Fatal Myocarditis in Course of<i>Plasmodium falciparum</i>Infection: Case Report and Review of Cardiac Complications in Malaria

Costenaro, Paola; Benedetti, Paolo; Facchin, Chiara; Mengoli, Carlo; Pellizzer, Giampietro

doi:10.1155/2011/202083

Cited by 20 publications

(17 citation statements)

References 24 publications

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“…and Plasmodium falciparum is the most pathogenic species causing severe form and high mortality rate. Clinical manifestation of severe malaria can include damages on central nervous system (Idro et al 2005), severe anaemia (Stoute et al 2003), kidney failure (Plewes et al 2017), pulmonary dysfunction (Maguire et al 2008), disseminated intravascular coagulation, hepatic dysfunction and shock (Jain et al 2016), and also cardiovascular abnormalities (Costenaro et al 2011). There are different pathways which P. falciparum infection can trigger cardiac disorders.…”

Section: Introductionmentioning

confidence: 99%

“…There are different pathways which P. falciparum infection can trigger cardiac disorders. Parasitized red blood cells can occlude myocardial capillaries, leading to ischaemic cardiomyopathy and dilated heart (Mohsen et al 2001; Costenaro et al 2011); high levels of tumour necrosis factor (TNF- α ) may play a role in inflammatory process at heart, impairing myocardial function (Torre-Amione et al 1996); and hypoxia induced by severe anaemia may cause ischaemic myocardial injury with prolonged QTc interval of electrocardiogram (ECG), as frequently observed in children (Sadoh and Uduebor, 2016).…”

Section: Introductionmentioning

confidence: 99%

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Reduced cardiotoxicity and increased oral efficacy of artemether polymeric nanocapsules in Plasmodium berghei-infected mice

et al. 2017

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Artemether (ATM) cardiotoxicity, its short half-life and low oral bioavailability are the major limiting factors for its use to treat malaria. The purposes of this work were to study free-ATM and ATM-loaded poly-ε-caprolactone nanocapules (ATM-NC) cardiotoxicity and oral efficacy on Plasmodium berghei-infected mice. ATM-NC was obtained by interfacial polymer deposition and ATM was associated with polymeric NC oily core. For cardiotoxicity evaluation, male black C57BL6 uninfected or P. berghei-infected mice received, by oral route twice daily/4 days, vehicle (sorbitol/carboxymethylcellulose), blank-NC, free-ATM or ATM-NC at doses 40, 80 or 120 mg kg-1. Electrocardiogram (ECG) lead II signal was obtained before and after treatment. For ATM efficacy evaluation, female P. berghei-infected mice were treated the same way. ATM-NC improved antimalarial in vivo efficacy and reduced mice mortality. Free-ATM induced significantly QT and QTc intervals prolongation. ATM-NC (120 mg kg-1) given to uninfected mice reduced QT and QTc intervals prolongation 34 and 30%, respectively, compared with free-ATM. ATM-NC given to infected mice also reduced QT and QTc intervals prolongation, 28 and 27%, respectively. For the first time, the study showed a nanocarrier reducing cardiotoxicity of ATM given by oral route and it was more effective against P. berghei than free-ATM as monotherapy.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Reduced cardiotoxicity and increased oral efficacy of artemether polymeric nanocapsules in Plasmodium berghei-infected mice

et al. 2017

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“…The malaria pathogens have been related to cause detrimental effects on skeletal muscles of animals and humans [3][4][5][6][7][8][9]. In addition of affecting skeletal muscles, severe malaria may cause damage on cardiac muscles [10][11][12]. Circulation levels of cardiac proteins increases with the severity of malaria, indicating myocardial impairment in complicated falciparum malaria [13,14].…”

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confidence: 99%

The skeletal muscles of mice infected with Plasmodium berghei and Plasmodium chabaudi reveal a crosstalk between lipid mediators and gene expression

Marrelli

Wang

Huang

et al. 2020

Malar J

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Background: Malaria is one of the most prevalent infectious disease in the world with 3.2 billion humans at risk. Malaria causes splenomegaly and damage in other organs including skeletal muscles. Skeletal muscles comprise nearly 50% of the human body and are largely responsible for the regulation and modulation of overall metabolism. It is essential to understand how malaria damages muscles in order to develop effective preventive measures and/or treatments. Using a pre-clinical animal model, the potential molecular mechanisms of Plasmodium infection affecting skeletal muscles of mice were investigated. Methods: Mouse Signal Transduction Pathway Finder PCR Array was used to monitor gene expression changes of 10 essential signalling pathways in skeletal muscles from mice infected with Plasmodium berghei and Plasmodium chabaudi. Then, a new targeted-lipidomic approach using liquid chromatography with tandem mass spectrometry (LC-MS/MS) to profile 158 lipid signalling mediators (LMs), mostly eicosanoids derived from arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), was applied. Finally, 16 key LMs directly associated with inflammation, oxidative stress, and tissue healing in skeletal muscles, were quantified. Results: The results showed that the expression of key genes altered by Plasmodium infection is associated with inflammation, oxidative stress, and atrophy. In support to gene profiling results, lipidomics revealed higher concentrations of LMs in skeletal muscles directly related to inflammatory responses, while on the levels of LMs crucial in resolving inflammation and tissue repair reduced significantly. Conclusion: The results provide new insights into the molecular mechanisms of malaria-induced muscle damage and revealed a potential mechanism modulating inflammation in malarial muscles. These pre-clinical studies should help with future clinical studies in humans aimed at monitoring of disease progression and development of specific interventions for the prevention and mitigation of long-term chronic effects on skeletal muscle function.

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“…The occurrence of the cardiac event relates in time with residual parasitaemia during curative Malarone treatment post-CHMI that might be suggestive of a causal relationship. A few cases of malaria and concomitant myocarditis have been reported in the literature, albeit restricted to patients with severe or fatal infection with P. falciparum [16][17][18][19][20][21][22] and Plasmodium vivax malaria [23]. In literature, myocarditis has never been reported in patients with uncomplicated P. falciparum malaria, even in those patients who present with P. falciparum parasite densities 20 to 30 times higher than the parasite density in this volunteer.…”

Section: Discussionmentioning

confidence: 99%

Idiopathic acute myocarditis during treatment for controlled human malaria infection: a case report

Meer

Bastiaens

Boulaksil

et al. 2014

Malar J

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A 23-year-old healthy male volunteer took part in a clinical trial in which the volunteer took chloroquine chemoprophylaxis and received three intradermal doses at four-week intervals of aseptic, purified Plasmodium falciparum sporozoites to induce protective immunity against malaria. Fifty-nine days after the last administration of sporozoites and 32 days after the last dose of chloroquine the volunteer underwent controlled human malaria infection (CHMI) by the bites of five P. falciparum-infected mosquitoes. Eleven days post-CHMI a thick blood smear was positive (6 P. falciparum/μL blood) and treatment was initiated with atovaquone/proguanil (Malarone®). On the second day of treatment, day 12 post-CHMI, troponin T, a marker for cardiac tissue damage, began to rise above normal, and reached a maximum of 1,115 ng/L (upper range of normal = 14 ng/L) on day 16 post-CHMI. The volunteer had one ~20 minute episode of retrosternal chest pain and heavy feeling in his left arm on day 14 post-CHMI. ECG at the time revealed minor repolarization disturbances, and cardiac MRI demonstrated focal areas of subepicardial and midwall delayed enhancement of the left ventricle with some oedema and hypokinesia. A diagnosis of myocarditis was made. Troponin T levels were normal within 16 days and the volunteer recovered without clinical sequelae. Follow-up cardiac MRI at almost five months showed normal function of both ventricles and disappearance of oedema. Delayed enhancement of subepicardial and midwall regions decreased, but was still present. With the exception of a throat swab that was positive for rhinovirus on day 14 post-CHMI, no other tests for potential aetiologies of the myocarditis were positive. A number of possible aetiological factors may explain or have contributed to this case of myocarditis including, i) P. falciparum infection, ii) rhinovirus infection, iii) unidentified pathogens, iv) hyper-immunization (the volunteer received six travel vaccines between the last immunization and the CHMI), v) atovaquone/proguanil treatment, or vi) a combination of these factors. Definitive aetiology and pathophysiological mechanism for the myocarditis have not been established.

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Fatal Myocarditis in Course ofPlasmodium falciparumInfection: Case Report and Review of Cardiac Complications in Malaria

Cited by 20 publications

References 24 publications

Reduced cardiotoxicity and increased oral efficacy of artemether polymeric nanocapsules in Plasmodium berghei-infected mice

Reduced cardiotoxicity and increased oral efficacy of artemether polymeric nanocapsules in Plasmodium berghei-infected mice

The skeletal muscles of mice infected with Plasmodium berghei and Plasmodium chabaudi reveal a crosstalk between lipid mediators and gene expression

Idiopathic acute myocarditis during treatment for controlled human malaria infection: a case report

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