Stress-Associated Neurobiological Pathway Linking Socioeconomic Disparities to Cardiovascular Disease

Tawakol, Ahmed; Osborne, Michael T.; Wang, Ying; Hammed, Basma; Tung, Brian; Patrich, Tomas; Oberfeld, Blake; Ishai, Amorina; Shin, Lisa M.; Nahrendorf, Matthias; Warner, Erica T.; Wasfy, Jason H.; Fayad, Zahi A.; Koenen, Karestan C.; Ridker, Paul M.; Pitman, Roger K.; Armstrong, Katrina

doi:10.1016/j.jacc.2019.04.042

Cited by 120 publications

(97 citation statements)

References 50 publications

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“…5 Multiple mechanisms have been proposed to explain this association, including impeding cognitive function, 6 inability to purchase access to health care, worse nutritional quality, worse neighborhoods, and higher psychosocial stress. 2,7 Low SES is also associated with depression, 8 which is in turn associated with cardiovascular disease (CVD) risk. 9 However, it does not necessarily cost money to engage in some cardioprotective behaviors.…”

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confidence: 99%

Longitudinal Associations Between Income Changes and Incident Cardiovascular Disease

et al. 2019

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IMPORTANCE Higher income is associated with lower incident cardiovascular disease (CVD). However, there is limited research on the association between changes in income and incident CVD. OBJECTIVE To examine the association between change in household income and subsequent risk of CVD. DESIGN, SETTING, AND PARTICIPANTS The Atherosclerosis Risk In Communities (ARIC) study is an ongoing, prospective cohort of 15 792 community-dwelling men and women, of mostly black or white race, from 4 centers in the United States (Jackson, Mississippi; Washington County, Maryland; suburbs of Minneapolis, Minnesota; and Forsyth County, North Carolina), beginning in 1987. For our analysis, participants were followed up until December 31, 2016. EXPOSURES Participants were categorized based on whether their household income dropped by more than 50% (income drop), remained unchanged/changed less than 50% (income unchanged), or increased by more than 50% (income rise) over a mean (SD) period of approximately 6 (0.3) years between ARIC visit 1 (1987-1989) and visit 3 (1993-1995). MAIN OUTCOMES AND MEASURES Our primary outcome was incidence of CVD after ARIC visit 3, including myocardial infarction (MI), fatal coronary heart disease, heart failure (HF), or stroke during a mean (SD) of 17 (7) years. Analyses were adjusted for sociodemographic variables, health behaviors, and CVD biomarkers. RESULTS Of the 8989 included participants (mean [SD] age at enrollment was 53 [6] years, 1820 participants were black [20%], and 3835 participants were men [43%]), 900 participants (10%) experienced an income drop, 6284 participants (70%) had incomes that remained relatively unchanged, and 1805 participants (20%) experienced an income rise. After full adjustment, those with an income drop experienced significantly higher risk of incident CVD compared with those whose incomes remained relatively unchanged (hazard ratio, 1.17; 95% CI, 1.03-1.32). Those with an income rise experienced significantly lower risk of incident CVD compared with those whose incomes remained relatively unchanged (hazard ratio, 0.86; 95% CI, 0.77-0.96). CONCLUSIONS AND RELEVANCE Income drop over 6 years was associated with higher risk of subsequent incident CVD over 17 years, while income rise over 6 years was associated with lower risk of subsequent incident CVD over 17 years. Health professionals should have greater awareness of the influence of income change on the health of their patients.

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confidence: 99%

Longitudinal Associations Between Income Changes and Incident Cardiovascular Disease

et al. 2019

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“…Inter-organ communication, the heart-brain axis, and systems biology are increasingly recognized as important contributors to the copresentation of disease in the aging population [11,23]. We have previously established concomitant neuroinflammation after acute myocardial infarction and in chronic heart failure which was attenuated by continuous enalapril therapy [12].…”

Section: Discussionmentioning

confidence: 97%

Angiotensin-converting enzyme inhibitor treatment early after myocardial infarction attenuates acute cardiac and neuroinflammation without effect on chronic neuroinflammation

Borchert

Hess

Lukacevic

et al. 2020

Eur J Nucl Med Mol Imaging

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Purpose Myocardial infarction (MI) triggers a local inflammatory response which orchestrates cardiac repair and contributes to concurrent neuroinflammation. Angiotensin-converting enzyme (ACE) inhibitor therapy not only attenuates cardiac remodeling by interfering with the neurohumoral system, but also influences acute leukocyte mobilization from hematopoietic reservoirs. Here, we seek to dissect the anti-inflammatory and anti-remodeling contributions of ACE inhibitors to the benefit of heart and brain outcomes after MI. Methods C57BL/6 mice underwent permanent coronary artery ligation (n = 41) or sham surgery (n = 9). Subgroups received ACE inhibitor enalapril (20 mg/kg, oral) either early (anti-inflammatory strategy; 10 days treatment beginning 3 days prior to surgery; n = 9) or delayed (anti-remodeling; continuous from 7 days post-MI; n = 16), or no therapy (n = 16). Cardiac and neuroinflammation were serially investigated using whole-body macrophage-and microglia-targeted translocator protein (TSPO) PET at 3 days, 7 days, and 8 weeks. In vivo PET signal was validated by autoradiography and histopathology. Results Myocardial infarction evoked higher TSPO signal in the infarct region at 3 days and 7 days compared with sham (p < 0.001), with concurrent elevation in brain TSPO signal (+ 18%, p = 0.005). At 8 weeks after MI, remote myocardium TSPO signal was increased, consistent with mitochondrial stress, and corresponding to recurrent neuroinflammation. Early enalapril treatment lowered the acute TSPO signal in the heart and brain by 55% (p < 0.001) and 14% (p = 0.045), respectively. The acute infarct signal predicted late functional outcome (r = 0.418, p = 0.038). Delayed enalapril treatment reduced chronic myocardial TSPO signal, consistent with alleviated mitochondrial stress. Early enalapril therapy tended to lower TSPO signal in the failing myocardium at 8 weeks after MI (p = 0.090) without an effect on chronic neuroinflammation. Conclusions Whole-body TSPO PET identifies myocardial macrophage infiltration and neuroinflammation after MI, and altered cardiomyocyte mitochondrial density in chronic heart failure. Improved chronic cardiac outcome by enalapril treatment derives partially from acute anti-inflammatory activity with complementary benefits in later stages. Whereas early ACE inhibitor therapy lowers acute neuroinflammation, chronic alleviation is not achieved by early or delayed ACE inhibitor therapy, suggesting a more complex mechanism underlying recurrent neuroinflammation in ischemic heart failure.

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“…The reasons for the elevated CVD risk in this population is a multifactorial public health issue and involves a variety of physiological, cultural, socioeconomic, and psychosocial factors. [4][5][6][7] From a physiological perspective, the mechanism(s) responsible for the elevated CVD risk in BL women remains incompletely understood, but impairments in macro-and micro-vascular function likely play a role. Indeed, vascular dysfunction is a precursor to pathophysiological conditions that are most prevalent in BL women, including hypertension, coronary artery disease, and stroke.…”

Section: Cardiovascular Diseasementioning

confidence: 99%

“…Non-Physiological Factors Contributing to Elevated Disease Risk: Although additional studies of the vasculature and cardiovascular physiology, in general, are needed, it will also be crucial to investigate the contribution of cultural and psychosocial factors in the elevated CVD risk in the BL population as has been recently described. 7…”

Section: Investigate Other Potential Mechanisms Associated Withmentioning

confidence: 99%

Influence of sex on heightened vasoconstrictor mechanisms in the non‐Hispanic black population

et al. 2020

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Cardiovascular disease (CVD) affects individuals of all races and ethnicities; however, its prevalence is highest in non-Hispanic black individuals (BL) relative to other populations. While previous research has provided valuable insight into elevated CVD risk in the BL population, this work has been almost exclusively How to cite this article: Brothers RM, Stephens BY, Akins JD, Fadel PJ. Influence of sex on heightened vasoconstrictor mechanisms in the non-Hispanic black population.

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Stress-Associated Neurobiological Pathway Linking Socioeconomic Disparities to Cardiovascular Disease

Cited by 120 publications

References 50 publications

Longitudinal Associations Between Income Changes and Incident Cardiovascular Disease

Longitudinal Associations Between Income Changes and Incident Cardiovascular Disease

Angiotensin-converting enzyme inhibitor treatment early after myocardial infarction attenuates acute cardiac and neuroinflammation without effect on chronic neuroinflammation

Influence of sex on heightened vasoconstrictor mechanisms in the non‐Hispanic black population

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