Circulation. 2002;106:286-288
doi: 10.1161/01.CIR.0000019884.36724.D9
doi: 10.1161/01.CIR.0000019884.36724.D9
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(Circulation. 2002;106:286.)
© 2002 American Heart Association, Inc.
Clinician Update |
Metabolic Syndrome
Pathophysiology and Implications for Management of Cardiovascular Disease
From Falk Cardiovascular Research Center, Stanford Medical Center, Stanford, Calif.
Correspondence to Gerald Reaven, MD, Falk Cardiovascular Research Center, Stanford Medical Center, 300 Pasteur Dr, Stanford, CA 94305. E-mail greaven@cvmed.stanfor.edu
Key Words: metabolic syndrome • insulin resistance • coronary disease
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Case Presentation: E.C. is a 53-year-old postmenopausal female, referred for treatment of hypertension, with a family history of type 2 diabetes, hypertension, and coronary heart disease (CHD). Until learning that her blood pressure was "too high" during a routine physical examination, she felt well, and her postmenopausal symptoms had responded to hormone replacement therapy. She was not overweight (her body mass index [BMI] was 23.7 kg/m2), and the only abnormality on physical examination was a blood pressure of 145/95 RAR. Laboratory results revealed a normal blood count and urinalysis, with the following fasting plasma concentrations of relevant metabolic variables (in mg/dL): glucose 102, triglycerides (TG) 238, low-density lipoprotein cholesterol (LDL-C) 147, and high-density lipoprotein cholesterol (HDL-C) 52.
E.C. is hypertensive and hypertriglyceridemic and at increased risk for CHD. Less obvious is that these metabolic abnormalities are highly likely to be the manifestations of a more fundamental defect—resistance to insulin-mediated glucose disposal and compensatory hyperinsulinemia, changes that greatly increase CHD risk.1,2 The importance of insulin resistance as a CHD risk factor was first explicated in 1998, and the cluster of abnormalities likely to appear as manifestations of the defect in insulin action designated as syndrome X.1 Support for this notion has grown almost as fast as the names used to describe the phenomenon. The Adult Treatment Panel III (ATP III) has recently3 recognized the importance as CHD risk factors of a "constellation of lipid and nonlipid risk factors of metabolic origin," designated this cluster of abnormalities as "the metabolic syndrome,"
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