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1 nctive polymorphic ventricular tachycardia ('torsades de pointes').
2 ciated arrhythmias (eg, long QT syndrome and torsade de pointes).
3 ome with QT-related ventricular arrhythmias (torsades de pointes).
4 ion of the QT interval and/or development of torsades de pointes).
5 y-high-dose methadone may be associated with torsade de pointes.
6 European market after being associated with torsade de pointes.
7 ary outcome was QT prolongation resulting in Torsade de pointes.
8 sion of atrial arrhythmias, but it can cause torsade de pointes.
9 o prolongs the QT interval but rarely causes torsade de pointes.
10 s, and thus the potential for development of torsade de pointes.
11 h from ventricular arrhythmias, specifically torsade de pointes.
12 interval and an increased propensity toward torsade de pointes.
13 to explain the link between hypokalemia and torsade de pointes.
14 affecting susceptibility to arrhythmias like Torsade de Pointes.
15 o a life-threatening ventricular arrhythmia, Torsade de Pointes.
16 d is a significant predictor of drug-induced torsade de pointes.
17 T syndrome and the lethal cardiac arrhythmia torsade de pointes.
18 at of antiarrhythmic agents known to promote torsade de pointes.
19 may cause abnormal heart rhythms, including torsade de pointes.
20 gned to examine the risk of rare events like torsade de pointes.
21 load, early afterdepolarizations (EADs), and torsade de pointes.
22 ype 2, women are more vulnerable than men to torsade de pointes.
23 QT prolongation with the associated risk of torsade de pointes.
24 redispose individuals to QT prolongation and torsade de pointes.
25 rs), can prolong the QT interval and provoke torsades de pointes.
26 es, which are thought to trigger episodes of torsades de pointes.
27 f repolarization are not capable of inducing torsades de pointes.
28 ar tachycardia displaying characteristics of torsades de pointes.
29 nduce potentially lethal arrhythmia known as torsades de pointes.
30 ally the polymorphic ventricular tachycardia torsades de pointes.
31 predisposes to drug-induced QT prolongation/torsades de pointes.
32 enic afterdepolarizations thought to trigger torsades de pointes.
33 ciated with the potentially fatal arrhythmia torsades de pointes.
34 duced long QT interval syndrome (diLQTS) and torsades de pointes.
35 lead to interventions to reduce the risk of torsades de pointes.
36 sociated with the rare adverse drug reaction torsades de pointes.
37 adverse events including QT prolongation and torsades de pointes.
38 to hyperfunction of L-type channels, such as Torsades de Pointes.
39 quired and drug-induced long QT syndrome and torsades de pointes.
40 ation and is associated with case reports of torsades de pointes.
42 ons in a cohort of consecutive patients with Torsades de Pointes; (3) the relationship between K(+) c
44 enic can prolong the QT interval and lead to torsade de pointes, a life-threatening ventricular arrhy
46 mary suspect in cases of QTc prolongation or torsade de pointes after dofetilide (a known proarrhythm
47 n in the placebo group (0.3% versus 0.1% for torsade de pointes and 0.9% versus 0.2% for severe neutr
51 iew the mechanisms and establish the risk of torsade de pointes and sudden death with antipsychotic d
52 nd haloperidol have been documented to cause torsade de pointes and sudden death, the most marked ris
56 ssociated with complex arrhythmias including torsades de pointes and 2 degrees atrioventricular block
57 ndrome, adult women carry a greater risk for Torsades de pointes and sudden cardiac death than do men
63 n between familial and drug-induced cases of torsade de pointes, and the recognition of the role of n
64 ardiac events defined as syncope, documented torsades de pointes, and aborted cardiac arrest or sudde
69 0400 is effective against dofetilide-induced torsade de pointes arrhythmias (TdP), while maintaining
71 interval on the electrocardiogram and cause torsade de pointes arrhythmias not by direct block of th
72 is commonly associated with life-threatening torsade de pointes arrhythmias that develop as a consequ
73 ties that have been associated with syncope, torsade de pointes arrhythmias, and sudden cardiac death
76 ontractions and fibrillations reminiscent of Torsades des Pointes arrhythmias, and they exhibit sever
77 se in the intracellular calcium may underlie torsades de pointes associated with intravenous tacrolim
81 lt to predict which patients are at risk for torsade de pointes, careful assessment of the risk to be
83 ENDO, causing a persistent increase in TDR; Torsade de Pointes developed or could be induced only in
84 bradycardia per se, determines the risk for torsade de pointes during atrioventricular block (AVB).
85 nd Europe with diLQTS, defined as documented torsades de pointes during treatment with a QT-prolongin
86 ated in causing QT interval prolongation and torsades de pointes, errors in the use of medications th
87 clinical observation of QT prolongation and torsade de pointes found with astemizole intake may prin
89 terval prolongation, potassium channels, and torsade de pointes from both the long QT syndrome and dr
90 ars, and cases of prolonged QTc interval and torsades de pointes have been described in HIV-infected
92 arrhythmias developed in 7 patients (5.8%) (torsade de pointes in 2), significant bradycardia in 20
93 clinical observation of QT prolongation and torsade de pointes in a patient with undetectable serum
94 was a significant predictor of drug-induced torsade de pointes in an independent sample of 216 cases
95 APD(90,) reduced BVR (P<0.01), and abolished torsade de pointes in hearts treated with either 20 nmol
96 o the cell surface cause QT prolongation and torsade de pointes in patients treated with As(2)O(3).
97 , which has been recognized as a hallmark of torsade de pointes in the acquired LQTS, plays a major r
98 to describe the mode of onset of spontaneous torsade de pointes in the congenital long QT syndrome.
99 The in vivo electrophysiologic mechanism of torsade de pointes in the long QT syndrome is described,
100 ervals and higher incidences of drug-induced torsade de pointes in women than in men are incompletely
101 eats after aftercontractions occurred before torsades de pointes in an in vivo dog model of drug-indu
102 s used to examine susceptibility to acquired torsades de pointes in chronic atrioventricular block an
103 voke the life-threatening cardiac arrhythmia torsades de pointes in some, but not all, individuals.
104 proved predictors of risk for progression to torsade de pointes, in addition to the degree of QT prol
105 ing of noncardiac medications known to cause torsades de pointes, including fluoroquinolones and intr
107 A common effect of many drugs producing torsade de pointes is block of the rapidly activating co
109 ion of the QT interval and the occurrence of torsades de pointes is similar to more expensive alterna
111 cially amiodarone, and drugs associated with torsade de pointes may have contributed to poor outcomes
112 dult gender differences in propensity toward torsade de pointes may reflect the relatively greater pr
113 c ventricular tachycardia, Brugada syndrome, torsades de pointes) may result in serious consequences,
114 over, the data suggest that cisapride caused torsade de pointes not only by blocking IKr but also by
119 /31; 61%) versus WT (8/26; 31%; P<0.05), and Torsades de Pointes occurred more frequently (73% Cav3.1
121 nic atrioventricular block animals exhibited torsades de pointes on dofetilide, the arrhythmia was in
123 None of the patients on sotalol developed Torsade de pointes or sustained ventricular arrhythmias.
125 ychloroquine+/-azithromycin, no instances of Torsade de pointes, or arrhythmogenic death were reporte
126 entified 24 patients with QT prolongation or torsade de pointes, or both, associated with protease in
128 netheless, drug-induced long QT syndrome and torsade de pointes pose unique challenges for clinicians
129 en identified in a patient with drug-induced torsade de pointes precipitated by the IKr blocker cisap
131 s system vasculitis and leukoencephalopathy, torsades de pointes, pulmonary vasculopathy, and pulmona
132 g class IC drugs, patients with low risk for torsades de pointes receiving selected class III agents,
136 ind QT prolongation to be common (24%), with Torsade de Pointes representing 6% of in-hospital cardia
137 icited seizure was followed by an episode of torsade de pointes requiring immediate cardioversion.
143 rhythmic agent with the propensity to induce torsades de pointes, substantially inhibits the current.
144 5 micromol/L totally suppressed spontaneous torsade de pointes (TdP) and reduced the vulnerable wind
145 or inherited and acquired long-QT associated torsade de pointes (TdP) arrhythmias, and sympathetic di
148 tricular tachycardia with characteristics of torsade de pointes (TdP) developed in the presence of dl
149 hat women are more prone than men to develop torsade de pointes (TdP) in a defined cohort of patients
150 Female rabbit hearts are more susceptible to torsade de pointes (TdP) in acquired long QT type 2 than
151 functional electrical instability leading to torsade de pointes (TdP) in LQTS are poorly understood.
152 repolarization (TDR) and the development of Torsade de Pointes (TdP) in models of LQT1, LQT2 and LQT
153 ation (TDR) may be related to the genesis of torsade de pointes (TdP) in patients with the long-QT (L
154 ural dispersion of repolarization (TDR), and torsade de pointes (TdP) induced by beta-adrenergic agon
158 ion of repolarization (TDR) and induction of torsade de pointes (TdP) under conditions mimicking the
159 rigins of EADs and the mechanisms underlying Torsade de Pointes (TdP) were investigated in a model of
161 ion (EAD) in producing a trigger to initiate torsade de pointes (TdP) with QT prolongation induced by
162 that the calmodulin inhibitor W-7 suppresses torsade de pointes (TdP) without shortening the QT inter
163 induced long-QT syndromes (diLQTS) can cause torsade de pointes (TdP), a life-threatening ventricular
164 iac repolarization and increases the risk of Torsade de Pointes (TdP), a potentially lethal arrhythmi
165 SIDS), one with documented prolonged QTc and Torsade de Pointes (TdP), and in an adult woman with QTc
166 proarrhythmic risk and in particular risk of Torsade de Pointes (TdP), as indicated by prolongation o
173 T, n = 18 123) and VA (n = 29 193) including torsade de pointes (TdP, n = 8163) reporting for 663 ant
175 cteristic of long QT syndrome (LQTS) include torsades de pointes (TdP) and/or 2 degrees atrioventricu
176 healthy subjects and may be associated with torsades de pointes (TdP) arrhythmia, we tested the hypo
177 teria that are associated with initiation of torsades de pointes (TdP) in patients with acquired (a-)
178 oal of this study was to identify markers of torsades de pointes (TdP) in patients with drug-associat
179 e used for AF, excessive QT prolongation and torsades de pointes (TdP) often occur shortly after sinu
180 nse to hERG ion channel specific blocker was Torsades de Pointes (TdP) reentrant arrhythmia activatio
183 a higher risk of lethal arrhythmias, called Torsades de pointes (TdP), compared to the opposite sex.
184 QT-prolonging medications with known risk of torsades de pointes (TdP), which is associated with high
187 safety, including the risk of drug-induced 'torsades de pointes' (TdP) arrhythmia, is a major concer
189 and some patients present with short-coupled torsade de pointes, the genetics of which are poorly und
190 ac conduction disorders, or risk factors for torsade de pointes, there have been no serious cardiovas
191 QT-prolonging medications can predispose to torsades de pointes, there is a relative paucity of info
192 een shown to correlate with a higher risk of torsades de pointes, there is no established threshold b
193 ine can induce acquired long QT syndrome and torsade de pointes through its interaction with the Purk
195 it is not known if the risk of drug-induced torsades de pointes varies during the menstrual cycle.
200 sustained ventricular tachycardia (VT), and torsade de pointes VT) in the antiarrhythmic drug arm of
206 iac death was recorded in five patients, and torsade de pointes was recorded in seven other patients.
211 ent with relapsed APL developed asymptomatic torsade de pointes, which resolved spontaneously and did
213 ly fatal polymorphic ventricular tachycardia torsade de pointes, with drugs or other environmental st