PubMed · 14697487
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William Clifford Roberts. 2004-01-01. Miscellany.. https://doi.org/10.1016/j.amjcard.2003.09.001
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The present paper provides a review of 45 studies on the Effort-Reward Imbalance (ERI) Model published from 1986 to 2003 (inclusive). In 1986, the ERI Model was introduced by Siegrist et al. (Biological and Psychological Factors in Cardiovascular Disease, Springer, Berlin, 1986, pp. 104-126; Social Science & Medicine 22 (1986) 247). The central tenet of the ERI Model is that an imbalance between (high) efforts and (low) rewards leads to (sustained) strain reactions. Besides efforts and rewards, overcommitment (i.e., a personality characteristic) is a crucial aspect of the model. Essentially, the ERI Model contains three main assumptions, which could be labeled as (1) the extrinsic ERI hypothesis: high efforts in combination with low rewards increase the risk of poor health, (2) the intrinsic overcommitment hypothesis: a high level of overcommitment may increase the risk of poor health, and (3) the interaction hypothesis: employees reporting an extrinsic ERI and a high level of overcommitment have an even higher risk of poor health. The review showed that the extrinsic ERI hypothesis has gained considerable empirical support. Results for overcommitment remain inconsistent and the moderating effect of overcommitment on the relation between ERI and employee health has been scarcely examined. Based on these review results suggestions for future research are proposed.
Complex cellular and inflammatory interactions are involved in the progress of vascular diseases. Endothelial cells, upon exposure to cytokines, undergo profound alterations of function that involve gene expression and de novo protein synthesis. The functional reprogramming of endothelial cells by cytokines is of importance especially in patients with chronic vascular inflammation. The intercellular network of dendritic cells, T-lymphocytes, macrophages and smooth muscle cells generates a variety of stimulatory cytokines [e.g. TNF-alpha (tumour necrosis factor-alpha), IL (interleukin)-1, IL-6 and IFN-gamma (interferon-gamma)] and growth factors that promote the development of functional and structural vascular changes. High concentrations of proinflammatory cytokines increase oxidative stress, down-regulate eNOS (endothelial nitric oxide synthase) bioactivity and induce endothelial cell apoptosis. Chemoattractant cytokines [e.g. VEGF (vascular endothelial growth factor), TGF-beta1 (transforming growth factor-beta1) and IL-8] are important regulators of inflammation-induced angiogenesis and are directly modulated by nitric oxide. This review will focus on the vascular mechanisms orchestrated by cytokines and summarizes the current knowledge concerning the contribution of cytokines to cardiovascular diseases.
PURPOSE OF REVIEW: Statins significantly reduce cholesterol synthesis and reduce cardiovascular morbidity and mortality. In addition, they appear to have beneficial effects independent of their ability to lower cholesterol. Recent publications suggesting a potential role for statin therapy in chronic renal insufficiency, hypertension and following organ transplantation are reviewed. RECENT FINDINGS: Pharmacokinetic studies have shown statins to be well-tolerated and effective in patients on long-term haemodialysis, providing equivalent control of lipid levels to that seen in matched controls. Preliminary clinical trials suggest that statins may have beneficial disease-modifying effects in chronic inflammatory disease. Furthermore, immunosuppressive and immunomodulatory actions may confer benefit following cardiac transplantation, but this remains to be demonstrated definitively in renal transplant patients. Data to date suggest that, in addition to reduction of cardiovascular risk, statins may help slow the progress of chronic renal insufficiency, particularly in patients with proteinuria. Addition of statin therapy may also contribute to the control of systemic and pulmonary hypertension. SUMMARY: Encouraging data in support of a wider spectrum of use for statins are emerging. In addition to reduction of cardiovascular risk through lipid lowering, they may represent an important adjunctive therapy in patients with chronic kidney diseases and post-transplantation. However, further large, well-designed clinical trials are required before their widespread use can be recommended in this setting.