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临床试验/NCT01548768
NCT01548768已完成4 期

RHYTHM (RHeumatoid Arthritis studY of THe Myocardium): How Rheumatoid Arthritis (RA) and Tumor Necrosis Factor (TNF) Inhibitors Affect the Myocardial Structure and Function.

Columbia University1 个研究点 分布在 1 个国家目标入组 149 人开始时间: 2011年10月10日最近更新:
适应症
干预措施
相关药物

试验速览

阶段
4 期
状态
已完成
入组人数
149
试验地点
1
主要终点
Number of Participants With Myocardial FDG Uptake

研究概览

简要总结

For aim 1, the proposed studies will be performed in 150 patients with RA and 25 subjects without RA (healthy volunteers) who will function as controls.

For aim 2, 25 of the patients enrolled in aim 1 (who are in need for further treatment due to increased RA activity despite their current treatment) will be recruited to continue in the study for an additional 24 (+/- 2) weeks (or 6 months). These patient will receive a TNF inhibitor in addition to their current treatment in an open label protocol for increased disease activity and in the context of standard of care.

The investigators hypothesize that anti-TNF agents in RA patients without heart disease will not adversely affect the heart (will not cause a detrimental change in heart structure or its function).

详细描述

Patients with Rheumatoid Arthritis (RA) have a shortened life expectancy compared to the general population. Cardiovascular disease (CVD), including heart failure (HF), is the primary cause of the extra deaths in RA. HF, in general, results from failure of the heart muscle to pump adequately. In other words the heart muscle in HF becomes "weak". In patients without RA, the heart muscle gets larger before symptoms of HF appear. Contrary to that, patients with RA have reduced heart size and reduced heart strength. This may mean that in RA the pathway to heart failure may be different compared to what happens in patients without RA. It is possible - for example - that in RA the heart muscle becomes smaller before it becomes weak (while in non-RA patients the heart muscle becomes larger before it becomes weak). It is possible that cells that create inflammation in the joints may also do the same in the heart muscle making it smaller, thinner and eventually weaker.

Patients with RA nowadays can be treated with a variety of medications for their joint inflammation. These medications are powerful and have reduced the risk of permanent joint damage and disability. However it is unknown what is the effect of these medications on the heart size and strength and whether they increase or decrease the risk for cardiovascular disease and heart failure.

Among the medications used for RA are medications called TNF inhibitors. They are usually prescribed to patients who have joint inflammation that has not responded to treatment with the first line medication Methotrexate. Data in non-RA patients with advanced heart failure suggest that anti-TNF agents may not help heart failure and may even be harmful. However, the effect of these agents on the hearts of RA patients has never been directly studied. Some observational studies suggest that RA patients treated with TNF inhibitors have a lower risk of developing heart disease. Overall the knowledge regarding the effect of TNF inhibitors on RA patients heart function is limited.

研究设计

研究类型
Interventional
分配方式
Non Randomized
干预模型
Parallel
主要目的
Prevention
盲法
None

入排标准

年龄范围
18 Years 至 —(Adult, Older Adult)
性别
All
接受健康志愿者

入选标准

  • 未提供

排除标准

  • 未提供

研究组 & 干预措施

Patients - DMARDs + TNF Inhibitors

Experimental

Patients will receive a TNF inhibitor in addition to their current treatment in an open label protocol for increased disease activity and in the context of standard of care.

干预措施: TNF inhibitors (Drug)

Patients - DMARDs + TNF Inhibitors

Experimental

Patients will receive a TNF inhibitor in addition to their current treatment in an open label protocol for increased disease activity and in the context of standard of care.

干预措施: DMARDs (Drug)

Patients - DMARDs only

Active Comparator

Patients will receive their current treatment in an open label protocol in the context of standard of care.

干预措施: DMARDs (Drug)

结局指标

主要结局

Number of Participants With Myocardial FDG Uptake

时间窗: Baseline

This is designed to evaluate the baseline characteristics of the cross sectional RA cohort to understand the correlation of disease activity measured by the Clinical Disease Activity Index (CDAI) with myocardial inflammation measured by fluorodeoxyglucose (FDG) uptake in positron emission tomography (PET) scan at the baseline visit. Myocardial FDG uptake is classified as "diffuse" or "focal."

次要结局

  • Number of Participants With Myocardial FDG Uptake After Escalation of RA Pharmacotherapy(Baseline, 6-Month Follow-up)
  • LV Structure (Mean EDVI) in Association With Myocardial FDG Uptake(Baseline)
  • LV Function (Mean Stroke Volume Index) in Association With Myocardial FDG Uptake(Baseline)

研究者

申办方类型
Other
责任方
Principal Investigator
主要研究者

Joan M. Bathon

Professor Medicine, Rheumatology

Columbia University

研究点 (1)

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