Key result
Achieving LDL-C <55 mg/dL post-PCI is linked to ~56% lower MACE in ACS versus CCS.
Why the study?
Current guidelines recommend the same LDL-C goals for both ACS and CCS despite ACS having greater risks of recurrent atherosclerotic cardiovascular disease, necessitating evaluation of cardiovascular outcomes by LDL-C control in these populations.
Does achieving lower LDL-C levels (<55 mg/dL) after PCI reduce MACE differently in patients with ACS compared to CCS?
Observational (n=2,560)
Yes
Does achieving lower LDL-C levels (<55 mg/dL) after PCI reduce MACE differently in patients with ACS compared to CCS?
Achieving stricter LDL-C goals (<55 mg/dL) after PCI provides substantially greater absolute risk reduction for MACE in ACS patients compared to CCS patients, challenging current guidelines that advocate identical goals.
BACKGROUND: Acute coronary syndrome (ACS) exhibits greater risks of recurrent atherosclerotic cardiovascular disease compared to chronic coronary syndrome (CCS), suggesting the need for more intensified preventive management, including low-density lipoprotein cholesterol (LDL-C) control. However, current guidelines advocate the "same" LDL-C goals in both ACS and CCS. OBJECTIVES: The authors aimed to compare cardiovascular outcomes following attainment of guideline-recommended LDL-C control between ACS and CCS. METHODS: This multicenter retrospective observational study (ACTION-LDLC; jRCT 1050260064) analyzed 2,560 Japanese patients with coronary artery disease (ACS/CCS = 1,682/878). Risk of major adverse cardiovascular events (MACE; cardiac-caused death + nonfatal MI + coronary revascularization in nonculprit segments) was compared according to achieved LDL-C levels 8 weeks after percutaneous coronary intervention (<55, 55-69 and ≥70 mg/dL) in ACS and CCS, respectively. RESULTS: LDL-C <55 mg/dL was achieved in 29.4% and 32.5% of patients with ACS and CCS, respectively (P = 0.124). During the 3.7- and 3.8-year observation, achieving lower LDL-C levels was associated with reduced MACE risks in ACS (P < 0.001) and CCS (P = 0.040). Notably, lower standardized 3-year MACE rates (ACS = 4.4%, CCS = 9.9%, P < 0.001) and greater absolute risk differences (from ≥70 to <55 mg/dL: ACS = -26.5%, CCS = -5.3%, P < 0.001; from 55-69 to <55 mg/dL: ACS = -11.5%, CCS = -1.1%, P < 0.001) following achieved LDL-C <55 mg/dL were observed in ACS compared to CCS. Furthermore, in patients with achieved LDL-C <55 mg/dL (n = 780), an even lower risk of standardized 3-year MACE existed in ACS patients achieving LDL-C <40 mg/dL (log-rank P = 0.017). In contrast, in those who did not achieve LDL-C <70 mg/dL, risks of standardized 3-year MACE substantially increased in ACS compared to CCS (30.9% vs 15.2%, P < 0.001). CONCLUSIONS: Distinct cardiovascular risks with LDL-C control exist in ACS compared to CCS, suggesting the potential importance of achieving stricter LDL-C goals in ACS patients.
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Kataoka et al. (2026) conducted an observational in Coronary artery disease (ACS and CCS) (n=2,560). Achieved LDL-C <55 mg/dL vs. Achieved LDL-C ≥70 mg/dL and CCS patients was evaluated on Major adverse cardiovascular events (cardiac-caused death, nonfatal MI, coronary revascularization in nonculprit segments) (p=<0.001). Achieving LDL-C <55 mg/dL after PCI yielded a lower 3-year MACE rate in ACS than in CCS (4.4% vs 9.9%, P<0.001) and a greater absolute risk reduction compared to levels ≥70 mg/dL (-26.5% vs -5.3%).
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