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1 al electrocardiogram findings (arrhythmia or QT prolongation).
2 ood pressure control on the risk of incident QT prolongation.
3 drugs may be an important aspect of acquired QT prolongation.
4 ir2.1 and hERG potassium channels, causal to QT prolongation.
5 otassium conductance, more commonly known as QT prolongation.
6 tant before prescribing drugs known to cause QT prolongation.
7  inversely correlated with ibutilide-induced QT prolongation.
8 ng to frequent EADs and electrocardiographic QT prolongation.
9 a trigger to initiate the onset of TdP under QT prolongation.
10 o the need for careful predrug screening for QT prolongation.
11 tion abnormalities, consistent with clinical QT prolongation.
12 se events of abuse potential, suicidality or QT prolongation.
13  Older age was independently associated with QT prolongation.
14 ons involving AADs commonly involve additive QT prolongation.
15  long QT syndrome (LQTS) is characterized by QT prolongation.
16 lace during AVB with the bradycardia-induced QT prolongation.
17  effects of cardiac memory lead to excessive QT prolongation.
18 entricular fibrillation, but did not prevent QT prolongation.
19 , and the dose-limiting toxicity was grade 3 QT prolongation.
20 ontrol arm did not have an increased risk of QT prolongation.
21 es the odds for mortality then those without QT prolongation.
22 icking of mutant proteins, thus exacerbating QT prolongation.
23 pertrophy, resulting in action potential and QT prolongation.
24 inding to this channel leads to drug-induced QT prolongation.
25 d for heart rate using Fridericia's formula (QT) prolongation.
26 vely) and DHT-treated animals exhibited less QT prolongation (11.4 +/- 3.8% increase; P < .03).
27 hrombocytopenia (13%), and electrocardiogram QT prolongation (13%).
28 hrombocytopenia (13%), and electrocardiogram QT prolongation (13%).
29 re hospital discharge in 46 (27%) because of QT prolongation (14%), torsades de pointe or polymorphic
30  syndrome (17%), all-grade electrocardiogram QT prolongation (26%), and grade >= 3 leukocytosis (9%).
31  syndrome (17%), all-grade electrocardiogram QT prolongation (26%), and grade 3 leukocytosis (9%).
32 nic exposure is consistently associated with QT prolongation, a risk factor for arrhythmia and sudden
33              Despite the absence of manifest QT prolongation, adolescent anorexic females have impair
34  by diffuse symmetrical T wave inversion and QT prolongation after recovery from an episode of cardio
35 ry edema may cause deep T wave inversion and QT prolongation after resolution of the symptoms.
36                                 Drug-induced QT prolongation after successful inpatient loading of cl
37 ependently (1 to 100 micromol/L), leading to QT prolongation and an increase in TDR.
38 ed with baseline QT interval to drug-induced QT prolongation and arrhythmias is not known.
39 ise mechanism by which the mutations lead to QT prolongation and arrhythmias is uncertain, however.
40 ardiac hypertrophy, which is associated with QT prolongation and arrhythmias.
41 ssociated with acquired electrocardiographic QT prolongation and arrhythmic activity initiated by pre
42 resent study examines the cellular basis for QT prolongation and arrhythmogenesis after reversal of t
43      A simplified approach to monitoring for QT prolongation and arrythmia was implemented on April 5
44 ographically, CKD mice developed significant QT prolongation and episodes of bradycardia.
45 e IKs channel), who presented with excessive QT prolongation and high serum levels of norfluoxetine,
46  Long-QT syndrome (LQTS) is characterized by QT prolongation and increased risk for syncope, seizures
47 roportion of the variability in drug-induced QT prolongation and is a significant predictor of drug-i
48 ocyte ID are likely to provide insights into QT prolongation and its associated disorders.
49 ave implications regarding the definition of QT prolongation and its use in predicting arrhythmias an
50 ial Ca(2+) uptake has been implicated in the QT prolongation and lethal arrhythmias associated with n
51 normal resting QTc values and only developed QT prolongation and malignant arrhythmias after exposure
52  during AVB is independently associated with QT prolongation and may be arrhythmogenic during AVB.
53 e slow component of I(to) (I(to,s)), have no QT prolongation and no spontaneous arrhythmias, and (c)
54 keted drugs, and this inhibition may lead to QT prolongation and possibly fatal cardiac arrhythmia.
55 hile sotalol requires initial monitoring for QT prolongation and proarrhythmia, dronedarone does not.
56 This review focuses on mechanisms underlying QT prolongation and proarrhythmia, risk factors, includi
57                     The predictive values of QT prolongation and QTD were assessed in 1839 participan
58 ough V4, with either persistent or transient QT prolongation and severe disease expression of exercis
59 us results in a clinical phenotype combining QT prolongation and ST segment elevation, indicating a c
60 alpain may contribute to ischemia-associated QT prolongation and sudden cardiac death.
61                                              QT prolongation and TdP are a risk in men receiving enza
62                  The clinical observation of QT prolongation and torsade de pointes found with astemi
63        We report the clinical observation of QT prolongation and torsade de pointes in a patient with
64 g of hERG channels to the cell surface cause QT prolongation and torsade de pointes in patients treat
65 e inhibitors could predispose individuals to QT prolongation and torsade de pointes.
66 iarrhythmic drugs are used for AF, excessive QT prolongation and torsades de pointes (TdP) often occu
67                                 Drug-induced QT prolongation and torsades de pointes remain significa
68 ncidence of serious adverse events including QT prolongation and torsades de pointes.
69 cell model, the KCNQ1-G589D mutation induced QT prolongation and transient afterdepolarizations, know
70     Left untreated, CAVB patients experience QT prolongation and ventricular overload, increasing sus
71 yndrome type 3 child experienced paradoxical QT prolongation and worsening of arrhythmias after mexil
72 ely used antibiotic that infrequently causes QT-prolongation and torsades de pointes cardiac arrhythm
73 T syndrome characterized by deafness, marked QT prolongation, and a high risk of sudden death.
74 with early childhood cardiac arrest, extreme QT prolongation, and a negative family history.
75 est were potential liver toxicity, corrected QT prolongation, and adrenal insufficiency.
76 tion, increased mitochondrial Ca(2+) uptake, QT prolongation, and arrhythmia, suggesting c-Src or MCU
77 ly discontinue any of the medications due to QT prolongation, and arrhythmogenic death.
78 foot syndrome, hypertension, rectal fistula, QT prolongation, and asymptomatic hypomagnesaemia, and t
79 fects causing hypertension, thromboembolism, QT prolongation, and atrial fibrillation.
80 including those related to treatment-induced QT prolongation, and bradyarrhythmias can also occur.
81 tive genes, family history of SCD, transient QT prolongation, and misinterpretation of the QTc interv
82  events, frequent premature beats, corrected QT prolongation, and more heart rate variability after e
83 ed by extensive T-wave inversions, transient QT prolongation, and severe disease expression of exerci
84 t lack both I(to,f) and I(to,s), have AP and QT prolongation, and spontaneous ventricular tachyarrhyt
85 t failure (aOR 2.64; 1.86-3.76; p < 0.0001), QT prolongation (aOR 1.40; 1.04-1.88; p = 0.025), MI (aO
86                Wide QRS/T angle, ECG-MI, and QT prolongation appeared as dominant predictors when eva
87 ulation and delineates mechanisms underlying QT prolongation, arrhythmia, and cardiomyopathy caused b
88                Indeed, progressive corrected QT prolongation, arrhythmias, and ischemic changes were
89 ociated systemic and pulmonary hypertension, QT prolongation, arrhythmias, pericardial disease, and r
90 t ventricular dysfunction, hypertension, and QT prolongation/arrhythmias.
91 se in HRV over 24h at 10 dpa, accompanied by QT prolongation as well as diurnal variations, followed
92 v4.2W362FxKv1.4(-/-) animals revealed marked QT prolongation, atrioventricular block, and ventricular
93    We examine the frequency and incidence of QT prolongation based on duration of Bdq and/or Dlm use
94                     L1825P fails to generate QT prolongation because it does not reach the cell surfa
95  lethal cardiac consequences of drug-induced QT prolongation because they have a substantial cardiova
96  ischemia, hypotension, hypertension, edema, QT prolongation, bradyarrhythmia, and thromboembolism.
97 ent, I(to,f), have action potential (AP) and QT prolongation, but no spontaneous arrhythmias, (b) Kv1
98 menon occurs in the heart and contributes to QT prolongation by altering cardiac sodium current prope
99 747+/-36 ms (+40%, P<0.0001), similar to the QT prolongation by dofetilide (511+/-22 to 703+/-45 ms [
100 e hypothesis that the extent of drug-induced QT prolongation by dofetilide is greater in sinus rhythm
101 on of SR, there was increased sensitivity to QT prolongation by this I(Kr)-specific blocker.
102 d NAA10 variant p.(Arg4Ser) segregating with QT-prolongation, cardiomyopathy, and developmental delay
103 8057 prevented action potential duration and QT prolongation caused by dofetilide.
104        Additionally, chronotropic as well as QT-prolongation causing reference compounds were used fo
105 lthough use of these medications resulted in QT prolongation, clinicians seldomly needed to discontin
106 owever, it is unclear whether to what extent QT prolongation coexisting with ECG-LVH can explain the
107 S1 independently of sex, including corrected QT prolongation, conduction defects, and increased arrhy
108 ivo telemetric recordings also reveal marked QT prolongation, consistent with a defect in ventricular
109 atment outcome and QT interval prolongation (QT prolongation), defined as any QT interval corrected b
110             Underlying abnormalities include QT prolongation, delayed repolarization from downregulat
111                                 Drug-induced QT prolongation (diLQT) is a feared side effect that cou
112 y cardiovascular liabilities associated with QT prolongation due to hERG activity or endothelial NOS
113 el antagonists will be useful in normalizing QT prolongation during As(2)O(3) therapy.
114                              Consistent with QT prolongation, epileptic rats had longer ventricular a
115 RR-TB regimens with most clinically relevant QT prolongation events occurring in the first 6 months.
116 nts [7%]), sepsis or septic shock (11 [5%]), QT prolongation (five [2%]), and nausea (five [2%]) in t
117 wave inversions, and 10 (53%) have transient QT prolongation &gt; 480 ms.
118 ls were used to compare the risk of incident QT prolongation (&gt;460 ms in women or >450 ms in men) in
119                                Patients with QT prolongation had longer hospitalization (276 hrs vs.
120             Attenuation of ibutilide-induced QT prolongation has been observed in a small number of p
121 patients without structural heart disease or QT prolongation has been reported.
122 ever, innate susceptibility to PM-associated QT prolongation has not been characterized.
123                    Acutely ill patients with QT prolongation have longer lengths of hospitalization a
124 ce, management, and clinical consequences of QT prolongation in a large cohort of patients treated wi
125 rize genetic susceptibility to PM-associated QT prolongation in a multi-racial/ethnic, genome-wide as
126                                    A case of QT prolongation in a patient receiving protease inhibito
127      Exercise testing is useful in unmasking QT prolongation in disorders associated with abnormal re
128 was to develop and validate a risk score for QT prolongation in hospitalized patients.
129  Danio rerio, we found that drugs that cause QT prolongation in humans consistently caused bradycardi
130 sis was conducted to determine the degree of QT prolongation in patients treated with arsenic trioxid
131  may alter susceptibility to PM10-associated QT prolongation in populations protected by the U.S. Env
132                             The magnitude of QT prolongation in response to bradycardia, rather than
133 nversions in the precordial leads, transient QT prolongation in some, and recurrent ventricular arrhy
134                                Predictors of QT prolongation in the acutely ill population are simila
135 olarization at the single cell level but not QT prolongation in the intact animal.
136 y associated with giant negative T waves and QT prolongation in the postevent electrocardiogram.
137                                      Grade 3 QT prolongation in the quizartinib group was uncommon (e
138 hERG inhibition (IC(50) = 44 muM for 7a) and QT prolongation in vivo.
139 th erythromycin caused significantly greater QT-prolongation in female rabbit hearts (mean [SD], 11.8
140 voltage, reduced heart rate variability, and QT prolongation (in the cardiovascular disease-free grou
141 74.20, p<0.1) were independent predictors of QT-prolongation.Incidence of LTA during hospitalization
142 ic ventricular tachycardia in the absence of QT prolongation, indicating a novel proarrhythmic syndro
143 er to initiate torsade de pointes (TdP) with QT prolongation induced by dl-sotalol and azimilide.
144                                              QT prolongation is a risk factor for ventricular arrhyth
145 ed with prolongation of the QT interval that QT prolongation is an accepted surrogate marker for arrh
146                                              QT prolongation is an important pharmacodynamic interact
147 udden death, and the increased prevalence of QT prolongation is an independent risk factor for cardio
148                                              QT prolongation is associated with increased risk of sud
149                                              QT prolongation is commonly associated with life-threate
150 etic testing of individuals with unexplained QT prolongation is restricted to examination of monogeni
151                                 Drug-induced QT prolongation is usually caused by block of human ethe
152 morphic ventricular tachycardia (VT) without QT prolongation is well described in patients without st
153 CCORD trial is not likely to be explained by QT prolongation leading to lethal ventricular arrhythmia
154 ed to LQTS (n = 46; 16%), isolated/transient QT prolongation (n = 44; 15%), or misinterpretation of t
155 up, n=1 [1%]; imatinib group, n=1 [1%]), and QT prolongation (nilotinib group, n=1 [1%]; imatinib gro
156    These results provide a mechanism for the QT prolongation observed clinically with administration
157                                              QT prolongation occurred in 49 (3%) patients given nerat
158                                              QT prolongation occurred in 7 patients (1.5%).
159 n, urinary tract infection, and asymptomatic QT prolongation occurred with pimavanserin.
160 ring intravenous tacrolimus infusion, marked QT prolongation occurred.
161 t AF at the time of drug discontinuation for QT prolongation (odds ratio 0.14, 95% confidence interva
162 pital mortality compared to patients without QT prolongation (odds ratio 2.99 95% confidence interval
163 mycin held or discontinued due to an average QT prolongation of 60.5+/-40.5 ms from a baseline QTc of
164 e 4 thrombocytopenia [cohort 2], one grade 3 QT prolongation on electrocardiogram [cohort 3], and one
165           Although no clinical events due to QT prolongation on electrocardiography were observed, QT
166 nterval despite LQTS often being detected by QT prolongation on resting electrocardiography (ECG).
167                  Arrhythmias associated with QT prolongation on the ECG often lead to sudden unexpect
168               We identified 24 patients with QT prolongation or torsade de pointes, or both, associat
169 which is consistent with other findings that QT prolongation, per se, is insufficient to generate TdP
170 ater presence in men of a factor that blunts QT prolongation responses, especially at slow heart rate
171                      The primary outcome was QT prolongation resulting in Torsade de pointes.
172 creased action potential duration, mimicking QT prolongation seen in the index patient on mexiletine
173 rdiovascular effects, such as bradycardia or QT prolongation, supporting its development as a safe im
174 are Na- and K-channel mutations in Mendelian QT prolongation syndromes.
175 e do not know why some patients develop more QT prolongation than others, despite similar bradycardia
176  de pointes may be less related to degree of QT prolongation than to drug effects on transmural dispe
177 , we report a mechanism for diabetes-induced QT prolongation that involves an increase in INaP caused
178                  Secondary outcomes included QT prolongation, the need to prematurely discontinue any
179 4.20; P < .1) were independent predictors of QT prolongation.The incidence rate of LTA during hospita
180                                      We find QT prolongation to be common (24%), with Torsade de Poin
181              Its clinical use is burdened by QT prolongation, torsade de pointes, and sudden cardiac
182                                     Cases of QT prolongation, torsades de pointes, and sudden death h
183 tion reserve and predisposes to drug-induced QT prolongation/torsades de pointes.
184 d the association of citalopram with cardiac QT prolongation, use of this agent to treat agitation ma
185  was also a prerequisite for aging-dependent QT prolongation, ventricular fibrillation and SCD immedi
186 ary python script to identify any mention of QT prolongation, ventricular tachy-arrhythmias and cardi
187  at 0.10 mug/kg per minute and borderline if QT prolongation was 1 to 29 ms.
188                         Electrocardiographic QT prolongation was common (63%).
189                                              QT prolongation was neither more common nor more severe
190 e, new large or global T wave inversion with QT prolongation was observed after resolution of acute c
191 cular contractions at onset (300-360 ms); no QT prolongation was observed.
192                                              QT prolongation was present in 24%.
193 (AF) at the time of drug discontinuation for QT prolongation was protective despite similar heart rat
194 gation on electrocardiography were observed, QT prolongation was reported significantly more frequent
195 nt EADs in rabbits, in which more pronounced QT prolongation was seen.
196  events occurred in 26 (8%) of 329 patients; QT prolongation was the most common serious adverse even
197                                       Severe QT prolongation was uncommon and did not require permane
198 reason, rates of ventricular arrhythmias and QT prolongation were assessed.
199                                Predictors of QT prolongation were female sex, QT-prolonging drugs, hy
200                                  Episodes of QT prolongation were manually over-read.
201 ade de pointes, in addition to the degree of QT prolongation, which is an imperfect predictor.
202 ntensive glycemic control is associated with QT prolongation, which may lead to ventricular arrhythmi
203 arization but increases the risk of manifest QT prolongation with I(Kr) block in variant carriers.
204       A wide array of drugs can cause marked QT prolongation with the associated risk of torsade de p
205 version to normal rhythm was associated with QT prolongation yet absent proarrhythmia markers for Tor

 
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