Myocardial Inflammation, Measured Using 18‐Fluorodeoxyglucose Positron Emission Tomography With Computed Tomography, Is Associated With Disease Activity in Rheumatoid Arthritis

Abstract

Objective To determine the prevalence and correlates of subclinical myocardial inflammation in patients with rheumatoid arthritis (RA). Methods RA patients (n = 119) without known cardiovascular disease underwent cardiac 18‐fluorodeoxyglucose (FDG) positron emission tomography with computed tomography (PET‐CT). Myocardial FDG uptake was assessed visually and measured quantitatively as the standardized uptake value (SUV). Multivariable linear regression was used to assess the associations of patient characteristics with myocardial SUVs. A subset of RA patients who had to escalate their disease‐modifying antirheumatic drug (DMARD) therapy (n = 8) underwent a second FDG PET‐CT scan after 6 months, to assess treatment‐associated changes in myocardial FDG uptake. Results Visually assessed FDG uptake was observed in 46 (39%) of the 119 RA patients, and 21 patients (18%) had abnormal quantitatively assessed myocardial FDG uptake (i.e., mean of the mean SUV [SUVmean] ≥3.10 units; defined as 2 SD above the value in a reference group of 27 non‐RA subjects). The SUVmean was 31% higher in patients with a Clinical Disease Activity Index (CDAI) score of ≥10 (moderate‐to‐high disease activity) as compared with those with lower CDAI scores (low disease activity or remission) (P = 0.005), after adjustment for potential confounders. The adjusted SUVmean was 26% lower among those treated with a non–tumor necrosis factor–targeted biologic agent compared with those treated with conventional (nonbiologic) DMARDs (P = 0.029). In the longitudinal substudy, the myocardial SUVmean decreased from 4.50 units to 2.30 units over 6 months, which paralleled the decrease in the mean CDAI from a score of 23 to a score of 12. Conclusion Subclinical myocardial inflammation is frequent in patients with RA, is associated with RA disease activity, and may decrease with RA therapy. Future longitudinal studies will be required to assess whether reduction in myocardial inflammation will reduce heart failure risk in RA.

Coronary Microvascular Dysfunction in Rheumatoid Arthritis Compared to Diabetes Mellitus and Association With All‐Cause Mortality

“…Treatment of RA patients with anakinra, an interleukin‐1 antagonist, was associated with improved flow‐mediated dilation, as well as CFR, further supporting the hypothesis linking inflammation with CMD (32). Inflammation of the myocardium can also be detected on imaging, which may impact endothelial function of the microvascular bed (28,33,34). Persistent or recurrent flares over time may therefore lead to endothelial dysfunction, resulting in CMD, which in turn can cause subclinical myocardial injury.…”

Pathogenesis of ischaemic and non-ischaemic heart diseases in rheumatoid arthritis

“…Active inflammatory processes in the heart may lead to excessive myocardial fibrosis causing stiffening of the ventricles and thus contribute to systolic and diastolic dysfunctions and to cardiac arrhythmia. Cardiac MRI and PET-CT data indeed confirmed a correlation between RA disease activity and increased myocardial inflammation and fibrosis 7 38. Structural changes in the myocardium observed with cardiac MRI also correlate with diagnostic markers of systemic inflammation 38.…”

“…Technical advantages and limitations of the specific imaging techniques are described elsewhere 5. Data of cardiac MRI and positron emission tomography–computed tomography (PET-CT) in patients with RA with no diagnosis of cardiovascular disease demonstrated that up to half showed signs of cardiac fibrosis or inflammation 6 7. These changes in the myocardium might be responsible for the observed increased left ventricular mass in patients with RA 8.…”

Chronic Heart Failure in Rheumatoid Arthritis Patients (Part III): Effects of Antirheumatic Drugs

“…Динамика параметров эхокардиографии и уровня биомаркеров также свидетельствует о положительном влиянии иФНО-α на сердечную функцию у больных РА. Терапия иФНО-α при краткосрочном наблюдении (до 12 мес) приводила к увеличению ФВЛЖ у пациентов с нормальной фракцией выброса, улучшению диастолической функции ЛЖ (E/E') и снижению концентрации эндотелина-1, ИЛ-6, N-концевого предшественника мозгового натрийуретического пептида (NTproBNP) [55][56][57]. В работе I. Amigues и соавт.…”

“…В работе I. Amigues и соавт. [57] патологическое накопление фтордезоксиглюкозы по данным позитронно-эмиссионной томографии выявлено у 21 (18%) из 119 больных РА без ССЗ. Через 6 мес наблюдения накопление фтордезоксиглюкозы снизилось в 2 раза параллельно со снижением активности РА, преимущественно на фоне терапии иФНО-α.…”