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Study reports on abnormal heart muscle function in severely obese patients


HOUSTON—(Aug. 08, 2006)—A new study by The University of Texas Medical School at Houston is yielding some of the earliest clinical evidence of abnormal heart function in clinically severe obesity.

In findings published in the August 2006 edition of the American Journal of Clinical Nutrition, principal investigator Heinrich Taegtmeyer, M.D., D.Phil., professor of cardiology at the UT Medical School, and Joshua Leichman, M.D., UT Medical School clinical fellow, report on early changes in heart function related to the oversupply of fat, with a focus on the heart’s ability to pump blood. Results are based on the extensive examination of the hearts of 64 patients.

A build-up of fat inside heart muscle cells weakens the heart muscle and prevents the heart from functioning properly. “Everybody talks about fat and cholesterol building up in the arterial walls, but fat metabolism does not stop in the arterial walls,” said Taegtmeyer. “It continues inside the heart muscle cells. The heart fails in the midst of plenty, having more fat than it can handle.” Specifically, Taegtmeyer is referring to free fatty acids, the precursor to triglycerides (the storage forms for fatty acids), in the bloodstream, which maintain higher levels in obese patients.

Taegtmeyer says obesity creates a “masking effect” that makes impaired heart pump function difficult to detect. He explains that because obese patients are generally not as physically active as healthy-weight patients, they do not notice that they are short of breath “until the heart is really far gone.”

“Obese patients are not likely to run to catch the bus or chase after their three-year-old,” Taegtmeyer said.

The study began with blood work for all patients as Taegtmeyer’s team sought to establish baseline insulin sensitivity by measuring patients’ glucose, insulin, cholesterol and free fatty acid levels after fasting. They also measured two types of proteins, known as adipokines, specifically derived from fat: leptin (responsible for regulating energy or food intake and the partitioning of fat into fat cells or organs like the heart or liver) and adiponectin (associated with insulin sensitivity). “Interestingly, when people become obese, their adiponectin levels drop, which is a little counter-intuitive because it’s made by the fat cell, so you’d think if you have more or bigger fat cells, you’d make more adiponectin,” said Leichman, the study’s first author. “Adiponectin has also been shown to correlate inversely with insulin sensitivity, so that if you have higher normal adiponectin levels, you probably have normal insulin sensitivity, meaning insulin signals the cell to take up glucose and to utilize it appropriately. Whereas in the obese population, if you have a low adiponectin level, you may have insulin resistance, meaning that the cell doesn’t recognize or respond to insulin and glucose runs through the bloodstream, becoming potentially toxic to the body.” The study found very high levels of leptin in the obese patients.

In addition to blood chemistries, patients also received echocardiograms to measure systolic heart function (the way the muscle squeezes) and diastolic function (the way the muscle relaxes right before pumping blood). “Tissue Doppler imaging, a relatively new mode of echocardiography, was used to measure how the myocardium moves rather than how the blood flows through a valve,” Leichman said.

In the study, Taegtmeyer and Leichman report finding sub-clinical dysfunction in about 40 percent of their patients. That is, in diastole, there is impairment in heart relaxation. “This negatively correlates with the amount of free fatty acids in the bloodstream,” said Leichman.

“At baseline, we observed that the higher free fatty acid level in a patient, the more likely he or she would have diastolic impairment, whereas the lower the level, the more likely he or she would have normal diastolic function,” explained Leichman. Furthermore, investigators believe it is unlikely that age or co-morbid states, such as diabetes, hypertension or medications, contributed to the findings of the relationship between free fatty acids and diastolic function.

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