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Oversized Heart Chamber Result of Obesity

NEW YORK (Reuters Health) - Obesity is a predominant factor contributing to enlargement of the upper-left chamber of the heart, a known risk factor for heart disease and death, a team of Canadian researchers reports.

``Obesity, a preventable disorder and a current epidemic, is the strongest determinant of left ventricular mass,'' Dr. Zion Sasson of the Mount Sinai Hospital in Toronto and his colleagues write in the June 1st issue of the Journal of the American College of Cardiology.

Diabetics have been shown to have a higher risk for enlargement of the heart's left ventricle--a condition known as left ventricular hypertrophy--which raises the risk of cardiovascular death.

But Sasson's team believed much of this association can be explained by the fact that people with type 2 diabetes tend to be older, obese and have high blood pressure. The increase in ventricle size is believed to be a result of excess pressure or increased blood flow to the heart muscle.

To examine factors influencing the enlargement of the left ventricle, the researchers studied 875 men and women who had been referred for an echocardiogram by their primary care physicians. They measured the size of the patients' hearts and noted the patients' weight and the presence of diabetes or high blood pressure.

It turned out that obesity was the main factor associated with an enlarged left ventricle, followed by the presence of coronary artery disease, high blood pressure and old age.

Diabetes in and of itself was still a predictor of an enlarged left ventricle, but the association was magnified when the patient was obese or older.

More than half of the patients who were diabetic, obese and had high blood pressure suffered from left ventricular hypertrophy, compared with fewer than 4% of patients without these conditions.

``The increased left ventricular mass found in diabetics is mainly due to the interaction of diabetes with obesity, which is amplified by the aging process,'' the researchers conclude.

SOURCE: Journal of the American College of Cardiology 2001;37:1957-1962.

Reference Source 89

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