AHA Scientific Sessions 2026 Abstract · Nov 2, 2026
Cardiovascular Health and Lipoprotein(a)/Oxidized Phospholipids in Relation to Subclinical and Clinical Cardiovascular Disease: The Framingham Heart Study
By Qian F, Prescott B, McMenamin K et al.
Background: Cardiovascular health, defined using the American Heart Association’s Life’s Essential 8 (LE8), is associated with lower risk of clinical cardiovascular disease (CVD). However, its associations with subclinical measures of vascular and valvular heart disease are less studied. Additionally, whether LE8 modifies the association between lipoprotein(a) [Lp(a)] or oxidized phospholipids (OxPL) with subclinical or clinical CVD is unknown. Methods: We examined 2,777 participants (mean age 50 years; 50% women) from the Framingham Heart Study Offspring, New Offspring Spouses, Generation Three, Omni 1, and Omni 2 cohorts, who were free of CVD, attended a clinical examination, and underwent multi-detector computed tomography to evaluate for subclinical vascular disease [coronary artery calcium (CAC), thoracic aortic calcium (TAC), and abdominal aortic calcium (AAC)] and valvular disease [aortic valve calcium (AVC) and mitral valve calcium (MVC)], quantified in Agaston units (AU). In a subset (N=1,207) of these participants, Lp(a) and OxPL were measured using standard assays. Multivariable logistic regressions were performed to evaluate the relations of LE8, Lp(a), and OxPL with presence (>0 AU) of each subclinical disease measure as well as having severe subclinical disease (CAC≥300, TAC≥500, and AAC≥3000; separate models). Additionally, we prospectively evaluated the joint association of LE8 and Lp(a) or OxPL with CVD risk [composite of coronary heart disease (CHD), stroke, and peripheral arterial disease, and as separate outcomes] using multivariable-adjusted Cox models among 2,366 participants in the Offspring and Omni 1 cohorts. We tested for effect modifications of the relations between Lp(a) or OxPL and subclinical phenotypes and incident CVD by LE8. Results: Higher LE8 scores were associated with lower odds of subclinical atherosclerosis and subclinical valvular heart disease ( Table 1 ). Similarly, higher LE8 scores were associated with lower odds of severe subclinical vascular disease. For Lp(a) and OxPL, we only observed significant associations with odds of AVC. We observed similar patterns of associations using dichotomized Lp(a) (≥125 nmol/L) and OxPL (≥10.6 nmol/L). LE8 did not modify the association of Lp(a) or OxPL with odds of AVC ( P interactions >0.05). During follow-up, 557 incident CVD events were observed (including 165 CHD events). Higher LE8 scores were associated with lower risk of incident CVD and CHD, including among individuals with elevated Lp(a) (≥125 nmol/L) or OxPL (≥10.6 nmol/L) ( P interaction >0.05) ( Table 2 ). Conclusion: Higher LE8 scores were associated with lower odds of subclinical vascular and valvular disease as well as CVD risk, regardless of Lp(a) or OxPL levels. Our findings underscore the potential of cardiovascular health optimization for prevention across the spectrum of Lp(a) and OxPL-related risk.