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1 ger and substrate for atrial and ventricular proarrhythmia.
2 en withdrawn for their ability to cause such proarrhythmia.
3 nonfailing hearts and absence of ventricular proarrhythmia.
4 g to increased conduction in homogeneity and proarrhythmia.
5 titute an important mechanism of ventricular proarrhythmia.
6 e device longevity, and avoid device-induced proarrhythmia.
7 of non-PV foci are sufficient to treat this proarrhythmia.
8 ac abnormalities secondary to a high risk of proarrhythmia.
9 hythm disorders with an acceptable degree of proarrhythmia.
10 and should minimize the risk of ventricular proarrhythmia.
11 fficacy and/or carry the risk of ventricular proarrhythmia.
12 raindications and adverse effects, including proarrhythmia.
13 development of long-QT-mediated ventricular proarrhythmia.
14 may be futile or lead to atrial scarring or proarrhythmia.
15 antiarrhythmic drugs carries a high risk for proarrhythmias.
16 ions under which autonomic imbalance induces proarrhythmia and can be modified to prevent or inhibit
17 l mechanism for individual susceptibility to proarrhythmia and highlight the need for a new paradigm
19 en mainly by hospitalizations for arrhythmia/proarrhythmia and other cardiovascular causes, but not b
21 clinical consequences-arrhythmia recurrence, proarrhythmia, and death-that have now been reported in
22 s under which adverse event rates, including proarrhythmia, are expectedly low, would favor outpatien
23 nded for the evolving Comprehensive In Vitro Proarrhythmia Assay (CiPA) coordinated by the Health and
28 infection, unnecessary shocks, potential for proarrhythmia, device malfunction, highly publicized man
32 scar was significantly more frequent in the proarrhythmia group (60% versus 9% P=0.03 on epicardial
41 review some methodologies employed to assess proarrhythmia liability of drugs, discuss the challenges
46 disease, for patients receiving a drug whose proarrhythmia may be idiosyncratic (e.g., quinidine), an
47 e the potential mechanism for the flecainide proarrhythmia observed in CAST, the voltage dependence o
53 l storm (100% versus 39% of patients with no proarrhythmia; P<0.01), requiring temporary biventricula
58 on mechanisms underlying QT prolongation and proarrhythmia, risk factors, including the role of genet
62 cardiac action potential as an indicator of proarrhythmia, supposing that these shape changes might
64 ses the new concepts of arrhythmogenesis and proarrhythmia; the long QT interval syndrome; newer, mor
65 ocyte action potentials, AF, and ventricular proarrhythmia, to determine the relationship between the
69 dy provides mechanistic insights into atrial proarrhythmia with SQT3 Kir2.1 mutations and highlights