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Updated: Jan 18, 2026
Evaluation of Left Ventricular Structure and Function using 3D Echocardiography
Published on: October 28, 2020
Association of Cardiovascular Health and Genetic Risk for Left Ventricular Mass with Left Ventricular Structure,
Marcela Cuellar-Lobo1, Musong Gao2, Maria M Ruda1,3
1Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Insights
Poor cardiovascular health combined with high genetic risk significantly increases the risk of adverse heart remodeling and cardiovascular disease (CVD). This highlights the importance of both lifestyle and genetics in CVD development.
Area of Science:
- Cardiology
- Genetics
- Public Health
Background:
- Cardiovascular health (CVH) and genetic susceptibility to adverse left ventricular (LV) remodeling are independently linked to cardiovascular diseases (CVD).
- The combined impact of CVH and genetic predisposition on CVD risk and LV remodeling remains incompletely understood.
Purpose of the Study:
- To investigate the synergistic effects of modifiable cardiovascular health factors and genetic risk on LV structure, function, and incident cardiovascular disease.
- To assess how combinations of Life's Essential 8 (LE8) scores and a Polygenic Risk Score (PRS) for LV mass index (LVMI) relate to adverse cardiovascular outcomes.
Main Methods:
- Utilized Framingham Heart Study data from Offspring and Generation 3 cohorts.
- Assessed modifiable risk factors using the American Heart Association's Life's Essential 8 (LE8) score and calculated a Polygenic Risk Score (PRS) for LV mass index (LVMI).
- Created 9 risk groups based on LE8 and PRS tertiles and analyzed their association with LVMI, LVEF, E/e' ratio, and incident CVD using regression models.
Main Results:
- Participants had intermediate CV health (mean LE8 score 70) and normal baseline LV structure and function.
- Over 19 years, individuals with low LE8 scores and high PRS exhibited significantly higher LVMI and E/e' ratios.
- The low LE8-high PRS group showed over a three-fold increased risk for incident CVD and coronary heart disease (CHD) compared to the optimal risk group.
Conclusions:
- Worse cardiovascular health (lower LE8 scores) synergizes with high genetic risk (high PRS) to elevate risks for adverse LV structure and function.
- Combined assessment of lifestyle-based CVH and genetic predisposition is crucial for predicting and potentially mitigating cardiovascular disease development.
Background:
Cardiovascular health (CVH) and genetic susceptibility to adverse left ventricular (LV) remodeling are each linked to cardiovascular diseases (CVD); however, their combined role remains unclear.
Methods:
Framingham Heart Study participants [n=1,255 Offspring-Exam 8 (2005-2008), n=2,835 Generation 3-Exam 1 (2002-2005)] had assessment of modifiable risk factors comprising the American Heart Association's Life's Essential 8 (LE8) score with higher scores indicating better CVH health. A Polygenic Risk Score (PRS) for LV mass index (LVMI) was also calculated based on published PRS(PGS003427). We created 9 groups combining LE8 and PRS tertiles (high LE8+low PRS served as referent group reflecting optimal risk) and related these groups to presence of LVMI, LV ejection fraction (LVEF), and the ratio of the peak early diastolic mitral inflow velocity (E wave) to the peak early diastolic mitral annular velocity (e' wave; E/e'; separate model for each outcome), and incident cardiovascular disease (CVD; a composite of coronary heart disease [CHD], heart failure, stroke, peripheral arterial disease). We applied linear mixed regression and Cox regression models to evaluate the relation of LE8-PRS groups with all outcomes mentioned above.
Results:
Participants (56% women, mean age 47 years) had mean LE8 score 70 (SD=13), indicating intermediate CV health and normal LVMI and systolic function (LVMI 76±13 g/m2, LVEF 65±5%, E/e' 6 ±1.8 cm/s). Over 19 years of follow-up, composite CV events and CHD occurred in n=188 and n=99, respectively, of Offspring and n=83 and n=49 respectively, of Gen 3 participants. Compared to the referent group, individuals in the low LE8-high PRS group had high LVMI, E/e', and over three-fold higher risks for CVD and CHD, with incidence rates of approximately 1.84 versus 4.06 per 1,000 person-year, respectively.
Conclusion:
Lower LE8 scores (indicating worse CVH) combined with high genetic risk confer higher conjoint risks for adverse LV structure, function, and CVD development.
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