title: Does contrast echocardiography induce increases in markers of myocardial necrosis, inflammation and oxidative stress suggesting myocardial injury?
abstract: BACKGROUND
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Universitätsmedizin Berlin, Medical Clinic for Cardiology, Angiology, Pulmology, Charité Campus Mitte, Germany. fabian.knebel@charite.de
authors.forename: Fabian
authors.initials: F
authors.lastname: Knebel
authors.forename: Ingolf
authors.initials: I
authors.lastname: Schimke
authors.forename: Stephan
authors.initials: S
authors.lastname: Eddicks
authors.forename: Torsten
authors.initials: T
authors.lastname: Walde
authors.forename: Reinhard
authors.initials: R
authors.lastname: Ziebig
authors.forename: Sebastian
authors.initials: S
authors.lastname: Schattke
authors.forename: Gert
authors.initials: G
authors.lastname: Baumann
authors.forename: Adrian Constantin
authors.initials: AC
authors.lastname: Borges
mesh_terms: D000293:Adolescent; D000328:Adult; D000418:Albumins / Q000009:adverse effects*; D003287:Contrast Media / Q000009:adverse effects*; D016207:Cytokines / Q000276:immunology*; D004452:Echocardiography / Q000009:adverse effects*; D005260:Female; D005466:Fluorocarbons / Q000009:adverse effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009205:Myocarditis / Q000139:chemically induced* / Q000175:diagnosis / Q000276:immunology*; D018384:Oxidative Stress / Q000187:drug effects / Q000276:immunology; D018570:Risk Assessment; D012307:Risk Factors; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
chemical_list: D000418:Albumins; D003287:Contrast Media; D016207:Cytokines; C099458:FS 069; D005466:Fluorocarbons; D017392:Thiobarbituric Acid Reactive Substances