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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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