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Lipoprotein(a) and Type 2 Diabetes: Findings in Acute Myocardial Infarction
Session:
Sessão de Posters 56 - Risco metabólico e lipoproteínas na doença coronária
Speaker:
David Matos
Congress:
CPC 2026
Topic:
E. Coronary Artery Disease, Acute Coronary Syndromes, Acute Cardiac Care
Theme:
13. Acute Coronary Syndromes
Subtheme:
13.6 Acute Coronary Syndromes - Clinical
Session Type:
Posters Eletrónicos
FP Number:
---
Authors:
David Matos Monteiro; Sofia Martinho; Ana Rita Ramalho; Mariana Salvador; Pedro Miguel Ventura; Tiago Garcia; Lino Gonçalves
Abstract
<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:"Times New Roman",serif"><strong><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">Introduction:</span></span></strong><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif"> Lipoprotein(a) [Lp(a)] is a genetically determined, predominantly stable biomarker and a causal driver of atherosclerotic cardiovascular disease (ASCVD). Unlike traditional lipids, its plasma concentrations are minimally affected by metabolic disorders. Paradoxically, recent genetic and epidemiological studies have suggested an inverse relationship between Lp(a) and type 2 diabetes mellitus (T2D), hinting that lower Lp(a) levels may confer higher diabetes risk. Despite this, current cardiovascular guidelines treat Lp(a) and T2D as independent ASCVD risk factors, leaving uncertainty about whether clinically measured Lp(a) differs in diabetic patients.</span></span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:"Times New Roman",serif"><strong><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">Objectives:</span></span></strong><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif"> We aimed to investigate whether patients with T2D display distinct Lp(a) concentrations compared with non-diabetic individuals in a cohort of acute myocardial infarction (AMI) survivors.</span></span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:"Times New Roman",serif"><strong><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">Methods:</span></span></strong><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif"> In this retrospective study, all consecutive patients admitted to a coronary care unit with AMI between March and October 2025 were evaluated. T2D status, Lp(a), and HbA1c levels were recorded during admission and at six-week follow-up. Continuous variables were compared using independent-samples t-tests, and correlations between Lp(a) and glycaemic markers were assessed.</span></span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:"Times New Roman",serif"><strong><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">Results:</span></span></strong><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif"> Of 89 patients, 24 (27%) had T2D. Non-diabetic patients exhibited numerically higher mean Lp(a) (58.5 ± 46.7 mg/dL) than those with T2D (32.8 ± 33.8 mg/dL), though this difference was not statistically significant (p = 0.073). The HbA1c was elevated in T2D patients, yet no statistically-significant correlation was observed between HbA1c and Lp(a) at either time point (r= -0.246, p=0.073 at acute phase and r= -0.212, p= 0.121 at ≥6 weeks post-infarction).</span></span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:"Times New Roman",serif"><strong><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">Conclusion:</span></span></strong><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif"> In this AMI cohort, Lp(a) levels did not differ significantly between patients with and without T2D, reinforcing the concept that Lp(a) is predominantly genetically determined and largely independent of established diabetes. These findings suggest that the inverse Lp(a)–T2D association reported in genetic studies may not translate into clinically meaningful differences. Our results support universal, once-in-a-lifetime Lp(a) testing, regardless of diabetic status, to optimise personalised ASCVD risk stratification and guide targeted prevention strategies.</span></span></span></span></p>
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