Neighborhood social vulnerability associated with early onset and accelerated development of incident heart failure
M Torpoco Rivera, A Al-Bazaz, I Hassan, M Abdou Awad Elsayed, S AbohashemAbstract
Background
Heart failure (HF) is a major global public health challenge, reflecting cumulative biological and social stress across the life course. Social vulnerability, capturing neighborhood-level socioeconomic adversity, has been linked to cardiovascular disease (CVD) development, yet its role in predicting long-term incident HF and earlier disease onset, remains uncertain. We examined the association between Social Vulnerability and incident HF (overall and subtypes) and tested whether higher vulnerability is associated with earlier HF development.
Methods
We analyzed longitudinal data from the Mass General Brigham Biobank (MGBB) including participants free of HF at baseline. Neighborhood social vulnerability was quantified using the CDC-developed Social Vulnerability Index (SVI), which integrates multiple socioeconomic and demographic domains at the census-tract level; five-year pre-2010 estimates were used. SVI was modeled as a standardized continuous variable and by quartiles. Incident HF (any HF, systolic HF, and diastolic HF), age at HF onset, and covariates were ascertained from electronic health records and survey data. Multivariable Cox regression, Kaplan–Meier analyses, linear regression, and restricted cubic splines (RCS) were performed. Effect modification by sex was examined.
Results
Among 87,498 adults enrolled in MGBB (2010-2020), 6853 develop HF over 10 years of follow up. In fully adjusted analyses, higher SVI was independently associated with greater risk of incident HF. Per 1-SD increase in SVI, the hazard ratio (HR) was 1.11 (95% CI 1.08–1.15) for any HF, 1.17 (1.12–1.23) for systolic HF, and 1.16 (1.12–1.21) for diastolic HF. A graded association was observed across SVI quartiles. For any HF, HRs were 1.08 (0.99–1.16), 1.22 (1.12–1.32), and 1.29 (1.19–1.41) for Q2–Q4 (Table). Associations were more pronounced for women (Q4 vs. Q1: 1.38 (1.21–1.57) compared to men (Q4 vs. Q1: 1.23 (1.10–1.38), with a relative increased risk of 65%. RCS analyses demonstrated a linear dose–response relationship (p-nonlinearity>0.05). Higher SVI was also associated with younger age at HF onset. Per 1-SD increase in SVI, HF occurred 1.68 years earlier for any HF (β −1.68, p<0.001), 2.14 years earlier for systolic HF (β −2.14, p<0.001), and 2.01 years earlier for diastolic HF (β −2.01, p<0.001; Figure). Quartile analyses demonstrated a stepwise reduction in age at HF across increasing SVI categories.
Conclusions
Neighborhood social vulnerability independently predicts incident HF, with stronger associations observed among women, and is associated with significantly earlier disease onset. These findings suggest that social disadvantage contributes to accelerated HF development independent of clinical and environmental risk factors. Addressing social vulnerability may represent a critical lever for preventing premature HF and reducing inequities in cardiovascular outcomes.SVI_HF_Figure 1SVI_HF_Figure 2