Unbound MEDLINE

Does contrast echocardiography induce increases in markers of myocardial necrosis, inflammation and oxidative stress suggesting myocardial injury? Cardiovascular ultrasound [electronic resource]. [Cardiovasc Ultrasound] Journal article

 
TitleDoes contrast echocardiography induce increases in markers of myocardial necrosis, inflammation and oxidative stress suggesting myocardial injury?
Author(s)Knebel F, Schimke I, Eddicks S, Walde T, Ziebig R, Schattke S, Baumann G, Borges AC 
InstitutionUniversitätsmedizin Berlin, Medical Clinic for Cardiology, Angiology, Pulmology, Charité Campus Mitte, Germany. fabian.knebel@charite.de
SourceCardiovasc Ultrasound 2005.:21.
MeSHAdolescent
Adult
Albumins
Contrast Media
Cytokines
Echocardiography
Female
Fluorocarbons
Humans
Male
Middle Aged
Myocarditis
Oxidative Stress
Risk Assessment
Risk Factors
Thiobarbituric Acid Reactive Substances
AbstractBACKGROUND: Contrast echocardiography is a precise tool for the non-invasive assessment of myocardial function and perfusion. Side effects of contrast echocardiography resulting from contrast-agent induced myocardial micro-lesions have been found in animals. The goal of this study is to measure markers of myocardial necrosis, inflammation and oxidative stress in humans to evaluate potential side-effects of contrast echocardiography.
METHODS: 20 patients who underwent contrast echocardiography with Optison as the contrast medium were investigated. To evaluate myocardial micro-necrosis, inflammation and oxidative stress, cardiac troponin I (cTnI), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, -8 and thiobarbituric acid reactive substances (TBARS) were measured at baseline and at 2, 4, 8 and 24 hours after contrast echocardiography.
RESULTS: At baseline, 50% of the patients had cTnI and TBARS values outside the reference range. TNF-alpha, IL-6, IL-8 levels were within the reference range. Patients with cTnI above the RR clustered to significantly higher levels of TNF-alpha and IL-6. After contrast echocardiography, no statistically significant increase of cTnI, cytokines and TBARS was found. However, for nearly 50% of the patients, the intra-individual cTnI kinetics crossed the critical difference (threefold of methodical variation) which indicates a marker increase. This was neither predicted by the baseline levels of the cytokines nor the markers of oxidative stress.
CONCLUSION: There are no clinically relevant increases in serum markers for micro-necrosis, inflammation and oxidative stress in humans after contrast echocardiography. Future studies have to address whether cTnI increase in some patients represent a subset with increased risk for side effects after contrast echocardiography.
Languageeng
Pub Type(s)Journal Article
PubMed ID16107209
  
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