(Circulation. 2006;113:1.)
© 2006 American Heart Association, Inc.
Issue Highlights
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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SLEEP AND EXERTIONAL PERIODIC BREATHING IN CHRONIC HEART FAILURE: PROGNOSTIC IMPORTANCE AND INTERDEPENDENCE, by Corrà et al. |
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The prediction of prognosis in patients with heart failure has important implications for therapy. Measurements of peak oxygen uptake during exercise testing provide useful information in that regard, yet such an analysis often stratifies patients into a gray zone of intermediate risk. In this issue of Circulation, Corrà et al move the field beyond peak oxygen uptake and prompt us to evaluate breathing patterns during exercise and sleep. Periodic breathing, as assessed via the apnea-hypopnea index during sleep and cyclic fluctuations in minute ventilation during exercise, was measured in 133 patients with heart failure. The authors report the incremental value of each measure when used alone or in combination in predicting adverse cardiac events. In an accompanying editorial (p 9), Ribeiro highlights the importance of these data in the context of other variables that can be obtained from gas exchange analysis in patients with heart failure. See p 44.
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INHIBITION OF HISTONE DEACETYLATION BLOCKS CARDIAC HYPERTROPHY INDUCED BY ANGIOTENSIN II INFUSION AND AORTIC BANDING, by Kee et al. |
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Class II histone deacetylases (HDACs) have been shown to antagonize a variety of pathways that lead to myocardial hypertrophy. Surprisingly, myocardial hypertrophy induced by chronic angiotensin infusion or aortic banding was inhibited by simultaneous administration of several HDAC inhibitors, including those that are nonselective with regard to class I versus class II HDACs as well as a class I–selective inhibitor. Inhibition of myocardial hypertrophy was paralleled by salutary effects on fetal gene expression and interstitial fibrosis. These observations suggest that the predominant effect of HDAC inhibition is to attenuate myocardial hypertrophy that is mediated by class I HDACs, and
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