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Updated: May 3, 2026
In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
Published on: February 16, 2016
Myocardial perfusion MRI shows impaired perfusion of the mouse hypertrophic left ventricle
Bastiaan J van Nierop1, Bram F Coolen, Noortje A Bax
1Biomedical NMR, Department of Biomedical Engineering, Eindhoven University of Technology, PO Box 513, 5600 MB, Eindhoven, The Netherlands.
Insights
Myocardial perfusion deficits are key in heart failure. This study shows reduced perfusion in mice with pressure overload-induced heart failure, correlating with cardiac dysfunction.
Area of Science:
- Cardiovascular Research
- Medical Imaging
- Animal Models
Background:
- Myocardial perfusion deficits are increasingly recognized as critical in the progression of cardiac hypertrophy to decompensated heart failure.
- Previous studies have not systematically investigated these deficits in a pressure overload-induced hypertrophy and heart failure model.
Purpose of the Study:
- To systematically evaluate myocardial perfusion deficits in a mouse model of pressure overload-induced hypertrophy and heart failure using transverse aortic constriction (TAC).
- To longitudinally assess myocardial perfusion and its correlation with left ventricular (LV) function and morphology.
Main Methods:
- Utilized a dual-bolus first-pass perfusion magnetic resonance imaging (MRI) technique to quantify regional LV myocardial perfusion in healthy and TAC-induced heart failure mice over 10 weeks.
- Assessed LV function and morphology using cinematographic MRI.
Main Results:
- TAC mice exhibited significantly reduced myocardial perfusion (4.2 ± 0.9 mL/min/g) compared to controls (7.6 ± 1.8 mL/min/g).
- Decreased myocardial perfusion in TAC mice correlated strongly with increased LV volumes and mass, and decreased ejection fraction.
- Total LV blood flow was significantly lower in TAC mice (0.5 ± 0.1 mL/min) versus controls (0.7 ± 0.2 mL/min).
Conclusions:
- Myocardial perfusion is significantly reduced in a mouse model of pressure overload-induced heart failure.
- Quantitative first-pass contrast-enhanced MRI is a valuable tool for studying perfusion deficits in diseased hearts.
- Perfusion deficits are linked to cardiac remodeling and impaired LV function in this model.
Abstract:
There is growing consensus that myocardial perfusion deficits play a pivotal role in the transition from compensated to overt decompensated hypertrophy. The purpose of this study was to systematically study myocardial perfusion deficits in the highly relevant model of pressure overload induced hypertrophy and heart failure by transverse aortic constriction (TAC), which was not done thus far. Regional left ventricular (LV) myocardial perfusion (mL/min/g) was assessed in healthy mice (n = 6) and mice with TAC (n = 14). A dual-bolus first-pass perfusion MRI technique was employed to longitudinally quantify myocardial perfusion values between 1 and 10 weeks after surgery. LV function and morphology were quantified from cinematographic MRI. Myocardial rest perfusion values in both groups did not change significantly over time, in line with the essentially constant global LV function and mass. Myocardial perfusion was significantly decreased in TAC mice (4.2 ± 0.9 mL/min/g) in comparison to controls (7.6 ± 1.8 mL/min/g) (P = 0.001). No regional differences in perfusion were observed within the LV wall. Importantly, increased LV volumes and mass, and decreased ejection fraction correlated with decreased myocardial perfusion (P < 0.001, in all cases). Total LV blood flow was decreased in TAC mice (0.5 ± 0.1 mL/min, P < 0.001) in comparison to control mice (0.7 ± 0.2 mL/min). Myocardial perfusion in TAC mice was significantly reduced as compared to healthy controls. Perfusion was proportional to LV volume and mass, and related to decreased LV ejection fraction. Furthermore, this study demonstrates the potential of quantitative first-pass contrast-enhanced MRI for the study of perfusion deficits in the diseased mouse heart.
