Case Report Revista da Sociedade Brasileira de Medicina Tropical 47(6):810-813, Nov-Dec, 2014

http://dx.doi.org/10.1590/0037-8682-0126-2014

Myocarditis associated with Plasmodium vivax malaria:

a case report
Ana Maria Revoredo da Silva Ventura[1],[2], Tnia do Socorro Souza Chaves[1],
Julius Caesar Mendes Monteiro[3], Carina Guilhon Sequeira[2],
Maria Deise de Oliveira Ohnishi[2], Rosana Maria Feio Libonati[4],
Rita Catarina Medeiros Sousa[4],[5] and Jose Maria de Souza[1]

[1]. Laboratrio de Ensaios Clnicos em Malria, Instituto Evandro Chagas, Secretaria de Vigilncia em Sade, Ministrio da Sade, Belm, PA. [2]. Departamento
de Medicina Integrada, Universidade do Estado do Par, Belm, PA. [3]. Faculdade de Medicina, Universidade Federal do Par, Belm, PA. [4]. Ncleo de
Medicina Tropical, Universidade Federal do Par, Belm, PA. [5]. Clnica Mdica, Hospital Porto Dias, Belm, PA.

ABSTRACT
Malaria remains a major public health problem in Brazil where Plasmodium vivax is the predominant species, responsible
for 82% of registered cases in 2013. Though benign, P. vivax infection may sometimes evolve with complications and a fatal
outcome. Here, we report a severe case of P. vivax malaria in a 35-year-old Brazilian man from a malaria endemic area, who
presented with reversible myocarditis.
Keywords: Malaria. Reversible myocarditis. Severe Plasmodium vivax malaria.

and was again hospitalized. In the hospital, a thick blood smear

INTRODUCTION was positive to P. vivax (30,000 asexual parasite forms/mm3),
and he was treated with 150mg chloroquine (4 tablets on the
Brazil, where malaria is endemic in the Amazon region1, rst day and 3 tablets on the second and third days) plus 15mg
is one of the few countries around the world with Plasmodium primaquine (2 tablets/day for 7 days) according to the treatment
vivax predominance. We report a case of P. vivax malaria in a regime proposed by the Health Ministry of Brazil4.
35-year-old patient from Anajs, a province in the Island of In the third day of hospitalization, primaquine was
Maraj, State of Par (0098'S, 4993'W), which is considered discontinued and the patient transferred to the intensive care
a high-risk area for malaria. unit due to worsening respiratory distress concomitant with
Severe malaria is caused mainly by Plasmodium falciparum. signs of heart failure and petechial hemorrhagic suffusion on
Severe cases similar to those that have been described for the thorax, abdomen and lower limbs (Figure 1). Normal white
P. falciparum malaria have been reported with P. vivax malaria, blood cell count observed at admission evolved to leukopenia
but few cases have been reported with cardiac involvement2,3. (3,000/L/mm3), and hemoglobin decreased from 12.8g/dL
to 8.9g/dL. Thrombocytopenia was present both at admission
CASE REPORT (20,000 platelets/mm3) and in day 3 (15,000 platelets/mm3).
Chest radiography revealed pulmonary edema and cardiomegaly
(Figures 2A and 2B), Ecocardiography revealed left ventricular
The 35-year-old male patient was an electrician and 5-year dilatation during systole (5mm, normal = 4mm) and diastole
resident of Anajs, State of Par, Brazil. He had no previous (73mm, normal = 56mm), decreased left ventricular ejection
history of malaria or cardiovascular system disorders. fraction (LVEF) (47%, normal > 58%), diffuse hypokinesia and
After discharge from the hospital following spinal cord mild mitral regurgitation (Figure 3). Blood and urine cultures
injury due to an occupational accident, the patient presented were negative. Results of serological tests for dengue, yellow
with a 5-day history of fever, chills, headache, and asthenia, fever, infectious mononucleosis, Chagas disease, enterovirus
(Coxsackie and Echovirus), human immunodeciency virus
(HIV) and human T-lymphotropic virus (HTLV) were also
Address to: Dra. Ana Maria Revoredo da Silva Ventura. Laboratrio de Ensaios negative. Polymerase chain reaction (PCR) to conrm P. vivax
Clnicos em Malria/IEC. Rodovia BR-316, km 7 s/n, Levilndia, 67030-000 infection was not performed.
Ananindeua, PA, Brasil. The patient gradually improved with antibiotic therapy
Phone: 55 91 3226-5880; 55 91 8146-7723
e-mail: [email protected]
(oxacillin and ceftriaxone), administered with antimalarials
Received 30 May 2014 due to the clinical severe condition. He was also administered
Accepted 21 August 2014 diuretics (furosemide and spironolactone), digoxin and

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 Ventura AMRS et al. - Myocarditis associated with P. vivax malaria

FIGURE 1 - Petechial hemorrhagic suffusion, on the thorax and

abdomen of a patient with Plasmodium vivax malaria.

carvedilol and was maintained in negative uid balance. A

thick blood smear was negative to Plasmodium sp to day 5, and
after 12 days of treatment, he was discharged (February, 11th,
2009) in regular health and administered carvedilol (1 tablet,
2 times/day).
Thereafter, he did not return to Anajs and was monitored
on a monthly basis in the Laboratory of Clinical Malaria
Essay at the Evandro Chagas Institute, in Ananindeua, State
of Par, Brazil, relapsing on the 46th day post-treatment, with
3,500 asexual P. vivax parasite forms/mm3. At this time, the
standard treatment was reintroduced. A negative blood smear
was observed on day 4, which persisted for up to 90 days with
monthly controls. In May - 2009, radiography showed normal
lung transparency and normal cardiac area; electrocardiography
showed normal sinus rhythm; and echocardiography showed a
B
34-mm ventricular diameter in systole, 50-mm left ventricular
diameter in diastole, LVEF of 60%, and heart valves without
morphologic or dynamic abnormalities.
FIGURES 2A and 2B - Chest radiography showing cardiomegaly
and acute edema of the lung in a patient with Plasmodium vivax
DISCUSSION malaria.

The worldwide prevalence of severe P. vivax malaria cases is

not well known, probably because there are no dened severity
criteria for malaria caused by P. vivax. However, the World in addition to the rst P. vivax malaria episode in six patients
Health Organization (WHO) criteria for severe P. falciparum who presented with cardiac involvement (from a series of 22
malaria seem to apply to the broad spectrum of the most severe malaria cases admitted in a German hospital)2. Similarly a case
P.vivax malaria cases described3,5. of myocarditis associated with primary P. vivax malaria has
A Plasmodium vivax malaria case complicated with been reported in a woman from South Korea3. Though these
myocardial failure and hemorrhagic diathesis in an adult man primary cases were related to the absence of specic immunity
from a malaria endemic area (Anajs) in the Amazon region to the parasite, severe cases, including cardiac damage, may
(Brazil) without a previous history of malaria, was reported occur in patients with previous malaria who have some degree

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Rev Soc Bras Med Trop 47(6):810-813, Nov-Dec, 2014

FIGURE 3 - Echocardiography showing left ventricular dilatation in systole and diastole and mild mitral regurgitation in a patient
with Plasmodium vivax malaria.

of immunity, making this relationship between myocarditis and Besides cardiac involvement, the present patient manifested
malaria unclear2. signs of septic shock. Myocardial dysfunction is one of the
Our patient presented with high parasitemia (30,000 asexual diagnostic criteria for severe sepsis and septic shock and frequently
parasite forms/mm3), which might have inuenced the severity, accompanies these conditions, presenting as ventricular dilatation
although additional studies are necessary to determine to what and reduced ejection fraction; when properly managed, it is
extent high parasite density may be considered a marker of reversible. An infection stimulus, generally an endotoxin or another
severity in P. vivax infections, as indicated by Lacerda et al.6. microbiological element (e.g., malaria endotoxins), - induces the
In a recent review of cardiac involvement in parasitic release of local and systemic inammatory mediators, especially
infection, Hidron et al. reported that Trypanosoma cruzi is the alpha-TNF and interleukin (IL)-1, from monocytes/macrophages
main parasite to compromise the heart; however the authors and other cells. These cytokines stimulate polymorphonuclear
did not mention malaria7. Myocardial involvement in malaria leukocytes, macrophages, and endothelial cells to release a
seems uncommon, with unclear physiopathology in the majority number of downstream inflammatory mediators, including
of cases associated with P. falciparum. Autopsy ndings have platelet activating factor and nitric oxide, further amplifying the
shown parasites and parasitized red blood cells blocking inammatory response. Several anti-inammatory mediators,
myocardial capillaries, leading to ischemic cardiomyopathy, such as IL-10, transforming growth factor-beta, and IL-1 receptor
and a dilated heart has also been observed. In addition, the toxic antagonist, are also released as part of this amplication cascade9.
effects of high levels of tumor necrosis factor (TNF) may play The myocardial involvement in the present patient
a role in the inammatory process in the heart, with migration was probably caused by the parasite itself and/or due to an
of lymphocytes and plasma cells, among others3,8. inammatory-trigged response; the physiopathology of the events

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 Ventura AMRS et al. - Myocarditis associated with P. vivax malaria

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