Background: Transthoracic echocardiography provides a non-invasive approach for in-vivo evaluation of the mouse heart. The present study examines its use in assessing the functional phenotype of the left ventricle (LV) in a model of chronic coronary heart disease (CHD). Methods: 26 male apolipoprotein E knockout mice (ApoE-/-) were fed either a western-type high-fat diet (n=13; 21% lard and 0.15% cholesterol) or chow diet (n=13) for 12 weeks from weaning. High-fat diet ApoE-/- mice develop progressive atherosclerosis including in their coronary arteries (CHD). In contrast, littermates fed a chow diet exhibit no coronary disease (control). Animals underwent echocardiography with a Vevo 770 (Visualsonics, Canada) at 12 weeks of age. Heart rate and core temperature were continuously monitored. Normothermic mouse core temperatures were maintained using a heated platform. Mice were anaesthetised with isoflurane at a concentration of 2% (induction) and 1-1.5% (maintenance) in 100% Oxygen. To minimize the confounding effects of anaesthesia between experiments, recordings were taken when the heart rate was in the range 400-500 beats/min. LV systolic function was evaluated with the fractional area shortening (FAS%) in a parasternal long axis. Pulsed wave and tissue doppler modes were used to assess the diastolic function. Data were analysed using an unpaired Student’s t-test. Results: 12-wk old apoE -/- mice when fed an atherogenic diet had comparable body mass (31.1 ± 1.46 g; CHD vs. 31.7 ± 2.6 g control), corrected cardiac mass (96 ± 23 mg; CHD vs. 100 ± 21 mg control) and cardiac output (16.7 ± 4 ml/min; CHD vs. 16.2 ± 5.6 ml/min control). There were no significant differences in short-axis B- and M-mode measurements: Aortic root (1.56 ± 0.028 mm; CHD vs. 1.542 ± 0.035 mm control); LV internal systolic diameter (2.24 ± 0.39 mm; CHD vs. 2.3 ± 0.3 mm control); LV internal diastolic diameter (3.59 ± 0.31 mm; CHD vs. 3.46 ± 0.49 mm control), fractional shortening (38.4 ± 4 %; CHD vs. 34.4 ± 6 %), and ejection fraction (68.5 ± 6 %; CHD vs. 62.1 ± 8 % control). There was no change in long axis FAS% (65 ± 5 %; CHD vs. 68 ± 9 %), peak aortic velocity (905 ± 144 mm/s; CHD vs. 890 ± 88 mm/s and mitral valve early and late diastolic filling (E/A) ratio (1.8 ± 0.5; CHD vs. 2 ± 0.6) between the two groups. Conclusions: We have performed a complete characterisation of the left ventricular function in a mouse model of coronary disease in its early stage of atheroma deposition. These reference values will enable a serial study of the heart as the disease progresses.