Survival, Exercise Capacity, and Left Ventricular Remodeling in a Rat Model of Chronic Mitral Regurgitation: Serial Echocardiography and Pressure-Volume Analysis.
10.4070/kcj.2011.41.10.603
- Author:
Kyung Hee KIM
1
;
Yong Jin KIM
;
Seung Pyo LEE
;
Hyung Kwan KIM
;
Jeong Wook SEO
;
Dae Won SOHN
;
Byung Hee OH
;
Young Bae PARK
Author Information
1. Department of Internal Medicine, Cardiovascular Center, Seoul National University College of Medicine, Seoul, Korea. kimdamas@snu.ac.kr
- Publication Type:Original Article
- Keywords:
Mitral regurgitation;
Hemodynamic study;
Exercise test;
Rat model
- MeSH:
Animals;
Echocardiography;
Exercise Test;
Fibrosis;
Heart Failure;
Mitral Valve Insufficiency;
Models, Animal;
Needles;
Rats;
Rats, Sprague-Dawley;
Reference Values;
Salicylamides;
Ventricular Remodeling
- From:Korean Circulation Journal
2011;41(10):603-611
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND AND OBJECTIVES: The aims of this study were to establish a reliable model of chronic mitral regurgitation (MR) in rats and verify the pathophysiological features of this model by evaluating cardiac function using serial echocardiography and a pressure-volume analysis. MATERIALS AND METHODS: MR was created in 37 Sprague-Dawley rats by making a hole with a 23 gauge needle on the mitral leaflet through the left ventricular (LV) apex under the guidance of transesophageal echocardiography. RESULTS: Serial echocardiograms revealed that the LV began to dilate immediately after the MR operation and showed progressive dilation until the 14th week (LV end-systolic dimension at 14 weeks, 4.71+/-0.25 mm vs. 6.81+/-0.50 mm for sham vs. MR, p<0.01; LV end-diastolic dimension, 8.32+/-0.42 mm vs. 11.01+/-0.47 mm, p<0.01). The LV ejection fraction tended to increase immediately after the MR operation but started to decrease thereafter and showed a significant difference with the sham group from the 14th week (70.0+/-2.2% vs. 62.1+/-3.1% for sham vs. MR). In a pressure-volume analysis performed at the 14th week, the LV end-systolic pressure-volume relationship and +dp/dt decreased significantly in the MR group. A serial treadmill test revealed that exercise capacity remained in the normal range until the 14th week when it began to decrease (exercise duration, 406+/-45 seconds vs. 330+/-27 seconds, p<0.01). A pathological analysis showed no significance difference in interstitial fibrosis between the two groups. CONCLUSION: We established a small animal model of chronic MR and verified its pathophysiological features. This model may provide a useful tool for future research on MR and volume overload heart failure.
