Rheumatoid Arthritis Disease Activity and Sub Clinical Atherosclerosis
Last updated on July 2021Recruitment
- Recruitment Status
- Not yet recruiting
- Estimated Enrollment
- Same as current
Summary
- Conditions
- Rheumatoid Arthritis
- Type
- Observational
- Design
- Observational Model: Case-ControlTime Perspective: Other
Participation Requirements
- Age
- Between 20 years and 125 years
- Gender
- Both males and females
Description
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease characterized by progressive joint destruction, associated with extra-articular manifestations, affecting different internal organs . Interestingly, these patients show an increased risk of mortality when compared to general popu...
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease characterized by progressive joint destruction, associated with extra-articular manifestations, affecting different internal organs . Interestingly, these patients show an increased risk of mortality when compared to general population and recent evidence clearly confirmed that this risk is largely due to cerebro-cardiovascular events (CV Es), this may be explained by the greater prevalence, severity, burden and different composition of occult coronary lesions in RA compared with age- and gender-matched controls. RA is associated with traditional CV risk factors ,subclinical atherosclerosis,arrhythmias , and coronary calcifications . Increased subclinical atherosclerosis, mainly carotid artery plaques, may be observed in RA patients, the increased carotid intima-media thickness (cIMT) and presence of plaques are accepted as strong predictors of generalized atherosclerosis and major CVEs in both non-RA and RA subjects. The evidence of traditional CV risk factors and subclinical atherosclerosis does not fully explain the increased incidence of CVEs in these patients; suggesting that the CV risk may be independently associated with RA and in fact, this risk has been shown to be associated with additional features specific of RA, such as the systemic inflammatory process, disease duration and therapeutic strategies . Chronic inflammation and high disease activity are reportedly associated with atherosclerotic burden, higher incidence of cerebrovascular disease (CVD), chronic heart failure (CHF), and mortality of patients with RA . Residual disease activity may further associate with more advanced, complex and prone-to-rupture coronary plaques . Pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-?), reflect clinical activity and structural damage in RA and are elevated in the blood of RA patients compared with controls , the same cytokine have been identified in atherosclerotic plaque and correlated with subclinical atherosclerosis independent of cardiac risk factors coronary plaque complexity , plaque destabilization and CVEs in subjects without autoimmune disease . Cardiac troponins (cTn) are components of the cardiomyocyte contractile apparatus, and circulating concentrations are elevated in the setting of myocardial injury, such as acute coronary syndromes (ACS) . High-sensitivity (hs) cTn assays allow measurement of troponin concentrations below conventional levels of detection and have revealed a spectrum of circulating cTn concentrations spanning low and high levels in both healthy subjects and in patients with overt cardiovascular disease Additionally, both high-sensitivity cardiac troponin T (hs-cTnT) and high-sensitivity cardiac troponin I (hs-cTnI) predicted a greater risk of fatal and non-fatal coronary heart disease, heart failure hospitalization and overall mortality in the general population . Aim of the study Detection of subclinical atherosclerosis in RA patients by means of carotid Doppler Detection of level of high sensitive cardiac troponin I in RA patients and it?s relation to sub clinical atherosclerosis and disease activity Correlation between high sensitive cardiac troponin I and TNF ? as a pro inflammatory cytokine to the presence of subclinical atherosclerosis in RA patients
Tracking Information
- NCT #
- NCT03821090
- Collaborators
- Not Provided
- Investigators
- Not Provided