title: Is the risk of cardiovascular disease altered with anti-inflammatory therapies? Insights from rheumatoid arthritis.
abstract: Cardiovascular disease (CVD) remains the leading cause of mortality worldwide. Atherosclerosis is the most common form of CVD, which is complex and multifactorial with an elevated risk observed in people with either metabolic or inflammatory diseases. Accumulating evidence now links obesity with a state of chronic low-grade inflammation and has renewed our understanding of this condition and its associated comorbidities. An emerging theme linking disease states with atherosclerosis is the increased production of myeloid cells, which can initiate and exacerbate atherogenesis. Although anti-inflammatory drug treatments exist and have been successfully used to treat inflammatory conditions such as rheumatoid arthritis (RA), a commonly observed side effect is dyslipidemia, inadvertently, a major risk factor for the development of atherosclerosis. The mechanisms leading to dyslipidemia associated with anti-inflammatory drug use and whether CVD risk is actually increased by this dyslipidemia are of great therapeutic importance and currently remain poorly understood. Here we review recent data providing links between inflammation, hematopoiesis, dyslipidemia and CVD risk in the context of anti-inflammatory drug use.
authors.affiliation: Department of Haematopoiesis and Leukocyte Biology, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, USA.
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Kraakman
authors.affiliation: Department of Haematopoiesis and Leukocyte Biology, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia; Department of Immunology, Monash University, Melbourne, Victoria, Australia.
authors.forename: Dragana
authors.initials: D
authors.lastname: Dragoljevic
authors.affiliation: Department of Haematopoiesis and Leukocyte Biology, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia; Department of Immunology, Monash University, Melbourne, Victoria, Australia.
authors.forename: Helene L
authors.initials: HL
authors.lastname: Kammoun
authors.affiliation: Department of Haematopoiesis and Leukocyte Biology, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia; Department of Immunology, Monash University, Melbourne, Victoria, Australia.
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Murphy