SPC365

Lipoprotein(a) role in acute myocardial infarction: real-world data of a tertiary care centre

Session: Sessão de Posters 10 - Dislipidémia e metabolismo lipídico
Speaker: Catarina Amaral Marques

Congress: CPC 2024
Topic: J. Preventive Cardiology
Theme: 28. Risk Factors and Prevention
Subtheme: 28.14 Risk Factors and Prevention - Other
Session Type: Cartazes
FP Number: ---
Authors: Catarina Amaral Marques; André Cabrita; Cátia Oliveira; Luís Santos; Ana Isabel Pinho; Miguel Rocha; Pedro Palma; Helena Santos Moreira; Paulo Maia Araújo; Cristina Cruz; Rui André Rodrigues

<p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Introduction:</strong> Growing evidence points to lipoprotein(a) [Lp(a)] role in cardiovascular (CV) risk modulation. However, its clinical practice assessment and utility are poorly studied, particularly in acute myocardial infarction (AMI). Our aim was to evaluate Lp(a) behavior in a real-world cohort of AMI patients (pts). </span></span></span></p>

<p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Methods:</strong> Tertiary care centre retrospective study of pts admitted with type one AMI between 2020 and 2023, in whom Lp(a) was assessed (n=162). Data was based on pts&rsquo; medical records review. Lp(a) values &ge; 30 mg/dL denoted higher CV risk pts (Lp30 pts), in accordance with current literature. &nbsp;&nbsp;</span></span></span></p>

<p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Results:</strong> 162 pts were included: 19% female; median age at AMI was 54 years; 95% presented &ge;1 CV risk factor (CVRF). <span style="color:black">Non-ST/ST segment elevation AMI frequency&nbsp;was </span>46% and 54%, respectively. Median Lp(a) was 37.5 mg/dL; 58% presented Lp(a) &ge; 30 mg/dL. Median follow-up (FU) time was 24 months.</span></span></span></p>

<p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Regarding baseline characteristics, no differences were found across the spectrum of Lp(a) values in terms of CVRF (p=0.6), sex (p=0.8), age (p=0.3), or previous CV events (p=0.6). Notably, Lp30 pts presented more family history of premature coronary heart disease (CHD) (30% vs 13% in non-Lp30; p=0.01). Lipid panel at admission was comparable between groups, namely for low-density lipoprotein (LDL) values (median LDL of 118 mg/dL in Lp30 vs 110 mg/dL; p=0.2). However, higher Lp(a) pts were more frequently on pre-AMI antidyslipidemic treatment (p=0.02), as well as on higher-intensity drug regimens (p=0.003) (Table 1). </span></span></span></p>

<p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Concerning in-hospital management and outcomes, multivessel disease was more commonly identified in higher Lp(a) (p=0.05). No other differences were found. Similarly, no differences were observed in CV outcomes on FU across the whole range of Lp(a) values. Still, higher Lp(a) pts presented worse lipidic control on FU (non-LDL-target pts with median Lp(a) of 44 mg/dL vs 33 mg/dL in LDL-target pts; p=0.03). Nonetheless, FU antidyslipidemic treatment was not different (Table 1) across the Lp(a) spectrum (p=0.13). </span></span></span></p>

<p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Genetic testing for familial hypercholesterolemia was performed in 7%, and more commonly requested in higher Lp(a) pts (median Lp(a) of 98 mg/dL on tested pts vs 35 mg/dL on non-tested; p=0.009).</span></span></span></p>

<p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Conclusion:</strong> Reflecting about our real-world data on AMI pts, important messages stand out: 1) lipidic panel at admission was comparable in Lp30 vs non-Lp30, likely reflecting higher frequencies and higher-intensity regimens of treatment presented by Lp30; 2) worse lipidic control was observed in higher Lp(a), conferring a well-known increased CV risk in non-LDL-target pts; 3) genetic testing frequency was clearly discrepant from the proportion of pts with family history of premature CHD. </span></span></span></p>

<p style="text-align:justify"><span style="font-size:medium"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Our data raises awareness for this higher CV risk and vulnerable subgroup of AMI pts, highlighting the need for a rigorous evaluation and management. Additional larger and longer FU studies are needed.&nbsp;&nbsp;&nbsp;&nbsp; &nbsp;</span></span></span></p>