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Review
. 2014:2014:367359.
doi: 10.1155/2014/367359. Epub 2014 Jul 22.

Cardiovascular involvement in autoimmune diseases

Jenny Amaya-Amaya  1 , Laura Montoya-Sánchez  1 , Adriana Rojas-Villarraga  1
Affiliations
Review

Cardiovascular involvement in autoimmune diseases

Jenny Amaya-Amaya et al. Biomed Res Int. 2014.

Abstract

Autoimmune diseases (AD) represent a broad spectrum of chronic conditions that may afflict specific target organs or multiple systems with a significant burden on quality of life. These conditions have common mechanisms including genetic and epigenetics factors, gender disparity, environmental triggers, pathophysiological abnormalities, and certain subphenotypes. Atherosclerosis (AT) was once considered to be a degenerative disease that was an inevitable consequence of aging. However, research in the last three decades has shown that AT is not degenerative or inevitable. It is an autoimmune-inflammatory disease associated with infectious and inflammatory factors characterized by lipoprotein metabolism alteration that leads to immune system activation with the consequent proliferation of smooth muscle cells, narrowing arteries, and atheroma formation. Both humoral and cellular immune mechanisms have been proposed to participate in the onset and progression of AT. Several risk factors, known as classic risk factors, have been described. Interestingly, the excessive cardiovascular events observed in patients with ADs are not fully explained by these factors. Several novel risk factors contribute to the development of premature vascular damage. In this review, we discuss our current understanding of how traditional and nontraditional risk factors contribute to pathogenesis of CVD in AD.

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Figures

Figure 1
Figure 1
Traditional and nontraditional risk factors for cardiovascular disease in rheumatoid arthritis. AD: autoimmune disease; CVD: cardiovascular disease; IMT: intima-media thickness; RA: rheumatoid arthritis; RF: rheumatoid factor. aCVD includes a broad spectrum of subphenotypes: stroke/transient ischemic attack, coronary artery disease, myocardial infarction, angina, congestive heart failure, arrhythmias, ventricular diastolic dysfunction, hypertension, pulmonary embolism, deep vein thrombosis, and peripheral arterial/venous disease. bMainly HLA-DRB1∗0404 shared epitope alleles. cThe presence of any diagnosed AD in first-degree relatives of proband. dThe presence of two concomitant AD in a single patient on the basis of international criteria. eRheumatoid factor, anti-cyclic citrullinated peptides antibodies, anti-oxidized low-density lipoprotein, anticardiolipins, anti-phosphorylcholine, anti-modified citrullinated vimentin, anti-apolipoprotein A-1, and anti-cytokeratin 18 antibodies. fHigh levels of c-reactive protein and erythrocyte sedimentation rate. gMethotrexate, leflunomide, and nonsteroidal anti-inflammatory drugs. hPatients (females and males) with RA working on household duties. ivon Willebrand factor, plasminogen activator inhibitor-1, and tissue plasminogen activator. jHypothyroidism, periodontal disease, and other markers such as mannose-binding lectin, serum pentraxin 3, osteopontin, osteoprotegerin, and seric uric acid.
Figure 2
Figure 2
Traditional and autoimmune-related mechanisms of cardiovascular disease in systemic lupus erythematosus and antiphospholipid syndrome. A complex interaction between traditional and disease-specific traits leads to premature atherosclerosis process. Several risk factors (left) have been described since the Framingham heart study, known as classic risk factors, which over time conduce to endothelial dysfunction, subclinical atherosclerosis, and CV event manifest. In the autoimmune setting (right), several novel risk factors contribute to development of premature vascular damage. This damage is represented by impaired endothelial function and early increase of intima-media thickness, which are surrogates of the accelerated atherosclerosis process. These associations are even more pronounced in this case of polyautoimmunity (SLE and APS in the same individual), where risk factors have additive effects and atherosclerosis develops earlier. The cornerstone of management of CV risk includes an aggressive treatment of disease activity, the continuous monitoring and treatment of modifiable CV risk factors, and the use of other medications in order to diminish the CV burden. ACE-I: angiotensin-converting enzyme inhibitors; AMs: antimalarials; APS: antiphospholipid syndrome; AT-II blockers: angiotensin II receptor blockers; Auto-Ab: autoantibodies; AZA: azathioprine; CIC: circulating immune complex; CYC: cyclophosphamide; CVD: cardiovascular disease; HDL: high-density lipoprotein; HRT: hormone replacement therapy; IR: insulin resistance; MetS: metabolic syndrome; MMF: mycophenolate mofetil; oxLDL/β2GPI complex: oxidized low-density lipoprotein/2 glycoprotein I; SLE: systemic lupus erythematosus; T2DM: type 2 diabetes mellitus.
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