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Circulation. 2004;110:103

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(Circulation. 2004;110:103.)
© 2004 American Heart Association, Inc.


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An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

POSTMENOPAUSAL HORMONE THERAPY IS ASSOCIATED WITH ATHEROSCLEROTIC PROGRESSION IN WOMEN WITH ABNOMAL GLUCOSE TOLERANCE, by Howard et al.

The influence of postmenopausal hormone therapy (PHT) on cardiovascular disease and its risk factors is complex. Whereas PHT has been demonstrated to increase the risk of heart disease, stroke, and thromboembolic events in the Women’s Health Initiative Trial, in that trial PHT also reduced the incidence of diabetes. Hence, the Women’s Angiographic Vitamin and Estrogen (WAVE) study examined the influence of PHT on angiographic progression in 140 women with versus 181 women without abnormal glucose tolerance (defined as diabetes or impaired glucose tolerance). The investigators observed that PHT was associated with increased atherosclerotic progression and increased CRP in women with abnormal glucose tolerance to a greater extent than those without. The authors conclude that PHT is not warranted in diabetic women, despite improvements in insulin resistance and glycemia. See p 201.

REGRESSION OF CAROTID ATHEROSCLEROSIS BY CONTROL OF POSTPRANDIAL HYPERGLYCEMIA IN TYPE 2 DIABETES MELLITUS, by Esposito et al.

Most prior studies examining the relation between glycemic control and cardiovascular disease risk focused on fasting glucose level. Esposito and colleagues examined postprandial glucose levels in patients with type II diabetes mellitus and observed a correlation with early carotid artery atherosclerosis assessed by ultrasound. In a randomized intervention study comparing 2 hypoglycemic therapies, they observed that the strategy designed to produce a greater reduction in postprandial glucose levels was associated with a greater reduction in carotid intimal thickness. These findings further emphasize the importance of postprandial glucose levels as an indicator of risk and a potential target for therapy. See p 214.

ALTERED TITIN EXPRESSION, MYOCARDIAL STIFFNESS, AND LEFT VENTRICUALR FUNCTION IN PATIENTS WITH DILATED CARDIOMYOPATHY, by Nagueh et al.

The giant myofilament protein titin, the so-called "third myofilament," spans the half sarcomere and regulates both systolic . . . [Full Text of this Article]




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