Near-universal combined oral LLT with ezetimibe and selective PCSK9 inhibitors enabled optimal LDL-C control (<55 mg/dL) in 84.9% of post-MI patients by Phase 2 CRP end.
Does lipid-lowering therapy optimization during a cardiac rehabilitation program improve the achievement of target LDL-C (<55mg/dL) in patients after myocardial infarction?
Proactive lipid-lowering therapy optimization during cardiac rehabilitation, including high rates of ezetimibe and selective PCSK9i use, enables the vast majority of post-MI patients to achieve strict LDL-C targets.
Absolute Event Rate: 0% vs 0%
Abstract Background Lipid control is one of the main secondary prevention goals after myocardial infarction (MI). Cardiac Rehabilitation Programs (CRP) can improve low-density lipoprotein cholesterol (LDL-C) through exercise interventions and lipid-lowering therapy (LLT) optimization. Purpose We aim to analyse, within our local CRP after MI, LDL-C control and the organizational and pharmacotherapeutic strategies that facilitate this goal. Methods Patients with MI between November 2021 and April 2024 who completed our Phase 2 CRP were included in a prospective registry. We recorded basal LDL-C before MI, corrected for LLT if any, as well as LDL-C during admission. Lipid testing was performed at least 4 to 6 weeks after discharge and at the end of Phase 2 CRP. LLT optimization and subsequent lipid testing were performed sequentially to reach target LDL-C (55mg/dL). LLT was documented at discharge and at the end of Phase 2 CRP, and theoretical models accounting for LLT efficacy were computed. Results Our cohort comprised 166 patients. The mean age was 62.86±11.13 years, most patients were male (n=138, 83.1%), and hypercholesterolemia was the most prevalent cardiovascular risk factor (n=156, 94%). Basal LDL-C levels were 162.79±45.23mg/dL, significantly higher than LDL-C levels during admission (100.12±36.42mg/dL, p0.001). LLT at discharge mainly consisted of high-intensity statin monotherapy or combination therapy with ezetimibe (n=89, 53.6%), which resulted in LDL-C levels of 59.88±22.68mg/dL 4-6 weeks after discharge (with 46.4% achieving LDL-C 55mg/dL). Considering LDL-C levels during admission, most patients (86.1%) should be expected to achieve LDL-C 55mg/dL with LLT prescribed at discharge (mean 41.68±18.42mg/dL), but the theoretical model accounting for basal LDL-C correlated more accurately with observed LDL-C 4-6 weeks after discharge (mean 66.47±22.49mg/dL, with 30.7% expected to achieve LDL-C 55mg/dL). Up-titration of statin therapy, near-universal combination with ezetimibe (n=151, 91%), and selective use of advanced therapies such as pro-protein convertase subtilisin kexin-9 inhibitors (PCSK9i, n=26, 15.7%) allowed for optimal LDL-C in 141 (84.9%) patients at the end of Phase 2 CRP. Conclusion LLT at discharge, likely prescribed based on LDL-C during admission, proved insufficient for early LDL-C control in more than half of our post-MI cohort. Near-universal combined oral LLT, mainly with ezetimibe, and selective use of parenteral LLT, mainly with PCSK9i, allowed for optimal LDL-C control in most patients after Phase 2 CRP. Careful revision or estimation of basal LDL-C levels, along with proactive follow-up and LLT up-titration, may help optimize lipid control after MI.LDL-C during CRP after MI. LDL-C 4 to 6 weeks after MI.
Garces et al. (Sat,) reported a other. Near-universal combined oral LLT with ezetimibe and selective PCSK9 inhibitors enabled optimal LDL-C control (<55 mg/dL) in 84.9% of post-MI patients by Phase 2 CRP end.