Title:Accelerated Atherosclerosis in Rheumatoid Arthritis: Mechanisms and Treatment
VOLUME: 25 ISSUE: 9
Author(s):Allison B. Reiss*, Andrew Silverman, Muhammed Khalfan, Nicholas A. Vernice, Lora J. Kasselman, Steven E. Carsons and Joshua De Leon
Affiliation:Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 Mineola Boulevard, Suite 4-004, Mineola, NY 11501, Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 Mineola Boulevard, Suite 4-004, Mineola, NY 11501, Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 Mineola Boulevard, Suite 4-004, Mineola, NY 11501, Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 Mineola Boulevard, Suite 4-004, Mineola, NY 11501, Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 Mineola Boulevard, Suite 4-004, Mineola, NY 11501, Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 Mineola Boulevard, Suite 4-004, Mineola, NY 11501, Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 Mineola Boulevard, Suite 4-004, Mineola, NY 11501
Keywords:Rheumatoid arthritis, tumor necrosis factor, atherosclerosis, inflammation, biologics, DMARD, methotrexate.
Abstract:
Background: Rheumatoid arthritis (RA) is a chronic systemic autoimmune inflammatory disorder that
increases the risk of developing cardiovascular disease. There is accumulating evidence that the RA disease state
accelerates the formation of atherosclerotic plaques. Treatments for RA improve joint symptomatology and may
reduce inflammation, but consideration of their effects on the cardiovascular system is generally low priority.
Objective: Since cardiovascular disease is the leading cause of mortality in RA patients, the impact of RA therapies
on atherosclerosis is an area in need of attention and the focus of this review.
Results: The drugs used to treat RA may be analgesics, conventional disease-modifying anti-rheumatic drugs,
and/or biologics, including antibodies against the cytokine tumor necrosis factor-α. Pain relievers such as nonselective
non-steroidal anti-inflammatory drugs and cyclooxygenase inhibitors may adversely affect lipid metabolism
and cyclooxygenase inhibitors have been associated with increased adverse cardiovascular events, such as
myocardial infarction and stroke. Methotrexate, the anchor disease-modifying anti-rheumatic drug in RA treatment
has multiple atheroprotective advantages and is often combined with other therapies. Biologic inhibitors of
tumor necrosis factor-α may be beneficial in preventing cardiovascular disease because tumor necrosis factor-α
promotes the initiation and progression of atherosclerosis. However, some studies show a worsening of the lipid
profile in RA with blockade of this cytokine, leading to higher total cholesterol and triglycerides.
Conclusion: Greater understanding of the pharmacologic activity of RA treatments on the atherosclerotic process
may lead to improved care, addressing both damages to the joints and heart.
