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12-04-2016 | Comorbidities | Article

Is the risk of cardiovascular disease altered with anti-inflammatory therapies? Insights from rheumatoid arthritis

Authors: Michael J Kraakman, Dragana Dragoljevic, Helene L Kammoun, Andrew J Murphy

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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.

Clin Trans Immunol 2016;5,e84. doi:10.1038/cti.2016.31

Cardiovascular disease (CVD) is currently the leading cause of death worldwide. Atherosclerosis is the major form of CVD and is characterized by a chronic inflammatory build up, driven largely by lipid accumulation within the artery wall. Unlike acute inflammation, atherosclerosis is hallmarked by a state of unresolved low-grade chronic inflammation. Importantly, low-grade inflammation is also a feature of several diseases known to increase the risk of CVD. Obesity is a prime example of a low-grade chronic inflammatory disease that can promote insulin resistance and type 2 diabetes (T2D), and can increase the risk of CVD.1 Indeed, people with T2D have up to fourfold the risk of developing CVD compared with non-diabetic individuals. Hence, strategies targeting insulin resistance and glucose homeostasis through inflammation modulation or other mechanisms are important for the treatment of CVD. Conversely, therapies that are associated with triggering known CV risk factors including weight gain, insulin resistance and dyslipidemia are met with caution.

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