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Ticagrelor to Reduce Myocardial Injury in Patients With High-Risk Coronary Artery Plaque
Alastair J Moss1, Marc R Dweck1, Mhairi K Doris1
1British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom.
Insights
Ticagrelor did not reduce troponin levels in patients with high-risk coronary plaque. This suggests that subclinical plaque thrombosis is not the cause of ongoing myocardial injury in this patient group.
Area of Science:
- Cardiology
- Pharmacology
Background:
- High-risk coronary atherosclerotic plaque is linked to elevated troponin levels, indicating myocardial injury.
- This myocardial injury may be a potential target for dual antiplatelet therapy.
Purpose of the Study:
- To investigate if ticagrelor can decrease high-sensitivity troponin I concentrations in patients with established coronary artery disease and high-risk coronary plaque.
- To assess the impact of ticagrelor on myocardial injury markers in the context of high-risk coronary plaque.
Main Methods:
- A randomized, double-blind, placebo-controlled trial involving patients with multivessel coronary artery disease.
- Coronary imaging (18F-fluoride PET/CT) and high-sensitivity cardiac troponin I measurements were performed.
- Patients received either ticagrelor 90 mg twice daily or placebo, with troponin I levels assessed at 30 days and 1 year.
Main Results:
- In patients with increased coronary 18F-fluoride uptake, ticagrelor showed no significant effect on plasma troponin I concentrations at 30 days (ratio 1.11, p=0.32).
- Over one year, ticagrelor also did not alter troponin concentrations in patients with increased coronary 18F-fluoride uptake (ratio 0.86, p=0.33).
Conclusions:
- Dual antiplatelet therapy with ticagrelor did not reduce plasma troponin concentrations in patients with high-risk coronary plaque.
- The findings suggest that subclinical plaque thrombosis may not be a significant contributor to ongoing myocardial injury in this patient population.
Objectives:
The goal of this study was to determine whether ticagrelor reduces high-sensitivity troponin I concentrations in patients with established coronary artery disease and high-risk coronary plaque.
Background:
High-risk coronary atherosclerotic plaque is associated with higher plasma troponin concentrations suggesting ongoing myocardial injury that may be a target for dual antiplatelet therapy.
Methods:
In a randomized, double-blind, placebo-controlled trial, patients with multivessel coronary artery disease underwent coronary 18F-fluoride positron emission tomography/coronary computed tomography scanning and measurement of high-sensitivity cardiac troponin I. Patients were randomized (1:1) to receive ticagrelor 90 mg twice daily or matched placebo. The primary endpoint was troponin I concentration at 30 days in patients with increased coronary 18F-fluoride uptake.
Results:
In total, 202 patients were randomized to treatment, and 191 met the pre-specified criteria for inclusion in the primary analysis. In patients with increased coronary 18F-fluoride uptake (120 of 191), there was no evidence that ticagrelor had an effect on plasma troponin concentrations at 30 days (ratio of geometric means for ticagrelor vs. placebo: 1.11; 95% confidence interval: 0.90 to 1.36; p = 0.32). Over 1 year, ticagrelor had no effect on troponin concentrations in patients with increased coronary 18F-fluoride uptake (ratio of geometric means: 0.86; 95% confidence interval: 0.63 to 1.17; p = 0.33).
Conclusions:
Dual antiplatelet therapy with ticagrelor did not reduce plasma troponin concentrations in patients with high-risk coronary plaque, suggesting that subclinical plaque thrombosis does not contribute to ongoing myocardial injury in this setting. (Dual Antiplatelet Therapy to Reduce Myocardial Injury [DIAMOND]; NCT02110303).
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