Temporal remodeling of atherosclerotic lipoprotein profiles and inflammatory markers after percutaneous coronary intervention: a real-world longitudinal study.

BACKGROUND

Patients who undergo percutaneous coronary intervention (PCI) remain exposed to residual lipid and inflammatory risk despite contemporary secondary prevention. Real-world longitudinal data describing how conventional lipids, apolipoproteins, small dense low-density lipoprotein (sdLDL), lipoprotein(a) [Lp(a)], and C-reactive protein (CRP) remodel together after PCI are limited. We evaluated serial post-PCI changes in a broad atherosclerotic biomarker panel and explored the dissociation between cholesterol control and inflammatory control.

METHODS

We performed a retrospective longitudinal study using a clinical laboratory dataset. Adults with at least one PCI-coded encounter and serial laboratory follow-up were included. The index date was defined as the first PCI-coded visit. Angiography-only patients without PCI were excluded. Biomarkers included triglycerides, total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB), Lp(a), apolipoprotein E (ApoE), sdLDL, free fatty acids, glycation, and CRP. Paired baseline-to-latest comparisons were performed in 397 patients. The prespecified primary endpoint was the paired change in LDL-C from index PCI to latest follow-up. Secondary endpoints included paired changes in other lipid and inflammatory biomarkers. Longitudinal associations across follow-up windows were explored using generalized estimating equations adjusted for age, sex, body mass index, diabetes, hypertension, smoking, baseline statin intensity, and time-updated lipid-lowering regimen category.

RESULTS

Among 1082 encounters from 526 individuals, 397 patients with PCI contributed 813 observations from index onward. Mean age was 62.0 ± 10.3 years, 77.8% were men, 69.5% had hypertension, and 35.0% had diabetes. Median follow-up was 393 days. Compared with index PCI, latest follow-up showed lower LDL-C (2.42 to 1.63 mmol/L; mean change - 0.79, 95% confidence interval [CI] -0.90 to -0.68; p < 0.001), non-HDL-C (3.07 to 2.11 mmol/L; mean change - 0.96, 95% CI -1.09 to -0.83; p < 0.001), ApoB (0.82 to 0.63 g/L; mean change - 0.19, 95% CI -0.22 to -0.16; p < 0.001), ApoB/ApoA1 ratio (0.74 to 0.59; p < 0.001), and CRP (4.94 to 2.71 mg/L; mean change - 2.23, 95% CI -3.36 to -1.09; p < 0.001). HDL-C rose modestly (1.07 to 1.11 mmol/L; p < 0.001). Lp(a), sdLDL, triglycerides, free fatty acids, and glycation changed little in paired analyses. In adjusted longitudinal models, lower LDL-C, ApoB, non-HDL-C, and log (CRP) persisted through 1 year, 1-2 years, and > 2 years, whereas Lp(a) showed little overall change, with only a modest decrease in the 1-2-year window. In expanded multivariable analyses, combination or PCSK9-containing regimen at latest follow-up was independently associated with dual attainment of LDL-C < 1.4 mmol/L and CRP < 2 mg/L at latest follow-up. The proportion with both high LDL-C and high CRP fell from 42.3% at index to 15.4% at follow-up, but isolated residual inflammatory risk rose from 6.0% to 11.8%.

CONCLUSION

After PCI, real-world biomarker remodeling was characterized by durable reductions in LDL-C, ApoB, non-HDL-C, and CRP, but incomplete convergence of cholesterol-related and inflammatory biomarker profiles. Lp(a) and several nontraditional lipid measures appeared relatively resistant to routine care pathways. Because conventional CRP rather than hsCRP was available and no adjudicated clinical outcome data were available, the translational relevance of these findings is limited and they should be interpreted cautiously as biomarker-level and hypothesis-generating observations.