Rheumatoid arthritis was associated with a 26 gm (18%) lower mean left ventricular mass compared with non-RA controls (P<0.001).
Cohort (n=300)
Does rheumatoid arthritis alter left ventricular structure and function compared to non-RA controls?
Rheumatoid arthritis is associated with reduced left ventricular mass and modestly lower systolic function, suggesting that progression to heart failure in this population may occur through myocardial mass reduction rather than hypertrophy.
Estimación del efecto: 26 gm lower
valor p: p=<0.001
OBJECTIVE: Heart failure is a major contributor to cardiovascular morbidity and mortality in patients with rheumatoid arthritis (RA), but little is known about myocardial structure and function in this population. This study was undertaken to assess the factors associated with progression to heart failure in patients with RA. METHODS: With the use of cardiac magnetic resonance imaging, measures of myocardial structure and function were assessed in men and women with RA enrolled in the Evaluation of Subclinical Cardiovascular Disease and Predictors of Events in Rheumatoid Arthritis study, a cohort study of subclinical cardiovascular disease in patients with RA, in comparison with non-RA control subjects from a cohort enrolled in the Baltimore Multi-Ethnic Study of Atherosclerosis. RESULTS: Measures of myocardial structure and function were compared between 75 patients with RA and 225 frequency-matched controls. After adjustment for confounders, the mean left ventricular mass was found to be 26 gm lower in patients with RA compared with controls (P < 0.001), an 18% difference. In addition, the mean left ventricular ejection fraction, cardiac output, and stroke volume were modestly lower in the RA group compared with controls. The mean left ventricular end systolic and end diastolic volumes did not differ between the groups. In patients with RA, higher levels of anti-cyclic citrullinated peptide (anti-CCP) antibodies and current use of biologic agents, but not other measures of disease activity or severity, were associated with significantly lower adjusted mean values for the left ventricular mass, end diastolic volume, and stroke volume, but not with ejection fraction. The combined associations of anti-CCP antibody level and biologic agent use with myocardial measures were additive, without evidence of interaction. CONCLUSION: These findings suggest that the progression to heart failure in RA may occur through reduced myocardial mass rather than hypertrophy. Both modifiable and nonmodifiable factors may contribute to lower levels of left ventricular mass and volume.
Giles et al. (Thu,) conducted a cohort in Rheumatoid arthritis (n=300). Rheumatoid arthritis vs. Non-RA control subjects was evaluated on Mean left ventricular mass (26 gm lower, p=<0.001). Rheumatoid arthritis was associated with a 26 gm (18%) lower mean left ventricular mass compared with non-RA controls (P<0.001).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: