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Cardiovascular disease evidence in chronic inflammatory rheumatic diseases Dr. Miguel Gonzรกlez-Gay

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Cardiovascular disease evidence in chronic inflammatory rheumatic diseases Dr. Miguel González-Gay Rheumatology Service The Marqués de Valdecilla University Hospital Santander, Spain.

1. Clinical evidences of cardiovascular diseases in rheumatoid arthritis and spondyloarthropathies Patients with inflammatory disease have a higher risk of cardiovascular (CV) events and mortality1. In rheumatoid arthritis (RA) : • CV disease is the most common cause of early mortality and myocardium infarction in patients with RA, with a relative risk (RR) of 2, which reaches up to 3 when RA has more than a 10-year evolution. • CV mortality in RA is a consequence of an accelerated atherosclerosis process.

• The increase in ankylosing spondylitis (AS) mortality is independent of possible complications, such as cardiac failure, cardiomyopathy and conduction defects, and it is a consequence of an accelerated atherogenesis4.

2, 3

In spondyloarthropathies: • Patients with spondyloarthropathies have a higher CV mortality rate which is explained only partially, due to the classical cardiovascular risk factors (CRF). 2

In psoriatic arthritis (PsA): • Patients with PsA have a higher mortality rate due to cardiovascular complications, such as myocardium infarction RR of 2.57 (95% CI: 1.73-3.80)5. • The severity of psoriasis cutaneous affection is a predictive factor of CV risk. 2. Subclinical CV disease presence in RA and spondyloarthropathies: In RA, PsA and AS, we can find: Endothelial dysfunction: • Initial atherosclerosis process under development

• It is a functional alteration • It can be diagnosed by ultrasound of the brachial artery through flow-mediated (endothelium dependent) vasodilatation. Subclinical (morphological) atherosclerosis: • It can be detected with a noninvasive method via carotid ultrasound, with the determination of: * Increased intima-media thickness (IMT) * Presence of atheroma plaques. The mechanisms of the accelerated atherogenesis in RA are summarized in the following table (see Table 1). Endothelial dysfunction in patients with RA appears at early stages and independently of the conventional CRF.

In addition, the endothelial dysfunction in “healthy” patients from the cardiovascular point of view has also been found in patients with PsA and AS. A simple way to assess the subclinical atherosclerosis is through high resolution carotid ultrasound. In the general population, an elevated IMT, or the presence of plaques, predicts the development of CV events. In RA, a meta-analysis showed that, in different population groups, there exist an increase of carotid IMT. Another study, comparing echo-graphical studies of patients with RA without CRF with healthy controls, found that patients with RA had a higher IMT and twice the quantity of carotid lesions. The predictive factor for the presence of plaques was the

most extended duration of rheumatic disease. This same pattern has been found in patients with PsA and AS. 3. Classical CRF influence on these chronic inflammatory diseases: Classical CRFs in RA have an additive effect, especially at the onset of the rheumatic disease, while, in subsequent stages, the inflammatory condition would have a more significant relevance6. On the other hand, these diseases are correlated with an increase of the CRF prevalence. 4. Role of the genetic factors in RA cardiovascular risk: A decrease in the endothelialdependent vasodilatation, positive for the HLA-DRB1*04 shared epitope in patients with RA has been found, and this is even

more severe in patients with HLADRB1*0404. The presence of HLA-DRB1 and persistent chronic inflammation contribute to the increase of the cardiovascular event and mortality risks in patients with RA. The TNF-α-308 polymorphism is associated to an increase of the CV risk in patients with RA. In addition, the CCR5 mutation associated to the protection against RA has also been found to have a preventive effect of cardiovascular events and endothelial dysfunction. 5. Inflammation as non-classical risk factor in the development of CV disease in chronic inflammatory diseases: Inflammation is the most important non-classical risk factor that should be treated in order to prevent CV disease in patients with

Rheumatoid arthritis: mechanisms accelerated atherogenesis

Table 1



Cytokines TNF-α IL1ß- , IL-6

PCR fibrinógeno

Adipose tissue Lipolysis

Dyslipidemia Skeletal muscle

Insulin Resistance


Endothelial dysfunction

Stress pro-oxidative Gonzalez-Gay et al. SeminArthritis Rheum 2005;35:8-17.

Prothrombotic state


chronic inflammatory diseases.In the general population, high CRF levels are associated to a higher CV morbi-mortality. In the same way, the highest CRF levels in patients with RA or AS present a higher prevalence of an increase of IMT and of carotid atherosclerosis, which is correlated to an increase of CV risk.


References 1.

• Chronic inflammatory rheumatic diseases are associated to an increase of the subclinical atherosclerosis and CV events. • An early diagnosis of the CV disease is necessary in chronic inflammatory rheumatic diseases.

2. 3. 4. 5. 6.

Goodson NJ et al. Arthritis Rheum 2005;52:2293-2299. Solomon et al. Circulation 2003;107:13031307. Maradit-Kremes et al. Arthritis Rheum 2005;52:402-411. Peters MJ, et al. Seminars in Arthritis and Rheumatism 2004, 34(3):585-592. Dafna Gladman et al. Arthritis Rheum 1997;40:1868-1872. Dessein PH, et al. J Rheumatol 2005;32:435442.


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The data and results presented herein were obtained from a conference on Medicine and the information summarized might be preliminary and subject to changes. This information is exclusively included for physician’s training and educational purposes only. The opinions here reflected belong to the authors and lecturers and do not comprise any suggestion or recommendation on the part of the sponsoring laboratory. Summary prepared by the Staff of Circle Press based on their attendance to the Symposium


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Cardiovascular disease evidence in chronic inflammatory rheumatic diseases  

Cardiovascular disease evidence in chronic inflammatory rheumatic diseases

Cardiovascular disease evidence in chronic inflammatory rheumatic diseases  

Cardiovascular disease evidence in chronic inflammatory rheumatic diseases