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CLINICAL STATEMENTS AND GUIDELINES April 1, 2025 Circulation. 2025;151:e771–e862. DOI: 10.1161/CIR.0000000000001309 e830 (ie, prasugrel and ticagrelor) excluded patients requiring long-term anticoagulation; therefore, clopidogrel is generally favored as the P2Y12 inhibitor in this setting for most patients. The decision whether to continue anticoagulant with or without antiplatelet therapy >12 months after ACS is addressed in the “2023 AHA/ACC/ACCP/ ASPC/NLA/PCNA Guideline for the Management of Patients with Chronic Coronary Disease.”8 Recommendation-Specific Supportive Text 1 Several RCTs have demonstrated that the dis- continuation of aspirin 1 to 4 weeks after PCI reduces the risk of bleeding in patients with AF with an indication for DAPT and an oral anticoagulant.1–5 Although individual studies were not powered for ischemic endpoints, meta-analyses across randomized trials suggest no difference in mortality, stroke, and overall MACE when aspirin is discontinued for patients on an oral anticoagulant, albeit with a marginal apparent increase in MI and stent thrombosis.9–14 An analysis of stent thrombosis rates suggested that 80% of events occurred within 30 days of PCI, with stent thrombosis events numerically less frequent in those receiving aspirin (randomization was approximately 1 week after PCI) compared with placebo in the AUGUSTUS (Antithrombotic Therapy After Acute Coronary Syndrome or PCI in Atrial Fibrillation) trial.15,16 Therefore, in patients with a high risk of stent thrombosis, aspirin for up to 30 days after PCI could be considered. P2Y12 inhibitor therapy should be continued for at least 12 months after PCI following aspirin discontinuation but could be discontinued earlier in those with multiple risk factors for bleeding.17,18 11.2 Reassessment of Lipid Levels Postdischarge Recommendation for Reassessment of Lipid Levels Postdischarge COR LOE Recommendation 1 C-LD 1 In patients after ACS, a fasting lipid panel is recommended 4 to 8 weeks after initiation or dose adjustment of lipid-lowering therapy to assess response or adherence to therapy.*1,2 *Modified from the “2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/ AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol.”3 Synopsis Aggressive LDL-C lowering is an important component of secondary CVD prevention. For every 1.0-mmol/L (∼39 mg/dL) reduction of LDL-C, an approximate 22% relative reduction in cardiovascular events is observed over a period of 4 to 5 years.2 Despite the growing number of lipid- lowering therapies currently available, many patients with ACS do not achieve target LDL-C levels.4,5 The reasons are varied but include underprescribing by providers, cost or insufficient coverage by medical insurance companies, and intolerance to therapies. Many patients are also unwilling or unable to readily fill prescriptions at pharmacies or patients self-discontinue therapy early. Providers are not always aware of the barriers that patients may be experiencing; therefore, a conversation between clinician and patient is important to help improve adherence. If adverse effects are experienced, consideration should be given to subsequent rechallenge at each visit or changing to a different type of statin or class of lipid-lowering therapy. Statin intolerance requires exposure to at least 2 different statins with 1 prescribed at the lowest available dose. Because risk of MACE is elevated in the early months after ACS, early follow-up visits are important for making appropriate changes to lipid-lowering therapy to help achieve desired LDL-C targets (Section 4.5, “Lipid Management”). Importantly, lipid-lowering therapies should not be downtitrated in response to very low LDL-C concentrations, because current evidence supports that those with very low LDL-C concentrations are at lowest risk of MACE without any clear safety concern.6–9 Recommendation-Specific Supportive Text 1 Use of high-potency statin therapy has been shown to reduce MACE with the benefit appearing early after ACS and persisting with time.10 To date, evidence suggests the benefit of lowering LDL-C concentrations may be irrespective of whether it is achieved through high-potency statins or other lipid-lowering therapies; however, the largest body of evidence exists with statin therapies. As such, early intensification of lipid-lowering therapy after ACS is justified. In clinical practice, statin-eligible patients remain undertreated or untreated.1,11 Early and frequent follow-up, including lipid testing, is associated with improved adherence to lipid-lowering therapies.1 In the PALM (Provider Assessment of Lipid Management) registry, less than one-half of adults were on the statin intensity recommended by the guidelines.12 In a study of US veterans with a history of ACS or coronary revascularization, less than one-half of patients received intensification of lipid-lowering therapy (41.9% at 3 months versus 47.3% at 1-year postdischarge).5 High patient copays and poor coverage of newer lipid-lowering therapies by some prescription plans are factors contributing to suboptimal LDL target attainment. To that end, out-of-pocket costs should be verified and discussed with patients before they fill a prescription for a new lipid-lowering therapy. Education about the importance of lipid-lowering therapies should be discussed with patients at visits to allow Downloaded from http://ahajournals.org by on October 7, 2026