Lipoprotein(a) and Coronary Plaque in Asymptomatic Individuals: The Miami Heart Study at Baptist Health South Florida

Author:

Mszar Reed1ORCID,Cainzos-Achirica Miguel2ORCID,Valero-Elizondo Javier2ORCID,Lahan Shubham2ORCID,Al-Kindi Sadeer G.2ORCID,Quispe Renato3,Ali Shozab S.4,Arias Lara4,Saxena Anshul4ORCID,Shah Svati H.5ORCID,Cury Ricardo C.46ORCID,Budoff Matthew J.78ORCID,Blaha Michael J.3ORCID,Shapiro Michael D.9ORCID,Sharma Garima3ORCID,Santos Raul D.1011ORCID,Blankstein Ron12ORCID,Feldman Theodore4,Fialkow Jonathan4,Nasir Khurram2ORCID

Affiliation:

1. Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT (R.M.).

2. Division of Cardiovascular Prevention and Wellness, Department of Cardiology, Houston Methodist DeBakey Heart & Vascular Center, Houston, TX (M.C.-A., J.V.-E., S.L., S.G.A.-K., K.N.).

3. Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, MD (R.Q., M.J. Blaha., G.S.).

4. Miami Cardiac and Vascular Institute, Baptist Health South Florida, Miami (S.S.A., L.A., A.S., R.C.C., T.F., J.F.).

5. Division of Cardiology, Department of Medicine, Duke University School of Medicine, Durham, NC (S.H.S.).

6. Herbert Wertheim College of Medicine, Florida International University, Miami (R.C.C.).

7. Lundquist Institute at Harbor-University of California, Los Angeles Medical Center, Torrance, CA (M.J. Budoff.).

8. David Geffen School of Medicine, University of California, Los Angeles (M.J. Budoff.).

9. Center for Prevention of Cardiovascular Disease, Section on Cardiovascular Medicine, Wake Forest University School of Medicine, Winston-Salem, NC (M.D.S.).

10. Heart Institute (INCOR), University of São Paulo Medical School Hospital, Brazil (R.D.S.).

11. Hospital Israelita Albert Einstein, São Paulo, Brazil (R.D.S.).

12. Cardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston Cardiovascular Imaging Program, Cardiovascular Division (Department of Medicine) and Department of Radiology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA (R.B.).

Abstract

BACKGROUND: Elevated levels of lipoprotein(a) (Lp(a)) are independently associated with an increased risk of atherosclerotic cardiovascular disease events. However, the mechanisms driving this association are poorly understood. We aimed to evaluate the association between Lp(a) and coronary plaque characteristics in a contemporary US cohort without clinical atherosclerotic cardiovascular disease, undergoing coronary computed tomography angiography, the noninvasive gold standard for the assessment of coronary atherosclerosis. METHODS: We used baseline data from the Miami Heart Study—a community-based, prospective cohort study—which included asymptomatic adults aged 40 to 65 years evaluated using coronary computed tomography angiography. Those taking any lipid-lowering therapies were excluded. Elevated Lp(a) was defined as ≥125 nmol/L. Outcomes included any plaque, coronary artery calcium score >0, maximal stenosis ≥50%, presence of any high-risk plaque feature (positive remodeling, spotty calcification, low-attenuation plaque, napkin ring), and the presence of ≥2 high-risk plaque features. RESULTS: Among 1795 participants (median age, 52 years; 54.3% women; 49.6% Hispanic), 291 (16.2%) had Lp(a) ≥125 nmol/L. In unadjusted analyses, individuals with Lp(a) ≥125 nmol/L had a higher prevalence of all outcomes compared with Lp(a) <125 nmol/L, although differences were only statistically significant for the presence of any coronary plaque and ≥2 high-risk features. In multivariable models, elevated Lp(a) was independently associated with the presence of any coronary plaque (odds ratio, 1.40, [95% CI, 1.05–1.86]) and with ≥2 high-risk features (odds ratio, 3.94, [95% CI, 1.82–8.52]), although only 35 participants had this finding. Among participants with a coronary artery calcium score of 0 (n=1200), those with Lp(a) ≥125 nmol/L had a significantly higher percentage of any plaque compared with those with Lp(a) <125 nmol/L (24.2% versus 14.2%; P <0.001). CONCLUSIONS: In this contemporary analysis, elevated Lp(a) was independently associated with the presence of coronary plaque. Larger studies are needed to confirm the strong association observed with the presence of multiple high-risk coronary plaque features.

Publisher

Ovid Technologies (Wolters Kluwer Health)

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