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.
Intravenous Administration of Allogenic Cell-Derived Microvesicles of Healthy Origins Defends Against Atherosclerotic Cardiovascular Disease Development by a Direct Action on Endothelial Progenitor Cells
