Features of cardiac remodeling in Patients with Acute Coronary Syndrome Complicated with Rheumatoid Arthritis

Abstract

Cardiovascular diseases are important factors to increased morbidity and mortality in patients with rheumatoid arthritis (RA). The aim of this study is to investigate the effects of RA on cardiac remodeling in patients with acute coronary syndrome (ACS). Sixty-one patients with ACS complicated with RA (RA group) and 55 age- and sex-matched patients with ACS without RA (control group) were enrolled. We compared the parameters of laboratory and echocardiogram across the 2 groups. Levels of serum brain natriuretic peptide in patients with RA were significantly higher than control group. Prevalence of left ventricular hypertrophy (LVH), and LV diastolic dysfunction (E/A < 1) were significantly higher in the RA patients, while the LV ejection fraction (EF%) was significantly lower in RA patients. Incidence of tricuspid regurgitation and pulmonary regurgitation were significantly higher in ACS patients with RA than in the ACS patients without RA. In RA group, levels of serum high density lipoprotein cholesterol were negatively correlated with C reactive protein (CRP), EF% was also negatively correlated with CRP. The prevalence of LVH and mitral regurgitation showed positive correlations with ESR. Early intervention for controlling the inflammation associated with RA can play a significant role in preventing cardiac remodeling in ACS patients.

The Impact of Ischemic Heart Disease on Rheumatoid Arthritis

“…From the moment that RA patients had AMI, those present a higher prevalence of worse cardiac remodeling parameters such as: Ventricular hypertrophy, diastolic dysfunction, lower ejection fraction, higher incidence of tricuspid and pulmonary valve regurgitation than patients breathless. To minimize these deleterious effects, inflammatory control of arthritis should occur as rapidly as possible [44]. Another significant difference that may contribute to the worst outcome after AMI was documented in Australia after data analysis from 1995 to 2005.…”

Left ventricular hypertrophy predicts poorer cardiovascular outcome in normotensive normoglycemic patients with rheumatoid arthritis

“…We found that this condition was not uncommon in our normotensive normoglycemic RA patients. Clinical data showed that hypertension and/or hyperglycemia did not represent the needed condition promoting LVH in RA patients, and that inflammation during active RA had long‐term consequences on molecular cardiac remodeling and mass growth 32‐36 . Norton et al 33 reported that in RA humans, a pro‐inflammatory state (ie higher circulating serum tumor necrosis factor[TNF]‐α levels) was more closely related to concentric LVH than a systemic hypertensive state.…”

The Key Comorbidities in Patients with Rheumatoid Arthritis: A Narrative Review

“…Systemic inflammation may, at least in part, explain the remaining risk, and this theory is supported by a multitude of studies demonstrating an association between high RA disease activity and increased CVD risk (Table 2) [24,28,[39][40][41][42][43][44]. The relationship between chronic inflammation and CVD remains to be fully delineated, but it has been reported that the proinflammatory mechanisms underlying the pathogenesis of RA may contribute to the development of atherosclerosis [45][46][47], promotion of cardiac remodelling [48], alterations in lipid blood profiles [49] and changes to the morphology of red blood cells [50] (Figure 1). RA-related inflammation can also be exacerbated by cytomegalovirus infection and is linked to coronary artery damage through the actions of a population of cytotoxic T-cells (reviewed in detail by Broadley et al [51]).…”

“…Chronic inflammation in rheumatoid arthritis as a risk factor for cardiovascular disease. The proinflammatory mechanisms underlying RA may contribute to the development of atherosclerosis [45][46][47], promotion of cardiac remodelling [48], alterations in lipid blood profiles [49] and changes to the morphology of red blood cells [50]. RA can be exacerbated by cytomegalovirus infection and is linked to coronary artery damage via cytotoxic T-cells [51].…”