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Cardiovascular magnetic resonance detects the progression of impaired myocardial perfusion reserve and increased left-ventricular mass in mice fed a high-fat diet

View Article: PubMed Central - PubMed

ABSTRACT

Background: Impaired myocardial perfusion reserve (MPR) is prevalent in obesity and diabetes, even in the absence of obstructive coronary artery disease (CAD), and is prognostic of adverse events. We sought to establish the time course of reduced MPR and to investigate associated vascular and tissue properties in mice fed a high-fat diet (HFD), as they are an emerging model of human obesity, diabetes, and reduced MPR without obstructive CAD.

Methods: C57Bl/6 mice fed a HFD or a low-fat diet (control) were imaged at 6, 12, 18 and 24 weeks post-diet. The cardiovascular magnetic resonance (CMR) protocol included multi-slice cine imaging to assess ejection fraction (EF), left-ventricular (LV) mass, LV wall thickness (LVWT), and LV volumes, and first-pass perfusion CMR to quantify MPR. Coronary vascular reactivity, aortic atherosclerosis, myocardial capillary density and tissue fibrosis were also assessed.

Results: Body weight was increased in HFD mice at 6–24 weeks post-diet (p < 0.05 vs. control). MPR in HFD mice was reduced and LV mass and LVWT were increased in HFD mice at 18 and 24 weeks post-diet (p < 0.05 vs. control). Coronary arteriolar vascular reactivity to adenosine and acetylcholine were reduced in HFD mice (p < 0.05 vs. control). There were no significant differences in cardiac volumes, EF, or capillary density measurements between the two groups. Histology showed interstitial fibrosis in HFD and no aortic atherosclerosis in either group.

Conclusions: C57Bl/6 mice fed a HFD for 18–24 weeks have progressively increased LV mass and impaired MPR with fibrosis, normal capillary density and no aortic plaque. These results establish C57Bl/6 mice fed a HFD for 18–24 weeks as a model of impaired MPR without obstructive CAD due to obesity and diabetes.

No MeSH data available.


a Example black-blood cine images in the control and HFD mice at end-diastole and end-systole at 18 weeks post-diet. b LV mass measurements in the control and HFD mice at 6–24 weeks post-diet (*p < 0.05 vs. age-matched control, $p < 0.05 vs. HFD at 6 weeks, #p < 0.05 vs. HFD at 12 weeks, &p < 0.05 vs. HFD at 18 weeks). c LV end-diastolic wall thickness (LVEDWT) measurements in the control and HFD mice at 6–24 weeks post-diet (*p < 0.05 vs. age-matched control, $p < 0.05 vs. HFD at 6 weeks, #p < 0.05 vs. HFD at 12 weeks). d LV end-systolic wall thickness (LVESWT) measurements in the control and HFD mice at 6–24 weeks post-diet (*p < 0.05 vs. age-matched control, $p < 0.05 vs. HFD at 6 weeks, #p < 0.05 vs. HFD at 12 weeks)
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Fig3: a Example black-blood cine images in the control and HFD mice at end-diastole and end-systole at 18 weeks post-diet. b LV mass measurements in the control and HFD mice at 6–24 weeks post-diet (*p < 0.05 vs. age-matched control, $p < 0.05 vs. HFD at 6 weeks, #p < 0.05 vs. HFD at 12 weeks, &p < 0.05 vs. HFD at 18 weeks). c LV end-diastolic wall thickness (LVEDWT) measurements in the control and HFD mice at 6–24 weeks post-diet (*p < 0.05 vs. age-matched control, $p < 0.05 vs. HFD at 6 weeks, #p < 0.05 vs. HFD at 12 weeks). d LV end-systolic wall thickness (LVESWT) measurements in the control and HFD mice at 6–24 weeks post-diet (*p < 0.05 vs. age-matched control, $p < 0.05 vs. HFD at 6 weeks, #p < 0.05 vs. HFD at 12 weeks)

Mentions: Figure 3a shows example black-blood cine images obtained from a control and a HFD mouse at ED and ES at 18 weeks post-diet. LV mass was significantly higher in the HFD mice as compared to the control mice at 18 and 24 weeks post-diet (Fig. 3b, p < 0.05 vs. age-matched control). LV mass progressively increased in the HFD mice from the start of the diet to the end of the study. We also saw a slight increase in LV mass in the control group at 24 weeks post-diet (p < 0.05 vs. control at 6 and 12 weeks post-diet), probably due to normal growth at their age. LV EDWT and ESWT were also significantly increased in the HFD mice at 18 and 24 weeks post-diet (Fig. 3c–d, p < 0.05 vs. age-matched control, p < 0.05 vs. HFD at 6 and 12 weeks post-diet). There were no statistically significant differences in LV EDV, LV ESV, LV EF, LV Ecc-subendo, LV Ecc-subepi, LV global Ecc or CURE measurements between the two groups of mice over the time course (Table 1).Fig. 3


Cardiovascular magnetic resonance detects the progression of impaired myocardial perfusion reserve and increased left-ventricular mass in mice fed a high-fat diet
a Example black-blood cine images in the control and HFD mice at end-diastole and end-systole at 18 weeks post-diet. b LV mass measurements in the control and HFD mice at 6–24 weeks post-diet (*p < 0.05 vs. age-matched control, $p < 0.05 vs. HFD at 6 weeks, #p < 0.05 vs. HFD at 12 weeks, &p < 0.05 vs. HFD at 18 weeks). c LV end-diastolic wall thickness (LVEDWT) measurements in the control and HFD mice at 6–24 weeks post-diet (*p < 0.05 vs. age-matched control, $p < 0.05 vs. HFD at 6 weeks, #p < 0.05 vs. HFD at 12 weeks). d LV end-systolic wall thickness (LVESWT) measurements in the control and HFD mice at 6–24 weeks post-diet (*p < 0.05 vs. age-matched control, $p < 0.05 vs. HFD at 6 weeks, #p < 0.05 vs. HFD at 12 weeks)
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Fig3: a Example black-blood cine images in the control and HFD mice at end-diastole and end-systole at 18 weeks post-diet. b LV mass measurements in the control and HFD mice at 6–24 weeks post-diet (*p < 0.05 vs. age-matched control, $p < 0.05 vs. HFD at 6 weeks, #p < 0.05 vs. HFD at 12 weeks, &p < 0.05 vs. HFD at 18 weeks). c LV end-diastolic wall thickness (LVEDWT) measurements in the control and HFD mice at 6–24 weeks post-diet (*p < 0.05 vs. age-matched control, $p < 0.05 vs. HFD at 6 weeks, #p < 0.05 vs. HFD at 12 weeks). d LV end-systolic wall thickness (LVESWT) measurements in the control and HFD mice at 6–24 weeks post-diet (*p < 0.05 vs. age-matched control, $p < 0.05 vs. HFD at 6 weeks, #p < 0.05 vs. HFD at 12 weeks)
Mentions: Figure 3a shows example black-blood cine images obtained from a control and a HFD mouse at ED and ES at 18 weeks post-diet. LV mass was significantly higher in the HFD mice as compared to the control mice at 18 and 24 weeks post-diet (Fig. 3b, p < 0.05 vs. age-matched control). LV mass progressively increased in the HFD mice from the start of the diet to the end of the study. We also saw a slight increase in LV mass in the control group at 24 weeks post-diet (p < 0.05 vs. control at 6 and 12 weeks post-diet), probably due to normal growth at their age. LV EDWT and ESWT were also significantly increased in the HFD mice at 18 and 24 weeks post-diet (Fig. 3c–d, p < 0.05 vs. age-matched control, p < 0.05 vs. HFD at 6 and 12 weeks post-diet). There were no statistically significant differences in LV EDV, LV ESV, LV EF, LV Ecc-subendo, LV Ecc-subepi, LV global Ecc or CURE measurements between the two groups of mice over the time course (Table 1).Fig. 3

View Article: PubMed Central - PubMed

ABSTRACT

Background: Impaired myocardial perfusion reserve (MPR) is prevalent in obesity and diabetes, even in the absence of obstructive coronary artery disease (CAD), and is prognostic of adverse events. We sought to establish the time course of reduced MPR and to investigate associated vascular and tissue properties in mice fed a high-fat diet (HFD), as they are an emerging model of human obesity, diabetes, and reduced MPR without obstructive CAD.

Methods: C57Bl/6 mice fed a HFD or a low-fat diet (control) were imaged at 6, 12, 18 and 24&nbsp;weeks post-diet. The cardiovascular magnetic resonance (CMR) protocol included multi-slice cine imaging to assess ejection fraction (EF), left-ventricular (LV) mass, LV wall thickness (LVWT), and LV volumes, and first-pass perfusion CMR to quantify MPR. Coronary vascular reactivity, aortic atherosclerosis, myocardial capillary density and tissue fibrosis were also assessed.

Results: Body weight was increased in HFD mice at 6&ndash;24 weeks post-diet (p&thinsp;&lt;&thinsp;0.05 vs. control). MPR in HFD mice was reduced and LV mass and LVWT were increased in HFD mice at 18 and 24&nbsp;weeks post-diet (p&thinsp;&lt;&thinsp;0.05 vs. control). Coronary arteriolar vascular reactivity to adenosine and acetylcholine were reduced in HFD mice (p&thinsp;&lt;&thinsp;0.05 vs. control). There were no significant differences in cardiac volumes, EF, or capillary density measurements between the two groups. Histology showed interstitial fibrosis in HFD and no aortic atherosclerosis in either group.

Conclusions: C57Bl/6 mice fed a HFD for 18&ndash;24 weeks have progressively increased LV mass and impaired MPR with fibrosis, normal capillary density and no aortic plaque. These results establish C57Bl/6 mice fed a HFD for 18&ndash;24 weeks as a model of impaired MPR without obstructive CAD due to obesity and diabetes.

No MeSH data available.