Echocardiographic evidence of left ventricular hypertrophy in obese dogs

Cardiomyopathy of obesity occurs in humans, but the gross and cellular myocardial response to obesity in dogs is not well defined.

To characterize in vivo myocardial morphology and function in normotensive obese dogs, and quantitate collagen, triglyceride and myocyte cross-sectional area (CSA) in postmortem tissues from obese dogs.

Echocardiographic-Doppler measurements of normotensive obese dogs (n = 19) without historical or physical examination evidence of disease, and lean healthy dogs (n = 19) matched for age and ideal weight. Postmortem data were obtained from a separate population of 4 obese and 12 lean dogs without evidence of cardiac disease.

A prospective, observational study of myocardial morphology and function was conducted by echocardiographic-Doppler measurement. Left ventricular (LV) tissue was collected for quantitation of triglyceride, collagen, and myocyte CSA.

Compared with lean control dogs, obese dogs had increased systolic blood pressure (obese 153 ± 19 mm Hg; lean 133 ± 20 mm Hg; P = .003), and increased LV free wall thickness at end-diastole (obese 9.9 ± 1.8 mm, lean 8.7 ± 1.5 mm; P = .03) and end-systole (obese 15.2 ± 2.3 mm, lean 12.9 ± 2.3 mm; P = .004). Isovolumic relaxation time was prolonged in 7/19 (37%) of obese dogs, compared with normal ranges. Myocardial triglyceride and collagen content and myocyte CSA were similar between groups.

As in humans, LV hypertrophy and diastolic dysfunction can be an early myocardial change in some obese dogs.