What is the clinical evidence from this study?

Study design: Cohort. Population: Cardiovascular disease risk (n=18694). Intervention: AHA PREVENT equations and Social Determinants of Health (SDOH) burden. Primary outcome: all-cause mortality per 5-percentage-point higher PREVENT-estimated risk (HR 1.55, 95% CI 1.47-1.64).

What question did this study set out to answer?

The research aims to investigate how social determinants of health influence mortality risks related to cardiovascular disease as estimated by the AHA PREVENT equations.

May 12, 2026

Social Determinants of Health Reveal Heterogeneity in Associations Between AHA PREVENT Cardiovascular Disease Risk Equations and Mortality and Provide Incremental Discrimination for Mortality in US Adults

Key Result

Higher PREVENT-estimated CVD risk was associated with increased all-cause mortality (HR 1.55 per 5% increase; 95% CI 1.47-1.64), with the association attenuated by higher SDOH burden.

Key Points

The research aims to investigate how social determinants of health influence mortality risks related to cardiovascular disease as estimated by the AHA PREVENT equations.
Linked 18,694 adults aged 40–75 years from NHANES 2003–2018 to the National Death Index until December 31, 2019.
Assigned SDOH burden by summing 8 adverse SDOH components and utilized Cox models for mortality associations.
Evaluated incremental discrimination with receiver operating characteristic curves after incorporating SDOH into PREVENT equations.
5-percentage-point increase in PREVENT risk correlates with higher all-cause mortality (HR = 1.55, 95% CI, 1.47–1.64, p < 0.001).
Stronger associations of PREVENT risk were found in the low SDOH group (HR = 2.01, 95% CI, 1.79–2.25) compared to the high SDOH group (HR = 1.38, 95% CI, 1.26–1.50).
Added SDOH to PREVENT improved mortality discrimination (AUC increased from 0.747 to 0.778, p < 0.001).

Study Design

Type

Cohort (n=18,694)

Multicenter

Yes

Structured PICO

Does adding social determinants of health (SDOH) to the AHA PREVENT equations improve discrimination for all-cause and cardio-cerebrovascular mortality in US adults?

Population

18,694 adults aged 40–75 years in NHANES 2003–2018, mean age 54.3 years, 52.6% women.

Intervention

AHA PREVENT equations estimated 10-year CVD risk combined with Social Determinants of Health (SDOH) burden

Comparator

AHA PREVENT equations alone

Outcome

All-cause mortality and cardio-cerebrovascular disease (CCD) mortality (composite of cardiovascular and cerebrovascular mortality)hard clinical

Adding social determinants of health to the AHA PREVENT equations modestly improves mortality discrimination, supporting the incorporation of social risk in cardiovascular risk stratification.

Main Result

Effect estimate: HR 1.55 (95% CI 1.47-1.64)

Abstract

ABSTRACT Background The American Heart Association (AHA) PREVENT equations provide contemporary estimates of 10‐year cardiovascular disease (CVD) risk. Although PREVENT was developed to estimate incident CVD risk, its relation to subsequent mortality in nationally representative US adults has not been well characterised. It also remains unclear whether social determinants of health (SDOH) modify these associations and improve discrimination beyond PREVENT. Methods Adults aged 40–75 years in NHANES 2003–2018 were linked to the National Death Index through December 31, 2019. SDOH burden was derived by summing 8 unfavourable SDOH components and categorised as 0, 1–2, 3–4 or ≥ 5. Survey‐weighted Cox models were used to evaluate associations with all‐cause and cardio‐cerebrovascular disease (CCD) mortality, defined as a composite of cardiovascular and cerebrovascular mortality. Effect modification was assessed using multiplicative interaction terms. Incremental discrimination after adding SDOH to PREVENT was evaluated using time‐dependent receiver operating characteristic (ROC) curves. Results Among 18 694 adults (mean age, 54.3 years; 52.6% women), 1646 all‐cause deaths and 392 CCD deaths occurred over a median follow‐up of 8.2 years (IQR, 4.3–12.3). In multivariable models, each 5–percentage‐point higher PREVENT‐estimated risk was associated with higher all‐cause mortality (HR = 1.55; 95% CI, 1.47–1.64) and CCD mortality (HR = 1.62; 95% CI, 1.52–1.74). Heterogeneity by SDOH burden was demonstrated ( p for interaction < 0.001 for both outcomes), with stronger associations in the 0‐unfavourable group (all‐cause: HR = 2.01; 95% CI, 1.79–2.25; CCD: HR = 2.35; 95% CI, 1.91–2.88) and attenuated associations in the ≥ 5‐unfavourable group (all‐cause: HR = 1.38; 95% CI, 1.26–1.50; CCD: HR = 1.46; 95% CI, 1.31–1.62). At 10 years, discrimination improved after adding SDOH to PREVENT (all‐cause AUC: 0.747 to 0.778; p < 0.001; CCD AUC: 0.790 to 0.812; p = 0.042). Conclusions SDOH burden was associated with graded mortality and modified the strength of the association between PREVENT‐estimated 10‐year CVD risk and mortality. Adding SDOH modestly improved mortality discrimination beyond PREVENT alone, supporting incorporation of social risk in risk stratification.

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