Restoring repolarization in LQT3

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Transmural dispersion of repolarization as a key factor of arrhythmogenicity in a novel intact heart model of LQT3.

BACKGROUND Congenital and acquired long QT syndrome (LQTS) are caused by abnormalities of ionic currents underlying ventricular repolarization. For a better understanding of the mechanisms by which functional electrical instability at the level of the whole heart leads to torsade de pointes (TdP), a novel model of LQT3 was developed and the role of transmural dispersion of repolarization for th...

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Transmural dispersion in LQT3 and arrhythmogenesis.

At the end of the 19th century Einthoven described the configuration of the human ECG [1] and in later papers he elaborated on the magnitude and direction of its components [2]. From an intellectual point of view it is in fact unacceptable that we still do not know exactly how the T wave emerges. More precisely, we may understand how (dispersion in) repolarization within the ventricles transfor...

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Transmural dispersion in LQT3 and arrhythmogenesis

We thank Dr. Opthof and Dr. Coronel for the interest in our recently published work [1] and appreciate their comments. We aimed at developing a novel intact heart model of LQT3 for a better understanding of the mechanisms by which functional electrical instability at the level of the whole heart leads to torsade de pointes (TdP). The potassium concentration was repeatedly lowered to design an e...

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Gene-specific response of dynamic ventricular repolarization to sympathetic stimulation in LQT1, LQT2 and LQT3 forms of congenital long QT syndrome.

AIMS Differences in the sensitivity of the genotype of the congenital long QT syndrome to sympathetic stimulation have been suggested. This study compared the influence of sympathetic stimulation on continuous corrected QT (QTc) intervals between LQT1, LQT2 and LQT3 forms of the congenital long QT syndrome. METHODS AND RESULTS We recorded a 12-lead electrocardiogram continuously before and af...

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Effects of a K(+) channel opener to reduce transmural dispersion of repolarization and prevent torsade de pointes in LQT1, LQT2, and LQT3 models of the long-QT syndrome.

BACKGROUND This study examines the effects of nicorandil, a K(+) channel opener, on transmural dispersion of repolarization (TDR) and induction of torsade de pointes (TdP) under conditions mimicking the LQT1, LQT2, and LQT3 forms of the congenital long-QT syndrome (LQTS). METHODS AND RESULTS Transmembrane action potentials of epicardial, M, and endocardial cells were recorded simultaneously f...

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ژورنال

عنوان ژورنال: Heart Rhythm

سال: 2009

ISSN: 1547-5271

DOI: 10.1016/j.hrthm.2008.10.037