EUR HEART J-CARD PHA: Results of antiplater board therapy in patients with smoking and acute coronary artery syndrome

Previous studies have revealed differences in antiplatet drug reactions and clinical outcomes between smokers and nonsmoleors, so the safety and effectiveness of any dual antiplate plateboard therapy (DAPT) downgrade strategy may be related to smoking status.
, this study assessed the clinical outcomes of smoking in patients with acute coronary syndrome (ACS) and the effects of adenosine phosphate induced plate plateboard aggregation.
multi-center tropical-ACS trial grouped 2,610 biomarker-positive ACS patients at a 1:1 scale and under the guidance of Pragre standard treatment for 12 months (control group) or platea function testing.
current smokers (n s 1182) showed comparability of event rates between the study groups . . . 6.6% vs. 6.6%; Risk ratio (HR) 1.0, 95% confidence interval (CI) 0.64-1.56, P .gt; 0.99.
in non-smokers (n s 1428), the lead DAPT downgrade was compared to the control group (7.9% to 11.0%; HR 0.71, 95% CI 0.50-0.99, P = 0.048)。
this is mainly due ≥ of BARC and level 2 bleeding rate (5.2% vs. 7.7%; HR 0.68, 95% CI 0.45-1.03, P = 0.066)。
no significant interaction between smoking status and the effect of leading DAPT downgrading therapy (Pint s 0.23).
adenosine diphosphate-induced plateboard aggregation value is higher than that of smokers (average 28 U, quarter range (IQR: 20 - 40)) and non-smoking (average 24 UIQR (16-25), P slt; 0.0001), control group and smokers (average 42 U, IQR (27 - 68)) and non-smoking (median 37 U, IQR (25-55), monitoring group P .lt; 0.001).
that guiding DAPT downgrades appears to be just as safe and effective for smokers and nonsmoists.
whether or not you smoke, especially in patients who are not considered suitable for 1 year of strong plateplate suppression, DAPT strategies may be used as an alternative to antiplate plateplate therapy.
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