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Published on: May 31, 2016
Independent Association of Lipoprotein(a) and Coronary Artery Calcification With Atherosclerotic Cardiovascular Risk
Anurag Mehta1, Nestor Vasquez2, Colby R Ayers3
1Emory Clinical Cardiovascular Research Institute, Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, USA.
Insights
Elevated lipoprotein(a) [Lp(a)] and coronary artery calcium (CAC) score independently increase atherosclerotic cardiovascular disease (ASCVD) risk. Combining Lp(a) and CAC assessments can enhance primary prevention strategies.
Area of Science:
- Cardiovascular Medicine
- Preventive Cardiology
- Biomarkers of Atherosclerosis
Background:
- Elevated lipoprotein(a) [Lp(a)] and coronary artery calcium (CAC) score are known independent risk factors for atherosclerotic cardiovascular disease (ASCVD).
- The combined impact of Lp(a) and CAC on ASCVD risk has not been previously investigated.
Purpose of the Study:
- To evaluate the independent and joint associations of Lp(a) and CAC with ASCVD risk.
- To determine if Lp(a) and CAC can be used together to refine ASCVD risk assessment.
Main Methods:
- Analysis of asymptomatic participants from the MESA (n=4,512) and DHS (n=2,078) cohorts.
- Measurement of plasma Lp(a) and CAC scores at baseline.
- Utilized risk factor-adjusted Cox regression models to assess associations with incident ASCVD events over 13.2 years of follow-up.
Main Results:
- Both elevated Lp(a) and higher CAC scores (1-99 and ≥100) were independently associated with increased ASCVD risk.
- Participants with elevated Lp(a) and CAC ≥100 had the highest ASCVD risk (HR: 4.71).
- No significant Lp(a)-by-CAC interaction was observed, but combined assessment provided additive risk information.
Conclusions:
- Lipoprotein(a) and coronary artery calcium are independently linked to ASCVD risk.
- Concurrent assessment of Lp(a) and CAC may improve the guidance of primary prevention therapy decisions.
Background:
Elevated lipoprotein(a) [Lp(a)] and coronary artery calcium (CAC) score are individually associated with increased atherosclerotic cardiovascular disease (ASCVD) risk but have not been studied in combination.
Objectives:
This study sought to investigate the independent and joint association of Lp(a) and CAC with ASCVD risk.
Methods:
Plasma Lp(a) and CAC were measured at enrollment among asymptomatic participants of the MESA (Multi-Ethnic Study of Atherosclerosis) (n = 4,512) and DHS (Dallas Heart Study) (n = 2,078) cohorts. Elevated Lp(a) was defined as the highest race-specific quintile, and 3 CAC score categories were studied (0, 1-99, and ≥100). Associations of Lp(a) and CAC with ASCVD risk were evaluated using risk factor-adjusted Cox regression models.
Results:
Among MESA participants (61.9 years of age, 52.5% women, 36.8% White, 29.3% Black, 22.2% Hispanic, and 11.7% Chinese), 476 incident ASCVD events were observed during 13.2 years of follow-up. Elevated Lp(a) and CAC score (1-99 and ≥100) were independently associated with ASCVD risk (HR: 1.29; 95% CI: 1.04-1.61; HR: 1.68; 95% CI: 1.30-2.16; and HR: 2.66; 95% CI: 2.07-3.43, respectively), and Lp(a)-by-CAC interaction was not noted. Compared with participants with nonelevated Lp(a) and CAC = 0, those with elevated Lp(a) and CAC ≥100 were at the highest risk (HR: 4.71; 95% CI: 3.01-7.40), and those with elevated Lp(a) and CAC = 0 were at a similar risk (HR: 1.31; 95% CI: 0.73-2.35). Similar findings were observed when guideline-recommended Lp(a) and CAC thresholds were considered, and findings were replicated in the DHS.
Conclusions:
Lp(a) and CAC are independently associated with ASCVD risk and may be useful concurrently for guiding primary prevention therapy decisions.
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