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1 c status of the heart (inhomogeneity of left ventricular repolarization).
2 or activity of any other channel involved in ventricular repolarization.
3 tion scar, atrial fibrillation, and abnormal ventricular repolarization.
4 tion system, as well as heterogeneity of the ventricular repolarization.
5 defining gender-related differences in mouse ventricular repolarization.
6 ng the densities of K(+) currents underlying ventricular repolarization.
7 te with long QT syndrome (LQTS), a defect in ventricular repolarization.
8 nd electrocardiographic evidence for delayed ventricular repolarization.
9 rate, which likely contributes to prolonged ventricular repolarization.
10 al flutter or fibrillation without affecting ventricular repolarization.
11 d re-entrant excitation arising from delayed ventricular repolarization.
12 nown whether alpha-linolenic acid influences ventricular repolarization.
13 hythmia associated with abnormally prolonged ventricular repolarization.
14 been proposed as a more valid way to assess ventricular repolarization.
15 d, or both) of the ionic currents underlying ventricular repolarization.
16 T interval is prolonged due to dysfunctional ventricular repolarization.
17 informative in pathophysiological studies of ventricular repolarization.
18 dal factors contribute to the differences in ventricular repolarization.
19 eflect different underlying abnormalities of ventricular repolarization.
20 icate that DCM leads to temporal lability in ventricular repolarization.
21 T-wave changes imply an abnormal sequence of ventricular repolarization.
22 al-specific lymphocyte infiltration, impairs ventricular repolarization.
24 ng-QT syndrome is characterized by prolonged ventricular repolarization and a variable clinical cours
25 and tissue excitability, while it prolonged ventricular repolarization and refractoriness by 7.5% to
26 responsible for the abnormal prolongation of ventricular repolarization and revealed associations bet
28 function in sedated mice in vivo, prolonged ventricular repolarization, and provoked ventricular arr
29 he effects of restitution in single cells on ventricular repolarization at the level of the intact he
31 to identify the ionic and cellular basis for ventricular repolarization components on the body surfac
33 use a spectrum of diminished IKr and delayed ventricular repolarization, consistent with the prolonge
34 ed the hypothesis that heterogeneity of left ventricular repolarization creates an arrhythmogenic sub
35 3 deletion also caused aldosterone-dependent ventricular repolarization delay (19.6% mean QTc prolong
36 low delayed rectifier K+ current, in cardiac ventricular repolarization has been a subject of debate.
37 rrhythmia characterized in part by prolonged ventricular repolarization, has been linked to 5 loci, 4
38 significantly modulate spatial gradients of ventricular repolarization (ie, modulated dispersion), w
39 rhythmias by modulating spatial gradients of ventricular repolarization (ie, modulated dispersion).
40 during atrial and ventricular activation and ventricular repolarization in (i) normal heart (ii) hear
44 QT prolongation, consistent with a defect in ventricular repolarization, in Kv2.1N216FLAG-expressing
46 is the electrocardiographic manifestation of ventricular repolarization, is variable under physiologi
47 for suppressing hypertrophy (Hdac9) and for ventricular repolarization (Kcnd2) and conduction (Hcn4)
48 yndrome (LQTS) is a disease in which delayed ventricular repolarization leads to cardiac arrhythmias
49 to determine spatial and dynamic changes in ventricular repolarization may help to understand arrhyt
51 ndividuals developing marked prolongation of ventricular repolarization on exposure to an offending d
52 upts the electrophysiological homogeneity of ventricular repolarization, predisposing to arrhythmia.
54 , atrioventricular conduction (PR interval), ventricular repolarization (QT interval), and ventricula
56 Long QT syndrome (LQTS) is a disorder of ventricular repolarization that predisposes affected ind
57 Ks and cause long-QT syndrome, a disorder of ventricular repolarization that predisposes affected ind
58 tigated the impact of reduced sialylation on ventricular repolarization through gene deletion of the
59 ain (beta-MHC) gene mutations exhibit labile ventricular repolarization using beat-to-beat QT variabi
62 ome is characterized by abnormally prolonged ventricular repolarization, which predisposes patients t
63 A transmural voltage gradient during initial ventricular repolarization, which results from the prese
64 ting in vivo, and a role for MiRP1 in murine ventricular repolarization with parallels to that propos
65 heart rate, atrioventricular conduction, and ventricular repolarization, with potential implications
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