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Does contrast echocardiography induce increases in markers of myocardial necrosis, inflammation and oxidative stress suggesting myocardial injury?

Fabian Knebel1 email, Ingolf Schimke1 email, Stephan Eddicks1 email, Torsten Walde2 email, Reinhard Ziebig3 email, Sebastian Schattke1 email, Gert Baumann1 email and Adrian Constantin Borges1 email

Universitätsmedizin Berlin, Medical Clinic for Cardiology, Angiology, Pulmology, Charité Campus Mitte, Germany

Paritätisches Krankenhaus Lichtenberg, Fanningerstraße 32, 10365 Berlin, Lichtenberg, Germany

Universitätsmedizin Berlin, Institute for Laboratory Medicine and Pathobiochemistry, Charité Campus Mitte, Germany

author email corresponding author email

Cardiovascular Ultrasound 2005, 3:21doi:10.1186/1476-7120-3-21

Published: 17 August 2005

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-α (TNF-α), 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-α, IL-6, IL-8 levels were within the reference range. Patients with cTnI above the RR clustered to significantly higher levels of TNF-α 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.


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