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CLINICAL STATEMENTS AND GUIDELINES Circulation. 2023;148:e9–e119. DOI: 10.1161/CIR.0000000000001168 August 29, 2023 Virani et al 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Chronic Coronary Disease Guideline Triglyceride levels ≥500 mg/dL should be treated pharmacologically to reduce the risk of pancreatitis. Drug-drug interactions with protease inhibitors can also occur with antiplatelet drugs like ticagrelor because of its CYP3A metabolism,23 which may increase the risk of bleeding. 3. Because lovastatin and simvastatin are metabo- lized by intestinal and liver CYP3A4, the concomitant use of protease inhibitors can increase levels of these statins and may increase the risk of rhabdomyolysis.6,7,24 4 Patients with rheumatoid arthritis and other auto- immune disease have residual inflammatory risk, beyond that conferred by traditional CVD risk factors. For patients with rheumatoid arthritis, disease-modifying antirheumatoid drugs such as methotrexate are associated with lower risk of cardiovascular events in observational studies.10 A single-center observational study found that use of biologic disease–modifying antirheumatoid drugs in patients with rheumatoid arthritis stabilized and decreased plaque as measured by CCTA.25 5 Janus kinase inhibitors, tumor necrosis factor inhibi- tors, and other immunomodulators for the treatment of autoimmune diseases (eg, rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and ulcerative colitis) may reduce cardiovascular events by reducing disease activity and inflammation.11,26,27 These treatments should be used in combination with intensive management of traditional risk factors (see Section 4.2.6, “Lipid Management,” Section 4.2.7, “Blood Pressure Management,” and Section 4.2.8, “Sodium Glucose Cotransporter 2 Inhibitors and Glucagon-Like Peptide-1 Receptor Agonists”). 6. Observational studies suggest that long-term use of higher doses of glucocorticoids (≥5 mg of prednisone) in patients with rheumatoid arthritis are associated with a higher risk of cardiovascular events.12 This association has not been described with the use of steroid-sparing agents11 or shorter duration use of steroids (<81 days in 6 months or cumulative doses of <751 mg in 6 months).12 Using short courses of glucocorticoids for autoimmune disease flares is unlikely to increase cardiovascular risk. 6.9 Cardiac Allograft Vasculopathy in Heart Transplant Recipients Recommendations for Management of Cardiac Allograft Vasculopathy in Heart Transplant Recipients Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations 1 C-LD 1. In patients with cardiac allograft vasculopathy, statins are recommended for secondary prevention to reduce MACE.1 2a C-LD 2. In patients with cardiac allograft vasculopathy, aspirin can be beneficial for secondary prevention to reduce MACE.2 2a C-LD 3 In patients with severe cardiac allograft vasculopathy, revascularization is reasonable in those with suitable anatomy to potentially mitigate the adverse long-term consequences of cardiac allograft vasculopathy.*3–6 *Modified from the 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization.7 Synopsis Post–heart transplant cardiac allograft vasculopathy is the leading cause of long-term mortality and retransplantation among heart transplant recipients.8 The incidence of cardiac allograft vasculopathy increases over time after heart transplant, developing in ∼30% of patients at 5 years and ∼50% of patients at 10 years.8 Coronary angiography is the accepted clinical standard for screening and diagnosis of cardiac allograft vasculopathy.3,9 Intravascular ultrasound is a useful adjunct to angiography and can improve detection of angiographically occult cardiac allograft vasculopathy.10 Lifestyle modifications and optimal control of cardiovascular risk factors are important for the primary and secondary prevention of cardiac allograft vasculopathy.3,11 In patients after heart transplant with or without established cardiac allograft vasculopathy, statins, aspirin, and high-intensity interval training delay cardiac allograft vasculopathy progression.1,2,12 In patients with cardiac allograft vasculopathy, PCI can be beneficial in those with severe, proximal, discrete lesions, and the use of second-generation DES is associated with decreased rates of in-stent restenosis.4-7 CABG is rarely used in highly selected patients with suitable anatomy, and retransplantation is reserved for patients with severe cardiac allograft vasculopathy not amenable to revascularization.3 In heart transplant recipients with established cardiac allograft vasculopathy, early substitution of mycophenolate mofetil, azathioprine, or calcineurin inhibitor with a proliferation signal inhibitor can slow cardiac allograft vasculopathy progression but is associated with an increased risk of grade ≥2R rejection.13–17 CR is addressed in Section 4.2.10. Recommendation-Specific Supportive Text 1 Multiple RCTs have shown decreased incidence of cardiac allograft vasculopathy with simvastatin or pravastatin initiated early after heart transplant.18,19 However, in patients with cardiac allograft vasculopathy, RCTs evaluating the safety and efficacy of statins for secondary prevention are lacking. In a retrospective observational study of 409 heart Recommendations for Management of Cardiac Allograft Vasculopathy in Heart Transplant Recipients (Continued ) COR LOE Recommendations Downloaded from http://ahajournals.org by on October 7, 2026