Evidence map›Paper›PMID 18000714›Full record

ArticleMolecular imaging and biology

Phosphorus-31 two-dimensional chemical shift imaging in the myocardium of patients with late onset of Friedreich ataxia.

Christian Wolf, Sylvia Boesch, Bernhard Metzler, Helga Weirich-Schwaiger, Thomas Trieb, Michael F H Schocke

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Article in Molecular imaging and biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

What it found

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Christian WolfDepartment of Radiology I, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria.
Sylvia Boesch
Bernhard Metzler
Helga Weirich-Schwaiger
Thomas Trieb
Michael F H Schocke

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeFriedreich ataxia (FRDA) is characterized by GAA expansions in the intron 1 of the frataxin gene correlating with disease onset and progression as well as cardiac affection. Accordingly, FRDA patients with early disease onset show a clear impairment of mitochondrial function in the myocardium. The purpose of this study was to investigate cardiac function and high-energy phosphate metabolism in FRDA patients with late disease onset. PROCEDURES: Using a 1.5 T magnetic resonance scanner, cardiac phosphorus-31 two-dimensional chemical shift imaging was performed in ten patients (seven male, three female) with a late onset of FRDA and in 35 healthy, male controls. Ejection faction (EF) and interventricular septum thickness (IST) were determined by echocardiography.

resultsThe differences in left ventricular phosphocreatine (PCr) to beta-adenosine triphosphate (beta-ATP) ratios between both groups were not significant. FRDA patients had increased ISTs (10.8+/-1.6 vs. 9.7+/-0.9 mm; p=0.048), which correlated significantly with the left ventricular PCr to beta-ATP ratios (r= -0.644; p=0.04), and decreased EFs (52.24+/-7.72% vs. 64.09+/-4.25%; p=0.001) compared to normal controls.

conclusionsIn contrast to FRDA patients with early disease onset, our patients collective exhibited a normal, probably compensated cardiac mitochondrial function, whereby IST and EF were mildly altered.

Indexed as

Adenosine TriphosphateAdultAge of OnsetDemographyFemaleFriedreich AtaxiaHeart VentriclesHumansMagnetic Resonance ImagingMaleMyocardiumPhosphocreatinePhosphorus IsotopesAdenosine TriphosphatePhosphocreatinePhosphorus Isotopes

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.