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Enlarged Heart Not Always a Sign of Trouble

Type of stress determines how the heart reacts, researchers report

FRIDAY June 2, 2006 (HealthDay News) -- An enlarged heart is usually considered a sign of cardiac trouble. But the cause of the enlargement is critical in determining whether there's actual heart disease, researchers are reporting.

In fact, the nature of the stress that created the enlargement is more important than the duration of the stress, according to the researchers.

"We set out to answer a longstanding question in cardiac biology, which is what happens to the heart during periods of stress," said lead researcher Dr. Howard Rockman, a cardiologist at Duke University Medical Center.

The researchers looked at different types of stress, such as stress from exercise, as well as so-called pathological stress that causes damage to the heart. High blood pressure is an example of pathological stress, Rockman said.

Although both types of stress can be severe, the way the heart responds to exercise or high blood pressure is very different, Rockman said. "Exercise is beneficial. The heart adapts in a good way," he said.

Endurance runners have large hearts, Rockman noted, but without damage to the function of the heart. "In contrast, someone with longstanding high blood pressure can develop a dilatated heart and heart failure," he said.

To test the reactions of the heart to these different types of stress, Rockman's team did a series of experiments in mice.

The findings appear in the June 1 issue of the Journal of Clinical Investigation.

The experiments demonstrated that intermittent cardiac stress from high blood pressure starts a series of events that eventually leads to abnormalities in heart muscle cells as well as damage to blood vessels. The researchers also found that these harmful responses can begin before the heart itself begins to get bigger.

To induce high blood pressure in the mice, Rockman's group tied a slipknot around each mouse's aorta. Then they manipulated the knot from outside the mouse through a small incision in the back. The researchers tied off the aortas in one group of mice for 90 minutes twice a day. A second group of mice exercised for 90 minutes twice a day, either by swimming or running in a wheel.

"After seven days, the hearts of the swimming mice were gorgeous," Rockman said.

The hearts of the mice with high blood pressure were similarly enlarged and appeared to be functioning normally, but individual heart muscle cells showed significant structural and cellular abnormalities, the researchers found.

"The heart is more sophisticated than we thought," Rockman said. "The type of stress you apply on the heart determines whether it's going to develop a deleterious phenotype or whether it's going to be an adaptive and beneficial phenotype," he added.

Rockman speculated that the same findings would hold for humans. Exercise is beneficial for the heart, he said, adding that "it increases the number of blood vessels in the heart, and the cells activated in the heart are all on the good side.

"The opposite things that you do, the things that raise blood pressure, even intermittently, may not be good," he added.

Dr. Gregg C. Fonarow, a professor of cardiology at the University of California, Los Angeles, said, "This study provides important new insights into the mechanisms behind cardiac hypertrophy (enlarged heart)."

The study addresses a common theory on why cardiac stress induced by exercise does not produce changes in the heart similar to the cardiac stress from high blood pressure, Fonarow noted. "The theory was that stress from exercise was intermittent, whereas that from high blood pressure was more continuous," he said.

"Better understanding of these mechanisms may lead to new treatments that can better protect the heart from hypertrophy and heart failure," Fonarow said.

More information

The American Heart Association can tell you more about enlarged hearts.

SOURCES: Howard Rockman, M.D., cardiologist, Duke University Medical Center, Chapel Hill, N.C.; Gregg C. Fonarow, M.D., professor, cardiology, University of California, Los Angeles; June, 1, 2006, Journal of Clinical Investigation
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