Key result
Elevated Lipoprotein(a) levels were associated with higher MACE after PCI (HR 1.5; 95% CI 1.3-1.7), greater coronary anatomical complexity, and increased risk of restenosis.
Why the study?
The impact of lipoprotein(a) on coronary anatomy, plaque biology, and outcomes after PCI remained incompletely defined from an interventional perspective.
Do high Lp(a) levels increase coronary anatomical complexity, plaque vulnerability, and adverse outcomes after PCI compared to low Lp(a) levels?
Meta-Analysis (n=40,000)
Do high Lp(a) levels increase coronary anatomical complexity, plaque vulnerability, and adverse outcomes after PCI compared to low Lp(a) levels?
Hazard Ratio: 1.5 (95% CI 1.3–1.7)
Elevated Lp(a) is significantly associated with greater coronary anatomical complexity, vulnerable plaque phenotypes, and worse clinical and stent-related outcomes following PCI.
Background Lipoprotein(a) [Lp(a)] is a genetically determined cardiovascular risk factor. However, its impact on coronary anatomy, plaque biology, and outcomes after percutaneous coronary intervention (PCI) remains incompletely defined from an interventional perspective. Methods We performed a systematic review and random–effects meta–analysis of observational studies comparing high versus low Lp(a) levels in a pooled population of more than 40,000 patients. Prespecified outcomes included coronary anatomica! complexity (binary high SYNTAX, continuous SYNTAX, and Gensini score), major adverse cardiovascular events (MACE) after PCI, stent–related outcomes (in–stent and stent–edge restenosis, target vessel revascularization), and coronary plaque characteristics assessed by multimodality imaging (OCT, IVUS, CCTA). Pooled estimates were derived using random–effects models. Results Elevated Lp(a) was associated with greater coronary anatomica! complexity (pooled OR 1.5, 95% Cl 1.3– 1.6). High Lp(a) predicted worse post–PCI prognosis with higher MACE (pooled HR 1.5, 95% Cl 1.3– 1.7). From a procedura! perspective, elevated Lp(a) significantly increased in–stent and stent–edge restenosis (OR 3.2, 95% Cl 2.2– 4.8) and the need far target vessel revascularization (OR 2.6, 95% Cl 1.6–4 .4). Lp(a) was not associated with coronary calcific plaque but was significantly linked to vulnerable plaque phenotypes, including lipid–rich plaque and thin–cap fibroatheroma (high–risk plaque OR 2.1, 95% Cl 1.4– 3.1; TCFA OR 2.0, 95% Cl 1.3– 3.0). Conclusions Lp(a) bridges laboratory data and interventional decision–making, supporting a biologically infarmed approach that integrates anatomica! complexity, procedura! risk, and plaque vulnerability into PCI planning and fallow–up. These findings reinfarce the raie of Lp(a) as a key biomarker in advanced dyslipidemia and multimodality coronary imaging far personalized risk stratification.
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Cereda et al. (2026) conducted a meta-analysis in Cardiovascular disease requiring PCI (n=40,000). High Lipoprotein(a) levels vs. Low Lipoprotein(a) levels was evaluated on Major adverse cardiovascular events (MACE) after PCI (HR 1.5, 95% CI 1.3-1.7). Elevated Lipoprotein(a) levels were associated with higher MACE after PCI (HR 1.5; 95% CI 1.3-1.7), greater coronary anatomical complexity, and increased risk of restenosis.
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