The Influence of Low (81 mg) Versus High (325 mg) Doses of ASA
The Influence of Low (81 mg) Versus High (325 mg) Doses of ASA
Background: Conflicting opinion exists regarding the optimal dose of acetyl salicylic acid (ASA) to be given after percutaneous coronary intervention (PCI) with drug-eluting stents (DES). We sought to evaluate the influence of ASA dose on the incidence of unexplained subacute and late stent thrombosis in the era of DES.
Methods: We performed a retrospective analysis of the incidence of subacute and late stent thrombosis in our patient population over a 2-year period. The analysis was limited to patients being discharged and maintained on a daily ASA dose of either 81 mg or 325 mg and having received at least 1 sirolimus-eluting stent.
Results: During the study period, 1,093 patients (1,807 separate PCI procedures) met the inclusion criteria. The incidence of unexplained subacute and late stent thrombosis was 1.1% in the study population (12 out of 1,093 patients). When considering the total number of individual procedures performed on the study population during the study period (1,807 procedures), the incidence of unexplained subacute or late stent thrombosis was 0.7%. Six were subacute and 6 were late thrombosis. No significant difference was observed in the incidence of stent thrombosis between the 2 ASA dose groups. Seven patients had stent thrombosis in the 81 mg group (1.2% of 583 patients), while 5 had thrombosis in the 325 mg group (1% of 510 patients); p = 0.727.
Conclusion: In conclusion, we found no significant difference in the incidence of unexplained subacute or late stent thrombosis with the use of an 81 mg versus 325 mg dose of aspirin post-PCI with sirolimus-eluting stents.
Conflicting opinions exist regarding the optimal dose of acetyl salicylic acid (ASA) to be given after percutaneous coronary intervention (PCI) with drug-eluting stents (DES). The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy suggested a daily dose of 75-100 mg of ASA with concomitant clopidogrel, without differentiating between bare-metal and DES. Recent PCI guidelines state that patients without ASA allergy, resistance or increased risk of bleeding should receive a daily dose of 325 mg for 3 to 6 months depending on the type of DES implanted. However, higher doses of ASA in combination with clopidogrel are proven to increase the risk of bleeding. Hence, despite the recent PCI guidelines, the optimal dose of ASA at the time of discharge is still a matter of debate. ASA is rapidly absorbed after ingestion, with platelet inhibition occurring within 30-40 minutes and lasting for the lifespan of the platelet (7-10 days). Low-dose ASA (75-100 mg/day) is sufficient for providing maintenance of chronic platelet inhibition by suppression of thromboxane A2 (TXA2) production. Since ASA does not prevent restenosis, its clinical benefits are derived in the prevention of stent thrombosis and long-term secondary prevention of cardiovascular events. Low-dose ASA has been proven efficacious in this latter regard, and it is thus the regimen of choice for long-term use. From a pharmacodynamic point of view, no reason exists to believe that a higher dose of ASA is necessary to confer sufficient antiplatelet effect after implantation of a DES. The purpose of the current study is to evaluate the influence of ASA dose on the incidence of unexplained subacute and late stent thrombosis in the era of DES.
Abstract and Introduction
Abstract
Background: Conflicting opinion exists regarding the optimal dose of acetyl salicylic acid (ASA) to be given after percutaneous coronary intervention (PCI) with drug-eluting stents (DES). We sought to evaluate the influence of ASA dose on the incidence of unexplained subacute and late stent thrombosis in the era of DES.
Methods: We performed a retrospective analysis of the incidence of subacute and late stent thrombosis in our patient population over a 2-year period. The analysis was limited to patients being discharged and maintained on a daily ASA dose of either 81 mg or 325 mg and having received at least 1 sirolimus-eluting stent.
Results: During the study period, 1,093 patients (1,807 separate PCI procedures) met the inclusion criteria. The incidence of unexplained subacute and late stent thrombosis was 1.1% in the study population (12 out of 1,093 patients). When considering the total number of individual procedures performed on the study population during the study period (1,807 procedures), the incidence of unexplained subacute or late stent thrombosis was 0.7%. Six were subacute and 6 were late thrombosis. No significant difference was observed in the incidence of stent thrombosis between the 2 ASA dose groups. Seven patients had stent thrombosis in the 81 mg group (1.2% of 583 patients), while 5 had thrombosis in the 325 mg group (1% of 510 patients); p = 0.727.
Conclusion: In conclusion, we found no significant difference in the incidence of unexplained subacute or late stent thrombosis with the use of an 81 mg versus 325 mg dose of aspirin post-PCI with sirolimus-eluting stents.
Introduction
Conflicting opinions exist regarding the optimal dose of acetyl salicylic acid (ASA) to be given after percutaneous coronary intervention (PCI) with drug-eluting stents (DES). The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy suggested a daily dose of 75-100 mg of ASA with concomitant clopidogrel, without differentiating between bare-metal and DES. Recent PCI guidelines state that patients without ASA allergy, resistance or increased risk of bleeding should receive a daily dose of 325 mg for 3 to 6 months depending on the type of DES implanted. However, higher doses of ASA in combination with clopidogrel are proven to increase the risk of bleeding. Hence, despite the recent PCI guidelines, the optimal dose of ASA at the time of discharge is still a matter of debate. ASA is rapidly absorbed after ingestion, with platelet inhibition occurring within 30-40 minutes and lasting for the lifespan of the platelet (7-10 days). Low-dose ASA (75-100 mg/day) is sufficient for providing maintenance of chronic platelet inhibition by suppression of thromboxane A2 (TXA2) production. Since ASA does not prevent restenosis, its clinical benefits are derived in the prevention of stent thrombosis and long-term secondary prevention of cardiovascular events. Low-dose ASA has been proven efficacious in this latter regard, and it is thus the regimen of choice for long-term use. From a pharmacodynamic point of view, no reason exists to believe that a higher dose of ASA is necessary to confer sufficient antiplatelet effect after implantation of a DES. The purpose of the current study is to evaluate the influence of ASA dose on the incidence of unexplained subacute and late stent thrombosis in the era of DES.
Source...