An experimental study of early cardiovascular disease and risk factors in a collagen-induced arthritis rat model
Chun Yun Jiang1, Da Li1, Quan Jiang1
1Department of Rheumatology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Introduction:
This study investigated the pathological characteristics and risk factors of early cardiovascular disease (CVD) associated with rheumatoid arthritis (RA) using a collagen-induced arthritis (CIA) rat model.
Methods:
A total of 120 SPF-grade male SD rats were used. Following CIA induction, echocardiography, histopathology, molecular biology, and lipid profile analysis were employed to dynamically monitor cardiac function, structural changes, and lipid profiles across disease stages (D0-D112) .
Results:
Sequential progression of cardiac dysfunction: Echocardiography revealed a significant decrease in the mitral valve E/A ratio (MVE/A) starting from D84 (P<0.05), indicating diastolic impairment preceding systolic dysfunction.Myocardial structural abnormalities: The heart-to-body weight ratio (HW/BW) in CIA rats was significantly higher than that in the control group starting from day 84 (*P < 0.01), indicating cardiac hypertrophy. Masson staining revealed progressive myocardial fibrosis with increasing collagen deposition from D56. Abnormal lipid profiles and biomarkers: LDL-C significantly increased from D84 to D112 (*P<0.01), while OX-LDL rose from D98 to D112 (P<0.05); B-type natriuretic peptide (BNP) significantly increased at D112 (*P<0.01), indicating heart failure risk. Negative atherosclerosis findings: No plaque formation was detected in the Oil Red O staining of the aorta and coronary arteries. While macroscopic atherosclerotic plaques were not apparent, microvascular endothelial dysfunction may play a role in the early stages of cardiovascular disease (CVD) .
Discussion:
Cardiovascular lesions in CIA rats exhibit sequential progression: diastolic dysfunction and myocardial fibrosis emerge first (from D56), followed by systolic dysfunction (from D98), accompanied by lipid metabolism disorders driven by LDL-C and OX-LDL. This model provides an experimental basis for studying the mechanisms of RA-associated cardiac lesions and early intervention.
