Cardiac function in Ghanaian children with severe malaria

Nguah, Samuel Blay; Feldt, Torsten; Hoffmann, Steffi; Pelletier, Daniel; Ansong, Daniel; Sylverken, Justice; Mehrfar, Parisa; Herr, Johanna; Thiel, Christian; Ehrhardt, Stephan; Burchard, Gerd; Cramer, Jakob P.

doi:10.1007/s00134-012-2676-z

Cited by 15 publications

(26 citation statements)

References 32 publications

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“…The pathogenesis mechanisms of several diseases caused by protozoan and nematode parasites have shown to cause detrimental effect on cardiac and skeletal muscles (i.e., Chagas disease, toxoplasmosis, trichinosis, leishmaniosis, and malaria) [4–7]. Parasitic infestations by Trypanossoma cruzi , Toxoplasma gondii and Trichinella spiralis cause cardiomyopathy in the immunocompetent and immunocompromised patients.…”

Section: Introductionmentioning

confidence: 99%

The effect of malaria and anti-malarial drugs on skeletal and cardiac muscles

Marrelli

Brotto

2016

Malar J

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Malaria remains one of the most important infectious diseases in the world, being a significant public health problem associated with poverty and it is one of the main obstacles to the economy of an endemic country. Among the several complications, the effects of malaria seem to target the skeletal muscle system, leading to symptoms, such as muscle aches, muscle contractures, muscle fatigue, muscle pain, and muscle weakness. Malaria cause also parasitic coronary artery occlusion. This article reviews the current knowledge regarding the effect of malaria disease and the anti-malarial drugs on skeletal and cardiac muscles. Research articles and case report publications that addressed aspects that are important for understanding the involvement of malaria parasites and anti-malarial therapies affecting skeletal and cardiac muscles were analysed and their findings summarized. Sequestration of red blood cells, increased levels of serum creatine kinase and reduced muscle content of essential contractile proteins are some of the potential biomarkers of the damage levels of skeletal and cardiac muscles. These biomarkers might be useful for prevention of complications and determining the effectiveness of interventions designed to protect cardiac and skeletal muscles from malaria-induced damage.

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Section: Introductionmentioning

confidence: 99%

The effect of malaria and anti-malarial drugs on skeletal and cardiac muscles

Marrelli

Brotto

2016

Malar J

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“…How these changes in the electrophysiology of the heart also influence cardiac function is difficult to say. While an impaired cardiac output in acidotic children could not be shown in the same study population [27] others indeed identified impaired cardiac function in relation to acidosis [27,28]. Children with hyperlactataemia and metabolic acidosis also showed increased HR.…”

Section: Discussionmentioning

confidence: 85%

Disease-associated QT-shortage versus quinine associated QT-prolongation: age dependent ECG-effects in Ghanaian children with severe malaria

Roggelin

Pelletier

Hill

et al. 2014

Malar J

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BackgroundWhile several anti-malarials are known to affect the electric conduction system of the heart, less is known on the direct effects of Plasmodium falciparum infection. Some earlier studies point to a direct impact of Plasmodium falciparum infection on the electric conduction system of the heart. The aim of this study was to analyse infection- and drug-induced effects on the electric conduction system.MethodsChildren aged 12 months to 108 months with severe malaria were included in Kumasi, Ghana. In addition to basic demographic, clinical, biochemical and parasitological, biochemical data were measured data upon hospitalization (day 0) and 12-lead electrocardiograms were recorded before (day 0) and after (day 1) initiation of quinine therapy as well as after 42 (±3) days.ResultsA total of 180 children were included. Most children were tachycardic on day 0 but heart rate declined on day 1 and during follow up. The corrected QT intervals were longest on day 1 and shortest on day 0. Comparison of QT intervals with day 42 (healthy status) after stratification for age demonstrated that in the youngest (<24 months) this was mainly due to a QT shortage on day 0 while a QT prolongation on day 1 was most pronounced in the oldest (≥48 months). Nearly one third of the participating children had measurable 4-aminoquinoline levels upon admission, but no direct effect on the corrected QT intervals could be shown.ConclusionSevere P. falciparum infection itself can provoke changes in the electrophysiology of the heart, independent of anti-malarial therapy. Especially in young - thus non immune - children the effect of acute disease associated pre-treatment QT-shortage is more pronounced than quinine associated QT-prolongation after therapy. Nevertheless, neither malaria nor anti-malarial induced effects on the electrophysiology of the heart were associated with clinically relevant arrhythmias in the present study population.

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“…The QT intervals were computed from the peak of the R to the peak of the T wave in a pseudo-ECG from Φ=a ∫(−∇V)(∇(1/x−x ′ ))dx (2) where Φ represents the unipolar potential recorded at an electrode 20 mm from the epi-cardial end of the strand, a is a scaling factor, and x − x′ is the distance from the electrode to any point in the tissue [11]. For both the adult and child models, the APD90s and QT intervals in ms were shorter in the malarial model than the normal, whereas the QTc was prolonged in the adult (from 257 to 310ms) and shortened in the child (from 274 to 172ms).…”

Section: Resultsmentioning

confidence: 99%

“…90% of these deaths are in were in sub-Saharan Africa, and 70% in children less than 5 years old. Cardiac function, in terms of rate, stroke volume, ejection fraction and haemodynamic indices is impaired in severe malaria [1][2][3], and some antimalarial agents (the quinolines) affect ventricular repolarization, observed as QT interval prolongation [4,5].…”

Section: Introductionmentioning

confidence: 99%