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Lowering Cardiovascular Risks in Patients with Rheumatoid Arthritis

Lowering Cardiovascular Risks in Patients with Rheumatoid Arthritis

Using four well known cardiovascular risk 'calculators' including the National Cholesterol Education Program (NCEP) and the Framingham risk score, a study done by Toms et al. from a single rheumatology clinic examined cardiovascular risk in 400 patients with rheumatoid arthritis (RA). This study is published in the Annals of the Rheumatic Diseases.

A minimum total cholesterol of 6.2 mmol/l, LDL-cholesterol level of least 4.13 mmol/l, HDL-cholesterol lower than 1.03 mmol/l or triglyceride level of at least 1.7 mmol/l is defined by the NCEP as lipid abnormalities. These lipid abnormalities were present in about half of the patients. Up to 26% of patients with RA and no apparent cardiovascular disease were classified as high risk despite variations among the algorithms used to estimate cardiovascular risk, and would have qualified from preventive statin treatment using conventional criteria (5% or greater risk of cardiovascular death over the next 10 years, and minimum total cholesterol 5 mmol/l, or LDL-cholesterol at least 3 mmol/l).


The fact that the majority (more than 58%) of these high-risk patients weren't receiving statin therapy was the principal finding of the study. The investigators speculate that reluctance to prescribe yet more medications to a population that already suffers from 'polypharmacy', a misconception that cardiovascular risk is low in females (who constituted most of the patients in this study), and a lack of attention to cardiovascular risk assessment among RA specialists, are some of the causes of this lack of therapy.


Considering the fact that patients with RA are at higher risk than the general population of acute cardiovascular events, including myocardial infarction, and that these events are associated with a poor prognosis, the apparent under-treatment of patients with RA is surprising. Toms et al. used cardiovascular risk calculators that were derived from unselected populations and will most probably underestimate the risk in RA. Because of this, the European League Against Rheumatism taskforce has recommended that a 1.5× risk-multiplier be applied to patients with RA and criteria associated with increased cardiovascular risk, including rheumatoid factor positive status and long disease duration.


Clustering of the 'traditional' cardiovascular risk factors such as hypertension, dyslipidemia and insulin resistance could be a partial cause of increased susceptibility to atherosclerosis in RA. Statins are the cornerstone of current lipid treatment, and despite the fact that they only weakly elevate HDL levels, usually by less than 5%, but they are effective at lowering LDL levels, usually by 20 to 30%.


High levels of atherogenis triglycerides, small and dense LDL particles, and low levels of protective HDL are included in the triad of harmful lipid abnormalities that dyslipidemia comprises in RA. Reverse cholesterol transport (from atherosclerotic plaques to the liver), and antioxidant and anti-inflammatory effects are some of the multiple functions from which arises the protective effect of HDL in cardiovascular disease. HDL undergoes marked compositional and functional changes in patients with RA, sometimes to the extent of becoming proinflammatory. However, in vitro studies have indicated that normal HDL function can be restored with high-dose statin treatment.


The progression of atherosclerosis is caused by the chronic inflammation in RA, which also promotes the development of unstable plaque morphology and behavior, with an increased risk of acute vascular events caused by plaque rupture. Elevated C-reactive protein (CRP) levels were associated with an increased risk of cardiovascular events in an otherwise apparently healthy population. In the JUPITER (Justification for the use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin) study, statin treatment considerably reduced a composite of cardiovascular events and deaths in patients with low LDL-cholesterol but high CRP levels. However, the suppression of inflammation in the patients of JUPITER might not be equivalent to suppressing disease activity in RA, because the inflammatory activity in the patients from JUPITER study was probably related to inflamed atherosclerotic vessels. Nevertheless, emerging evidence suggests that markers of cardiovascular risk including subclinical carotid atherosclerosis and endothelial function could be improved through both traditional treatments such as methotrexate and novel specific therapies such as anti-interleukin-1 agents. The statins that were used as an adjunct to conventional RA treatment were reported to cause reductions in RA disease activity in the TARA (Trial of Atorvastatin in Rheumatoid Arthritis) study, and they were also reported to have anti-inflammatory effects.


The combination of chronic inflammation and risk factor clustering invites comparison between the vascular disease in diabetes mellitus and the metabolic syndrome X, and that seen in RA. The former two diseases have considerable overlap and are increasingly considered as cardiovascular 'risk equivalents', the presence of which alone can be sufficient groups for initiating statin treatment. Several statin trials, including the Heart Protection Study, support the use of statin treatment for primary cardiovascular prevention in diabetes mellitus, despite the fact that not all patients with diabetes ultimately develop cardiovascular disease.


A question rises here:
Should all RA patients be treated with statins to reduce cardiovascular risk as in diabetes?
There isn't any conclusive data to this yet.


Ongoing studies measuring clinical cardiovascular endpoints such as TRACE-RA (Trial of Atorvastatin in the Primary Prevention of Cardiovascular. Endpoints in Rheumatoid Arthritis), a multicenter, placebo-controlled study aiming to enroll over 3,000 patients with RA without overt cardiovascular disease, should be able to answer the question mentioned above in the next few years.


Risk-prediction calculators that are specifically designed for patients with RA could have a role in this, and improved methods of assessing cardiovascular risk in RA to target those patients at highest risk are still needed. The use of advanced imaging techniques such as MRI and positron emission tomography, or optical coherence tomography, or intravascular ultrasound could be included in some of the other approaches to estimating risk. Further information could be provided with the help of these medications together with novel molecular contrast agents, including accurate measurement of atherosclerotic plaque burden and characterization of the composition and likely behavior of plaques, which could permit targeting and monitoring of the response to therapy.


The findings of Toms et al. will serve as a timely reminder that in addition to managing RA-specific therapy, clinicians should remain alert to and address cardiovascular risk in patients with RA according to current guidelines, at least until the results of ongoing trials are known. In addition to treatment with statins, other modifiable risk factors shouldn't be ignored, including optimum blood pressure control, exercise, weight management, smoking cessation and other lifestyle measures.

Prepared By: Dr. Mehyar Al-khashroum
Edited By: Miss Araz Kahvedjian

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