Chronic inflammatory disease (CID) causes major cardiovascular events such as coronary heart disease, stroke, peripheral vascular disease and cardiomyopathy. Rheumatoid arthritis (RA) is a chronic, autoimmune, systemic inflammatory disorders with secondary cardiovascular events.
Indeed, patients with RA have an increased cardiovascular risk independently of classical risk factors (i.e. dyslipidemia, aging, hypertension), linked to an accelerated atherosclerotic process, cardiac dysfunction with left ventricular hypertrophy and/or failure. More generally, CID patients also show increased inflammatory activity in vasculature, in micro-vessels as well as at the level of the cardiomyocytes themselves.
They also have a defective sympatho-vagal balance leading to decreased heart rate variability. Recently, alteration of the intestinal microbiota was shown to contribute to the development of cardiovascular diseases. Indeed, the microbiota can modulate the autonomic function (intestine-brain axis) which will modify the adaptability of the heart rate to the body’s needs.
The microbiota can also increase atherosclerosis by promoting the formation of foam cells through cytokines and chemokines secreted in response to bacterial lipopolysaccharide and is able to modify lipids metabolism. To date, no specific metabolite produced by microbiota has been identified to be responsible for a sympatho-vagal imbalance and impaired cardiac function in patients with RA.
Using RA models and clinical studies, we aim to establish the contribution of the gut microbiota and related inflammatory mechanisms to the cardiovascular events observed during RA. We explore new therapeutic perspectives either through dietary modifications, probiotics and/or targeted pharmacological treatments. With this translational approach, we will determine common denominators for the development of CID and associated cardiomyopathy. These knowledges can be used to suggest novel ways to treat and/or prevent myocardial dysfunction in CID or to improve current treatment.