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Table of Contents
Year : 2017  |  Volume : 54  |  Issue : 4  |  Page : 372-374

Malaria and the heart: Two rare case reports of Plasmodium falciparumassociated pericarditis

1 Department of Sciences for Health Promotion and Mother & Child Care, Section of Infectious Diseases, University of Palermo, Italy
2 Faculdade de Medicina, Universidade do Porto, Porto, Portugal

Date of Submission07-Dec-2016
Date of Acceptance11-Jul-2017
Date of Web Publication19-Feb-2018

Correspondence Address:
Claudia Colomba
Department of Sciences for Health Promotion and Mother and Child Care, Section of Infectious Diseases, University of Palermo
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-9062.225845

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Keywords: Malaria; Plasmodium falciparum; pericardial effusion; pericarditis

How to cite this article:
Colomba C, Trizzino M, Gioè C, Coelho F, Lopo I, Pinheiro P, Sousa J, Cascio A. Malaria and the heart: Two rare case reports of Plasmodium falciparumassociated pericarditis. J Vector Borne Dis 2017;54:372-4

How to cite this URL:
Colomba C, Trizzino M, Gioè C, Coelho F, Lopo I, Pinheiro P, Sousa J, Cascio A. Malaria and the heart: Two rare case reports of Plasmodium falciparumassociated pericarditis. J Vector Borne Dis [serial online] 2017 [cited 2021 Apr 19];54:372-4. Available from: https://www.jvbd.org/text.asp?2017/54/4/372/225845

Malaria is one of the most important parasitic diseases in the world, causing significant mortality and morbidity in the tropical regions[1]. Although symptoms can range from a mild fever to severe complicated forms, there are limited published data on cardiac involvement of malaria and only a few studies have been carried out regarding cardiac function in severe malaria[2],[3]. Cardiac involvement in the course of malaria ranges from severe forms with hypatension, shock, circulatory collapse and impaired haemodynamic function, to mild disorders documented by Electrocardiogram (ECG) and echocardiography[4],[5],[6]. Pericardial involvement in malaria is a very rare event[7],[8]. We report here two cases of falciparum malaria complicated with pericardial effusion.

Case 1: A 19-yr-old Nigerian female, resident of Sicily, was admitted with history of intermittent highgrade fever over three days, following her return from Nigeria, 10 days prior to the onset of the symptoms. The fever was associated with headaches as well as thoracic pain during the episodes. The patient denied neck stiffness. There was no history of diabetes, hypertension or dyslipidaemia. On examination the patient was apyretic, eupneic, blood pressure was 120/70 mmHg with a pulse rate of 105 bpm. Neck stiffness and peripheral oedema were absent and there was no active bleeding from any site. Neurological examination was normal. Hepatomegaly was absent and the spleen was palpable with a long axis of approximately 13 cm. Cardiovascular examination identified a systolic murmur and pericardial rub. White blood cells (WBCs) count was 6600/mm3, platelet count was 54000/mm3 indicating thrombocytopenia, haemoglobin was 8.2 g/dl, and blood glucose was 110 mg/dl; coagulation profile revealed an INR of 1.38, a D-dimer of 949 ng/dl and a fibrinogen of 502 mg/dl. Liver function tests displayed a GGT of 56 IU/L and LDH of 232 IU/L. Renal function tests showed a blood urea of 21 mg/ dl and a serum creatinine of 0.8 mg/dl. C-reactive protein levels were elevated at 14.95 mg/l. Blood smear was positive for Plasmodium falciparum with 1.5% parasitaemia. Virological screen was negative for human immunodeficiency virus (HIV) and cytomegalovirus (CMV).

ECG showed sinus tachycardia of 106 bpm and diffuse non-specific abnormality of ST-T wave. The echocardiogram, performed to investigate the cause of the thoracic pain, revealed an anterior non-compressive pericardial effusion (6 mm behind the right atrium, 9 mm in lateral) and a congenital intra-atrial and intra-ventricular communication with left-to-right shunt. Chest X-ray was normal.

The patient was treated with a co-formulation of dihydroartemisinin (DHA)-piperaquine (PPQ) 120 mg/960 mg orally (po) once daily for three days. The patient also started treatment for pericarditis under the supervision of a cardiologist with colchicine 1 mg po daily and ibuprofen 600 mg every 8 h (as attack dose for a week, then every 12 h for another week).

There was a favourable evolution throughout seven days of admission, with an improvement of symptomatology. Repeat blood smear at the end of antimalaria therapy showed no evidence of malarial parasites. Patient was discharged after 16 days in good and stable clinical condition, with colchicine therapy for a total period of three months. An appropriate follow-up plan was agreed upon as recommended.

Case 2:A 52-yr-old Ghanese woman, residing in Sicily, was admitted with history of abdominal pain and fever over five days, following her return from Ghana, 15 days prior to the onset of the symptoms. On admission, she appeared suffering, but without altered state of consciousness. On examination the patient was febrile (body temperature 39 °C), eupneic, with blood pressure 120/60 mmHg. There were no signs of meningeal irritation, cognitive impairment or any neurological deficit. She had no hepatosplenomegaly. A cardiac examination revealed soft heart sounds, with pericardial friction rub.

Laboratory studies showed a WBC count of 24200/ mm3 (neutrophils 89.7%, lymphocytes 5.5%); haemoglobin level 8.6 g/l, platelets count 17000/mm3, C-Reactive protein 198 mg/l, D-dimer 15.112 mg/l. Examination of a thin blood smear revealed ring trophozoites typical of P. falciparum including multiple infected cells with 3.7% of erythrocytes parasitized. Quanti FERON-TB-Gold test and viral serology for HIV were negative.

ECG showed sinus tachycardia of 110 bpm. Transthoracic echocardiography (TE) showed a left ventricular concentric hypertrophy with preserved global systolic function, absence of any segmental wall-motion abnormalities of the left ventricle; right sections were of normal size with preserved right ventricular function. It also showed pericardial effusion (8 mm behind the right atrium, 12 mm in lateral) without haemodynamic consequences [Figure 1]. The patient was treated for malaria infection with a co-formulation of dihydroartemisinin (DHA)-piperaquine (PPQ) 120 mg/960 mg po once daily for three days. In agreement with 2015 ESC guidelines[9] the patient was treated for pericarditis with ibuprofen 600 mg po every 8 h (as attack dose for a week, then every 12 h for another week) plus colchicine 1 mg po daily. Over four days after initiation of antimalaria therapy, the patient’s clinical condition improved. Repeat blood smear at the end of antimalaria therapy showed no evidence of malarial parasites. On Day 12 of hospitalization, a control TE confirmed the presence of a minor pericardial effusion (4 mm in lateral), with no signs of haemodynamic compromise. The patient was discharged on the 14th day in good condition, with colchicine therapy for a total period of three months.
Figure 1: Echocardiography showing a circumcardiac pericardial effusion (yellow arrow) in parasternal long axis (left) and apical 4 chamber (right).

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  Discussion Top

Falciparum malaria has a wide range of symptoms, and can be complicated by acute renal insufficiency, cerebral malaria, acidosis and acute respiratory distress syndrome[4]. Cardiac involvement is rarely seen and, when present, affects predominantly the myocardium and the myoelectric system[5],[10]. Features of myocarditis, ectopic ECG changes, conduction defects, tachy-brady-arrhythmias and acute heart failure with reduced cardiac output have been observed in a few cases of imported severe falciparum malaria[10],[11],[12],[13],[14]. In the present cases, both the patients developed pericardial effusion. Whilst myocardial damage appears to retain a multifactorial pathogenesis, being probably the result of mechanical (microcirculatory obstruction), metabolic (systemic acidosis and related tissue hypo-oxygenation), and humoral mechanisms; the mechanism underlying the causal relationship between the parasitic infection and the development of pericardial effusion is still unclear. One possible explanation may be the locally elevated cytokine levels. Day et al[15] have shown that cytokines produced locally in particular tissue during malarial infection may be regulated by the degree of regional parasitic sequestration; and the documentation of parasitic antigen, by Kohli et al[8], in the pericardial fluid has also confirmed the association of malaria and pericardial effusion.

Plasmodium falciparum has the unique capability of causing cytoadherence, where parasitised RBCs become sequestered in capillaries. It has been shown that the production of pro-inflammatory cytokines can be regulated by the extent of cytoadherence in specific areas[16]. The pro-inflammatory state created locally alters the dynamic equilibrium between the pericardial fluid and the blood serum. Local production of inflammatory mediators can bring about the extravasation of fluid from the visceral pericardium into the virtual space between the two layers. In addition, the exudation of large molecules increases the osmotic potential inside the pericardial sheets and perpetuates the vicious cycle installed.

In the light of earlier reports, it is reasonable to conclude that pericardial effusion must be deemed a serious complication of falciparum malaria. This is crucial insight to prevent cardiac tamponade, a potentially fatal complication of what is an otherwise curable disease[8].

Conflict of interest

There are not any affiliation, financial agreement, or other involvement of any author with the companies whose products figure prominently in the submitted typescript.

Ethical statement

Written informed consent was obtained from the patients for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor/Editor-in-Chief of this journal.

  References Top

World Malaria Report 2015. Geneva: World Health Organization 2015; p. 280.  Back to cited text no. 1
Ehrhardt S, Mockenhaupt FP, Anemana SD, Otchwemah RN, Wichmann D, Cramer JP, et al. High levels of circulating cardiac proteins indicate cardiac impairment in African children with severe Plasmodium falciparum malaria. Microbes Infect 2005; 7(11-12): 1204-10.  Back to cited text no. 2
Yacoub S, Lang HJ, Shebbe M, Timbwa M, Ohuma E, Tulloh R, et al. Cardiac function and hemodynamics in Kenyan children with severe malaria. Crit Care Med 2010; 38(3): 940-5.  Back to cited text no. 3
Severe falciparum malaria. World Health Organization, Communicable Diseases Cluster. Trans R Soc Trop Med Hyg 2000; 94 (Suppl 1): S1-90.  Back to cited text no. 4
Mishra SK, Behera PK, Satpathi S. Cardiac involvement in malaria: An overlooked important complication. J Vector Borne Dis 2013; 50(3): 232-5.  Back to cited text no. 5
Hooda AK, Varma PP, Dutta V. Fatal cardiac tamponade in malarial acute renal failure. Ren Fail 2007; 29(3): 371-3.  Back to cited text no. 6
Franzen D, Curtius JM, Heitz W, Höpp HW, Diehl V, Hilger HH. Cardiac involvement during and after malaria. Clin Investig 1992; 70(8): 670-3.  Back to cited text no. 7
Kohli R, Gulati S, Kapoor A, Singh S. Cardiac tamponade: An unusual complication of Plasmodium falciparum-induced acute renal failure. Nephrol Dial Transplant 2003; 18(8): 1678-9.  Back to cited text no. 8
Adler Y, Charron P, Imazio M, Badano L, Barón-Esquivias G, Bogaert J, et al. ESC guidelines for the diagnosis and management of pericardial diseases: The task force for the diagnosis and management of pericardial diseases of the European Society of Cardiology (ESC) Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J 2015; 36(42): 2921-64.  Back to cited text no. 9
Costenaro P, Benedetti P, Facchin C, Mengoli C, Pellizzer G. Fatal myocarditis in course of Plasmodium falciparum infection: Case report and review of cardiac complications in malaria. Case Rep Med 2011; 2011: 202083.  Back to cited text no. 10
Wichmann O, Löscher T, Jelinek T. Fatal malaria in a German couple returning from Burkina Faso. Infection 2003; 31(4): 260-2.  Back to cited text no. 11
Kumar D, Kapoor A. Cardiac involvement in falciparum malaria: A brief report. Clin Pediatr (Phila) 2013; 52(4): 362-3.  Back to cited text no. 12
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(4): 219-20.  Back to cited text no. 13
Bhat S, Alva J, Muralidhara K, Fahad S. Malaria and the heart. BMJ Case Rep 2012; 27; 2012  Back to cited text no. 14
Day NP, Hien TT, Schollaardt T, Loc PP, Chuong LV, Chau TT et al. The prognostic and pathophysiologic role of pro- and antiinflammatory cytokines in severe malaria. J Infect Dis 1999; 180(4): 1288-97.  Back to cited text no. 15
Craig AG, Khairul MF, Patil PR. Cytoadherence and severe malaria. Malays J Med Sci 2012; 19(2): 5-18.  Back to cited text no. 16


  [Figure 1]

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