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1 QTc interval >/=500 ms increased the risk of cardiac eve
2 QTc interval prolongation was defined as QTc interval >5
3 QTc intervals were analyzed according to age (< 16 or >
4 QTc intervals were measured in 241 patients with heart f
5 QTc intervals were prolonged (>440 ms) in 122 (51%) pati
6 C) runs (sertraline: 13.1%; placebo: 12.9%), QTc interval greater than 450 milliseconds at end point
7 ed the DSEC were more likely to experience a QTc interval increase of at least 30 milliseconds vs pla
11 pregnant women) with cardiac parameters, all QTc intervals were within normal limits, with no signifi
13 , PR intervals (P = 0.014), QRS duration and QTc interval (both P = 0.003), but Normal-VLDL did not.
15 ts (PR interval, QRS axis, QRS duration, and QTc interval) were evaluated for single-nucleotide polym
16 Tc) on drug therapy, the magnitude of QT and QTc interval prolongation, and the change in T(peak) to
19 ificantly greater symptoms, increased QT and QTc intervals and QTc dispersion, ventricular tachycardi
22 048 segments showed mean (+/- SD) RR, QT and QTc intervals of 830 +/- 100, 407 +/- 23 and 445 +/- 16
25 QTc interval prolongation was defined as QTc interval >500 ms or increase in QTc of >/=60 ms from
27 red with baseline, the heart rate-corrected (QTc) interval was prolonged by 30 to 60 milliseconds in
30 icant shortening of the electrocardiographic QTc interval and reduction of left ventricular systolic
31 athy, including cardiac isoenzyme elevation, QTc interval prolongation, and rapidly reversible cardia
33 iables predicts patients at highest risk for QTc interval prolongation and may be useful in guiding m
34 ed to a patient at moderate or high risk for QTc interval prolongation, a computer alert appeared on
38 binary outcome meta-analyses (human height, QTc interval and gallbladder disease); all previous repo
44 c repolarization disturbances with increased QTc intervals in both patients and controls, but with a
45 ing of the heart rate-corrected QT interval (QTc interval) in Kir2.1-transduced animals (n = 4) and a
46 ll patients developed corrected QT interval (QTc interval) prolongation (median QTc interval 504 ms,
49 prevalence and factors associated with long QTc interval in a cohort of opioid-dependent HIV-infecte
50 trophy (77% versus 58%; P=0.02) and a longer QTc interval (466+/-36 versus 453+/-41 milliseconds; P=0
51 Compared with men, women exhibit a longer QTc interval and an increased propensity toward torsade
54 ne and lansoprazole had significantly longer QTc intervals (up to 12 ms in white men) and were 1.4 ti
56 consumption of fish is associated with lower QTc interval in free-eating people without any evidence
58 uals receiving the DSEC had a longer maximal QTc interval (mean [SD], 419.4 [11.8] vs 396.1 [15.7] mi
63 riability between hourly minimal and maximal QTc intervals reached their circadian peak shortly after
68 +/- 23 and 445 +/- 16 ms, respectively (mean QTc interval for men 434 +/- 12 ms, 457 +/- 10 ms for wo
69 d relatives, men exhibited the shortest mean QTc interval in chromosome 7q- and 11p-linked blood rela
74 interval (QTc interval) prolongation (median QTc interval 504 ms, IQR: 477 to 568 ms) within 24 h of
77 n the JLNS family described here have normal QTc intervals (0.43 and 0.44 seconds, respectively).
78 QT-prolonging drugs and reduces the risk of QTc interval prolongation in hospitalized patients with
80 by examining dose dependency, the percent of QTc intervals higher than 500 msec, and the risk of drug
81 SNPs previously identified as modulators of QTc-interval in genome-wide association studies in the g
91 score comprising renal impairment, prolonged QTc interval, and age older than 52 was developed for pr
92 wing in recent years, and cases of prolonged QTc interval and torsades de pointes have been described
94 (</= 440 ms [n = 469]), LQTS with prolonged QTc interval (> 440 ms [n = 1,392]), and unaffected fami
96 implantation in 3) and excessively prolonged QTc intervals in 8 (6.7%) (dosage reduced or discontinue
97 ly, both these family members have prolonged QTc intervals and would have been classified as Romano-W
98 ificantly lower than in those with prolonged QTc intervals (15%) (p < 0.001) but higher than in unaff
99 r ACA or SCD only in patients with prolonged QTc intervals (female age > 13 years, hazard ratio: 1.90
100 bradycardia; palpitation; changing PR, QRS, QTc intervals in electrocardiogram; heart failure) for t
101 d >/=120 ms (1.75, 1.17-2.62); corrected QT (QTc) interval >/=450 ms in men or >/=460 ms in women (1.
103 gender differences in the rate-corrected QT (QTc) interval in the presence of a QT-prolonging gene.
104 stigate whether the heart rate-corrected QT (QTc) interval on the electrocardiogram (ECG) is associat
109 and variability of the QT and corrected QT (QTc) intervals over 24 h and to assess their pattern and
111 hisms (SNPs) that modulate the corrected QT (QTc)-interval and the occurrence of cardiac events in 63
113 SCD in patients with LQTS with normal-range QTc intervals (4%) was significantly lower than in those
114 ors ACA or SCD in patients with normal-range QTc intervals included mutation characteristics (transme
115 the baseline, the mean, and the most recent QTc interval recorded before age 10, were less significa
117 the LQT group had a 24% reduction in resting QTc interval (from 617 +/- 92 to 469 +/- 23 ms, P = .004
119 h the mutation was associated with a shorter QTc interval (P<0.05) and a reduced occurrence of cardia
124 +/-6 versus 115+/-11 beats/min; P=0.54), the QTc interval had prolonged significantly more in patient
125 To better understand it, we analyzed the QTc interval duration in patients with heart failure wit
129 COMMENDATION 4 (RISK STRATIFICATION): If the QTc interval is greater than 450 ms but less than 500 ms
132 rocardiogram for all patients to measure the QTc interval and a follow-up electrocardiogram within 30
133 4) and a 16.7% +/- 1.8% prolongation of the QTc interval (n = 3) in Kir2.1AAA-transduced animals 72
135 p < 0.001) as significant predictors of the QTc interval; and heart rate (p < 0.001), genotype (p <
136 gs that cause torsade de pointes prolong the QTc interval and bind to the potassium rectifier channel
137 opic drugs have been reported to prolong the QTc interval and increase the risk of ventricular dysrhy
142 However, recent studies indicate that the QTc interval is nonlinear with respect to heart rate dur
144 pectedly large effects of NOS1AP SNPs on the QTc-interval and a trend for effects on risk of cardiac
145 an analysis for quantitative effects on the QTc-interval, 3 independent SNPs at NOS1AP (rs10494366,
149 up and upward, the risk of AF increased with QTc interval duration in a dose-response manner, reachin
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