doi: 10.1161/01.CIR.0000069911.48261.CA
(Circulation. 2003;107:e9022.)
© 2003 American Heart Association, Inc.
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Circulation Newswriter
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Rapamycin and Murine Cardiac Hypertrophy
Inhibition of the action of a gene (mammalian target of rapamycin [mTOR]) associated with a biochemical pathway (the insulin-phosphoinositide 3-kinase pathway) important in determining the size of cells, organs, and the body reduced the increase in the size of myocytes associated by aortic constriction in mice, according to a team led by Tetsuo Shioi, MD, PhD, of Deaconess Medical Center in Boston, Mass. The report appears in this week’s issue of the journal Circulation (Circulation. 2003;107:1664–1670).
The researchers administered rapamycin (which inhibits mTOR) to mice with constriction of the ascending aorta. The researchers found that the drug suppressed by 67% the load-induced increase in heart weight compared with mice that did not receive the drug. Rapamycin did not cause body weight loss, death, or left ventricular dysfunction.
The researchers concluded that mTOR or its targets appear to play in important role in the development of this type of cardiac hypertrophy. "Because systemic administration of rapamycin has been used successfully for the treatment of transplant rejection in clinical practice, it may be a useful therapeutic modality to suppress cardiac hypertrophy in patients," the researchers wrote.
Silent Atrial Tachycardia Gives the MOST Data
Periods of atrial tachycardia or atrial high rate events in patients with sinus node dysfunction appear to be associated with a 2-fold increase in death or stroke and a 6-fold increase in atrial fibrillation, according to researchers involved in the Mode Selection Trial (MOST). A report of their study appears in this week’s issue of the journal Circulation (Circulation. 2003;107:1614–1619).
The MOST