Key result
Guided DAPT de-escalation had no significant interaction with smoking status (Pint=0.23) for the primary endpoint, occurring in 7.9% vs 11.0% of non-smokers and 6.6% vs 6.6% of smokers.
Why the study?
Because variations in antiplatelet drug response and clinical outcomes exist between smokers and non-smokers, the safety and efficacy of DAPT de-escalation may differ by smoking status.
Does platelet function testing guided de-escalation of DAPT improve clinical outcomes compared to standard prasugrel in invasively managed ACS patients, regardless of smoking status?
RCT (n=2,610)
1:1
Yes
Does platelet function testing guided de-escalation of DAPT improve clinical outcomes compared to standard prasugrel in invasively managed ACS patients, regardless of smoking status?
Hazard Ratio: 0.71 (95% CI 0.5–0.99)
Absolute Event Rate: 7.9% vs 11%
p-value: p=0.048
Guided DAPT de-escalation is a safe and effective alternative to 12 months of standard prasugrel therapy in ACS patients, irrespective of their smoking status.
Supports guided DAPT de-escalation in ACS regardless of smoking status; extends RCT evidence of consistent effect across subgroups.
AIMS: Prior analyses disclosed variations in antiplatelet drug response and clinical outcomes between smokers and non-smokers, thus the safety and efficacy of any dual antiplatelet therapy (DAPT) de-escalation strategy may differ in relation to smoking status. Hence, we assessed the impact of smoking on clinical outcomes and adenosine diphosphate-induced platelet aggregation following guided de-escalation of DAPT in invasively managed acute coronary syndrome (ACS) patients. METHODS AND RESULTS: The multicentre TROPICAL-ACS trial randomized 2610 biomarker-positive ACS patients 1:1 to standard treatment with prasugrel for 12 months (control group) or a platelet function testing guided de-escalation of DAPT. Current smokers (n = 1182) showed comparable event rates between study groups [6.6% vs. 6.6%; hazard ratio (HR) 1.0, 95% confidence interval (CI) 0.64-1.56, P > 0.99]. In non-smokers (n = 1428), a guided DAPT de-escalation was associated with a lower 1-year incidence of the primary endpoint [cardiovascular death, myocardial infarction, stroke, or bleeding ≥ Grade 2 according to Bleeding Academic Research Consortium (BARC) criteria] compared with control group patients (7.9% vs. 11.0%; HR 0.71, 95% CI 0.50-0.99, P = 0.048). This reduction was mainly driven by a lower rate of BARC ≥ Grade 2 bleedings (5.2% vs. 7.7%; HR 0.68, 95% CI 0.45-1.03, P = 0.066). There was no significant interaction of smoking status with treatment effects of guided DAPT de-escalation (Pint = 0.23). Adenosine diphosphate-induced platelet aggregation values were higher in current smokers [median 28 U, interquartile range (IQR: 20-40)] vs. non-smoker [median 24 U (16-25), P < 0.0001] in the control group and in current smokers [median 42 U, IQR (27-68)] vs. non-smoker [median 37 U, IQR (25-55), P < 0.001] in the monitoring group. CONCLUSION: Guided DAPT de-escalation appears to be equally safe and effective in smokers and non-smokers. Regardless of smoking status and especially for those patients deemed unsuitable for 1 year of potent platelet inhibition this DAPT strategy might be used as an alternative antiplatelet treatment regimen.
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Orban et al. (2019) conducted an RCT in acute coronary syndrome (ACS) (n=2,610). Platelet function testing guided de-escalation of DAPT vs. Standard treatment with prasugrel was evaluated on cardiovascular death, myocardial infarction, stroke, or bleeding ≥ Grade 2 according to Bleeding Academic Research Consortium (BARC) criteria (HR 0.71, 95% CI 0.50-0.99, p=0.048). Guided DAPT de-escalation had no significant interaction with smoking status (Pint=0.23) for the primary endpoint, occurring in 7.9% vs 11.0% of non-smokers and 6.6% vs 6.6% of smokers.
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