Why the study?
Does rheumatoid arthritis increase left ventricular mass or reduce ejection fraction in patients without clinical cardiovascular disease?
Does rheumatoid arthritis increase left ventricular mass or reduce ejection fraction in patients without clinical cardiovascular disease?
Rheumatoid arthritis is independently associated with increased left ventricular mass and hypertrophy, but not systolic dysfunction, suggesting a pathophysiologic link between chronic inflammation and structural heart changes.
RA-associated LVH may prompt earlier cardiac evaluation in asymptomatic patients; hypothesis-generating for inflammation-mediated remodeling pending prospective data.
OBJECTIVE: Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with premature atherosclerosis, vascular stiffening, and heart failure. This study was undertaken to investigate whether RA is associated with underlying structural and functional abnormalities of the left ventricle (LV). METHODS: Eighty-nine RA patients without clinical cardiovascular disease and 89 healthy matched controls underwent echocardiography, carotid ultrasonography, and radial tonometry to measure arterial stiffness. RA patients and controls were similar in body size, hypertension and diabetes status, and cholesterol level. RESULTS: LV diastolic diameter (4.92 cm versus 4.64 cm; P<0.001), mass (136.9 gm versus 121.7 gm; P=0.004 or 36.5 versus 32.9 gm/m2.7; P=0.01), ejection fraction (71% versus 67%; P<0.001), and prevalence of LV hypertrophy (18% versus 6.7%; P=0.023) were all higher among RA patients versus controls. In multivariate analysis, presence of RA was an independent correlate of LV mass (P=0.004). Furthermore, RA was independently associated with presence of LV hypertrophy (odds ratio 4.14 [95% confidence interval 1.24, 13.80], P=0.021). Among RA patients, age at diagnosis and disease duration were independently related to LV mass. RA patients with LV hypertrophy were older and had higher systolic pressure, damage index scores, C-reactive protein levels, homocysteine levels, and arterial stiffness compared with those without LV hypertrophy. CONCLUSION: The present results demonstrate that RA is associated with increased LV mass. Disease duration is independently related to increased LV mass, suggesting a pathophysiologic link between chronic inflammation and LV hypertrophy. In contrast, LV systolic function is preserved in RA patients, indicating that systolic dysfunction is not an intrinsic feature of RA.
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Rudominer et al. (2008) studied this question.
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