Role Of Inflammation In Cardiovascular Disease Research Articles

Abstract 11282: Meta-Analysis of Residential Portable Air Cleaner Use and Circulating Inflammatory Biomarkers

Introduction: Fine particulate matter air pollution (PM 2.5 ) exposure is associated with elevated circulating inflammatory biomarkers implicated in cardiovascular disease (CVD). Portable Air Cleaners (PAC)s reduce PM 2.5 exposure and may lower concentrations of inflammatory biomarkers. Methods: We performed a systematic review and meta-analysis of randomized crossover trials of in-home high efficiency particulate air (HEPA) PACs vs. sham control on changes in CRP, IL-6, and/or TNFα among adults with no smoking exposure using Medline, Embase, and Cochrane Central Register of Controlled Trials with the Ovid Platform, Inspec, Compendix, and Web of Science Core Collection. Two investigators (S.W, D.W.) independently screened and reviewed the studies. We used RevMan 5.3 to perform the meta-analysis. Results: Search results included 459 articles screened, 26 selected for full review, and 14 that met inclusion criteria, representing N=724 participants included in the meta-analysis. Ten studies reported CRP, 9 reported IL-6, and 5 reported TNFα. Based on WHO guidelines, 5 studies were in regions of extreme PM 2.5 exposure (>35 μg/m 3 ), 3 were high (10-35 μg/m 3 ), 3 were low (<10 μg/m 3 ), and 2 lacked baseline PM 2.5 . Median (± S.D.) duration of HEPA/sham use was 9 ± 6.6 days. Reductions in PM 2.5 ranged from 2.6 to 54.9 μg/m 3 (35-82%) and varied by baseline PM 2.5 , although reporting of baseline PM 2.5 was incomplete across trials. Compared to sham PAC use, active PACs were associated with a 7% lower CRP (95% CI -13%, 0%) and 12% lower IL-6 (-22%, -2%), P<0.05 for both (Figure). Subgroup analyses demonstrated consistency of effect of PACs across levels of baseline PM 2.5 . Conclusions: Our data demonstrate that PAC use is associated with significant reductions in circulating CRP and IL-6, with a magnitude of effect similar to clinical trials of statins and IL-1β inhibition. Given the role of inflammation in CVD, PACs may be useful to reduce systemic inflammation and cardiovascular risk.

Chronic Inflammatory Diseases and Atherosclerotic Cardiovascular Disease: Innocent Bystanders or Partners in Crime?

Inflammation plays a significant role in atherosclerosis and cardiovascular disease (CVD). Patients with chronic inflammatory diseases are at increased risk of CVD, but it is debated whether this association is causal or dependent on shared risk factors, other exposures, genes, and/or inflammatory pathways. The current review summarizes epidemiological, clinical, and experimental data supporting the role of shared inflammatory mechanisms between atherosclerotic CVD and rheumatoid arthritis, psoriasis, inflammatory bowel disease, and periodontitis, respectively, and provides insights to future prospects in this area of research. Awareness of the role of inflammation in CVD in patients with chronic inflammatory diseases and the potential for anti-inflammatory therapy, e.g., with tumor necrosis factor-α inhibitors, to also reduce atherosclerotic CVD has evolved into guideline- based recommendations. These include regular CVD risk assessment, aggressive treatment of traditional CVD risk factors, and recognition of reduced CVD as an added benefit of strict inflammatory disease control. At present, chronic inflammatory diseases would appear to qualify as partners in crime and not merely innocent bystanders to CVD. However, definite incremental contributions of inflammation versus effects of the complex interplay with other CVD risk factors may never be fully elucidated and for the foreseeable future, inflammation is posed to maintain its current position as both a marker and a maker of CVD, with clinical utility both for identification of patient at risk of CVD and as target for therapy to reduce CVD.

Associations between cardiovascular disease risk factors and IL-6 and hsCRP levels in the elderly

BackgroundAge-related diseases, including cardiovascular diseases (CVD) may be stimulated by microinflammation, marked by increased level of IL-6 and high-sensitivity CRP (hsCRP). We aimed to investigate whether aging “per se” independently contributes to the microinflammation, in addition to traditional and novel CVD risk factors. Methods/resultsThe research sample included 4979 participants from PolSenior Study, aged over 65years. The study consisted of three visits and included questionnaire survey, geriatric assessment and blood/urine sampling in 4101 participants (83.2% of the sample). Serum hsCRP and plasma IL-6 were measured in 4093 (99.8%) and 3895 (95.0%) subjects. Multiple logistic regression showed that advanced age (over 80years), obesity, actual/former smoking, decreased HDL-cholesterol, chronic kidney disease (CKD) and depression were associated with occurrence of increased level of IL-6 (>2.4pg/ml). For hsCRP we found that advanced age, overweight/obesity, decreased HDL-cholesterol, actual/former smoking and CKD were associated with increased level of hsCRP (>3mg/l), while high income and statins treatment were related to lower level of hsCRP. ConclusionsMicroinflammation in the elderly is not fully explained by traditional and novel CVD risk factors. Active smoking, obesity and low HDL-cholesterol among traditional risk factors, along with CKD, depression and low income among novel risk factors, are the strongest determinants of microinflammation. Also we found that statin therapy decreases hsCRP levels, which indicates a potential role of inflammation in CVD as a target for intervention in the elderly (e.g. statin use).

Vascular Inflammation: A Novel Access Route for Nanomedicine.

Despite an improved understanding of its pathophysiology and a wide range of new treatments, cardiovascular disease (CVD) remains a serious public health issue and the number one cause of mortality in the United States. Conditions that promote chronic systemic inflammation, such as obesity, cancer, and autoimmune and infectious diseases, are now known to play an important role in promoting CVD by inducing the expression of endothelial adhesion molecules and chemokines; these in turn promote leukocyte adherence and infiltration, which initiates and spurs the progression of CVD. In response to this new understanding, researchers are evaluating the potential cardiovascular benefits of new-generation therapies based on endogenous molecules with anti-inflammatory properties. Similarly, targeted approaches that leverage the phenotypic differences between non-inflamed and inflamed endothelia have the potential to selectively deliver therapeutics and decrease the morbidity and mortality of CVD patients. In this review, we discuss the role of inflammation in CVD and explore the therapeutic potential of targeting inflamed vasculature through conventional and biomimetic approaches.

Cardiovascular co-morbidity in rheumatic diseases

Patients with rheumatic disorders have an increased risk of cardiovascular disease (CVD). This excess co-morbidity is not fully explained by traditional risk factors. Disease severity is a major risk factor for CVD in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Shared disease mechanisms in atherosclerosis and rheumatic disorders include immune dysregulation and inflammatory pathways, which are potential targets for therapy. Lessons from RA and SLE may have implications for future research on the pathogenesis of atherosclerotic vascular disease in general. Recent data indicate that suppression of inflammation reduces the risk of CVD morbidity and mortality in patients with severe RA. The modest, but clinically relevant, efficacy of atorvastatin treatment in RA adds to the evidence for important anti-inflammatory properties for statins. There is increased recognition of the need for structured preventive strategies to reduce the risk of CVD in patients with rheumatic disease. Such strategies should be based on insights into the role of inflammation in CVD, as well as optimal management of life style related risk factors. In this review, the research agenda for understanding and preventing CVD co-morbidity in patients with rheumatic disorders is discussed.