TCT-260 Lipoprotein(a) and Endoluminal Disease Phenotype

Abstract

Background
Elevated lipoprotein(a) [Lp(a)] is associated with accelerated progression of coronary plaques, a high prevalence of thin-cap fibroatheroma, and an increased risk of spontaneous myocardial infarction; however, its impact on coronary artery disease (CAD) patterns is not fully defined. In this study, we sought to evaluate how elevated Lp(a) affects epicardial coronary flow and the endoluminal disease pattern (focal or diffuse).

Methods
This substudy of the ongoing PIONEER IV randomized controlled trial (NCT04923191) propensity-matched a cohort of patients with elevated Lp(a) (>0 mg/dL or 125 nmol/L) to control subjects based on traditional CAD risk factors. Epicardial flow velocity was quantified using quantitative flow ratio (QFR), with virtual QFR–pressure pullback gradient index (PPGi) characterizing the endoluminal phenotype. A QFR <0.80 indicated significant epicardial flow restriction.

Results
Lp(a) was elevated in 19% (n = 123/645) of patients. In 123 matched pairs, 77% (566/738) of vessels were suitable for QFR analysis. Significant flow limitation was more frequent in elevated Lp(a) vessels compared with matched controls (35% vs 21%; absolute risk difference: 14%; 95% CI: 6.9%-22.0%; P < 0.001) of a significantly more diffuse endoluminal disease phenotype (absolute difference, QFR-PPGi: −0.05; 95% CI: −0.08 to −0.03). Figure 1 shows the cumulative frequency distributions of QFR and QFR-PPGi values.

Conclusions
Elevated plasma levels of Lp(a) were associated with increased epicardial flow limitation and a diffuse endoluminal disease pattern.