Nov. 12, 2004 DALLAS, Nov. 2 – Overweight or obese people without obvious heart disease have changes in heart muscle structure and function that set the stage for heart failure, researchers report in Circulation: Journal of the American Heart Association.
“Weight control is an important issue not just in your risk of heart attack or high blood pressure, but in how your heart functions,” said Thomas H. Marwick, Ph.D., professor of medicine at the University of Queensland at Princess Alexandra Hospital in Brisbane, Australia.
Researchers measured the speed and extent of muscle contraction in the heart with recently developed ultrasound technology. The study included 73 women and 69 men, average age 44. None had existing heart disease, high blood pressure, diabetes or known symptoms of congestive heart failure. Researchers divided participants into four groups based on body mass index (BMI), a measure of body fatness. Thirty-three participants were normal-weight, meaning they had a BMI less than 25; 26 were overweight (BMI between 25–29.9); 37 were mildly obese (BMI between 30–34.9); and 46 were severely obese (BMI 35 or higher).
When compared with the left ventricles of people of normal weight, the left ventricles of severely obese participants had both a significantly weakened ability to contract (systolic dysfunction) and a reduced ability to fully relax to allow the ventricle to be refilled with blood during the rest period between heartbeats (diastolic dysfunction). Researchers found smaller but still significant impairments of left ventricle function in overweight or mildly obese volunteers.
“The study showed a direct relationship between the level of obesity and the degree of myocardial dysfunction. The impact was independent of other risk factors such as hypertension,” Marwick said. “We think this indicates a direct metabolic effect of obesity on the heart muscle.”
Using a conventional echocardiogram, researchers found that all participants had a normal ejection fraction, a measurement of the amount of blood pumped from the ventricles; so none would be considered to have heart failure.
“We detected subtle changes that we think are steps along the way to developing heart failure,” Marwick said.
In heart failure, the heart no longer pumps sufficient blood to the body’s organs. In the United States, physicians diagnose about 550,000 new cases of congestive heart failure annually, and about 53,000 people die of the condition as the primary cause of death each year. The annual deaths due to congestive heart failure would be more than 260,000 if statistics included cases when it was listed on death certificates as a contributing cause of death. Although heart failure can eventually affect the entire heart, it usually begins in the left ventricle, the largest chamber of the heart that pumps blood out to the rest of the body.
Two additional findings from the study suggest ways that physicians might intervene to help prevent the development of heart failure in obese patients. On treadmill testing, researchers found that those with the poorest myocardial function had the worst exercise capacity. Those with the most heart muscle dysfunction also had higher fasting levels of insulin, which is an indication that the body can’t properly use insulin (insulin resistance, one component of the metabolic syndrome that raises the risk of heart disease, stroke and type 2 diabetes).
Using those clues, the researchers initiated ongoing clinical trials to determine whether exercise training and/or medication to counter insulin resistance can improve heart muscle function and help forestall the development of heart failure. Results from these trials are not yet available.
“We know from other conditions that we lose the best opportunity to initiate treatment if we wait until late in the disease process, trying to close the stable door after the horse is gone,” Marwick said. “Once we learn more about these heart muscle changes, we would like to be able to intervene at an early stage.”
First author on the report is Chiew Y. Wong, M.B.B.S, FRACP. Other co-authors are Trisha O’Moore Sullivan, M.B.B.S., FRACP; Rodel Leano, B.S.; Nuala Byrne, Ph.D.; and Elaine Beller, Ph.D.
The research is funded by the National Health and Medical Research Program in Australia.
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