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1 ard ECG measures (heart rate, PQ-, QRS-, and QT-intervals).
2 myocardial scar is associated with a longer QT interval.
3 ing RING finger protein 207 (RNF207) and the QT interval.
4 s that shorten action potential duration and QT interval.
5 arts with an INaP blocker also shortened the QT interval.
6 hy by voltage and slight prolongation of the QT interval.
7 rtion of patients, most commonly a prolonged QT interval.
8 mia, as measured by the electrocardiographic QT interval.
9 extremely unlikely in the absence of a short QT interval.
10 sted by prolongation of the QRS duration and QT interval.
11 parent risk of prolongation of the corrected QT interval.
12 10 loci explain 5.4-6.5% of the variation in QT interval.
13 ent human genome-wide association studies of QT interval.
14 q21 locus, which is strongly associated with QT interval.
15 the action potential duration and corrected QT interval.
16 zation and repolarization as manifest in the QT interval.
17 in clinical settings, such as prediction of QT interval.
18 tadalafil produced equivalent effects on the QT interval.
19 action potential and by prolongation of the QT interval.
20 articularly when associated with a prolonged QT interval.
21 eatment of erectile dysfunction (ED), on the QT interval.
22 Q1-G589D mutation alone does not prolong the QT interval.
23 e (a proton-pump inhibitor) will prolong the QT interval.
24 achycardia but abolished the prolongation of QT interval.
25 ontrolling action potential duration and the QT interval.
26 layed repolarization and prolongation of the QT interval.
27 for this pediatric patient cohort with short QT interval.
28 iness was prolonged, along with both QRS and QT interval.
29 r exercise duration, and longer PR, QRS, and QT intervals.
30 al treatments for individuals with prolonged QT intervals.
31 enotype is combined with shorter-than-normal QT intervals.
32 of VT under conditions associated with short QT intervals.
33 10% incidence) were nausea (16%), prolonged QT interval (12%), vomiting (11%), and dysgeusia (11%);
34 is associated with an extremely abbreviated QT interval (200 ms) on ECG and paroxysmal atrial fibril
35 s (84% male; age, 26 +/- 15 years; corrected QT interval, 329 +/- 22 ms) were studied, and 62 were fo
36 over, patients with schizophrenia had longer QT-intervals (410.9 versus 393.1 and 401.9 ms; both P<0.
37 l/L, n=5) led to greater abbreviation of the QT interval, a further increase in TDR(max) (from 55.4+/
39 Prolongation of the electrocardiographic QT interval, a measure of cardiac repolarization, is ass
41 ments predict that, in addition to the short QT interval, absence of inward rectification in the E299
44 Furthermore, glucose ingestion increased QT interval and aggravated the cardiac repolarization di
46 s, such as palonosetron, does not affect the QT interval and has a half-life of 40 h that should be a
47 f ethanol) per day with heart rate-corrected QT interval and heart rate assessed from electrocardiogr
48 prognostic association between the baseline QT interval and incident cardiovascular events in indivi
49 the normal activation sequence prolongs the QT interval and increases the existing transmural disper
52 slight abbreviation (300 micromol/L) of the QT interval and no change in transmural dispersion of re
54 nate (SSG), has been reported to prolong the QT interval and produce life-threatening arrhythmias.
56 ients with higher sympathetic control of the QT interval and reduced vagal control of heart rate are
59 ed IKs inhibition necessary to normalize the QT interval and terminate re-entry in SQT2 conditions wa
60 st that the incidence of prolongation of the QT interval and the occurrence of torsades de pointes is
62 association between NOS1AP variants and the QT interval and to examine the association with SCD in a
63 adverse cardiac events (prolongation of the QT interval and/or development of torsades de pointes).
64 on of p90RSK (p90RSK-Tg) had prolongation of QT intervals and of ventricular myocyte action potential
65 these mice have prolongation of the QRS and QT intervals and spontaneous ventricular arrhythmias, in
67 omplexes (PVCs) from 40 patients with normal QT intervals and with PVCs in 24 of the 35 LQTS patients
68 rophysiologically (bradycardia and prolonged QT interval) and functionally (hyperdynamic left ventric
69 arrest (normal left ventricular function and QT interval) and selected family members from the Cardia
70 n (PR interval), ventricular repolarization (QT interval), and ventricular conduction (QRS interval).
72 ion-induced syncope since age 10, had normal QT interval, and displayed ventricular ectopy during str
73 rugs delays cardiac repolarization, prolongs QT interval, and is associated with an increased risk of
74 r hypertrophy, prolongation of the corrected QT interval, and repolarization changes (ST/T wave abnor
75 ght ventricular ejection fraction, prolonged QT interval, and total infarct size and resulted in impr
76 an extend action potential duration, prolong QT intervals, and ultimately contribute to life-threaten
77 own whether any of the components within the QT interval are responsible for its association with SCD
79 Electrocardiographic parameters, including QT intervals, as well as ventricular action potential wa
80 on age, sex, heart rate, frontal T axis, and QT interval assesses the risk for CVD and compares favor
81 epolarisation and electrocardiographic (ECG) QT interval, associated with increased age-dependent ris
83 n of common genetic variants contributing to QT interval at baseline, identified through genome-wide
84 diac PI3K signaling in diabetes prolongs the QT interval at least in part by causing an increase in I
85 ns, followed by normalization in mean HR and QT intervals at 26 days post ventricular amputation (dpa
86 ed the biological clock and normalization of QT intervals at 26 dpa, providing the first evidence of
88 e majority of LQTS patients have a corrected QT interval below this threshold, and a significant mino
89 of the channel are associated with the long QT (interval between the Q and T waves in electrocardiog
90 romes, representing the very extremes of the QT interval, both seem to have a high prevalence of AF.
92 pective analysis of an ECG identified a long QT interval, but sequencing of known LQT genes was uninf
93 on (APD) of individual myocytes and thus the QT interval by altering multiple ion currents, including
95 or 3.9-ms higher age-, sex- and RR-adjusted QT interval compared with GG individuals (P=0.00006).
96 18594 minor homozygotes had a 12.5-ms-longer QT interval compared with major homozygotes (P = 1.5 x 1
97 494366 minor homozygotes had a 9.3-ms-longer QT interval compared with major homozygotes (P = 5.7 x 1
98 e examined the association of the individual QT-interval components (R-wave onset to R-peak, R-peak t
100 Forty-three percent of TdP patients had a QT interval corrected by Bazett's formula, for heart rat
101 mine the association between prolongation of QT interval corrected for heart rate (QTc) with incident
104 the QT interval on electrocardiogram, with a QT interval corrected for heart rate ranging from 620 to
107 bjects at the extremes of a population-based QT interval distribution of 3,966 subjects from the KORA
109 neither associated with heart rate-corrected QT interval duration (QTc) nor cardiac events in any of
110 associated with MeanNN, heart-rate-corrected QT interval duration (QTc), deceleration capacity, and w
112 Two NOS1AP SNPs are strongly associated with QT interval duration in a predominately diabetic Europea
113 or protein (NOS1AP) gene are associated with QT interval duration in a type 2 diabetes-enriched sampl
114 e KCNH2 locus are associated with continuous QT interval duration in an unselected community-based sa
115 75 genotypes were associated with continuous QT interval duration in men and women (2-df P=0.002), wi
116 No association between the NOS1AP SNPs and QT interval duration was observed in the limited number
117 atures that, along with heart rate-corrected QT interval duration, may risk stratify perinatal manage
121 show that cardiac ion-channel expression and QT-interval duration (an index of myocardial repolarizat
123 stosterone levels may explain differences in QT-interval duration between men and women and could be
124 multivariate adjusted differences in average QT-interval duration comparing the highest quartiles wit
125 tween physiologic levels of sex hormones and QT-interval duration in humans was evaluated using data
126 Estradiol levels were not associated with QT-interval duration in men, but there was a marginally
130 A paradoxical increase in the uncorrected QT interval during infusion of low-dose epinephrine appe
132 vided a significant increase in variation in QT interval explained compared with a model with only no
135 trioventricular block, AZD1305 increased the QT interval from 535+/-28 to 747+/-36 ms (+40%, P<0.0001
138 ontaneous beat-to-beat variability of RR and QT intervals from standard 24-h electrocardiogram Holter
139 otal of 1,059 LQTS patients with a corrected QT interval > or =450 ms presenting with syncope as a fi
144 es, but were not associated with uncorrected QT interval, HR-corrected QT interval or high-density li
145 In this study, we sought to validate PGS for QT interval in 2 real-world cohorts of European ancestry
146 sought to determine the prevalence of short QT interval in a pediatric population and associated cli
147 genetic disease characterized by a prolonged QT interval in an electrocardiogram (ECG), leading to hi
148 in one; hypertension and prolonged corrected QT interval in another) occurred in patients initially e
149 shortened the action potential duration and QT interval in arterially perfused rabbit ventricular we
150 as longer than neonatal heart rate-corrected QT interval in both group 2 (491.2+/-27.6; P=0.004) and
151 002 mg/kg intravenously), and placebo on the QT interval in healthy men were compared (placebo and ta
153 ant role for propagation variation affecting QT interval in humans, we show that common polymorphisms
157 sociation studies (GWAS) of variation in the QT interval in population-based cohorts now report assoc
160 his analogue also led to prolongation of the QT interval in the dog that was linked to affinity for h
166 S1AP gene variants play a role in modulating QT intervals in healthy subjects and severity of present
168 However, increased miR-133a levels increased QT intervals in surface electrocardiographic recordings
169 vealed an age-dependent heart rate-corrected QT interval increase (1% per additional 10 years) irresp
170 ts investigated altered heart rate-corrected QT interval irrespective of mutation status, as well as
171 Prolongation of the electrocardiographic QT interval is a risk factor for sudden cardiac death (S
173 s have demonstrated that prolongation of the QT interval is associated with sudden cardiac death (SCD
175 fficient for diagnosis, unless the corrected QT interval is repeatedly >/=500 ms without an acquired
178 nts (20%) experienced a >/=60-ms increase in QT interval, leading to bedaquiline discontinuation in 2
180 pressure, heart rate variability, corrected QT interval, low density lipoprotein (LDL) cholesterol,
181 isplaying ST-segment elevation and corrected QT intervals < or = 360 ms had mutations in genes encodi
183 populations, appropriate use of ischemia and QT-interval monitoring among select populations, alarm m
184 t electrocardiogram occurrences of corrected QT interval more than 500 ms (an indicator of potential
185 effect estimates from association tests with QT interval obtained from prior genome-wide association
187 of onset of 10 months, an average corrected QT interval of 676 ms, and a high prevalence of cardiac
192 ex was increased (P<0.001) and the corrected QT interval on ECG was prolonged (P<0.001) in HFpEF rats
193 individuals had extreme prolongation of the QT interval on electrocardiogram, with a QT interval cor
195 pounds have been identified that prolong the QT interval on the electrocardiogram and cause torsade d
196 ally produce exaggerated prolongation of the QT interval on the electrocardiogram and the morphologic
198 PD) in cardiac myocytes, prolongation of the QT interval on the surface electrocardiogram (ECG), and
199 ondition characterized by abnormally 'short' QT intervals on the ECG and increased susceptibility to
200 ce of increased risks of prolongation of the QT interval or dysglycemia with the 4-month regimen.
201 men is not beneficial for heart function via QT interval or heart rate but could be detrimental.
202 d with uncorrected QT interval, HR-corrected QT interval or high-density lipoprotein-cholesterol.
204 h congenital or acquired prolongation of the QT interval, or long QT syndrome (LQTS), are at risk of
206 longer QTrr (i.e., age- and gender-adjusted QT interval; p = 0.0004), a more depressed ST-segment in
207 more reactive sympathetic modulation of the QT interval, particularly during daytime when arrhythmia
208 4991 in meta-analysis: increase in corrected QT interval per C allele: 9.1 +/- 3.2 ms, p = 1.7 x 10(-
209 points; 95% CI, -1.97 to -0.13; P = .03) and QT interval prolongation (18.1 ms; 95% CI, 6.1-30.1; P =
211 dentifying hospitalized patients at risk for QT interval prolongation could lead to interventions to
212 in APD and INaP in myocytes translated into QT interval prolongation for both types of diabetic mice
213 polarization is underscored by evidence that QT interval prolongation in diabetes mellitus also may r
221 base-line intervals may display exaggerated QT interval prolongation, and the potentially fatal poly
222 hat mutations cause action potential and ECG QT interval prolongation, consistent with clinical pheno
223 ents who receive medications associated with QT interval prolongation, including thioridazine, mesori
224 icant associations were seen among corrected QT interval prolongation, repolarization changes, and al
229 oportion of patients who developed corrected QT-interval prolongation (p = 0.16), extrapyramidal symp
232 nt of surrogate markers of TdP-risk, such as QT-interval prolongation or inhibition of the rapid dela
233 ositive for long-QT syndrome if the absolute QT interval prolonged by >/= 30 ms at 0.10 mug/kg per mi
235 tween methadone and other drugs that possess QT interval-prolonging properties or slow the eliminatio
236 ected, in TdP patients, many known corrected QT interval-prolonging risk factors were simultaneously
237 rate, P duration, PR interval, QRS duration, QT interval, QRS axis, Sokolow-Lyon and Cornell voltages
239 correlated significantly with the corrected QT interval (QTc) and clinical diagnostic score ranging
240 the predictive value of heart rate-corrected QT interval (QTc) for incident coronary heart disease (C
241 patients experienced dose-limiting corrected QT interval (QTc) prolongation, pneumonitis, or neuropat
243 cohort study, prolongation of the corrected QT interval (QTc) was associated with an independent inc
245 ts of AKAP9 variants on heart rate-corrected QT interval (QTc), cardiac events, and disease severity.
248 for TdP included absolute and rate-corrected QT intervals (QTc) on drug therapy, the magnitude of QT
250 electrocardiographically affected (corrected QT interval [QTc] > or = 470 ms), borderline (QTc 440 to
251 ac death during childhood included corrected QT interval [QTc] duration > 500 ms (hazard ratio [HR];
252 ian age 16 years, average referral corrected QT interval [QTc] of 481 ms) referred with a diagnosis o
253 rs (QRS voltage, QRS duration, and corrected QT interval [QTc]) were evaluated by using multivariable
255 diograms (ST-segment elevation and prolonged QT interval, respectively) and increased risk for malign
256 rious coding variants in TTN associated with QT interval show that TTN plays a role in regulation of
257 ), in a pre-defined set of 7 congenital long QT interval syndrome (cLQTS) genes encoding potassium ch
258 riants are associated with drug-induced long QT interval syndrome (diLQTS) and torsades de pointes.
260 arrhythmogenesis and proarrhythmia; the long QT interval syndrome; newer, more selective class 3 anti
261 (acLQTS), which is associated with prolonged QT intervals, tachycardias, and sudden cardiac arrest.
262 eins are more enriched for associations with QT interval than observed for genome-wide comparisons.
263 ified 35 common variant loci associated with QT interval that collectively explain approximately 8-10
264 al criteria to identify loci associated with QT interval that do not meet genome-wide significance an
266 lta), associated with shorter repolarization QT intervals (the time interval between the Q and the T
268 variants previously associated with baseline QT interval to drug-induced QT prolongation and arrhythm
269 sts that shifting the focus from the overall QT interval to its individual components will refine SCD
273 s study aimed to determine whether increased QT interval variability is associated with an increased
277 collectively explain approximately 8-10% of QT-interval variation and highlight the importance of ca
278 from the corresponding common complex trait, QT-interval variation, to identify candidate genes that
279 egulator, have recently been associated with QT interval variations in a human whole-genome associati
287 SNPs, and a genome-wide association study of QT interval was performed in 10 cohorts (n=13,105).
291 which was not correlated with rs16847548 or QT interval, was also independently associated with SCD
292 T axis, heart rate, and heart rate-corrected QT interval were the most significant ECG factors in the
296 atients, the ST-segment, the T-wave, and the QT-interval were analyzed using the MUSE (General Electr
297 the proband, including an exceedingly short QT interval with merging of the QRS and the T wave, abse
298 -deficient mice (ST3Gal4(-/-)) had prolonged QT intervals with a concomitant increase in ventricular
299 units were not associated with the corrected QT interval, with beta = 1.04 (95% confidence interval:
300 on of repolarization and prolongation of the QT interval, yet the mechanisms underlying CO-induced ar
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