Obesity is considered a worldwide epidemic in humans, and it is becoming epidemic in pets as well. It is currently estimated that obesity affects 20-40% of the canine population. A study conducted in São Paulo, Brazil, showed a prevalence of 16.5% of obesity among dogs.

Obesity is the result of an imbalance between caloric intake and energy expenditure, and may result from nutritional, genetic, and metabolic diseases.

The human-animal bond seems to be a contributing factor for the obesity "boom" in the canine population. The unique relationship between humans and dogs has existed for centuries, and sharing food is a characteristic of this bond. The sedentary lifestyle of the dog owners can influence the dog´s lifestyle and contribute to obesity. In the past, humans used to exercise more because their work was related to physical activity, and food was less processed and had less fat. The activity level is related to body mass index (BMI) in humans and with body score condition (BCS) in dogs, i.e., low activity level is associated with higher BCS, and less active owners generally have less active dogs.

It is known that in humans, the obesity may result in cardiac structural and functional changes, even in the absence of arterial hypertension or primary heart disease. Fat is a relatively nonvascular tissue, but requires perfusion, what leads to an increase in circulatory volume, and cardiac output, which is proportional to weight excess and obesity duration. Peripheral vascular resistance decreases to accommodate the increase in cardiac output. Increased blood volume translates into an increased preload and increased end diastolic volume, what leads to ventricular dilation. According to Laplace´s law, this dilation increases wall stress and as an adaptive measure, hypertrophy develops by the addition of contractile elements. This eccentric hypertrophy may lead to diastolic dysfunction.

Although literature cites heart disease as a problem related to obesity in dogs, there are only few studies that evaluate the actual cardiovascular sequelae of obesity in this species.

In people, insulin resistance is one of the consequences of obesity, which has a link with cardiovascular events. In dogs, it has been determined that weight gain causes a decrease in insulin sensitivity, and an increase in plasma Tumor Necrosis Factor (TNFα), Insulin-Like Growth Factor 1 (IGFl), Non-Esterified Fatty Acids (NEFA) concentrations.

Obesity is cited as having minor effects on systemic/systolic arterial blood pressure (SABP) in pets, but hypertension has been reported in 23% and 45% of obese dogs, and a recent study observed 67% of the obese dogs with SABP above 160mmHg, considered as hypertensive (and the obese had significantly higher blood pressure than controls). Hypertension was considered a risk factor associated with body condition score in dogs.

Heart rate has been reported to be elevated in obese dogs. Significant ECG and routine 2-D echocardiographic changes were not found in a Brazilian recent study. Although non-significant, cTnI was elevated in 24% of the obese, and the magnitude of elevation was higher among the obese.

Data published regarding cardiac function in obese humans show that obesity is consistently associated with mild, but significant reductions in systolic and diastolic functions of both left and right ventricles, detected by pulsed tissue Doppler imaging (PTDI), and the severity of the dysfunction is related to the magnitude of obesity. It is still not proven if these changes progress to heart failure over time, and the possible mechanisms that may contribute to heart failure development are not defined.

An ongoing study of our group, revealed that overweight dogs without overt heart disease present preclinical left myocardial systolic and diastolic function changes detected by PTDI. Even without a predisposition of dogs to ischemic heart disease, obesity has an impact on ventricular function.

References

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