scholarly journals 427How does childhood maltreatment influence cardiovascular disease? A sequential causal mediation analysis

2021 ◽  
Vol 50 (Supplement_1) ◽  
Author(s):  
Ana Goncalves Soares ◽  
Laura D Howe ◽  
Gemma Hammerton ◽  
Jon Heron ◽  
Janet Rich-Edwards ◽  
...  

Abstract Background Childhood maltreatment (CM) has been associated with cardiovascular disease (CVD), but the mechanisms of this relationship are not fully understood. We explored the relative contribution of anxiety/depression, smoking, body mass index (BMI) and C-reactive protein (CRP) to the association between CM and CVD in the United Kingdom (UK) and whether this differed by sex and type of maltreatment. Methods We used data from 40,596 men and 59,511 women from UK Biobank. To estimate the indirect effects of CM (physical, sexual and emotional abuse, and emotional and physical neglect) on incident CVD, we applied a sequential mediation approach using g-computation. Results Together anxiety/depression, smoking, BMI and CRP mediated 26%-90% of the association between CM and CVD, and the contribution of these mediators differed by type of maltreatment and sex. For sexual abuse, emotional abuse and emotional neglect, anxiety/depression was the most important mediator (accounting for 16%-43% of the total effect), especially in women. In men, BMI contributed the most in associations of physical abuse and physical neglect with CVD; in women anxiety/depression and BMI had similar contributions. Conclusions These findings add to the understanding of how CM affects CVD and highlight the potential to reduce the burden of CVD in people exposed to CM through targeting modifiable mediating factors. Key messages Anxiety/depression, smoking, BMI and inflammation mediated part of the association between CM and CVD, and the contribution of these mediators differed by type of maltreatment and sex.

2020 ◽  
Author(s):  
Ana Goncalves Soares ◽  
Laura D Howe ◽  
Gemma Hammerton ◽  
Jon Heron ◽  
Janet Rich-Edwards ◽  
...  

Background: Childhood maltreatment has been consistently associated with cardiovascular disease (CVD). However, the mechanisms of this relationship are not yet fully understood. We explored the relative contribution of anxiety/depression, smoking, body mass index (BMI) and inflammation (C-reactive protein, CRP) to the association between childhood maltreatment and CVD in men and women aged 40-69 years in the United Kingdom (UK). Methods: We used data from 40,596 men and 59,511 women from UK Biobank. To estimate the indirect effects of childhood maltreatment (physical, sexual and emotional abuse, and emotional and physical neglect) on incident CVD via each of the mediators, we applied a sequential mediation approach. Results: All forms of maltreatment were associated with increased CVD risk (hazard ratios (HR) ranging from 1.09 to 1.27). Together anxiety/depression, smoking, BMI and CRP mediated 26%-90% of the association between childhood maltreatment and CVD, and the contribution of these mediators differed by type of maltreatment and sex. Anxiety/depression mediated the largest proportion of the association of sexual abuse, emotional abuse and emotional neglect with CVD (accounting for 16%-43% of the total effect), especially in women. In men, BMI contributed the most to the indirect effect of associations of physical abuse and physical neglect with CVD; in women anxiety/depression and BMI had similar contributions. Conclusions: These findings add to the understanding of how childhood maltreatment affects CVD risk and identify modifiable mediating factors which could potentially reduce the burden of CVD in people exposed to maltreatment in early life.


1997 ◽  
Vol 17 (6) ◽  
pp. 1121-1127 ◽  
Author(s):  
Russell P. Tracy ◽  
Rozenn N. Lemaitre ◽  
Bruce M. Psaty ◽  
Diane G. Ives ◽  
Rhobert W. Evans ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Kenji Inoue ◽  
Tatsuhiko Kodama ◽  
Hiroyuki Daida

Numerous studies have recently examined the role of pentraxin 3 (PTX3) in clinical situations. The pentraxin family includes C-reactive protein (CRP); however, unlike CRP, PTX3 is expressed predominantly in atherosclerotic lesions that involve macrophages, neutrophils, dendritic cells, or smooth muscle cells. Interestingly, PTX3 gene expression in human endothelial cells is suppressed to a greater extent by pitavastatin than the expression of 6,000 other human genes that have been examined, suggesting that PTX3 may be a novel biomarker for inflammatory cardiovascular disease. The expression and involvement of PTX3 in cardiovascular diseases are discussed in this paper, along with the characteristics of PTX3 that make it a suitable biomarker; namely, that the physiological concentration is known and it is independent of other risk factors. The results discussed in this paper suggest that further investigations into the potential novel use of PTX3 as a biomarker for inflammatory cardiovascular disease should be undertaken.


2019 ◽  
Vol 65 (9) ◽  
pp. 1102-1114 ◽  
Author(s):  
Hiroaki Ikezaki ◽  
Virginia A Fisher ◽  
Elise Lim ◽  
Masumi Ai ◽  
Ching-Ti Liu ◽  
...  

AbstractBACKGROUNDIncreases in circulating LDL cholesterol (LDL-C) and high-sensitivity C-reactive protein (hsCRP) concentrations are significant risk factors for cardiovascular disease (CVD). We assessed direct LDL-C and hsCRP concentrations compared to standard risk factors in the Framingham Offspring Study.METHODSWe used stored frozen plasma samples (−80 °C) obtained after an overnight fast from 3147 male and female participants (mean age, 58 years) free of CVD at cycle 6 of the Framingham Offspring Study. Overall, 677 participants (21.5%) had a CVD end point over a median of 16.0 years of follow-up. Total cholesterol (TC), triglyceride (TG), HDL cholesterol (HDL-C), direct LDL-C (Denka Seiken and Kyowa Medex methods), and hsCRP (Dade Behring method) concentrations were measured by automated analysis. LDL-C was also calculated by both the Friedewald and Martin methods.RESULTSConsidering all CVD outcomes on univariate analysis, significant factors included standard risk factors (age, hypertension, HDL-C, hypertension treatment, sex, diabetes, smoking, and TC concentration) and nonstandard risk factors (non-HDL-C, direct LDL-C and calculated LDL-C, TG, and hsCRP concentrations). On multivariate analysis, only the Denka Seiken direct LDL-C and the Dade Behring hsCRP were still significant on Cox regression analysis and improved the net risk reclassification index, but with modest effects. Discordance analysis confirmed the benefit of the Denka Seiken direct LDL-C method for prospective hard CVD endpoints (new-onset myocardial infarction, stroke, and/or CVD death).CONCLUSIONSOur data indicate that the Denka Seiken direct LDL-C and Dade Behring hsCRP measurements add significant, but modest, information about CVD risk, compared to standard risk factors and/or calculated LDL-C.


Stroke ◽  
2006 ◽  
Vol 37 (7) ◽  
pp. 1720-1724 ◽  
Author(s):  
David Tanne ◽  
Michal Benderly ◽  
Uri Goldbourt ◽  
Moti Haim ◽  
Alexander Tenenbaum ◽  
...  

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Lei Zhao ◽  
Songnan Li ◽  
Chen Zhang ◽  
Jie Tian ◽  
Aijia Lu ◽  
...  

Abstract Background Myocardial strain assessed with cardiovascular magnetic resonance (CMR) feature tracking can detect early left ventricular (LV) myocardial deformation quantitatively in patients with a variety of cardiovascular diseases, but this method has not yet been applied to quantify myocardial strain in patients with atrial fibrillation (AF) and no coexistent cardiovascular disease, i.e., the early stage of AF. This study sought to compare LV myocardial strain and T1 mapping indices in AF patients and healthy subjects, and to investigate the associations of a portfolio of inflammation, cardiac remodeling and fibrosis biomarkers with LV myocardial strain and T1 mapping indices in AF patients with no coexistent cardiovascular disease. Methods The study consisted of 80 patients with paroxysmal AF patients and no coexistent cardiovascular disease and 20 age- and sex-matched healthy controls. Left atrial volume (LAV), LV myocardial strain and native T1 were assessed with CMR, and compared between the AF patients and healthy subjects. Biomarkers of C-reactive protein (CRP), transforming growth factor beta-1 (TGF-β1), collagen III N-terminal propeptide (PIIINP), and soluble suppression of tumorigenicity 2 (sST2) were obtained with blood tests, and compared between the AF patients and healthy controls. Associations of these biomarkers with those CMR-measured parameters were analyzed for the AF patients. Results For the CMR-measured parameters, the AF patients showed significantly larger LAV and LV end-systolic volume, and higher native T1 than the healthy controls (max P = 0.027). The absolute values of the LV peak systolic circumferential strain and its rate as well as the LV diastolic circumferential strain rate were all significantly reduced in the AF patients (all P < 0.001). For the biomarkers, the AF patients showed significantly larger CRP (an inflammation biomarker) and sST2 (a myocardium stiffness biomarker) than the controls (max P = 0.007). In the AF patients, the five CMR-measured parameters of LAV, three LV strain indices and native T1 were all significantly associated with these two biomarkers of CRP and sST2 (max P = 0.020). Conclusions In patients with paroxysmal AF and no coexistent cardiovascular disease, LAV enlargement and LV myocardium abnormalities were detected by CMR, and these abnormalities were associated with biomarkers that reflect inflammation and myocardial stiffness.


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