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Updated: Sep 2, 2026
Assessment of Right Ventricular Structure and Function in Mouse Model of Pulmonary Artery Constriction by Transthoracic Echocardiography
Published on: February 3, 2014
Sequential Changes in Right Ventricular Straein During the Development of Pulmonary Hypertension Assessed With
Na Young Kim1, Dong Jin Im1, Yoo Jin Hong1
1Department of Radiology, Research Institute of Radiological Science, Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea.
Objective:
To evaluate the sequential changes in right ventricular (RV) strain and histological vascular remodeling and their correlations during pulmonary hypertension (PH) development in a rat model by using cardiac magnetic resonance (CMR)-feature tracking (FT).
Materials And Methods:
Separate cohorts of six-week-old male Wistar rats (10 per group) were allocated to a baseline group, PH induction groups assessed at 1, 2, 3, or 4 weeks after monocrotaline injection, and vehicle-injected control groups assessed at 2 and 4 weeks. Each rat underwent a single magnetic resonance imaging (MRI) examination and was subsequently euthanized for histological analysis. Cine images were acquired using a 9.4T MRI scanner, and strain was analyzed using the FT technique. Histological analysis was used to quantify pulmonary arterial wall thickness percentage (PA %WT) and RV collagen density. Overall group differences were analyzed using the Kruskal-Wallis test, which was followed by the Mann-Whitney U test with Bonferroni correction for pairwise comparisons with the baseline group. Correlations between the variables were assessed using Spearman's correlation coefficients.
Results:
All CMR-derived RV parameters showed significant differences across the baseline and PH induction groups (all P < 0.001). RV free wall longitudinal strain (RVFWLS) showed the earliest impairment at 2 weeks, with a progressive decline thereafter. The RV free wall circumferential strain (RVFWCS) and RV ejection fraction were reduced beginning at 3 weeks, whereas the RV end-diastolic volume index increased significantly only at 4 weeks. The PA %WT increased progressively from week 2, whereas the RV collagen density did not change significantly. RVFWLS and RVFWCS showed strong positive correlations with PA %WT (r = 0.885 and r = 0.757, respectively; both P < 0.001), which were primarily driven by parallel changes across the post-induction time points. The control groups showed no significant temporal changes in the CMR or histological measurements.
Conclusion:
In this preclinical model of PH, staged CMR and histological assessments demonstrated sequential RV remodeling in parallel with PA remodeling, with RVFWLS impairment preceding overt RV dysfunction and enlargement.
