Multidimensional lipid and inflammatory risk control following evolocumab treatment in real-world ASCVD: a hospital-based cohort study.

Background: Evolocumab lowers low-density lipoprotein cholesterol (LDL-C) and reduces cardiovascular events in patients with established atherosclerotic cardiovascular disease (ASCVD). In routine care, however, the LDL-C course is observed through irregular laboratory testing, changing background therapy, and variable follow-up. We examined lipid response, inflammatory risk control, post-index laboratory abnormalities, and exploratory risk-index outcomes after evolocumab initiation in a hospital-based ASCVD cohort. Methods: This retrospective real-world cohort used routine hospital data from ASCVD patients with recorded evolocumab exposure. Patients were classified into documented statin and no documented statin groups according to whether concomitant statin therapy was recorded in available hospital medication records during the pre-index 30-day window. Baseline lipids were defined as the patient-level median of traceable pre-index hospital laboratory measurements. The primary lipid follow-up period was 30-120 days; later periods were 121-365 days and beyond 365 days. The primary endpoint was percentage change in LDL-C at 30-120 days. LDL-C goal attainment, LDL-C reduction ≥ 50%, other lipid markers, C-reactive protein-triglyceride glucose index (CTI), inflammatory markers, longer-term LDL-C patterns, and post-index laboratory abnormalities were analyzed as secondary or exploratory outcomes. Between-group comparisons used propensity-score overlap weighting with bootstrap confidence intervals and were interpreted as adjusted observational associations. Results: Of 250 patients with recorded evolocumab exposure, 183 were included in the main analysis cohort: 137 in the documented statin group and 46 in the no documented statin group. Median LDL-C fell from 2.85 to 1.08 mmol/L, a median reduction of 63.3%. LDL-C <1.4 mmol/L was achieved in 82/117 patients (70.1%), and LDL-C reduction ≥ 50% was achieved in 81/117 patients (69.2%). In the endpoint-specific core clinical propensity model, LDL-C percentage reduction favored the documented statin group (weighted difference, -10.34 percentage points [95% CI, -20.85 to -0.045]; P = 0.048); the expanded lipid-adjusted sensitivity model remained directionally consistent but crossed the null. In the predefined exploratory CTI analysis, hsCRP-TyG Delta CTI favored the documented statin group (adjusted difference, -0.423 [95% CI, -0.749 to -0.097]; P = 0.011), whereas CRP-TyG pointed in the same direction without reaching statistical significance (-0.247 [95% CI, -0.564 to 0.071]; P = 0.128). Dual-target control was achieved in 55/131 patients (42.0%) and was more frequent in the documented statin group. Conclusion: In this hospital-based real-world ASCVD cohort, evolocumab was associated with marked LDL-C lowering in routine care. A broader pattern of lipid and exploratory residual-risk marker improvement was observed in patients with documented concomitant statin therapy. These findings are consistent with guideline-recommended lipid management, although the between-group results should be interpreted as adjusted observational associations rather than causal relationships.