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  Table of Contents  
Year : 2013  |  Volume : 31  |  Issue : 2  |  Page : 180-181

Plasmodium vivax induced myocarditis: A rare case report

1 Department of Medicine, University College of Medical Sciences, Dilshad Garden, New Delhi, India
2 Department of Medicine, Maulana Azad Medical College, Bahadur Shah, Zafar Marg, Delhi University, New Delhi, India

Date of Submission21-Nov-2012
Date of Acceptance16-Apr-2013
Date of Web Publication19-Jul-2013

Correspondence Address:
N Gupta
Department of Medicine, University College of Medical Sciences, Dilshad Garden, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0255-0857.115224

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 ~ Abstract 

Malaria is one of the commonest parasitic disease in the tropics since ages. However the plasmodium still continues to give surprises to all of us. In the similar context we report a case of Plasmodium vivax induced myocarditis in a 20 year old male and review the literature related to this rare entitiy.

Keywords: Complication, malaria, myocarditis, Plasmodium vivax

How to cite this article:
Gupta N, Sahoo S K. Plasmodium vivax induced myocarditis: A rare case report. Indian J Med Microbiol 2013;31:180-1

How to cite this URL:
Gupta N, Sahoo S K. Plasmodium vivax induced myocarditis: A rare case report. Indian J Med Microbiol [serial online] 2013 [cited 2020 Oct 31];31:180-1. Available from:

 ~ Introduction Top

World Health Organization (WHO) in 2010 has estimated that about 250 million cases of malaria occur every year worldwide, causing 8,60,000 deaths. Plasmodium falciparum infection accounts for the majority of complications and deaths. However, during the last few years it has been seen that there has been an increase in the complications due to Plasmodium vivax infection. P. vivax is now no longer considered a benign infection. Myocarditis has been a well-known but rare complication of P. falciparum infection. Myocarditis as a complication of P. vivax infection is extremely rare.

 ~ Case Report Top

A 20-year-old boy presented with complains of fever with chills and rigor, which was intermittent since 6 days with associated breathlessness, chest pain and palpitations. There was no history of jaundice, decreased urine output, swelling over the body or bleed from any site. There was no significant history in the past or family. On examination, his blood pressure was 90/58 mmHg, pulse rate of 120/min, respiratory rate of 26/min and temperature of 103°F. The patient was pale and splenomegaly was present 3 cm below the costal margin. Rest of the examination was unremarkable. On workup, his haemoglobin was 85 g/L, total leukocyte count 7.5 × 10 9 /L, platelet count 78 × 10 9 /L. Peripheral smear showed ring and schizont stage of P. vivax. Optimal test was positive for P. vivax only. Liver and kidney functions were normal. Blood and urine cultures were sterile; Widal test and leptospira slide macro agglutination test being negative. Viral serology for adenovirus, cytomegalovirus, coxsackie virus and ECHO virus were negative. Serum Lactate dehydrogenasel (DH) was raised, being 15.8 μkat/L. Electrocardiography (ECG) showed ST-T changes in leads II, III, aVF and V4-V6 [Figure 1]. Chest X-ray suggested cardiomegaly. 2D-echocardiography was carried out, which was suggestive of mildly dilated left and right ventricle, LV ejection fraction of 25%, with moderate Mitral and tricuspid regurgitation (MR and TR) present and mild pericardial effusion. Cardiac enzymes were negative CREATINE KINASE (CK-MB and troponin T). A diagnosis of P. vivax induced myocarditis was made and the patient was treated with antipyretics, chloroquine and primaquine tablets after which, the patient improved clinically. A repeat echocardiography carried out after 5 days showed normal cardiac chambers with Ejection fraction (EF) of 60%, with no MR or TR. Also, the ECG changes reverted to normal after 5 days.
Figure 1: ST-T changes in lead II, III, aVF and V4-V6

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 ~ Discussion Top

Malarial fever continues to be an important public health problem in India. India contributes to about 70% of the total reported cases of malaria in South-East Asia. More than two-thirds of the Indian population lives in malaria endemic zone. P. vivax accounts for nearly 50% of total malaria cases.

WHO defines severe P. falciparum malaria as one or more of the following: Impaired consciousness with unarousable coma, jaundice, progressive renal impairment, metabolic acidosis, hyperlactataemia and hypoglycaemia, respiratory distress, pulmonary oedema and severe anaemia. Although rare, these complications have been described in P. vivax infection. [1] Nearly, all published cases regarding malaria with cardiac complications have been limited to P. falciparum infections. Various cardiac complications of malaria include: Pericardial effusion, bundle branch block, cardiomyopathy and myocarditis. Myocarditis is extremely rare complication of falciparum malaria, reported in 0.6% of patients. [2] Myocarditis as a complication of P. vivax has rarely been described in the literature.

Mechanism for plasmodium induced myocarditis includes blockage of capillaries by malarial parasite; parasitized red blood cells and pigment laden macrophages can cause myocardial damage. It has also been seen that there is a fatty change in the myocardium and capillary fibrin thrombi. Tumour necrosis factor may also play a significant role in this pathophysiological process by exerting its toxic effect. [3] These polypeptides increase thrombospondin secretion, thus enhancing the sequestration of knob-bearing parasitized red cells. P. vivax has been demonstrated to cause both sequestration related as well as non-sequestration related complications of severe malaria. [4] Acidosis and hypoglycaemia seen in severe malaria may impair the myocardial integrity and function leading to raised levels of cardiac enzymes. Cardiac toxicity of hydroxychloroquine has been well known. It can lead to conduction blocks as well as congestive heart failure. [5]

Our patient presented with fever with chills rigor, breathlessness and chest pain and palpitations. He also had anaemia and thrombocytopenia. Furthermore, the optimal test was positive for vivax only. Echocardiography carried out in view of chest pain and palpiation showed of mildly dilated left and right ventricle, LEFT VENTRICLE (LV) ejection fraction of 25%, with moderate MR and TR present and mild pericardial effusion. Cardiac enzymes such as CK-MB and troponin T were negative in our case.

Echocardiography is generally helpful in differentiating cardiac diseases and defining the nature of the myocardial dysfunction. A regional wall abnormality would suggest myocarditis or coronary artery disease. Treatment of myocarditis due to P. vivax is similar as that of myocarditis due to other causes. It is advised to take rest and avoid exertional activities.

In a study, it was seen that the serum concentration of cardiac troponin T was found to be elevated in only 0.6% of patients. [2] Our patient had ST -T SEGMENT (ST-T) changes on the ECG which normalized after 5 days of treatment. ECG may show conduction and/or T or ST changes which were seen in 14.3% of patients. This suggests that the electrophysiology of cardial myocites can be altered before myocytolysis occurs. [3]

A study of 22 adult cases of P. faciparum malaria by Franzen et al. involving the heart was carried out. It showed ECG abnormalities in 23% cases. Pericardial effusion and global hypokinesia were seen in 9% and 4.5% of cases respectively. [6] Cardiac complications due to vivax malaria are extremely rare. Herrera [7] reported a case of fatal ischemic myocarditis associated with vivax malaria in an 8 years boy. A case of myocarditis associated with P. vivax has been reported in a 27-year-old woman by Soon et al., [8] Mustafa et al. [9] also reported a case of P. vivax myocarditis in a child.

Now-a-days, we can see that malaria especially P. vivax is manifesting with uncommon complications, which are lethal to human life. Thus, P. vivax is not considered a benign infection anymore.

 ~ References Top

1.Zaki SA, Shanbag P. Atypical manifestations of malaria. Res Rep Trop Med 2011;2:9-22.  Back to cited text no. 1
2.Günther A, Grobusch MP, Slevogt H, Abel W, Burchard GD. Myocardial damage in falciparum malaria detectable by cardiac troponin T is rare. Trop Med Int Health 2003;8:30-2.  Back to cited text no. 2
3.Clark IA, Chaudhri G, Cowden WB. Roles of tumour necrosis factor in the illness and pathology of malaria. Trans R Soc Trop Med Hyg 1989;83:436-40.  Back to cited text no. 3
4.Kochar DK, Saxena V, Singh N, Kochar SK, Kumar SV, Das A. Plasmodium vivax malaria. Emerg Infect Dis 2005;11:132-4.  Back to cited text no. 4
5.Costedoat-Chalumeau N, Hulot JS, Amoura Z, Delcourt A, Maisonobe T, Dorent R, et al. Cardiomyopathy related to antimalarial therapy with illustrative case report. Cardiology 2007;107:73-80.  Back to cited text no. 5
6.Hooda AK, Varma PP, Dutta V. Fatal cardiac tamponade in malarial acute renal failure. Ren Fail 2007;29:371-3.  Back to cited text no. 6
7.Herrera JM. Cardiac lesions in vivax malaria. Study of a case with coronary and myocardial damage. Arch Inst Cardiol Mex1960;30:26-36.  Back to cited text no. 7
8.Kim SA, Kim ES, Rhee MY, Choi SI, Huh HJ, Chae SL. A case of myocarditis associated with Plasmodium vivax malaria. J Travel Med 2009;16:138-40.  Back to cited text no. 8
9.Mustafa SA, Patra V, Ali SS, Balaji PA. Plasmodium vivax myocarditis in a child. Int Multidiscip Res J 2011;1:45-6.  Back to cited text no. 9


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