Key result
Initial heparin dose and activated clotting time levels were not associated with the 30-day composite of death, MI, or bleeding during PCI for acute myocardial infarction (HR 1.0; 95% CI 0.99-1.01).
Why the study?
An established dosage of heparin has not yet been determined for PCI in acute myocardial infarction, though treatment may be optimized through activated clotting time monitoring.
Does heparin dose or ACT level affect the composite outcome of death, MI, or bleeding in patients with MI undergoing PCI treated with potent P2Y12-inhibitors without planned GPI?
RCT
Open-label
Yes
Does heparin dose or ACT level affect the composite outcome of death, MI, or bleeding in patients with MI undergoing PCI treated with potent P2Y12-inhibitors without planned GPI?
Hazard Ratio: 1 (95% CI 0.99–1.01)
p-value: p=0.22
In patients with MI undergoing PCI on potent P2Y12 inhibitors without planned GPI, varying heparin doses or ACT levels did not significantly impact 30-day clinical outcomes, questioning the need for mandatory ACT monitoring.
No association seen between heparin dose/ACT and outcomes in MI PCI on potent P2Y12 inhibitors; leaves open whether ACT monitoring adds value.
AIMS: Heparin is the preferred choice of anticoagulant in percutaneous coronary intervention (PCI) for acute myocardial infarction (MI). An established dosage of heparin has not yet been determined, but treatment may be optimized through monitoring of activated clotting time (ACT). The aim of this study was to determine the relationship between heparin dose or ACT with a composite outcome of death, MI, or bleeding using data from the registry-based, randomized, controlled, and open-label VALIDATE-SWEDEHEART trial, although patients were not randomized to heparin dose in this substudy. METHODS AND RESULTS: Patients with MI undergoing PCI and receiving treatment with a potent P2Y12-inhibitor and anticoagulation with heparin, without the planned use of glycoprotein IIb/IIIa inhibitor (GPI), were enrolled in this substudy. The primary endpoint was a composite endpoint of death, MI, and bleeding at 30 days. The individual components and stent thrombosis were analysed separately. We divided patients into groups according to the initial dose of unfractionated heparin during PCI (<70 U/kg, 70-100 U/kg, and >100 U/kg) or ACT (ACT <250 s, 250-350 s, and >350 s) as well as investigating them as continuous variables in Cox proportional hazards models using univariable and multivariable analyses. No major differences were noted between heparin stratified in groups (P = 0.22) or heparin as a continuous variable in relation to the primary composite endpoint hazard ratio (HR) 1.0 confidence interval (CI) (0.99-1.01) for heparin dose/kg. No differences were found between ACT stratified in groups (P = 0.453) or ACT in seconds HR 1.0 CI (0.99-1.00) regarding the primary endpoint. The individual components of death, MI, major bleeding, and stent thrombosis were not significantly different across heparin doses or ACT levels either. CONCLUSION: We found no association between heparin dose or ACT levels and death, MI bleeding complications, or stent thrombosis. Therefore, there is no strong support for a specific heparin dose or mandatory ACT monitoring in patients treated with potent P2Y12-inhibitors with no planned GPI.
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Sharma et al. (2019) conducted an RCT in Acute myocardial infarction. Heparin dose or activated clotting time (ACT) vs. Different dose groups or continuous variables was evaluated on Composite of death, MI, and bleeding at 30 days (HR 1.0, 95% CI 0.99-1.01, p=0.22). Initial heparin dose and activated clotting time levels were not associated with the 30-day composite of death, MI, or bleeding during PCI for acute myocardial infarction (HR 1.0; 95% CI 0.99-1.01).
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