The art of delivering evidence-based dual antiplatelet therapy
This review, which details 2 DAPT risk scoring systems and includes a treatment guide, can help ensure that you deliver the right treatment to the right patients.
PRACTICE RECOMMENDATIONS
› Use a dual antiplatelet therapy (DAPT) risk calculator to encourage patient-centric decisions when presenting information to the health care team and the patient. B
› Consider the potential benefit of a shorter duration of DAPT for patients who 1) have prior bleeding complications or 2) are taking an oral anticoagulant, chronic corticosteroid, or nonsteroidal anti-inflammatory drug. B
› Continue aspirin use upon completion of DAPT or if a P2Y12 inhibitor is being held for surgery. A
› Reduce the risk of recurrent stroke in patients who have had a mild ischemic stroke or transient ischemic attack by providing DAPT for 21 to 28 days, followed by aspirin indefinitely—so long as treatment can begin within 24 hours of the event. B
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
ASA, as a component of DAPT, is recommended at a dosage of 81 mg/d. In trials of ASA plus clopidogrel, lower ASA dosages had comparable ischemic event rates compared to higher ASA dosages.6,7 Patients given higher ASA dosages with ticagrelor had poorer outcomes when compared with low-dosage ASA.8 Higher dosages of ASA, alone or with DAPT, increase the risk of bleeding complications.9,10
Clopidogrel is the only P2Y12 inhibitor available as a generic medication in the United States. As a pro-drug, clopidogrel requires 2 metabolic transformations to its active metabolite after being hydrolyzed in the gut, which delays onset of platelet inhibition for several hours after ingestion.11 Furthermore, individual genetic variation in cytochrome P450 (CYP) 2C19 (CYP2C19), one of the hepatic enzymes in this metabolic process, may lead to less alteration of clinical platelet aggregation response, and increased drug interactions.12 Methods to assess platelet function have shown decreased inhibition of platelet aggregation for some CYP2C19 polymorphisms, although consistent clinical effects of this inhibition have not been identified to date; genetic testing for these polymorphisms is, therefore, not recommended routinely.13
Indications for DAPT treatment with clopidogrel are unstable angina or non-ST-segment elevation acute coronary syndrome (NSTE-ACS), whether planned treatment is medical or coronary revascularization. Other indications include acute ST-segment elevation MI (STEMI) with planned medical treatment, and recent MI, stroke, or established peripheral arterial disease.13,14
Prasugrel has faster onset of action and greater and more consistent P2Y12 inhibition than clopidogrel. After prasugrel is hydrolyzed in the gut, an intermediary metabolite is activated in the liver. Peak serum concentration is reached within 30 minutes.12 Unlike the case with clopidogrel, genetic variation in the CYP gene does not impart significant impact on forming the active metabolite.15
Indication for the use of prasugrel is ACS that is managed with percutaneous coronary intervention (PCI). Dual antiplatelet therapy with prasugrel results in reduced risk of cardiovascular death, nonfatal MI, and stroke, compared with ASA plus clopidogrel, with an increase in bleeding events.16 Thrombolysis patients and those who have a history of stroke had a greater risk of hemorrhage complications with prasugrel treatment, compared with clopidogrel. Prasugrel offered no benefit to patients older than 75 years or those who weigh <60 kg. If used in patients who weigh <60 kg, however, dosage reduction is recommended.16
Continue to: Ticagrelor
