indian state of Uttarakhand, the number of cases of malaria, in general, and those due to Plasmodium (Pl.) falciparum have decreased over the last decade. ¹ However, severe complications in vivax malaria have been reported. ² Cardiac complications (cardiac tamponade, myocarditis and conduction abnormalities) with Pl. falciparum ³ are rarely seen and are extremely rare with Pl. vivax malaria. ⁴ Most case reports have shown cardiac involvement in association with concomitant cerebral or renal involvement.

We report the first case of vivax infection from Uttarakhand with malaria induced acute myocarditis without cerebral or renal involvement. Pulmonary oedema manifested after parasite clearance and on-going haematological and biochemical improvement, a rather atypical occurrence.

Case report

A 19-year old girl had been hospitalized a week earlier with a 2–3 day history of fever associated with yellowish discoloration of her eyes and urine. She developed generalized weakness a day prior to hospitalization which was associated with the onset of pain in the right upper abdomen and the peri-umbilical region. She had received a single intravenous injection of artesunate before presenting to our hospital. On examination, she had tachycardia (140 bpm), tachypnoea (22/min), BP 120/80 mm Hg and was afebrile. She was extremely pale and had moderate icterus and hepato-splenomegaly was present. The rest of the examination was otherwise unremarkable. She was maintaining an oxygen saturation of 88% on room air. Although unrelated to the presentation, she had post-polio residual paralysis of left upper limb since 4 years of age.

She was investigated and tested positive for Pl. vivax on a peripheral blood smear as well as by rapid malaria lactate dehydrogenase (LDH) card test; serological markers of hepatitis (A, B, C, E) were negative. Her investigations were as follows: haemoglobin of 4.9 g/dL; packed cell volume 14.1%; total leucocyte count 2670/ mm³; platelet count of 45000/mm³; LDH 420 U/L; total and indirect bilirubin 9.81; and 6.04 g/dL respectively; serum albumin 2.6 g/dL; International Normalized Ratio (INR) 1.07; alanine aminotransferase (ALT) 22 IU/L; aspartate aminotransferase (AST) 61 IU/L; alkaline phosphate (ALP) 87 IU/L: blood urea nitrogen (BUN) 25.2 mg/dL; and creatinine 0.77 mg/dL. An arterial blood gas analysis revealed compensated metabolic acidosis and the chest X-ray was suggestive of acute respiratory distress syndrome (ARDS) without cardiomegaly.

Artesunate, in combination with doxycycline, was initiated with packed red cell support. Malarial parasite clearance was noted after 48 h from the peripheral blood and the platelet count, white blood cell count and bilirubin level showed improvement. However, the tachypnoea persisted and, on the fourth day of hospitalization, the patient became hypoxic and required mechanical ventilatory support. The chest X-ray was suggestive of pulmonary oedema, the electrocardiograph (ECG) was unremarkable and serum cardiac markers were negative. However, the ECG demonstrated global left ventricular hypokinesia with an ejection fraction of 40%. A diagnosis of malaria-induced myocarditis with pulmonary oedema was entertained and diuretics were administered. Her condition improved within 2 days and she was subsequently discharged. Her cardiac systolic function normalized over the next 10 days when she was followed up on an out-patient basis.

Discussion

This case reports an extremely uncommon cardiac complication without cerebral and renal involvement, in an otherwise improving patient with vivax malaria. The patho-physiology of cardiac involvement in severe malaria is unclear but mechanical blockage of capillaries by malarial parasites and parasitized red blood cells probably caused ischaemic myocardial dysfunction. Acidosis and hypoglycaemia impair the myocardial integrity and function and may raise the levels of cardiac enzymes, not seen in our case. Although the cardiac enzymes in this case were not elevated, the lack of any evidence of prior cardiac dysfunction on the basis of history, the detection of decreased left ventricular contractility and its normalization in relation to the occurrence of acute malaria favours the diagnosis of acute myocarditis.

Conclusion

Cardiac dysfunctions, though rare in malaria, have been reported mainly in infection with Pl. falciparum. However, cardiac complications due to vivax malaria are extremely rare in the literature. Franzen et al. reported ECG abnormalities in 23% cases followed by pericardial effusion and myocardial dysfunction in 9% and 4.5% of cases, respectively. ³ Recently, a case of myocarditis associated with Pl. vivax has been reported in a 27-year-old woman by Soon et al., who had no sequalae. ⁴ Mohapatra et al. described myocardial injury as evidenced by raised cardiac troponin T levels in 11.8% patients with cerebral malaria. ⁵ The present case had haematological involvement in the form of pancytopenia and cardiac involvement. However, cerebral involvement and hypoglycaemia were lacking. Also, the patient in question did not develop hypotension and recovered completely. Moreover, pulmonary oedema manifested despite clinical, haematological and biochemical improvement.