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CLINICAL STATEMENTS AND GUIDELINES Circulation. 2025;151:e771–e862. DOI: 10.1161/CIR.0000000000001309 April 1, 2025 e831 them the opportunity to ask questions and review potential barriers. For the management of lipidlowering therapy initiated prior to discharge and continued after hospital discharge, refer to Section 4.5, “Lipid Management.” 11.3 SGLT-2 Inhibitors and GLP-1 Receptor Agonists Synopsis The cardiovascular benefits of both sodium glucose cotransporter-2 (SGLT-2) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists are well documented in stable patients with ASCVD and type 2 diabetes,1–6 as well as in patients with HF regardless of diabetes status.7–11 GLP-1 receptor agonists may lead to weight loss in many patients, and semaglutide has been shown to reduce the risk of MACE in overweight or obese patients with stable ASCVD but has not been studied early after ACS.12 SGLT-2 inhibitors may increase the risk of urinary tract infection, genital mycotic infection, hypovolemia, and acute kidney injury (while offering longer term renal benefit in patients with diabetes). Due to a higher risk of diabetic and euglycemic ketoacidosis in the perioperative period, canagliflozin, dapagliflozin, and empagliflozin should be stopped ≥3 days and ertugliflozin ≥4 days prior to scheduled surgery, including CABG.13–15 The efficacy and safety of SGLT-2 inhibitors have now been studied in 2 large trials of patients after MI. In patients without diabetes or HF, dapagliflozin was not shown to reduce the risk of cardiovascular death or HF hospitalization in patients with AMI and impaired LV systolic function.16 Similarly, empagliflozin did not significantly reduce all-cause death or first HF hospitalization in patients without prior HF who were hospitalized with AMI and found to have impaired LV systolic function with or without signs of congestion. However, empagliflozin did reduce HF hospitalizations in this population.17 No new safety concerns were identified. Therefore, use of an SGLT-2 inhibitor does not need to be deferred in patients with an indication for its use at hospital discharge. 11.4 Use of Chronic Colchicine Recommendation for Use of Chronic Colchicine Referenced studies that support recommendation are summarized in the Evidence Table. COR LOE Recommendation 2b B-R 1. In patients after ACS, low-dose colchicine may be reasonable to reduce risk of MACE.1–5 Synopsis Colchicine is a botanical-derived anti-inflammatory agent that has been used for millennia in the treatment of gout. Colchicine reduces neutrophil adhesion to endothelial cells and platelets and has been shown to reduce highsensitivity C-reactive protein concentration and low-attenuation plaque volume in patients already on aspirin and statin therapy.6–9 Colchicine is associated with a lower risk of MI in patients with gout, as well as in patients with CAD, including those with prior MI.1,4,5,10,11 Although gastrointestinal events were historically reported at a higher rate in patients on colchicine, this rate does not differ from placebo at the lower once daily dosing.5 A meta-analysis of the studies examining colchicine in patients with CAD reported no difference in all-cause death with colchicine versus placebo, but a nonsignificant trend was observed toward an increased risk of noncardiovascular death that requires further study.5 To date, no potential pathogeneses of the noncardiovascular deaths have been consistently shown to explain the numerical differences in noncardiovascular death.5 Recommendation-Specific Supportive Text 1 COLCOT (Colchicine Cardiovascular Outcomes Trial) randomized patients ≤30 days (median, 14 days) after MI to low-dose colchicine versus placebo.2 Colchicine reduced the primary outcome of cardiovascular death, resuscitated cardiac arrest, MI, stroke, or urgent coronary revascularization by 32% (median follow-up, 22.6 months). Although directional consistency was seen across individual components, this benefit was driven by a reduction in hospitalizations for angina requiring revascularization and stroke. The smaller COPS (Colchicine in Patients With ACS) study randomized patients during their index hospitalization of ACS to colchicine versus placebo.3 The primary endpoint of all-cause death, ACS, unplanned ischemia-driven urgent revascularization, and noncardioembolic ischemic stroke was numerically, but not significantly, lower for patients on colchicine (P =0.09). Although deaths were infrequent, more deaths occurred for patients on colchicine than on placebo (8 versus 1; P =0.017) due to more noncardiovascular deaths. In a post hoc analysis, the composite outcome of cardiovascular death, ACS, stroke, or urgent revascularization was lower for colchicine than placebo. The LoDoCo2 (Low-Dose Colchicine-2) trial enrolled patients with stable (>6 months) coronary disease, demonstrating a reduction in the composite of cardiovascular death, MI, ischemic stroke, or ischemia-driven coronary revascularization with colchicine (median follow-up, 28.6 months); findings were consistent in the 84% of patients with prior ACS.4,12 Pooled data from these large trials confirmed a reduction in the incidence of MACE with colchicine versus placebo.5 Colchicine should not be administered in patients with blood Downloaded from http://ahajournals.org by on October 7, 2026