BACKGROUND: Mental stress-induced myocardial ischemia (MSIMI) is frequent in patients with coronary artery disease and is associated with worse prognosis. Young women with a previous myocardial infarction (MI), a group with unexplained higher mortality than men of comparable age, have shown elevated rates of MSIMI, but the mechanisms are unknown. METHODS: We studied 306 patients (150 women and 156 men) ≤61 years of age who were hospitalized for MI in the previous 8 months and 112 community controls (58 women and 54 men) frequency matched for sex and age to the patients with MI. Endothelium-dependent flow-mediated dilation and microvascular reactivity (reactive hyperemia index) were measured at rest and 30 minutes after mental stress. The digital vasomotor response to mental stress was assessed using peripheral arterial tonometry. Patients received 99mTc-sestamibi myocardial perfusion imaging at rest, with mental (speech task) and conventional (exercise/pharmacological) stress. RESULTS: The mean age of the sample was 50 years (range, 22-61). In the MI group but not among controls, women had a more adverse socioeconomic and psychosocial profile than men. There were no sex differences in cardiovascular risk factors, and among patients with MI, clinical severity tended to be lower in women. Women in both groups showed a higher peripheral arterial tonometry ratio during mental stress but a lower reactive hyperemia index after mental stress, indicating enhanced microvascular dysfunction after stress. There were no sex differences in flow-mediated dilation changes with mental stress. The rate of MSIMI was twice as high in women as in men (22% versus 11%, P=0.009), and ischemia with conventional stress was similarly elevated (31% versus 16%, P=0.002). Psychosocial and clinical risk factors did not explain sex differences in inducible ischemia. Although vascular responses to mental stress (peripheral arterial tonometry ratio and reactive hyperemia index) also did not explain sex differences in MSIMI, they were predictive of MSIMI in women only. CONCLUSIONS: Young women after MI have a 2-fold likelihood of developing MSIMI compared with men and a similar increase in conventional stress ischemia. Microvascular dysfunction and peripheral vasoconstriction with mental stress are implicated in MSIMI among women but not among men, perhaps reflecting women's proclivity toward ischemia because of microcirculatory abnormalities.
C-reactive protein (CRP), a marker of systemic inflammation, has been associated with major depressive disorder (MDD) and posttraumatic stress disorder (PTSD). Emotion dysregulation is a transdiagnostic risk factor for many psychological disorders associated with chronic inflammatory state. The objective of this study was to determine whether inflammation is associated with emotion dysregulation in women with type 2 diabetes mellitus (T2DM). We examined associations between trauma exposure, MDD, PTSD, emotion dysregulation, and CRP among 40 African-American women with T2DM recruited from an urban hospital. Emotion dysregulation was measured using the Difficulties in Emotion Regulation Scale. PTSD and MDD were measured with structured clinical interviews. Child abuse and lifetime trauma load were also assessed. Analyses showed that both emotion dysregulation and current MDD were significantly associated with higher levels of CRP (p < 0.01). Current PTSD was not significantly related to CRP. In a regression model, emotion dysregulation was significantly associated with higher CRP (p < 0.001) independent of body mass index, trauma exposure, and MDD diagnosis. These findings suggest that emotion dysregulation may be an important risk factor for chronic inflammation beyond already known risk factors among women with T2DM, though a causal relationship cannot be determined from this study.
Background: Somatic depressive symptoms and certain biomarkers are each associated with worse acute myocardial infarction (AMI) prognosis, but the relationship between depressive symptom domains and inflammatory, neurohormonal, and coagulation markers is unknown. Methods: We examined the relationship between depressive symptoms and 1-month biomarker levels (high-sensitivity C-reactive protein [hs-CRP], N-terminal pro-brain natriuretic peptide [NT-proBNP], white blood cell [WBC], platelet counts) in 1265 AMI patients. Depressive symptoms (9-item Patient Health Questionnaire) were assessed during index hospitalization and categorized as somatic or cognitive. Using median regression models, the upper quartile of somatic and cognitive depression scores and each biomarker were compared with the lower three quartiles, adjusting for site, demographics, and clinical characteristics. Results: Although hs-CRP values were higher in patients with somatic symptoms, this association was attenuated after adjustment (B per SD increase =.02, 95% confidence interval:.00;.05, p =.07). WBC count was independently associated with somatic depressive symptoms (B per SD increase =.28, 95% confidence interval:.12;.44, p <.001). Cognitive depressive symptoms were not associated with hs-CRP or WBC count. Neither dimension was associated with NT-proBNP or platelet levels. For each biomarker, the depression dimensions explained <1% of their variation. Conclusions: Neither somatic nor cognitive depressive symptoms were meaningfully associated with hs-CRP, NT-proBNP, WBC, or platelet counts 1 month after AMI, suggesting that the association between depression and long-term outcomes may be unrelated to these biomarkers. Future research should explore other biomarkers to better illuminate pathways by which depression adversely impacts AMI prognosis.