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(Circulation. 2006;114:985.)
© 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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WILD-TYPE AND MUTANT HCN CHANNELS IN A TANDEM BIOLOGICAL-ELECTRONIC CARDIAC PACEMAKER, by Bucchi et al. |
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and
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BIOARTIFICIAL SINUS NODE CONSTRUCTED VIA IN VIVO GENE TRANSFER OF AN ENGINEERED PACEMAKER HCN CHANNEL REDUCES THE DEPENDENCE ON ELECTRONIC PACEMAKER IN A SICK-SINUS SYNDROME MODEL, by Tse et al. |
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Advances in technology have improved reliability of pacemaker therapy for bradycardia due to sinus node dysfunction or complete atrioventricular block. However, these electronic devices remain imperfect and have finite battery longevity. Recent manufacturers’ advisories and US Food and Drug Administration recalls due to component failures highlight the need for continued improvement. In this issue of Circulation, 2 separate studies by Bucchi and colleagues and by Tse and colleagues report their findings of experiments using bioengineered pacemaker channel technology. Both groups found a decrease in electronic pacing when constructs with engineered modified HCN channels were transfected into cardiac tissue. Bucchi and colleagues demonstrated that a mutant biological pacemaker implanted in a canine atrioventricular block model conferred catecholamine-sensitive rate improvement and less reliance on electronic pacemaker. Tse and colleagues overexpressed a different mutant HCN channel in a porcine sinus node dysfunction model, and similarly showed that transduction in the atria induced spontaneous automaticity and a catecholamine-responsive physiological heart rate that reduced electronic pacing. Although not yet ready to render pacemakers obsolete, these studies further our understanding of cardiac impulse generation and conduction. These hybrid electronic-biological pacemaker systems illustrate important advances in gene therapy for electrophysiological abnormalities. See p 992 and p 1000 (editorial on p 986).
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SPECIFIC TEMPORAL PROFILE OF MATRIX METALLOPROTEINASE RELEASE OCCURS IN PATIENTS AFTER MYOCARDIAL INFARCTION: RELATION TO LEFT VENTRICULAR REMODELING, by Webb et al. |
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Experimental studies in animals have shown that matrix metalloproteinases (MMPs) and their endogenous inhibitors, the tissue inhibitors of MMPs (TIMPs), play an important role in regulating myocardial remodeling after myocardial infarction (MI). Webb et al measured plasma levels of MMP-8 and -9 and
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