Abstract
BackgroundObesity affects a third of adults in the US and results in an increased risk of cardiovascular mortality. While the mechanisms underlying this increased risk are not well understood, animal models of obesity have shown direct effects on the heart such as steatosis and fibrosis, which may affect cardiac function. However, the effect of obesity on cardiac function in animal models is not well-defined. We hypothesized that diet-induced obesity in mice reduces strain, torsion, and synchrony in the left ventricle (LV).MethodsTen 12-week-old C57BL/6 J mice were randomized to a high-fat or low-fat diet. After 5 months on the diet, mice were imaged with a 7 T ClinScan using a cine DENSE protocol. Three short-axis and two long-axis slices were acquired for quantification of strains, torsion and synchrony in the left ventricle.ResultsLeft ventricular mass was increased by 15% (p = 0.032) with no change in volumes or ejection fraction. Subepicardial strain was lower in the obese mice with a 40% reduction in circumferential strain (p = 0.008) a 53% reduction in radial strain (p = 0.032) and a trend towards a 19% reduction in longitudinal strain (p = 0.056). By contrast, subendocardial strain was modestly reduced in the obese mice in the circumferential direction by 12% (p = 0.028), and no different in the radial (p = 0.690) or longitudinal (p = 0.602) directions. Peak torsion was reduced by 34% (p = 0.028). Synchrony of contraction was also reduced (p = 0.032) with a time delay in the septal-to-lateral direction.ConclusionsDiet-induced obesity reduces left ventricular strains and torsion in mice. Reductions in cardiac strain are mostly limited to the subepicardium, with relative preservation of function in the subendocardium. Diet-induced obesity also leads to reduced synchrony of contraction and hypertrophy in mouse models.
Highlights
Obesity affects a third of adults in the US and results in an increased risk of cardiovascular mortality
These results are exciting as they show for the first time that mouse models of diet-induced obesity have changes in the heart that are similar to what has been reported in human studies: hypertrophy and reduced strains, torsion and synchrony in the setting of normal ejection fraction and normal ventricular volumes [27,28,38]
Diet-induced obesity leads to a reduction in cardiac function in mice as evidenced by reductions in left ventricular strains and torsion
Summary
Obesity affects a third of adults in the US and results in an increased risk of cardiovascular mortality. Some studies have shown cardiac dysfunction in mouse models of obesity [9,10,11,12,13,14,15,16], while others have shown no dysfunction [17,18,19,20,21,22,23,24] These studies only utilized routine measures of cardiac function such as ejection fraction and ventricular dimensions. Preliminary human studies focusing on these advanced measures show that patients with obesity have normal ejection fraction and ventricular dimensions with reduced cardiac strains and torsion [27,28]. It is important to overcome this limitation to 1) establish relevance of the mouse model to human disease in order to investigate therapies and mechanisms and 2) further our understanding of the important link between obesity and cardiovascular mortality
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