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Table of Contents
CASE REPORT
Year : 2019  |  Volume : 10  |  Issue : 1  |  Page : 39-41

Myocarditis with sinus exit block: A rare presentation of Plasmodium vivax malaria


Department of Medicine, VMMC and Safdarjung Hospital, New Delhi, India

Date of Submission07-Jul-2018
Date of Decision27-Aug-2018
Date of Acceptance28-Aug-2018
Date of Web Publication17-Oct-2018

Correspondence Address:
Dr. Aanchal Arora
113 F/F Meera Enclave, New Delhi - 110 018
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/INJMS.INJMS_6_18

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  Abstract 


Although malaria is caused most commonly by falciparum species, vivax malaria counts the second most common in India. Until recently, severe malaria infection was attributed to falciparum species. Various systemic complications including arrhythmia, heart failure, conduction disturbances, and myocarditis have been typically seen in association with Plasmodium falciparum infections. Nowadays, severe vivax malaria encompasses varied complications including cardiac complication as well. We report a case of sinus exit block due to myocarditis in a 40-year-old male infected with vivax malaria without any cardiovascular risk factors. Recovery was complete with a favorable outcome in this case.

Keywords: Myocarditis, sinus exit block, vivax malaria


How to cite this article:
Arora A, Mudalagiri M, Sharma D, Porwal YC. Myocarditis with sinus exit block: A rare presentation of Plasmodium vivax malaria. Indian J Med Spec 2019;10:39-41

How to cite this URL:
Arora A, Mudalagiri M, Sharma D, Porwal YC. Myocarditis with sinus exit block: A rare presentation of Plasmodium vivax malaria. Indian J Med Spec [serial online] 2019 [cited 2019 May 24];10:39-41. Available from: http://www.ijms.in/text.asp?2019/10/1/39/243627


  Introduction Top


Malaria is an important public health problem worldwide. It is a tropical disease. A total of 216 million cases of malaria among 91 countries were reported in the world malaria report 2017.[1] Most malaria cases in 2016 were in the WHO African Region (90%), followed by the WHO South-East Asia Region (7%) and the WHO Eastern Mediterranean Region (2%) with 445,000 deaths globally in 2016. Out of the total reported cases of malaria in South-East Asia, India contributes to about 70%. Out of the five known species of malarial parasite, Plasmodium falciparum is the most commonly associated with fatal complications of malaria including adverse cardiovascular outcomes such as myocarditis and heart failure.[2] However, nowadays, Plasmodium vivax malaria is no longer considered a benign infection as it is also associated with various serious systemic complications. Association of cardiac complications with P. vivax is extremely rare.[3] We report the case of a 40-year-old male infected with P. vivax malaria who presented with myocarditis and sinus exit block and showed complete recovery following treatment.


  Case Report Top


A 40-year-old male, vendor by occupation, resident of Dhaulpur, Rajasthan, presented to our hospital in the 3rd week of September 2017, with a history of fever for 5 days. Fever was intermittent and moderate-high grade fever without rigors. He was a nonsmoker but consumed alcohol occasionally. There was no history of diabetes, hypertension, or coronary artery disease. There was no history of cough, breathlessness, headache, or pain abdomen. On examination, he was conscious, oriented, and had mild pallor. He was febrile with temperature of 102.4 F, normotensive, pulse rate 100/minute, and respiratory rate 20/mt. Spleen was palpable 2 cm below left costal margin. Systemic examination was unremarkable with no rash or eschar.

In view of fever and splenomegaly, on day 1, routine investigations were sent which revealed anemia, thrombocytopenia, and raised erythrocyte sedimentation rate (ESR). Malarial antigen and dengue immunoglobulin M (Elisa) were also sent [Table 1]. Peripheral smear showed trophozoite of P. vivax and malarial antigen was also positive for P. vivax. Ultrasonography of the abdomen showed enlarged spleen (14 cm). Considering diagnosis of vivax malaria, he was started on intravenous artesunate 2.4 mg/kg, antipyretics, and crystalloids.
Table 1: Laboratory parameters on day 1

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On day 2, fever declined in intensity, but patient complained of lethargy and lightheadedness, especially on standing. Repeat systolic blood pressure was 80 mmHg and pulse was 60/mt, irregular with a pause after every 3–4 beats. Cardiac and respiratory auscultation was normal. Routine investigations were sent again [Table 2] including creatine phosphokinase (CPK MB) which was not raised (20 U/L), quantitative G6PD, antistreptolysin O (ASO), C-reactive protein (CRP), HIV, blood, and urine culture. ASO and CRP were not raised. Platelet count improved. Renal function was deranged, suggesting prerenal acute kidney injury. An electrocardiogram (ECG) [Figure 1] and chest radiograph were done on the same day. ECG showed sinoatrial exit block (second degree Type II) evident as a pause (wide PP interval) after every third QRS complex. Chest radiograph showed cardiomegaly (left atrial and ventricular enlargement). Considering hypotension and conduction disturbance on ECG, cardiology opinion confirmed second-degree Type II sinoatrial block and suggested for Holter monitoring. Blood pressure was not fluid responsive, hence inotropic (noradrenaline 0.05–0.1 μg/kg/min) support was instituted from day 2. Two-dimensional (2D) echocardiography was done on day 3 which showed enlargement of left atrium (LA 30 mm/m2) and left ventricle (LV 42 mm/m2) with hypokinesia and low ejection fraction (EF 35%). Hence, a diagnosis of malarial myocarditis was suspected.
Table 2: Laboratory parameters on day 2 and day 5

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Figure 1: Electrocardiogram on day 2 showing sinoatrial exit block. Black arrows indicate normal timing of each P wave and blue arrows represent blocked sinus P wave impulses. Red line indicates pause around dropped P wave which is exactly double the preceding P-P interval

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On day 3, he became afebrile and was switched to oral artesunate combination therapy. Blood pressure (BP) improved with inotropic support and pulse became regular. On day 5, BP was maintained on tapering dose of inotrope. Repeat CPK MB, platelets, renal function [Table 2], and ECG became normal [Figure 2]. By day 6, he became normotensive without inotropic support. On day 8, he was discharged on tablet primaquine 0.5 mg/kg for 2 weeks and was advised complete bed rest for 1 week. Two weeks following discharge, repeat 2D echocardiography showed normal sized cardiac chambers with normal left ventricular ejection fraction (55%).
Figure 2: Electrocardiogram on day 5 showing normal sinus rhythm

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  Discussion Top


India is a malaria endemic zone. P. falciparum is the causative species in 50% cases of malaria and vivax causes approximately in the rest 40%–50% of cases.[4] Falciparum malaria has been most commonly seen with serious complications such as coma, jaundice, renal dysfunction, metabolic acidosis, hypoglycemia, respiratory distress, pulmonary edema, and cardiac complications.[4] Among cardiac complications of falciparum infection, myocarditis is very rare (0.6%). Others include bundle branch block (23%), pericardial effusion (9%), and cardiomyopathy (5%).[5] Nearly 23% cases of falciparum malaria showed ECG abnormalities in a study of 22 adult cases by Franzen et al.

P. vivax infection is rarely associated with serious complications.[3],[6],[7],[8] In India, studies by Kaur et al.[9] at Delhi and Kochar et al.[10] at Bikaner showed an association of vivax malaria with acute renal failure and acute respiratory distress syndrome. However, cardiac complications due to vivax malaria are extremely rare. Herrera[11] reported a case on fatal ischemic myocarditis in an 8-year-old boy due to vivax malaria. Kim et al.[12] reported a case of reversible myocarditis due to P. vivax in a 27-year-old female.

Myocarditis due to malaria infection has been attributed to various mechanisms such as sequestration of parasitized red blood cells in capillaries, tumor necrosis factor-α-induced toxicity on myocardium, hypoglycemia, acidosis, and damage due to pigment-laden macrophages. These mechanisms result in hypokinesia, low ejection fraction, pericardial effusion, valvular regurgitation, and electrophysiological changes. ECG may show ST-T changes and conduction blocks such as sinoatrial exit block. Electrophysiological changes precede myocytolysis. Thus, ECG and echocardiography aid diagnostic feasibility.

Sinoatrial blocks can be caused by drugs such as beta blockers, digitalis, and calcium channel blockers. Patients of coronary artery disease and hypothyroidism can also manifest with such disturbances. We excluded significant above drug history and hypothyroidism in our case.

Gupta and Sahoo reported the case of a 20-year-old young boy with myocarditis and pericardial effusion due to vivax malaria.[13] Kim et al. reported a case of a 27-year-old young woman with myocarditis due to vivax malaria.[12] Mustafa et al.[14] also reported a case of myocarditis in a child. In our case, patient presented with complaints of fever, hypotension, arrhythmia along with cardiomegaly on chest radiograph, and sinus exit block on ECG. Echocardiography showed dilated left heart chambers with reduced ejection fraction. Cardiac enzymes were not raised, and troponin T was negative. Thus, in the presence of above findings, a diagnosis of myocarditis due to vivax malaria was made. Treatment of malarial myocarditis is supportive along with bed rest and avoidance of exertional activities as in our case. Recovery was full, and there was complete resolution of clinical, electrophysiological, and echocardiographical findings.


  Conclusion Top


Myocarditis and conduction abnormalities should be considered when a patient with vivax malaria presents with hypotension. One should be aware of cardiac complications of malaria as myocarditis is uncommon with P. vivax. This will help in early diagnosis and specific management of such cases.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

None.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
World Health Organization. World Malaria Report 2017. Geneva: World Health Organization; 2017.  Back to cited text no. 1
    
2.
Mohsen AH, Green ST, West JN, McKendrick MW. Myocarditis associated with Plasmodium falciparum malaria: A case report and a review of the literature. J Travel Med 2001;8:219-20.  Back to cited text no. 2
    
3.
Oh MD, Shin H, Shin D, Kim U, Lee S, Kim N, et al. Clinical features of vivax malaria. Am J Trop Med Hyg 2001;65:143-6.  Back to cited text no. 3
    
4.
Zaki SA, Shanbag P. Atypical manifestations of malaria. Res Rep Trop Med 2011;2:9-22.  Back to cited text no. 4
    
5.
Franzen D, Curtius JM, Heitz W, Höpp HW, Diehl V, Hilger HH, et al. Cardiac involvement during and after malaria. Clin Investig 1992;70:670-3.  Back to cited text no. 5
    
6.
Carlini ME, White AC Jr., Atmar RL. Vivax malaria complicated by adult respiratory distress syndrome. Clin Infect Dis 1999;28:1182-3.  Back to cited text no. 6
    
7.
Choi HJ, Lee SY, Yang H, Bang JK. Retinal haemorrhage in vivax malaria. Trans R Soc Trop Med Hyg 2004;98:387-9.  Back to cited text no. 7
    
8.
Kim A, Park YK, Lee JS, Chung MH, Kim ES. A case of symptomatic splenic infarction in vivax malaria. Korean J Parasitol 2007;45:55-8.  Back to cited text no. 8
    
9.
Kaur D, Wasir V, Gulati S, Bagga A. Unusual presentation of plasmodium vivax malaria with severe thrombocytopenia and acute renal failure. Journal of Tropical Pediatrics 2007;53:210-2.  Back to cited text no. 9
    
10.
Kochar DK, Das A, Kochar SK, Saxena V, Sirohi P, Garg S, et al. Severe Plasmodium vivax malaria: A report on serial cases from Bikaner in Northwestern India. Am J Trop Med Hyg 2009;80:194-8.  Back to cited text no. 10
    
11.
Herrera JM. Cardiac lesions in vivax malaria. Study of a case with coronary and myocardial damage. Arch Inst Cardiol Me×1960;30:26-36.  Back to cited text no. 11
    
12.
Kim SA, Kim ES, Rhee MY, Choi SI, Huh HJ, Chae SL, et al. A case of myocarditis associated with Plasmodium vivax malaria. J Travel Med 2009;16:138-40.  Back to cited text no. 12
    
13.
Gupta N, Sahoo SK. Plasmodium vivax induced myocarditis: A rare case report. Indian J Med Microbiol 2013;31:180-1.  Back to cited text no. 13
  [Full text]  
14.
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. 14
    


    Figures

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    Tables

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