Rheumatology: Current Research
Open Access

The Role of Inflammation in Cardiovascular Risk for Rheumatoid Arthritis Patients

Francis Guillemin^{* *}Correspondence: Francis Guillemin, Department of Rheumatology, University of Belgrade, Belgrade, Serbia, Email:

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About the Study

Rheumatoid Arthritis (RA) is a chronic autoimmune disorder characterized by joint inflammation and destruction. While it primarily affects the joints, RA is a systemic disease that can have far-reaching consequences beyond the musculoskeletal system. One of the most concerning comorbidities associated with RA is an increased risk of Cardiovascular Disease (CVD). Mounting evidence suggests that chronic inflammation, a hallmark of RA, plays a pivotal role in the development and progression of CVD in these patients.

Rheumatoid arthritis is a complex autoimmune disorder that affects approximately 1% of the world's population. It is characterized by synovial inflammation, leading to joint pain, swelling, and eventually, joint destruction if left untreated. RA is a systemic disease, meaning it can impact various organs and systems in the body, not just the joints. Some of the common symptoms and complications of RA include fatigue, joint deformities, and an increased risk of infections.

Cardiovascular disease and rheumatoid arthritis

Cardiovascular disease encompasses a range of conditions that affect the heart and blood vessels, including coronary artery disease, heart failure, and stroke. Over the years, numerous studies have highlighted a higher prevalence of CVD among RA patients compared to the general population. This elevated risk has prompted researchers to investigate the mechanisms linking RA and cardiovascular events, with inflammation emerging as a central player.

Chronic inflammation in rheumatoid arthritis

In RA, the immune system mistakenly attacks the synovium, a thin membrane lining the joints, triggering a cascade of inflammatory responses. This chronic inflammation is characterized by increased levels of proinflammatory cytokines such as Tumor Necrosis Factor-Alpha (TNF-α), Interleukin-1 (IL-1), and Interleukin-6 (IL-6). These cytokines play a crucial role in the pathogenesis of RA and contribute to joint damage and systemic inflammation.

Inflammation and atherosclerosis

Atherosclerosis is the underlying process responsible for most CVD events. It involves the buildup of fatty deposits (atherosclerotic plaques) within the arterial walls, leading to narrowing and hardening of the arteries. Chronic inflammation, as seen in RA, can accelerate atherosclerosis through several mechanisms:

Endothelial dysfunction: Inflammation impairs the function of the endothelium, the inner lining of blood vessels. This dysfunction reduces nitric oxide production and promotes vasoconstriction, facilitating plaque formation.

Oxidative stress: Inflammatory cytokines increase the production of Reactive Oxygen Species (ROS) within blood vessels, causing oxidative damage to lipids and proteins. Oxidative stress contributes to plaque instability.

Dyslipidemia: Inflammation can alter lipid metabolism, leading to unfavorable lipid profiles. Elevated levels of Low-Density Lipoprotein (LDL) cholesterol and decreased levels of High- Density Lipoprotein (HDL) cholesterol are common in RA patients, promoting atherosclerosis.

Plaque vulnerability: Inflammation can make atherosclerotic plaques more vulnerable to rupture. A ruptured plaque can trigger thrombosis, resulting in acute cardiovascular events such as myocardial infarction or stroke.

Biomarkers of Inflammation and Cardiovascular Risk

C-Reactive Protein (CRP): CRP is a well-established biomarker of inflammation and is routinely measured in clinical practice. Elevated CRP levels are associated with an increased risk of cardiovascular events in RA patients. High-sensitivity CRP (hs- CRP) assays can detect even subtle increases in CRP levels and are particularly useful for assessing cardiovascular risk.

Erythrocyte Sedimentation Rate (ESR): ESR measures the rate at which red blood cells settle in a tube of blood. Elevated ESR is indicative of inflammation and has been linked to cardiovascular risk in RA. It is often used alongside other clinical and laboratory assessments to monitor disease activity.

Interleukin-6 (IL-6): IL-6 is a proinflammatory cytokine that plays a central role in RA pathogenesis. Elevated IL-6 levels have been associated with increased cardiovascular risk and may serve as a valuable biomarker for assessing both RA disease activity and cardiovascular risk.

Tumor Necrosis Factor-Alpha (TNF-α): TNF-α is another key cytokine in RA inflammation. While TNF-α itself is not commonly measured as a biomarker, the response to TNF inhibitors, a class of medications used to treat RA, can indirectly indicate the level of TNF-α activity in a patient. TNF inhibitors have shown cardiovascular benefits in clinical trials, further implicating this cytokine in CVD risk.

Management of cardiovascular risk in rheumatoid arthritis

Disease-Modifying Antirheumatic Drugs (DMARDs): DMARDs are the cornerstone of RA treatment. They help control inflammation, reduce joint damage, and may have indirect cardiovascular benefits by lowering systemic inflammation.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): NSAIDs are commonly used to manage RA symptoms, but they should be used cautiously in individuals at high cardiovascular risk due to their potential to increase blood pressure and promote thrombosis.

Biologic DMARDs and JAK inhibitors: These are newer classes of RA medications that specifically target inflammatory pathways. Some of these drugs have shown cardiovascular benefits in clinical trials.

Lifestyle modifications: RA patients can reduce their cardiovascular risk by adopting a heart-healthy lifestyle, including smoking cessation, regular exercise, a balanced diet, and managing blood pressure and cholesterol levels.

Rheumatoid arthritis is more than just a joint disease; it is a systemic disorder with profound implications for cardiovascular health. Chronic inflammation, a hallmark of RA, is increasingly recognized as a key driver of cardiovascular risk in these patients. Understanding the intricate relationship between inflammation and CVD in RA is crucial for early intervention and personalized management strategies.