How Lower Socioeconomic Status May 'Get Inside the Body' to Raise CV Risk

Megan Brooks

July 02, 2019

Researchers say they have identified a potentially modifiable biological pathway that may contribute to the increased burden of cardiovascular disease (CVD) and risk for clinical events in the socioeconomically disadvantaged.

They found that lower socioeconomic status (SES), estimated by zip codes in the United States, correlated with increased activity of the amygdala, a brain region involved in emotions and the fight-or-flight response, and arterial inflammation. Both are known to be associated with CVD risk.

"These observations point to a biological mechanism by which lower SES may precipitate CVD risk," first author Ahmed Tawakol, MD, Massachusetts General Hospital and Harvard Medical School, Boston, told theheart.org | Medscape Cardiology.

The study was published online June 24 in the Journal of the American College of Cardiology.

"Fascinating and Important" Work

This "fascinating and important report...offers the most detailed mechanistic account to date of how low SES, a stress exposure, 'gets inside the body' to accelerate CVD progression," an accompanying editorial states.

However, "like all highly innovative studies, this one raises numerous questions," and the findings should be considered "promising rather than definitive," write Gregory E. Miller, Northwestern University, Evanston, Illinois, and his coauthors.

The study was based on 509 adults (median age, 55) without known CVD or active cancer who underwent clinically indicated whole-body 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) imaging. Cancer surveillance was the most common indication for imaging.

Hematopoietic-tissue metabolism and arterial inflammation as reflected by arterial wall 18F-FDG activity and, in a subset of 289 people, resting amygdalar metabolism were quantified at baseline. Markers of SES included zip code as proxy for household income and neighborhood crime statistics.

Over a median of 4 years, 40 people had one or more major adverse cardiac events (MACE), defined as cardiac death, myocardial infarction, unstable angina, cerebrovascular accident, revascularized peripheral artery disease, or heart failure.

Individuals from neighborhoods with lower household incomes or higher crime rates had a significantly increased risk of experiencing a MACE during follow-up.

The risk was nearly fourfold higher in individuals in the lowest versus highest quartile of neighborhood median income (hazard ratio [HR], 3.91; (95% CI, 1.30 - 11.77; log rank P = .009). The relation remained significant after adjustment for CVD risk factors.

Similar relations between SES and MACE were seen when individuals were categorized by neighborhood crime rate.

Living in a low-income neighborhood was strongly associated with increased resting amygdalar activity, elevated immune cell production, and arterial inflammation.

Using the statistical technique of mediation path analysis, which integrated data from all the diverse sources of the analysis, the path of lower neighborhood SES to higher amygdalar activity to higher bone marrow activity to higher arterial inflammation to higher risk for MACE was significant (P < .05).

Target Downstream Processes

These findings highlight a "stress-associated neurobiological mechanism by which SES disparities may potentiate adverse health outcomes," write the researchers.

They also "suggest new approaches for reducing the risk of CVD among individuals with lower SES. Specifically, the findings suggest that disparities in outcomes may be mitigated by targeting processes downstream of SES," Tawakol told theheart.org | Medscape Cardiology.

"Interventions could be developed that target the physiological cascade described in the paper, including the activated brain stress centers, heightened bone marrow production of immune cells, and the inflamed arteries. Some of those interventions may include lifestyle approaches, including adequate sleep, exercise and mediation," he explained.

"Existing drugs targeting the brain, bone marrow, or the arteries may be repurposed. Of course, novel treatments targeting this multiorgan path should also be investigated. Additionally, further research and effort is needed to improve the social conditions that result in chronically heightened stress," he added.

In their editorial, Miller and coauthors agree with the authors that it is tough to substantially alter SES, and that downstream processes offer "promising" targets for intervention.

In that regard, accumulating evidence suggests it may be possible to mitigate some of the pathological processes that this study highlights by improving the social conditions of young people with low SES, even without bolstering income or education, Miller and colleagues observe.

The study was supported by the National Institutes of Health and the American Heart Association. Tawakol discloses receiving grants from Genentech and Actelion and personal fees from Actelion and Amgen. Miller et al had no relevant disclosures.

J Am Coll Cardiol. Published online June 24, 2019. Abstract, Editorial

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