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1                                              QTc increase was inversely proportional to baseline QTc
2                                              QTc interval >/=500 ms increased the risk of cardiac eve
3                                              QTc interval prolongation was defined as QTc interval >5
4                                              QTc prolongation is associated with a significantly incr
5                                              QTc prolongation was observed in all patients (by 60 +/-
6                                              QTc was calculated using Framingham formula (QTc(Fram)).
7 e > 13 years, hazard ratio: 1.90; p = 0.002; QTc duration, 8% risk increase per 10-ms increment; p =
8 cope [1], symptoms on therapy [2], LQT3 [1], QTc>520 ms [6]).
9 th LQT1, LQT2, or LQT3 were genotyped for 61 QTc-associated genetic variants used in a prototype QTc-
10 atio (OR) for QTc prolongation, defined as a QTc >/= 450 msec in men and >/= 460 msec in women, was 1
11 nts receiving hydroxychloroquine developed a QTc interval of 500 ms or greater, but the proportion of
12 en) and were 1.4 times more likely to have a QTc interval above 500 ms.
13 erval: 1.52 to 3.54, p < 0.001) for having a QTc interval >/=99th percentile (>/=458 ms).
14                                     Having a QTc interval lower than the first percentile (</=372 ms)
15 IV, hepatitis B, or hepatitis C infection; a QTc Fridericia of more than 480 ms; and substantial card
16  10-year-old female patient with LQTS with a QTc of 500 milliseconds who experienced recurrent exerti
17                         LQTS patients with a QTc>=480 ms (n=120) had a significantly higher QTc-PRS (
18 er QTc-PRS (89.3+/-6.7) than patients with a QTc<480 ms (n=303, 87.6+/-7.4, difference-in-mean, 1.7+/
19 LQTS based on unequivocal ECG abnormalities (QTc, 472+/-33 ms).
20 20 ms), physicians should examine the actual QTc value displayed on the report before concluding that
21 +) <3.5 mEq/L (2.1 [1.5-2.9]), and admitting QTc >450 ms (2.3; confidence interval [1.6-3.2]).
22 sociation persisted after adjusting for age, QTc, exercise-induced wall motion abnormalities, and lef
23 pregnant women) with cardiac parameters, all QTc intervals were within normal limits, with no signifi
24 al QRS and T vectors, J-point deviation, and QTc prolongation.
25 s from patients with autoimmune diseases and QTc prolongation were tested on IKr using HEK293 cells e
26 , PR intervals (P = 0.014), QRS duration and QTc interval (both P = 0.003), but Normal-VLDL did not.
27        Median PR interval, QRS duration, and QTc interval were 156, 88, and 402 ms, respectively.
28 ts (PR interval, QRS axis, QRS duration, and QTc interval) were evaluated for single-nucleotide polym
29 enerated by the blow, mean QRS duration, and QTc variability remained significant correlates of risk,
30 ridol group vs six in the placebo group) and QTc prolongation (seven patients in the haloperidol grou
31 s: (1) Overview of Arrhythmia, Ischemia, and QTc Monitoring; (2) Recommendations for Indication and D
32  higher dose therapy increased lethality and QTc interval prolongation.
33 release were larger and action potential and QTc duration longer in LDLr(-/-) and ApoA1(-/-) than in
34 eviation; PR interval, QRS duration, QT, and QTc interval; P, Q, R, S, and T amplitudes in 12 leads;
35 sinus slowing and increased PR, QRS, QT, and QTc intervals, as seen with azithromycin overdose.
36 y the blow, mean QRS duration, mean QTc, and QTc variability.
37 n, estimated glomerular filtration rate, and QTc interval.
38  whereas clinical factors, including sex and QTc duration, were associated with a significant increas
39  uptake on positron emission tomography, and QTc prolongation on the ECG.
40 omarily associated with bedaquiline use, and QTc prolongation (43%).
41 omarily associated with bedaquiline use, and QTc prolongation 6/14 (43%).
42     QTc interval prolongation was defined as QTc interval >500 ms or increase in QTc of >/=60 ms from
43 d QT (QTc) interval prolongation (defined as QTc>500 ms or an increase of >60 ms from baseline) occur
44    The animal model of autoimmune-associated QTc prolongation is the first to provide strong evidence
45 osis and management of autoimmune-associated QTc prolongation.
46                                  The average QTc-PRS in LQTS was 88.0+/-7.2 and explained only ~2.0%
47 ender, paroxysmal atrial fibrillation, basal QTc values, basal heart rate and dual antiviral therapy,
48 olongation of 60.5+/-40.5 ms from a baseline QTc of 473.7+/-35.9 ms to a peak QTc of 532.6+/-31.6 ms.
49 rease was inversely proportional to baseline QTc levels and leukocyte count and directly to basal hea
50       Propranolol has a significantly better QTc shortening effect compared to metoprolol and nadolol
51 dy, a J-shaped association was found between QTc interval duration and risk of AF.
52 ttle is known about the relationship between QTc and risk of stroke.
53 SCD among subjects with normal or borderline QTc.
54 n general, vandetanib is well tolerated, but QTc prolongation remains a potential concern demanding c
55 .2% from males), a prolonged 12SL-calculated QTc value (ie, >/=470 ms in females >60 years old, and >
56 Kr , lengthen the action potential and cause QTc prolongation on the surface ECG.
57 generate pathogenic inhibitory Abs and cause QTc prolongation.
58  Of the remaining 199, all with either clear QTc prolongation and/or typical repolarization abnormali
59 performed at admission, after 7 and 14 days; QTc values were analyzed.
60 on in liver transaminases and dose-dependent QTc prolongation without apparent complications were obs
61 puter declared 3588 (42.1%) "Normal" despite QTc prolongation.
62 ly because of a higher propensity to develop QTc prolongation.
63 h heart rate-corrected QT interval duration (QTc) nor cardiac events in any of the 3 mutation groups.
64 , heart-rate-corrected QT interval duration (QTc), deceleration capacity, and white blood cell count
65 ine levels and a longer electrocardiographic QTc interval than did the sham group.
66 he phenotype (prolonged electrocardiographic QTc interval).
67 athy, including cardiac isoenzyme elevation, QTc interval prolongation, and rapidly reversible cardia
68 were more prevalent in people with epilepsy (QTc prolongation: 5% vs 0%; p=0.002; ERP: 34% vs 13%, p<
69  When added to the QTc (C statistic 0.68 for QTc alone), discrimination improved to 0.78.
70 ng/mL (43.52 to 53.51; paliperidone) and for QTc prolongation (15 467 participants) from -2.21 ms (-4
71             The adjusted odds ratio (OR) for QTc prolongation, defined as a QTc >/= 450 msec in men a
72 xhibited significantly reduced potential for QTc elongation in a cardiovascular safety model.
73 iables predicts patients at highest risk for QTc interval prolongation and may be useful in guiding m
74 ed to a patient at moderate or high risk for QTc interval prolongation, a computer alert appeared on
75 DSS incorporating a validated risk score for QTc prolongation influences the prescribing of QT-prolon
76 DSS incorporating a validated risk score for QTc prolongation was developed and implemented using inf
77 es were required to have an ECG suitable for QTc analysis before and unrelated to the occurrence of S
78 QTc was calculated using Framingham formula (QTc(Fram)).
79  ECG abnormalities with positive genotyping (QTc, 482+/-35 ms).
80 f 91(36.3%) patients, and 3 of 91 (3.2%) had QTc >500 ms.
81                         One patient (7%) had QTc prolongation >500 milliseconds and died 20 months af
82        Forty-five patients (35 men, 76%) had QTc </=340 ms, for a prevalence of 0.05%.
83 e correction formula, 102 patients (90%) had QTc greater than 470 ms, including 74 (65%) above 500 ms
84  binary outcome meta-analyses (human height, QTc interval and gallbladder disease); all previous repo
85 c>=480 ms (n=120) had a significantly higher QTc-PRS (89.3+/-6.7) than patients with a QTc<480 ms (n=
86 ecreased by >= 40 ms with a mean decrease in QTc of 91 ms ( P < 0.008).
87                   There was no difference in QTc-PRS between symptomatic (n=156, 88.6+/-7.3) and asym
88                   There was no difference in QTc-PRS or QTc between genotypes.
89 olongation was defined solely as increase in QTc >/=60 ms from baseline.
90 0.82, 6.8) and a 2.5-millisecond increase in QTc (95% confidence interval: 0.11, 4.9).
91 duced ejection fraction, and (4) increase in QTc from baseline.
92 fined as QTc interval >500 ms or increase in QTc of >/=60 ms from baseline; for patients who presente
93 rmal limits, with no significant increase in QTc prolongation with increasing courses of DP.
94 of stroke was estimated per 1-SD increase in QTc(Fram), (HR [95% CI]: 1.12 [1.03 to 1.21], p = 0.0053
95 mouse models show similar problems including QTc interval prolongation and hypothermia.
96           Dofetilide monotonically increased QTc and APD throughout 6.5-hour exposure.
97 c repolarization disturbances with increased QTc intervals in both patients and controls, but with a
98 ession models were used to obtain individual QTc, JTc, JTpc and Tpec intervals.
99 er-range QTc, in whom a patient's individual QTc may provide less incremental prognostic information.
100 < 0.0001]), whereas the patient's individual QTc was not associated with a significant risk increase
101 ibitory Abs to the HERG E-pore region induce QTc prolongation in immunized guinea-pigs by targeting t
102 ic QT score was correlated with drug-induced QTc prolongation.
103 is associated with a low incidence of infant QTc prolongation.
104 ll patients developed corrected QT interval (QTc interval) prolongation (median QTc interval 504 ms,
105 Gs were available for corrected QT interval (QTc) measurement, and levels of hydroxychloroquine were
106                   The corrected QT interval (QTc) should be assessed as a routine when obtaining elec
107 , prolongation of the corrected QT interval (QTc) was associated with an independent increased risk o
108 ngation of heart rate-corrected QT interval (QTc), an arrhythmia risk marker.
109 ariants on heart rate-corrected QT interval (QTc), cardiac events, and disease severity.
110 ified EMW, heart rate-corrected QT interval (QTc), female sex, and LQTS genotype as univariate predic
111  prolonged heart rate-corrected QT interval (QTc).
112 59, median heart rate-corrected QT interval [QTc] at diagnosis 557 ms (IQR, 529-605) with genetically
113 ge, QRS duration, and corrected QT interval [QTc]) were evaluated by using multivariable regression a
114 1A (QRS duration), NOS1AP, KCNH2, and KCNQ1 (QTc interval).
115 ntricular hypertrophy voltage criteria, long QTc, and T-wave inversion, all P<0.05) and predicted cli
116  prevalence and factors associated with long QTc interval in a cohort of opioid-dependent HIV-infecte
117 trophy (77% versus 58%; P=0.02) and a longer QTc interval (466+/-36 versus 453+/-41 milliseconds; P=0
118 d-type but not LOX-1(-/-) mice showed longer QTc compared to L1-injected animals in vivo with corresp
119 ne and lansoprazole had significantly longer QTc intervals (up to 12 ms in white men) and were 1.4 ti
120       The association with respect to longer QTc intervals was stronger for the outcome of lone AF, a
121 LV scar (n = 106) was associated with longer QTc (beta = 4.3 msec, P = .031).
122 C-CMs were generated from a 13-year-old man (QTc, >480 ms) with a family history of sudden cardiac de
123 ventricular repolarization delay (19.6% mean QTc prolongation in females; P<0.05) and aldosterone-dep
124 was 70 mg/day (range 15-250 mg/day) and mean QTc interval was 438 +/- 34 ms.
125 ped a prolonged-QTc (pQT) after 7 days (mean QTc increase 66+/-20msec, +16%, p<0.001); these patients
126 nerated by the blow, mean QRS duration, mean QTc, and QTc variability.
127 eated with LCSD alone (37 [58%] female, mean QTc 466+/-30 ms, 16 [25%] patients were symptomatic befo
128                                     The mean QTc intervals were longer at peak exercise in patients (
129 mean age at diagnosis, 10.0+/-10 years; mean QTc, 528+/-74 ms) with LQTS who underwent LCSD between 2
130 nts </=21 years with electronically measured QTc of 140 to 340 ms.
131                                       Median QTc did not change among patients with LQTS (461+/-60 to
132 s (interquartile range, 280-360), and median QTc 323 ms (IQR, 313-332).
133 ent with mexiletine was 22 years, and median QTc interval before therapy 509 ms.
134 interval (QTc interval) prolongation (median QTc interval 504 ms, IQR: 477 to 568 ms) within 24 h of
135                 After mexiletine, the median QTc decreased by 65+/-45 ms from 547 ms (IQR, 488-558) p
136              We revealed Amiodarone-mediated QTc prolongation, HR reduction and HRV increase otherwis
137 symptomatic, heart rate 76 +/- 16 beats/min, QTc 472 +/- 46 ms) were started on beta-blocker therapy
138 nd APD more at 6.5 hours than at 50 minutes (QTc) or 30 minutes (APD) dofetilide administration.
139 ed that among patients with mild to moderate QTc duration (<500 ms), the risk associated with TRP was
140 for patients who presented with QTc >500 ms, QTc prolongation was defined solely as increase in QTc >
141 ion: 102+/-4 and 106+/-3 versus 84+/-3.1 ms; QTc: 50.9+/-1.3 and 52.8+/-0.8 versus 43.5+/-1.2 ms).
142 evels of hydroxychloroquine and the neonatal QTc (R=0.02, P=0.86) or the mean of hydroxychloroquine v
143                              In nonathletes, QTc interval abnormalities comprised the majority (52%)
144 f all probands were asymptomatic with normal QTc duration.
145 almost 3 times the risk in those with normal QTc(Fram) (hazard ratio [HR] [95% confidence interval (C
146 ants that collectively explain ~8% to 10% of QTc variation in the general population.
147 s stopped for 105 patients (7.5%) because of QTc prolongation or TdP.
148 cond-most common primary suspect in cases of QTc prolongation or torsade de pointes after dofetilide
149 rrhythmia or cardiac arrest and 379 cases of QTc prolongation or torsade de pointes were associated w
150 A continued search for novel determinants of QTc prolongation such as genomic factors is likely to en
151 ic role of anti-Ro Abs in the development of QTc prolongation.
152  population controls uncovered enrichment of QTc-prolonging alleles in patients for 2 SNPs, located r
153            We evaluated (1) the frequency of QTc prolongation and its association with inflammatory m
154   In the validation group, the incidences of QTc prolongation were 15% (low risk); 37% (moderate risk
155 0(43%) patients, including five instances of QTc prolongation-assessed as possibly related to BDQ and
156  SNPs previously identified as modulators of QTc-interval in genome-wide association studies in the g
157                    Independent predictors of QTc prolongation included the following: female (odds ra
158 cal evidence demonstrates high prevalence of QTc prolongation and complex ventricular arrhythmias in
159 nce a day 21/7 had a grade 3 prolongation of QTc; and two patients on a schedule of vemurafenib 960 m
160                           Monthly reports of QTc prolongation or torsade de pointes increased from a
161  QT-prolonging drugs and reduces the risk of QTc interval prolongation in hospitalized patients with
162 ependently associated with a reduced risk of QTc prolongation (adjusted odds ratio, 0.65; 95% confide
163                    Despite the known risk of QTc prolongation with ziprasidone treatment, the finding
164 onfidence interval, 1.32 to 2.96) and use of QTc-prolonging drugs (odds ratio, 2.90; 95% confidence i
165 in use, aspirin use, QRS duration and use of QTc-prolonging drugs, the risk of stroke remained signif
166 s of innate and drug-induced IKs blockade on QTc prolongation.
167  mexiletine to evaluate the drug's effect on QTc.
168        To examine the direct effect of L5 on QTc, mice were intravenously injected with L5 or L1.
169 y medication use for either QT (P = 0.93) or QTc (P = 0.58).
170        There was no difference in QTc-PRS or QTc between genotypes.
171 multivariable-adjusted model) and when other QTc correction formulas including those of Hodge, Bazett
172                             EMW outperformed QTc in predicting symptomatic patients (area under the c
173  a baseline QTc of 473.7+/-35.9 ms to a peak QTc of 532.6+/-31.6 ms.
174 ion, while those with TdP and/or a postnatal QTc more than 500 ms have SCN5A, KCNH2 or uncharacterize
175 heart rate (r=0.700; P<0.001), and postnatal QTc (r=-0.762; P<0.001) were found.
176         Fetal rhythm phenotype and postnatal QTc can predict postnatal rhythm and suggest genotype: b
177 1 to 21 points, respectively, best predicted QTc prolongation (C statistic=0.823).
178 were on medications that may further prolong QTc.
179 nflammation per se can significantly prolong QTc during acute infections, via cytokine-mediated chang
180                                    Prolonged QTc interval (>450 ms) was documented in 33 of 91(36.3%)
181                                    Prolonged QTc interval and life-threatening arrhythmias (LTA) are
182                                    Prolonged QTc interval was an independent predictor of posttranspl
183                                  A prolonged QTc interval and Q wave were related to post-transplant
184                   Cirrhotics had a prolonged QTc interval, a Q wave, abnormal QRS axis deviation, ST
185 family members, none of whom had a prolonged QTc interval.
186 34 participants (6.4%) developed a prolonged QTc.
187 ndrome (SIDS), one with documented prolonged QTc and Torsade de Pointes (TdP), and in an adult woman
188 nt cardiac arrest and dramatically prolonged QTc interval who were both born to healthy parents.
189 ith likely pathogenic variants had prolonged QTc.
190 score comprising renal impairment, prolonged QTc interval, and age older than 52 was developed for pr
191 s with shared clinical features of prolonged QTc interval (range 505-725 ms) and documented ventricul
192 wing in recent years, and cases of prolonged QTc interval and torsades de pointes have been described
193                  The prevalence of prolonged QTc interval in opioid-dependent HIV-infected patients o
194 in a significant change in risk of prolonged QTc.
195 aive (P = .036) were predictive of prolonged QTc.
196 ly 7709 (47.5%) of these ECGs with prolonged QTc did the automated interpretation include an accompan
197  (</= 440 ms [n = 469]), LQTS with prolonged QTc interval (> 440 ms [n = 1,392]), and unaffected fami
198 iver transplantation together with prolonged QTc interval.
199 ificantly lower than in those with prolonged QTc intervals (15%) (p < 0.001) but higher than in unaff
200 r ACA or SCD only in patients with prolonged QTc intervals (female age > 13 years, hazard ratio: 1.90
201  stroke in study participants with prolonged QTc(Fram) was almost 3 times the risk in those with norm
202 riteria, in 8526 (52.5%) ECGs with prolonged QTc.
203 dolol, especially in patients with prolonged QTc.
204 Fifteen (14%) patients developed a prolonged-QTc (pQT) after 7 days (mean QTc increase 66+/-20msec, +
205  by norfluoxetine resulted in more prominent QTc prolongation in mutation carriers than in noncarrier
206 ociated genetic variants used in a prototype QTc-polygenic risk score (QTc-PRS).
207                               This prototype QTc-PRS does not distinguish/predict the clinical outcom
208 aE2/DeltaE2)) in 129 sv mice results in QRS, QTc widening, bundle block and STc narrowing at 2-4 mont
209  arsenic and QT and heart rate-corrected QT (QTc) durations and to examine effect modification by cal
210 d >/=120 ms (1.75, 1.17-2.62); corrected QT (QTc) interval >/=450 ms in men or >/=460 ms in women (1.
211 stigate whether the heart rate-corrected QT (QTc) interval on the electrocardiogram (ECG) is associat
212                                Corrected QT (QTc) interval prolongation (defined as QTc>500 ms or an
213 QT syndrome (LQTS) with normal corrected QT (QTc) intervals.
214  novel and are associated with corrected QT (QTc) prolongation and complex ventricular arrhythmias.
215 s with autoimmune diseases and corrected QT (QTc) prolongation directly target and inhibit the human
216 induced increase in heart rate-corrected QT (QTc) versus drug concentration.
217 the prolongation of heart rate-corrected QT (QTc), PR, and QRS intervals.
218 hisms (SNPs) that modulate the corrected QT (QTc)-interval and the occurrence of cardiac events in 63
219 ontrols; however, resting heart rates and QT/QTc intervals were similar at baseline.
220 ced effect among patients with a lower-range QTc, in whom a patient's individual QTc may provide less
221 tries, categorized as LQTS with normal-range QTc (</= 440 ms [n = 469]), LQTS with prolonged QTc inte
222  SCD in patients with LQTS with normal-range QTc intervals (4%) was significantly lower than in those
223 ors ACA or SCD in patients with normal-range QTc intervals included mutation characteristics (transme
224 etransplant QT-time corrected by heart rate (QTc) and left-ventricular dysfunction was also registere
225 ion of QT interval corrected for heart rate (QTc) with incident stroke.
226 vidual QT interval corrected for heart rate (QTc).
227 of the QT interval corrected for heart rate (QTc).
228 ependent transaminase elevation and relative QTc prolongation were observed with the highest doses of
229 tely 9% to 10% of total variation in resting QTc in EA individuals and approximately 12% to 18% in AA
230          Sixteen probands had normal resting QTc values and only developed QT prolongation and malign
231 sed in a prototype QTc-polygenic risk score (QTc-PRS).
232                                       Severe QTc prolongation and ERP were more prevalent in people w
233 RP (ORadj 2.4, 95% CI 1.1 to 5.5) and severe QTc prolongation (ORadj 9.9, 95% CI 1.1 to 1317.7).
234                               ERP and severe QTc prolongation appear to be more prevalent in people w
235 .05), increased proportion of mild or severe QTc prolongation (13.1% and 5.8% versus 3.4% and 0.0% [N
236 d ECGs for three markers of SCA risk: severe QTc prolongation (male >450 ms, female >470 ms), Brugada
237         INa-L block with lidocaine shortened QTc and APD more at 6.5 hours than at 50 minutes (QTc) o
238           Mexiletine significantly shortened QTc (by 63 +/- 6 ms; p < 0.0001) and reduced the percent
239                           Besides shortening QTc interval, mexiletine caused a major reduction of lif
240 h the mutation was associated with a shorter QTc interval (P<0.05) and a reduced occurrence of cardia
241 rol (4.8+/-0.30 and 4.5+/-0.23), and shorter QTc intervals (167+/-2.6 versus 182+/-6.4).
242              Women had significantly shorter QTc compared with men (312 versus 323 ms; P=0.03).
243  of African origin had significantly shorter QTc intervals than Caucasians (p < 0.001).
244  0.34 (0.19-0.61; P<0.0002) and with shorter QTc (P<0.0001) in the combined discovery and replication
245 -kDa Ro antigen-immunized guinea pigs showed QTc prolongation on ECG after developing high titers of
246 titres of E-pore peptide Abs and significant QTc prolongation after immunization.
247 icular electrical remodeling and significant QTc prolongation, regardless concomitant antimicrobial t
248 airment, sedation, or clinically significant QTc prolongation.
249 e heart weight (3.6+/-0.26), but had similar QTc (179+/-4.3) compared with HF control.
250       Although it is generally believed that QTc changes almost exclusively result from concomitant t
251                                          The QTc shortening was significantly less pronounced among p
252                                          The QTc shortening with propranolol was significantly greate
253                                          The QTc-PRS explained <2% of the QTc variability in our LQT1
254                                          The QTc-PRS in LQTS probands (n=137; 89.3+/-6.8) was signifi
255 +/-6 versus 115+/-11 beats/min; P=0.54), the QTc interval had prolonged significantly more in patient
256                     In 8 patients (67%), the QTc decreased by >= 40 ms with a mean decrease in QTc of
257 throughout each individual pregnancy and the QTc (R=0.04, P=0.80).
258 ear relationship between GRS(NOS1AP) and the QTc-interval (P=4.2x10(-7)).
259 breakthrough LQTS arrhythmic risk beyond the QTc value.
260 and 13 patients with no CAD to correlate the QTc interval respectively.
261 I, 4%-24%]) neonates had prolongation of the QTc >2 SD above historical healthy controls (2 markedly
262         Risk factors for prolongation of the QTc interval are chronic hepatitis C-induced cirrhosis,
263             The QTc-PRS explained <2% of the QTc variability in our LQT1, LQT2, and LQT3 cohort, cont
264 s 88.0+/-7.2 and explained only ~2.0% of the QTc variability.
265 pectedly large effects of NOS1AP SNPs on the QTc-interval and a trend for effects on risk of cardiac
266  an analysis for quantitative effects on the QTc-interval, 3 independent SNPs at NOS1AP (rs10494366,
267 with LQT2 and significantly outperformed the QTc (C statistic, 0.82 [0.71-0.93]).
268                       Ranolazine reduced the QTc at all heart rates but less so during extreme noctur
269                        Concern regarding the QTc interval in human immunodeficiency virus (HIV)-infec
270 he sinus rate or QRS width but shortened the QTc from 509+/-41 to 451+/-26 ms, a mean decrease of 56+
271 ents with LQT3, mexiletine also shortens the QTc significantly in two-thirds of a small subset of pat
272                            When added to the QTc (C statistic 0.68 for QTc alone), discrimination imp
273 .6x10(-7)) were strongly associated with the QTc-interval with marked effects (>12 ms/allele).
274 ormalization of the ECG abnormalities (their QTc shortened from 492+/-37 to 423+/-25 ms [P<0.001]; th
275 d LQT3 cohort, contributing 5x less to their QTc value than in the general population.
276 0001) in QRS duration but was not related to QTc interval or Sokolow-Lyon index.
277                                   Similar to QTc intervals, women had JTc, and JTpc intervals longer
278 was precluded by a low therapeutic window to QTc prolongation in cardiovascular models consistent wit
279 ia (24%), as well as dose-related, transient QTc prolongation (17%).
280 tant QT-prolonging antimicrobial treatments, QTc was significantly prolonged but rapidly normalized i
281                                   A weighted QTc-PRS (range, 0-154.8 ms) was calculated for each pati
282 m patients with autoimmune diseases and with QTc prolongation on the ECG target the human ether-a-go-
283               Height was not associated with QTc interval or the Sokolow-Lyon index.
284 66 in gnomAD) and was highly associated with QTc on electro-cardiogram (P=5.53E-24, beta=20.2 ms/alle
285 Examining the risk of stroke associated with QTc-prolonging drugs may be warranted.
286 typed based on either their association with QTc duration in healthy populations or on their role in
287 sed the risk of cardiac events compared with QTc <470 ms (HR, 3.32; P=0.001).
288 tration of L5 was higher and correlated with QTc in patients with CAD compared to controls.
289 ty lipoprotein (LDL), L5, is correlated with QTc prolongation in patients with coronary artery diseas
290  show that L5 was positively correlated with QTc prolongation in patients with ischemic heart disease
291 up and upward, the risk of AF increased with QTc interval duration in a dose-response manner, reachin
292                                Patients with QTc of 140 to 340 ms confirmed by a pediatric electrophy
293 i-SSA/Ro Ab-positive sera from patients with QTc prolongation.
294 om baseline; for patients who presented with QTc >500 ms, QTc prolongation was defined solely as incr
295 s in the total cohort and in the subset with QTc >480 ms.
296 val: 1.24 to 1.66, p < 0.001) for those with QTc intervals >/=99th percentile (>/=464 ms).
297 om routine ECG screening and that those with QTc prolongation should receive counseling about drugs t
298 onotherapy, MK-8776 was well tolerated, with QTc prolongation (19%), nausea (16%), fatigue (14%), and
299 de Pointes (TdP), and in an adult woman with QTc >500 ms, atrioventricular block and TdP.
300 f 17 patients (82% male, age 29 +/- 3 years, QTc before treatment 331 +/- 3 ms) received HQ therapy (

 
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