Social Determinants of Cardiovascular Disease

Abstract

Social determinants of health (SDoH), which encompass the economic, social, environmental, and psychosocial factors that influence health, play a significant role in the development of cardiovascular disease (CVD) risk factors as well as CVD morbidity and mortality. The COVID-19 pandemic and the current social justice movement sparked by the death of George Floyd have laid bare long-existing health inequities in our society driven by SDoH. Despite a recent focus on these structural drivers of health disparities, the impact of SDoH on cardiovascular health and CVD outcomes remains understudied and incompletely understood. To further investigate the mechanisms connecting SDoH and CVD, and ultimately design targeted and effective interventions, it is important to foster interdisciplinary efforts that incorporate translational, epidemiological, and clinical research in examining SDoH-CVD relationships. This review aims to facilitate research coordination and intervention development by providing an evidence-based framework for SDoH rooted in the lived experiences of marginalized populations. Our framework highlights critical structural/socioeconomic, environmental, and psychosocial factors most strongly associated with CVD and explores several of the underlying biologic mechanisms connecting SDoH to CVD pathogenesis, including excess stress hormones, inflammation, immune cell function, and cellular aging. We present landmark studies and recent findings about SDoH in our framework, with careful consideration of the constructs and measures utilized. Finally, we provide a roadmap for future SDoH research focused on individual, clinical, and policy approaches directed towards developing multilevel community-engaged interventions to promote cardiovascular health.

Keywords: cardiovascular diseases; health status disparities; social determinants of health; social justice; socioeconomic factors.

Figure 1.

A critical framework of social determinants of health. The trickle-down effects of the sociopolitical and economic context shape social position and subsequent lived experiences of marginalized groups through the application of laws and policies within the social and community context. The everyday experience of othering such as discrimination, implicit bias, and stigma stems from structural determinants that shape social risk and an individual’s perception. The chronic effects of these experiences influence human biology and subsequent cardiovascular disease (CVD) outcomes through psychosocial and environmental stressors.

Figure 2.

The social determinants of health and the biology of adversity. Social determinants of health encompass an individual’s economic stability, neighborhood and built environment, education access, health care access and their social and community relationships. These areas can be sources of chronic psychosocial stressors to individuals that suffer from low socioeconomic status, unsafe housing, neighborhood violence, limited access to health care, early childhood adversity, discrimination, increased noised exposure, food insecurity, and decreased sleep quality among others. Pathway to chronic inflammation: Biologic consequence of adversity promote pathways to chronic inflammation. Sympatho-adrenomedullary (SAM) axis and hypothalamic-pituitary-adrenal (HPA) axis: the SAM axis and the HPA axis are activated by psychosocial stress and regulate the production of catecholamines (dopamine, norepinephrine, and epinephrine) and glucocorticoids, respectively. Glucocorticoid and catecholamine signaling under chronic stress: (1) Glucocorticoid receptor (GR) shows impaired nuclear translocation and decreased anti-inflammatory gene transcription in chronic stress. (2) β-Adrenergic receptors (ARs) have been found to alter their gene signaling to a noncanonical pathway (via β-arrestin 2 scaffolding) that increases production of inflammatory cytokines which also upregulate NLRP3 (NLR family pyrin domain-containing 3) inflammasome activity. β3 Receptors have also been found to play a role in clonal hematopoiesis which may contribute to atherosclerotic plaque formation. Neurohematopoietic axis: Chronic amygdalar activation has been linked to clonal hematopoiesis, possibly by direct sympathetic nervous system (SNS) innervation of the bone marrow; stress-induced leukopoiesis has been directly linked to atherosclerotic plaques. All of these inflammatory processes lead to increased cardiovascular disease (CVD) risk factors, such as obesity, hypertension, diabetes, and atherosclerosis, ultimately contributing to major adverse cardiac events (MACE) and CVD mortality. ACTH indicates adrenocorticotropic hormone; AP-1, activating protein-1; CREB, cAMP response element-binding protein; CRH, corticotropin-releasing hormone; MAPK, mitogen-activated protein kinases; NF-κB, nuclear factor κ-light-chain-enhancer of activated B cells; and SNS, sympathetic nervous system. [Created with BioRender.com.]

Figure 3.

Integration of the social determinants of health (SDoH) into multilevel cardiovascular health interventions. Based on the previously presented critical framework of the social determinants of health, multiple levels of interventions at the policy, community, and individual levels are needed to address the sociopolitical, community, and lived experience contexts of cardiovascular health. Community input and engagement at all stages is necessary to develop well-informed interventions that provide available, accessible, and affordable resources to vulnerable populations. Ultimately, these successful multilevel interventions have direct impacts on cardiovascular disease (CVD) outcomes and health equity, such as reducing health disparities, improving health behaviors and access, and reducing the biologic impact of adverse conditions. [Created with BioRender.com.]