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

## TL;DR

This study investigates whether contrast echocardiography causes signs of heart muscle injury in humans by measuring specific blood markers before and after the procedure.

## Contribution

The study provides new evidence on the safety of contrast echocardiography in humans by analyzing multiple biomarkers of myocardial injury.

## Key findings

- No clinically significant increases in markers of myocardial necrosis, inflammation, or oxidative stress were observed after contrast echocardiography.
- Approximately 50% of patients showed cTnI increases exceeding the critical difference threshold, but this was not predicted by baseline cytokine or oxidative stress levels.
- Baseline cTnI levels were elevated in 50% of patients, and these patients had higher TNF-α and IL-6 levels.

## Abstract

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.

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.

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.

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.