SPC365

Lipoprotein(a) in Coronary Disease: the Clinical and Angiographic Impact

Session: Sessão de Posters 56 - Risco metabólico e lipoproteínas na doença coronária
Speaker: Joana Catarina Silva

Congress: CPC 2026
Topic: E. Coronary Artery Disease, Acute Coronary Syndromes, Acute Cardiac Care
Theme: 13. Acute Coronary Syndromes
Subtheme: 13.1 Acute Coronary Syndromes – Pathophysiology and Mechanisms
Session Type: Posters Eletrónicos
FP Number: ---
Authors: Joana Catarina Silva; Daniela Pinheiro; Francisco Rocha Cardoso; Ana Raquel Santos; Pedro Rio; Felipe Leao; Enf. Joana Pinto; Enf. Miguel Trindade; Enf Vania Martins; Enf Carlos Franco; Enf Rui Costa; Rui Cruz Ferreira

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Arial,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff"><strong>Background:</strong></span></span></span></span><br />
<span style="font-size:11pt"><span style="font-family:Arial,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff">Elevated lipoprotein(a) (Lp(a)) is recognized as an independent risk factor for atherosclerotic cardiovascular disease (</span></span></span></span><span style="font-size:11pt"><span style="font-family:Arial,sans-serif"><span style="color:#000000">ASCVD)</span></span></span><span style="font-size:11pt"><span style="font-family:Arial,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff">, yet its relationship with angiographic disease severity and functional capacity in patients with established coronary artery disease (CAD) remains uncertain. </span></span></span></span><span style="font-size:11pt"><span style="font-family:Arial,sans-serif"><span style="color:#000000">A 2020 study of 16,853 patients with coronary artery disease demonstrated a linear association between Lp(a) concentration and ASCVD risk.</span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Arial,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff"><strong>Objectives:</strong></span></span></span></span><br />
<span style="font-size:11pt"><span style="font-family:Arial,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff">To evaluate whether higher Lp(a) concentrations are associated with greater CAD burden&mdash;including number of diseased vessels, lesion distribution, chronic total occlusion (CTO), and troponin levels&mdash;and to determine whether this association differs by age. A secondary objective was to assess whether Lp(a) levels correlate with functional capacity, quantified by changes in six-minute walk distance (&Delta;6MWT) and oxygen consumption (&Delta;VO2).</span></span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Arial,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff"><strong>Methods:</strong></span></span></span></span><br />
<span style="font-size:11pt"><span style="font-family:Arial,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff">Clinical data from 204 patients undergoing evaluation&nbsp;were analyzed. Variables included Lp(a), age, angiographic findings (number of diseased vessels, CTO, left main and left anterior descending artery involvement), troponin, &Delta;6MWT, and &Delta;VO2. Lp(a) was classified as Minimal (&lt;62 nmol/L), Low (62&ndash;105 nmol/L), High (&gt;105 nmol/L), or Not Obtained. Statistical analyses included Pearson and Spearman correlations, Kruskal&ndash;Wallis tests, and multivariable logistic regression adjusting for age and &Delta;VO2.</span></span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Arial,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff"><strong>Results:</strong></span></span></span></span><br />
<span style="font-size:11pt"><span style="font-family:Arial,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff">Lp(a) demonstrated no significant association with angiographic severity based on number of diseased vessels, lesion distribution (left main/LAD involvement). Although the High Lp(a) group had a greater proportion of CTO cases (26.5%), the association was not statistically significant, and Lp(a) did not independently predict CTO in multivariable modeling (p=0.051). Lp(a) and age were independent. No relationship was observed between Lp(a) and &Delta;6MWT, while Lp(a) exhibited a modest linear association with &Delta;VO2 (p=0.035).</span></span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Arial,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff"><strong>Conclusions:</strong></span></span></span></span><br />
<span style="font-size:11pt"><span style="font-family:Arial,sans-serif"><span style="color:#000000"><span style="background-color:#ffffff">In this cohort of 204 patients with established CAD, higher Lp(a) levels were not associated with angiographic disease severity, CTO, or impaired functional improvement, and no age-dependent effect was observed. These findings underscore the need for larger, prospectively designed cohorts with complete Lp(a) profiling to more precisely characterize the clinical significance of Lp(a) in secondary prevention populations</span></span></span></span></p>