Impact of elevated lipoprotein(a) on coronary artery disease phenotype and severity

Author:

Leistner David M12345ORCID,Laguna-Fernandez Andres6,Haghikia Arash1234ORCID,Abdelwahed Youssef S123,Schatz Anne-Sophie123,Erbay Aslihan1235,Roehle Robert47,Fonseca Ana F6,Ferber Philippe6,Landmesser Ulf1234ORCID

Affiliation:

1. Department of Cardiology, Campus Benjamin Franklin (CBF), Charité–Universitätsmedizin Berlin , Hindenburgdamm 30, 12203 Berlin , Germany

2. Deutsches Zentrum für Herzkreislaufforschung (DZHK), partner site Berlin , DZHK-Geschäftsstelle, Potsdamer Str. 58, 10785 Berlin , Germany

3. Friede Springer Cardiovascular Prevention Center, Charité , Hindenburgdamm 30, 12203 Berlin , Germany

4. Berlin Institute of Health (BIH) , Anna-Louisa-Karsch-Straße 2, 10178 Berlin , Germany

5. University Hospital Frankfurt and Wolfgang Goethe University , Theodor-Stern-Kai 7, 60596 Frankfurt , Germany

6. Novartis Pharma AG , Fabrikstrasse 2, CH-4056 Basel , Switzerland

7. Institute of Biometry and Clinical Epidemiology, Charité–Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin , Berlin , Germany

Abstract

Abstract Aims A thorough characterization of the relationship between elevated lipoprotein(a) [Lp(a)] and coronary artery disease (CAD) is lacking. This study aimed to quantitatively assess the association of increasing Lp(a) levels and CAD severity in a real-world population. Methods and results This non-interventional, cross-sectional, LipidCardio study included patients aged ≥21 years undergoing angiography (October 2016−March 2018) at a tertiary cardiology centre, who have at least one Lp(a) measurement. The association between Lp(a) and CAD severity was determined by synergy between PCI with taxus and cardiac surgery (SYNTAX)-I and Gensini scores and angiographic characteristics. Overall, 975 patients (mean age: 69.5 years) were included; 70.1% were male, 97.5% had Caucasian ancestry, and 33.2% had a family history of premature atherosclerotic cardiovascular disease. Median baseline Lp(a) level was 19.3 nmol/L. Patients were stratified by baseline Lp(a): 72.9% had < 65 nmol/L, 21.0% had ≥100 nmol/L, 17.2% had ≥125 nmol/L, and 12.9% had ≥150 nmol/L. Compared with the normal (Lp(a) < 65 nmol/L) group, elevated Lp(a) groups (e.g. ≥ 150 nmol/L) had a higher proportion of patients with prior CAD (48.4% vs. 62.7%; P < 0.01), prior coronary revascularization (39.1% vs. 51.6%; P = 0.01), prior coronary artery bypass graft (6.0% vs. 15.1%; P < 0.01), vessel(s) with lesions (68.5% vs. 81.3%; P = 0.03), diffusely narrowed vessels (10.9% vs. 16.5%; P = 0.01) or chronic total occlusion lesions (14.3% vs. 25.2%; P < 0.01), and higher median SYNTAX-I (3.0 vs. 5.5; P = 0.01) and Gensini (10.0 vs. 16.0; P < 0.01) scores. Conclusion Elevated Lp(a) was associated with a more severe presentation of CAD. Awareness of Lp(a) levels in patients with CAD may have implications in their clinical management.

Funder

Novartis Pharma

Publisher

Oxford University Press (OUP)

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