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At least 19 recordsLinked to original sources
PubMed1991

QTc prolongation measured by standard 12-lead electrocardiography is an independent risk factor for sudden death due to cardiac arrest.

BACKGROUND: QTc prolongation has been implicated as a risk factor for sudden death; however, a controversy exists over its significance. METHODS AND RESULTS: In the Rotterdam QT Project, 6,693 consecutive patients who underwent 24-hour ambulatory electrocardiography were followed up for 2 years; of these, 245 patients died suddenly. A standard 12-lead electrocardiogram and clinical data at the time of 24-hour ambulatory electrocardiography were collected for all patients who died suddenly and for a random sample of 467 patients from the study cohort. In all patients without an intraventricular conduction defect (176 patients who died suddenly and 390 patients from the sample), QT interval duration was measured in leads I, II, and III and corrected for heart rate with Bazett's formula (QTc). In patients without evidence of cardiac dysfunction (history of symptoms of pump failure or an ejection fraction less than 40%), QTc of more than 440 msec was associated with a 2.3 times higher risk for sudden death compared with a QTc of 440 msec or less (95% confidence interval: 1.4, 3.9). In contrast, in patients with evidence of cardiac dysfunction, the relative risk of QTc prolongation was 1.0 (0.5, 1.9). Adjustment for age, gender, history of myocardial infarction, heart rate, and the use of drugs did not alter these relative risks. CONCLUSIONS: These data indicate that in patients without intraventricular conduction defects and cardiac dysfunction, QTc prolongation measured from the standard electrocardiogram is a risk factor for sudden death independent of age, history of myocardial infarction, heart rate, and drug use. In patients with cardiac dysfunction, QTc duration is not related to the risk for sudden death.

Death, Sudden↗
PubMed1992

Prediction of sotalol-induced maximum steady-state QTc prolongation from single-dose administration in healthy volunteers.

The relationship between racemic sotalol plasma concentrations and QTc interval prolongation after both single-dose and repeated administration of three sotalol oral doses was studied in a randomized crossover protocol performed in 10 healthy volunteers. QTc interval increase was significant after the three single-dose sotalol administrations and was significantly related to the administered dose (p < 0.0001). In 21 of 30 analyses, QTc interval was linearly correlated with sotalol plasma concentrations. After the 320 mg dose, the linear model was a best fit for 90% of the cases, and no hysteresis was observed. After repeated sotalol administration, 69 of 87 QTc interval measurements at steady state could be predicted from the plasma concentration versus effect relationship established after single-dose 320 mg administration. Seventeen of 18 errors (94%) corresponded to QTc intervals that were significantly lower than predicted. These findings suggest that a short-term individual linear model determined after a 320 mg test dose of sotalol allows a good prediction of expected maximal increase in QTc duration in healthy subjects.

Administration, Oral↗
PubMed1991

[Behavior and prognostic value of QTc intervals in surface ECG in acute and chronic cerebral processes].

Abnormal ECG-patterns in patients with acute and chronic cerebral processes are well known; the prognostic value, however, is still uncertain. Therefore, we examined 12 conventional ECG-leads retrospectively (at the day of admission to hospital) with respect to heart rate, occurrence of heart rhythm disturbances, and repolarization abnormalities in 131 patients (pts) with acute strokes and in 116 pts with cerebral tumors. Patients with atrial fibrillation or bundle branch blocks were excluded. In all pts the longest QTc-intervals (heart rate correction according to Bazett) were found in the precordial leads V2-V6 and Nehb D, A, I. Patients with strokes had the longest QTc-intervals: 418 +/- 43 ms (II) - 445 +/- 55 ms (V5). The differences in healthy persons (n = 25) and pts with cerebral tumors were significant (p less than or equal to 0.01). Between the standard and precordial leads the differences in this group were also significant. The QTc-values in non-survivors were significantly longer (429 +/- 45 ms in lead I, 458 +/- 45 ms in V4) than in survivors (409 +/- 35 ms in lead I, 436 +/- 52 ms in Nehb A). Initially, unconscious pts (n = 22) also revealed significantly longer QTc-intervals (485 +/- 58 ms, Nehb D) than conscious pts (440 +/- 45 ms, lead V5). 78.6% of pts with strokes had QTc-values in at least one lead longer than 420 ms, and in 64%, we registered QTc-intervals greater than 440 ms. Significant differences were found between non-survivors (n = 56) and survivors (n = 75).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2026

Evaluation of the difference between automated and measured QTc intervals in children.

BACKGROUND: The corrected QT interval (QTc) is obtained through automated ECG computations or manual physician measurements. We hypothesized that differences exist in children between the measured and automated QTc intervals within and between Healthy and hypertrophic cardiomyopathy (HCM) subjects with greater differences for HCM due to structural abnormalities. METHODS: QT measurements - Bazett correction- automated (aQTc) and measured (mQTc), were extracted from the GE MUSE database for 385 Healthy pediatric (single ECG) and 208 HCM subjects (2 ECGs), stratified by age&#xa0;<&#xa0;12 and&#xa0;&#x2265;&#xa0;12&#xa0;yrs., sex, race, and ethnicity. QTc means (SD), automated and measured differences, and the difference of the differences of aQTc and mQTc were analyzed overall and by subgroups. All ECGs were read by one pediatric cardiologist with a second cardiologist reading a random subset of HCM ECGs to evaluate intraclass correlations and agreement. RESULTS: The mQTc intervals were shorter than aQTc intervals within Healthy (p&#xa0;<&#xa0;0.001) and within first HCM ECGs (p&#xa0;<&#xa0;0.001) with both aQTc and mQTc shorter in Healthy than HCM (p&#xa0;<&#xa0;0.001). The difference in these differences was significant overall using HCM ECG 1 but not HCM ECG 2. Healthy subject aQTc and mQTc intervals differed by age, sex, and race (p&#xa0;<&#xa0;0.002). HCM ECG 1 aQTc- mQTc intervals differed for age&#xa0;<&#xa0;12&#xa0;yrs., as well as by sex and race. HCM ECG 2 intervals differed only for age&#xa0;<&#xa0;12&#xa0;yrs. CONCLUSIONS: Compared to measured values, automated QTc values were significantly longer in both Healthy and HCM subjects. Automated measurements may overestimate the QTc.

Humans↗
PubMed1991

The longitudinal time course of QTc in early infancy. Preliminary results of a prospective sudden infant death syndrome surveillance program.

Eleven hundred one healthy neonates in Charleston County, SC, were enrolled in a prospective, serial measurement sudden infant death syndrome/QT surveillance program. Automated computer-enhanced ECGs were recorded at 1 day of age in the hospital nursery and again at 1 week and 1, 2, and 3 months in the participant's home. At 1 year, the families were contacted by phone or mail and questioned as to the health of the child. Validation studies demonstrated the computer-enhanced ECGs to be 96% accurate, whereas traditional ECG recording and measurement was 94% accurate. No systematic differences in the QTc according to race and sex were observed. There were parallel longitudinal time courses for each race and sex group with a significant (P less than .001) shortening of the QTc at 1 week. There was no evidence of tracking of the QTc during the first 3 months of life. In conclusion, (1) automated, enhanced ECG QTc intervals are superior to traditional electrocardiography while retaining the advantages of automation; (2) there is a significant shortening of the QTc during the first month of life; and (3) a home follow-up sudden infant death syndrome surveillance program is feasible and produces accurate, reliable information.

Computers↗
PubMed1991

Effects of exercise on heart rate, QT, QTc and QT/QS2 in the Romano-Ward inherited long QT syndrome.

Patients with the Romano-Ward inherited long QT syndrome have an incompletely defined cardiac sympathetic system abnormality, and exhibit ventricular arrhythmias during exercise, fear and anxiety. Treadmill and bicycle exercise were used to modulate cardiac autonomic activity in 27 Romano-Ward subjects and 27 normal controls. The heart rate, and the QT, QTc and QT/QS2 (ratio of electrical to mechanical systole) intervals were compared. Subjects with long QT were compared with normals. Those with a long QT interval had the following results: similar resting heart rates; lower rates during moderate (151.6 vs 169.6 beats/min, p = 0.04) and maximal (155.9 vs 182.1 beats/min, p = less than 0.001) exercise; an abnormal QT cycle-length relationship, with failure of the QT to shorten normally with increasing heart rate; an increase in QTc versus a decrease in normals; supine rest QT/QS2 ratio of 1.12 vs 0.93, p = 0.001; and an exercise QT/QS2 that increased by 30%, from 1.12 at rest to 1.45, versus 15%, in normals, from 0.93 to 1.07, p = 0.001. The lower heart rates and excessively prolonged QT/QS2 ratios during exercise further support an abnormality of, or abnormal cardiac response to, sympathetic activity. A QT/QS2 greater than 1.0 at rest, an exercise QT/QS2 ratio greater than 1.17, and an increase in QTc during moderate exercise may be helpful diagnostic findings in patients with borderline long QTc intervals at rest.

Adult↗
PubMed1989

[The mean values and correlation between blood pressure, body weight, height, heart rate, the PQ, QT and QTc intervals, the QRS-complex and the echocardiographic dimensions of the left atrium and ventricle in 515 14-year-old students].

In five hundred and fifteen schoolchildren, the mean values of blood pressure, body weight, height, heart rate, PQ, QT, QTc-interval, QRS-duration and echocardiographic left ventricular (LV) and left atrial (LA) diastolic internal dimension as well as their correlations were measured. There were 224 girls and 291 boys of 14 years of age. Mean systolic blood pressure was 118 +/- 15 mmHg in boys, 115 +/- 10 mmHg in girls. Mean diastolic blood pressure was 74 +/- 9 mmHg in boys, 74 +/- 7 mmHg in girls. The prevalence of systolic hypertension was 3.4% in boys, 3.1% in girls. The prevalence of diastolic hypertension was 2% in boys and 4% in girls. No significant difference was observed between body weight, height, PQ, QT, QTc-interval, QRS-duration and echocardiographic LA and LV measurement in boys and girls. Mean heart rate in girls was 98 +/- 19.7 and 88 +/- 17 in boys. The difference was statistically significant (t = 6.06; P less than 0.01). A significant positive correlation was found between body weight and height and diastolic and systolic blood pressure. The body weight and height revealed a significant positive correlation to echocardiographic left ventricular and left atrial dimension. No correlation of body weight to heart rate was observed in neither boys nor girls. A significant negative correlation was found between height and heart rate (P less than 0.05) in boys, whereas no correlation between these two variables was noticed in girls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

[Usefulness of the measurement of corrected QT (QTc) for the diagnosis of diabetic neuropathy of the autonomic cardiovascular system].

Corrected QT interval was determined in diabetic patients and in a group of obese individuals with glucose intolerance. It was shown that the measurements of corrected QT (QTc) interval may be a reliable test in the diagnosis of the autonomic diabetic neuropathy. Its simplicity enables routine measurements in diabetic patients treated in out-patients clinics.

Adolescent↗
PubMed1978

The effect of oral magnesium chloride therapy on the QTc and QUc intervals of the electrocardiogram.

The effect of magnesium, given orally as enteric-coated magnesium chloride tablets, on the ECG of 25 randomly selected patients was investigated. Each patient, who served as his own control, was given 4--6 tablets, each containing 0,5 g MgCl26H2O, at night for periods varying from 6 weeks to 2 years. Findings included (i) a statistically significant decrease in OTc and QUc intervals; (ii) a progressive shortening of QTc and QUc intervals with continuing therapy; (iii) reversion to normal of ECG abnormalities, especially of ST segments and T waves.

Administration, Oral↗
PubMed1992

Effects of halothane and quinidine on intracardiac conduction and QTc interval in pentobarbital-anesthetized dogs.

To confirm in vitro data that halothane and quinidine depressed cardiac conduction and prolonged action potential (AP) duration, the electrocardiogram and His bundle electrogram were recorded in dogs during basal pentobarbital anesthesia, after 1% halothane or quinidine (2.38 +/- 0.22 micrograms/mL serum concentration [mean +/- SEM]), or both. Purkinje fibers from a second dog were superfused with blood from the intact (support) dog, and APs were recorded. In the intact dogs, 1% halothane caused no changes in the electrocardiogram or His bundle electrogram. Quinidine prolonged QRS duration, QT interval, and rate-corrected QT (P < 0.05). Ventricular conduction (HS interval) slowed, and atrial effective refractory period increased (P < 0.05). Quinidine combined with halothane widened QRS, QT, and rate-corrected QT, prolonged the HS interval, and increased the vulnerability of the atrioventricular node to conduction block. Three of 20 dogs developed torsades de pointes-type ventricular tachycardia during simultaneous quinidine and halothane administration. In cross-superfused Purkinje fibers, the AP duration to 50% repolarization was shortened, and conduction time was prolonged by 1% halothane (both P < 0.05). Quinidine decreased AP amplitude, prolonged AP duration to 90% repolarization, and slowed conduction (P < 0.05). Quinidine combined with halothane decreased AP amplitude, and prolonged both AP duration to 90% repolarization and conduction (P < 0.05). When 1% halothane and therapeutic concentrations of quinidine are administered in dogs, depressed conduction and an acquired long QT syndrome with malignant ventricular arrhythmias may develop.

Action Potentials↗
PubMed1985

QT interval prolongation in acute myocardial infarction.

The relationship between corrected QT (QTc) interval and clinical factors in acute myocardial infarction (AMI) was studied, as well as long-term prognostic implications of QTc after AMI. QTc was measured on admission to the coronary care unit (CCU). Patients with AMI who showed ventricular fibrillation or severe ventricular tachycardia (n = 27) had prolonged QTc in comparison to AMI patients without ventricular arrhythmias (VA) and noninfarction patients. QTc was measured at discharge from hospital in 463 survivors of AMI. Patients with anterior infarcts had longer QTc than those with inferior infarcts. Patients with VA in the CCU had longer QTc. Patients who died (3-6 years) had shorter QTc; explained by digitalis therapy. Among patients (less than 66 years) without bundle branch block digitalis and quinidine, those who died within six months tended to have longer QTc than the survivors. QTc intervals were measured on the first two days in the CCU, the first post-CCU day, at discharge, and at 1-3, 6 and 12 months after discharge, in 160 AMI patients (less than 66 years). The highest QTc values were registered in the CCU, the lowest at the 1-year control. During the acute phase, patients with anterior infarcts had longer QTc than those with inferior infarcts. Those with subendocardial infarcts had longer QTc intervals. Patients who reinfarcted or died (particularly when sudden) after discharge had longer QTc during the post-CCU period; QTc at discharge was of significant independent value for predicting major cardiac events. QTc intervals were measured as in study III. Metoprolol (n = 59) or placebo (n = 52) were given prior to discharge to AMI patients (less than 70 years). QTc decreased in both groups between discharge and the 3-month control; most marked in those on beta-receptor blockade with prolonged QTc. Patients on metoprolol had shorter QTc during the follow-up. Patients who died suddenly had longer QTc prior to discharge than those without major cardiac events. In a prospective collaborative study, QTc intervals were measured at discharge from hospital in 865 patients. All patients who died after discharge within 30 days after admission were on medication or pacemaker therapy which would influence QTc. When this was taken into consideration, QTc was significantly longer in patients who died within 180 days and 1 year.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1992

QT-interval abnormalities in hypertrophic cardiomyopathy.

To examine whether QTc and QTc dispersion across the leads of a surface electrocardiogram (ECG) are different in patients with hypertrophic cardiomyopathy (HCM) compared with normal subjects, we measured QT and calculated QTc in all 12 leads of a surface ECG in 24 patients with HCM and in 20 age- and sex-matched normal control subjects. Maximal QTc was prolonged in HCM patients (465 +/- 24 ms) compared with controls (410 +/- 20 ms) (p < 0.001). QTc dispersion defined as the difference of maximum-minimum QTc was also greater in HCM patients (71 +/- 21 ms) compared with normals (35 +/- 11 ms) (p < 0.001). A correlation was found between the degree of left ventricular hypertrophy expressed by the maximal wall thickness and maximal QTc (r = 0.48, p < 0.02). However, QTc dispersion did not correlate with maximal wall thickness. Thus, patients with HCM show a prolonged QTc (> 440 ms) and increased QTc dispersion compared with normal subjects. In addition, the degree of left ventricular hypertrophy correlates with maximal QTc. The presence of a prolonged QT with increased regional dispersion may be associated with the occurrence of serious ventricular arrhythmia and sudden death in HCM.

Adult↗
PubMed1990

Effects of bepridil and diltiazem on ventricular repolarization in angina pectoris.

To examine the time-course and potential predictors of prolongation of ventricular repolarization with the calcium antagonist bepridil, the effects of bepridil (300 to 500 mg/day; n = 45) and diltiazem (180 to 300 mg/day; n = 42) on QT and QTc interval duration were analyzed in a randomized double-blind study in patients with angina pectoris. Electrocardiograms were recorded before and 14, 28, 70 and 112 days after treatment was begun. After 14 days, bepridil prolonged QT interval by 26 +/- 35 ms (range, -60 to 120 ms) and QTc (Bazett's formula) by 17 +/- 33 ms (range, -73 to 107 ms) compared to baseline (both p less than 0.05). QT or QTc did not significantly increase thereafter. However, among the 30 patients who had less than 40 ms QTc prolongation at day 14 compared with baseline, 13 (43%) exceeded this limit on at least 1 of the following visits. Diltiazem did not significantly alter QT or QTc intervals. The absolute change in QTc interval from baseline observed after 14 days of bepridil therapy was inversely proportional to the baseline QTc interval (r = -0.68; n = 42; p less than 0.001). The degree of bepridil-induced QTc prolongation on day 14 correlated with pretreatment RR interval (r = 0.36; n = 42; p less than 0.02). In conclusion, chronic administration of bepridil but not of diltiazem prolongs ventricular repolarization in patients with angina pectoris. The overall effects of bepridil therapy on QT and QTc intervals can be assessed by an electrocardiogram recorded after 14 days of treatment but subsequent measurements may be required in individual patients. A short baseline QTc interval and a slow initial heart rate may be potentially useful predictors of a greater QTc prolongation with bepridil.

Angina Pectoris↗