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Prolongation of QTc interval after postoperative nausea and vomiting treatment by droperidol or ondansetron.

BACKGROUND: At dosages above 0.1 mg/kg, droperidol induces a dose-dependent QTc interval prolongation. Although subject to controversy, low-dose droperidol has recently been suspected to induce cardiac arrhythmias. Hence, 5-hydroxytryptamine type 3 antagonists have become the first-line drug for management of postoperative nausea and vomiting. These drugs are also known to prolong the QTc interval at high dosages. This study describes QTc interval changes associated with postoperative nausea and vomiting treatment by droperidol or ondansetron at low doses. METHODS: Eighty-five patients with postoperative nausea and vomiting were included in this prospective, single-blind study. Patients received either 0.75 mg intravenous droperidol (n = 43) or 4 mg intravenous ondansetron (n = 42). Electrocardiographic recordings were obtained before administration of antiemetic drug and then 1, 2, 3, 5, 10, and 15 min after. Electrocardiographic monitoring was maintained for 3 h in eight patients in each group. RESULTS: The QTc interval was prolonged (> 450 ms in men, > 470 ms in women) in 21% of the patients before antiemetic drug administration. This was significantly correlated with lower body temperature and longer duration of anesthesia. Compared with predrug QTc measurement, both antiemetics were associated with a significant QTc interval prolongation (P < 0.0001). The mean maximal QTc interval prolongation was 17 +/- 9 ms after droperidol occurring at the second minute and 20 +/- 13 ms after ondansetron at the third minute (both P < 0.0001). Compared with predrug measurement, the QTc interval was significantly lower after the 90th minute in both groups. CONCLUSIONS: Droperidol and ondansetron induced similar clinically relevant QTc interval prolongations. When used in treatment of postoperative nausea and vomiting, a situation where prolongation of the QTc interval seems to occur, the safety of 5-hydroxytryptamine type 3 antagonists may not be superior to that of low-dose droperidol.

Adult↗

Traumatic subarachnoid hemorrhage and QTc prolongation.

OBJECTIVE: Spontaneous subarachnoid hemorrhage (SAH) causes a prolonged corrected QT interval (QTc) in 25% to 90% of patients, but whether this occurs with traumatic SAH (tSAH) is unknown. This investigation was conducted to determine whether QTc prolongation occurs with tSAH and to evaluate QTc prolongation with respect to severity of tSAH. DESIGN: Records of 104 consecutive tSAH patients were reviewed. A QTc was calculated on posttrauma day (PTD) 0, 1, and 3. Cranial computed tomography (CT) scans were graded for severity using a previously validated scale. QTc intervals were compared based on CT scan severity. SETTING: Pennsylvania level II trauma center. PATIENTS: Trauma patients with tSAH. INTERVENTIONS: None MEASUREMENTS AND MAIN RESULTS: QTc prolongation occurred in 67% of those with tSAH. Mean QTc intervals for PTD0, PTD1, and PTD3 were 470 +/- 69 ms, 467 +/- 72 ms, and 465 +/- 50 ms, respectively. As the severity of the tSAH increased, the average QTc became more prolonged (Pearson's r = 0.855, P = 0.003). CONCLUSIONS: tSAH is a common cause of an acquired prolonged QTc syndrome. As the tSAH becomes more severe, the QTc becomes more prolonged.

Adult↗

QTc dispersion predicts cardiac mortality in the elderly: the Rotterdam Study.

BACKGROUND: Increased QTc dispersion has been associated with an increased risk for ventricular arrhythmias and cardiac death in selected patient populations. We examined the association between computerized QTc-dispersion measurements and mortality in a prospective analysis of the population-based Rotterdam Study among men and women aged > or = 55 years. METHODS AND RESULTS: QTc dispersion was computed with the use of the Modular ECG Analysis System as the difference between the maximum and minimum QTc intervals in 12 and 8 leads (ie, the 6 precordial leads, the shortest extremity lead, and the median of the 5 other extremity leads). After exclusion of those without a digitally stored ECG, the population consisted of 2358 men and 3454 women. During the 3 to 6.5 years (mean, 4 years) of follow-up, 568 subjects (9.8%) died. The degree of QTc dispersion was categorized into tertiles. Data were analyzed using the Cox proportional hazards model, with adjustment for age. For QTc dispersion in 8 leads, those in the highest tertile relative to the lowest tertile had a twofold risk for cardiac death (hazard ratio, 2.5; 95% confidence interval [CI], 1.6 to 4.0) and sudden cardiac death (hazard ratio, 1.9; 95% CI, 1.0 to 3.7) and a 40% increased risk for total mortality (hazard ratio, 1.4; 95% CI, 1.2 to 1.8). Additional adjustment for potential confounders, including history of myocardial infarction, hypertension, and overall QTc, did not materially change the risk estimates. Hazard ratios for QTc dispersion in 12 leads were comparable to those found for QTc dispersion in 8 leads. CONCLUSIONS: QTc dispersion is an important predictor of cardiac mortality in older men and women.

Age Factors↗

Rank power of metrics used to assess QTc interval prolongation by clinical trial simulation.

Monte Carlo simulation was used to assess the type I error rate and rank order of power for six different metrics using linear mixed-effect models, including two variables recommended by the European Agency for the Evaluation of Medicinal Products (EMEA) in the analysis of QTc interval data. The metrics analyzed were maximal change in QTc interval from baseline, maximal QTc interval, area under the QTc interval-time curve (AUC), average QTc interval, maximal QTc interval with baseline QTc interval as covariate, and AUC with baseline QTc interval as covariate. Two dosing regimens were studied: multiple-dose oral and multiple-dose continuous intravenous infusion. Both regimens were designed to produce similar maximal plasma concentrations, albeit with the infusion regimen maintaining maximal plasma concentrations for a longer period of time. The ability of the metrics to detect a drug effect was examined, assuming drug effect followed either an Emax or linear model. All statistics had a type I error rate near the nominal value. Regardless of pharmacokinetic or pharmacodynamic model, AUC with baseline QTc interval as a covariate had greater power than any other metric examined. The simulations also suggest that mean QTc interval data not be used.

Administration, Oral↗

Reassessing the role of QTc in the diagnosis of autonomic failure among patients with diabetes: a meta-analysis.

OBJECTIVE: A 1992 consensus statement on autonomic testing portrayed Bazett's heart rate-corrected QT interval (QT) prolongation as a specific yet insensitive indicator of diabetic autonomic failure. At that time, only a few small studies had evaluated the accuracy of QTc. To date, even fewer studies have evaluated whether its accuracy is influenced by patient characteristics. RESEARCH DESIGN AND METHODS: We critically appraised 17 studies reporting the sensitivity and specificity of QTc for diabetic autonomic failure. The studies represented 4,584 patients with diabetes (mean age 34.9 years, 46% female, 92% with type 1 diabetes, mean duration of diabetes 14.5 years). We summarized the accuracy of QTc prolongation for diabetic autonomic failure as an odds ratio (OR) (95% CI) and determined whether patient and study design characteristics influenced the accuracy of QTc prolongation by comparing summary receiver operating characteristic curves. RESULTS: Autonomic failure, defined as > or =1.2+/-0.4 (mean +/- SD) abnormal of 2.0+/-1.6 administered cardiovascular reflex tests, was found in 26% (25-28) of patients. The pooled sensitivity and specificity of QTc > 441+/-8 ms for autonomic failure were 28% (26-29) and 86% (85-87), respectively. Autonomic failure was 2.26 times (1.90-2.70) more likely to be present in patients with than in patients without QTc prolongation. At 86% specificity, the sensitivity of QTc prolongation was 46 vs. 12% for men versus women (P = 0.0077), respectively, and, after adjustment for sex, 66 vs. 17% among patients aged 25 vs. 55 years (P = 0.1902) and 61 vs. 27% at thresholds of >420 vs. >460 ms, respectively (P = 0.2964). CONCLUSIONS: QTc prolongation is a specific albeit insensitive indicator of autonomic failure. Although QTc prolongation is relatively accurate for men, accuracy may be even greater for young men at low QTc thresholds.

Adult↗

Prolongation of the QTc interval in African children treated for falciparum malaria.

Antimalarial drugs can affect the heart and trigger life-threatening arrhythmias. However, little is known about the frequency with which cardiac abnormalities occur during uncomplicated attacks of malaria. Therefore, we have studied the electrocardiograms of 139 Gambian children with uncomplicated falciparum malaria who were treated with co-artemether, pyrimethamine/sulfadoxine, or chloriquine. The QTc intervals were measured on presentation, and four and eight days after treatment. No significant differences in mean QTc or heart rate were found between children in the three treatment groups on days 0, 4, or 8. After adjustment for the type of antimalarial thearapy in an analysis of variance, the mean (SD) QTc intervals on days 0, 4, and 8 were 402 (22.6), 416 (23.1), and 405 (24.3) msec, respectively. The mean QTc on day 4 was significantly longer than the mean QTc on days 0 or 8 (P < 0.01 in both cases). A quadratic line was fitted for QTc against time for each antimalarial therapy. No significant differences were found between the quadratic lines of the three groups. A weak association was found between QTc and the degree of parasitemia (r = 0.17, P = 0.04) and temperature (r = -0.23, P = 0.01) measured on day 0. The QTcs were measured in 18 children who experienced a second episode of malaria. The changes in QTc observed during second episodes were similar to those observed during the first attack. Changes in QTc in five children who developed severe malaria were similar to those found in the remaining children who did not develop severe malaria. This study indicates that the QTc interval changes during the early phase of malaria and this change is independent of the type of antimalarial therapy given.

Child↗

The effect of acute hyperglycaemia on QTc duration in healthy man.

AIMS/HYPOTHESIS: Prolongation of heart rate-adjusted QT (QTc) is associated with an increased risk of coronary heart disease and sudden death. The objective of this study was to investigate whether acute increases of plasma glucose concentrations in healthy subjects could influence QTc and QTc dispersion. METHODS: Plasma glucose concentrations were quickly raised to 15 mmol/l in 20 healthy subjects (10 men/10 women) and maintained for 2 h. On another occasion, and in random order, all subjects underwent the same hyperglycaemic clamp as above and an infusion of the somatostatin analogue octreotide (25 microg as iv bolus followed by a 0.5 g/min infusion) to block the release of endogenous insulin. RESULTS: Systolic and diastolic blood pressures, heart rate and plasma catecholamine concentrations showed significant increases (p < 0.05) starting after 60 min of hyperglycaemia. QTc, QTc dispersion and PR interval also showed significant increments at 120 min of the hyperglycaemic clamp. The infusion of octreotide did not influence QTc duration, QTc dispersion, PR interval and the haemodynamic effects of acute hyperglycaemia. CONCLUSION/INTERPRETATION: The results show that acute hyperglycaemia produces significant increments of QTc and QTc dispersion in normal subjects. In this context, endogenously released insulin during acute hyperglycaemia seems to play a minor part.

Adult↗

Chromium supplementation shortens QTc interval duration in patients with type 2 diabetes mellitus.

BACKGROUND: We investigated the potential effects of chromium supplementation on QTc interval duration in type 2 diabetic patients. METHODS: Of 60 patients with type 2 diabetes mellitus, 30 were randomly assigned to group A, and 30 to group B. Group A received 1000 microg of chromium picolinate (CrPic) daily for 3 months, followed by placebo in the next 3 months; group B was treated with placebo for the first 3 months and CrPic in the next 3 months. At each visit, QT interval was measured on a standard electrocardiogram by averaging 3 consecutive beats in leads II and V4 and corrected for heart rate with Bazett formula. RESULTS: Although baseline QTc interval was similar in both groups (422 +/- 34 milliseconds in group A vs 425 +/- 24 milliseconds in group B, P = .77), QTc interval at 3 months was shorter in group A (406 +/- 35 milliseconds) than in group B (431 +/- 26 milliseconds, P = .01). In the following 3 months, QTc interval shortened in group B but not in group A, which resulted in a comparable QTc interval duration of both groups at the end of the study (414 +/- 28 milliseconds in group A vs 409 +/- 22 milliseconds in group B, P = .50). Apart from body mass index (31.4 +/- 4.2 kg/m2 in patients with QTc shortening vs 28.7 +/- 4.2 kg/m2 in patients without QTc shortening, P = .03), none of the clinical and laboratory variables predicted QTc interval shortening in our patient cohort. CONCLUSIONS: Short-term chromium supplementation shortens QTc interval in patients with type 2 diabetes mellitus.

Chromium↗

Acute non-selective beta-adrenergic blockade reduces prolonged frequency-adjusted Q-T interval (QTc) in patients with cirrhosis.

BACKGROUND/AIMS: Earlier studies have shown a prolonged frequency-adjusted Q-T interval (QTc>0.440 s(1/2)) in a substantial fraction of patients with cirrhosis. The effect of beta-blockade on QTc is unknown, and its determination was the aim of the study. METHODS: Seventeen patients with cirrhosis received 80 mg propranolol orally during a haemodynamic investigation with measurements at baseline and 90 min after propranolol ingestion. RESULTS: Beta-blockade reduced cardiac output (-21%, P<0.001), heart rate (-20%, P<0.001), and the hepatic venous pressure gradient (HVPG, -17%, P<0.02). The mean QTc=0.460 s(1/2) was prolonged compared to 0.410 s(1/2) in age-matched controls (P<0.01). Whereas QTc decreased during beta-blockade in the cirrhotic patients (from 0.460 to 0.440 s(1/2), P<0.01), no effect was found in the subgroup with normal QTc (0.429 vs. 0.422 s(1/2), ns), and a reduction was seen in the patients with prolonged QTc (from 0.488 to 0.456 s(1/2), P<0.01). The percentage decrease in QTc was related to the reduction in HVPG (r=0.48, P=0.03) and cardiac output (r=0.56, P=0.02). CONCLUSIONS: Acute non-selective beta-blockade reduces prolonged QTc towards normal values in patients with cirrhosis. The clinical significance of QTc reduction in arrhythmia is a topic for future research.

Administration, Oral↗

Role of antiretroviral treatment in prolonging QTc interval in HIV-positive patients.

OBJECTIVES: The aims of our study were to assess the prevalence of QTc prolongation in a group of HIV-infected individuals and to evaluate the associated risk factors. METHODS: All the 650 HIV-infected patients followed up at our outpatient clinic underwent ECG recording. A "nested" case-control study was performed using as cases 64 HIV-infected patients with QTc > 0.44 s and as controls (1:4) 256 HIV-positive subjects matched by gender and age with QTc interval < or = 0.44 s. RESULTS: A prolonged QTc interval was found in 9.8% of HIV-positive individuals (64/650). In the nested case-control study, an increased risk of having a prolonged QTc interval was observed among patients taking nelfinavir, efavirenz, methadone, cotrimoxazole or an excessive amount of alcohol. When a zidovudine (AZT)-containing backbone was associated with nelfinavir-based or efavirenz-based antiretroviral therapy, the risk of having a prolonged QTc interval was about three times higher than in patients taking nelfinavir or efavirenz without AZT. CONCLUSIONS: Several drugs administered to HIV-infected patients may cause a QTc interval prolongation increasing the risk of serious arrhythmias. An ECG follow-up for the assessment of QTc seems to be advisable for HIV-infected patients receiving drugs with a QTc prolonging potential.

Aged↗

Cardiovascular disease in chinese type 2 diabetic women is associated with a prolonged QTc interval.

We studied the relationships between QT interval and cardiovascular disease status in 192 Chinese type 2 diabetic patients. Of these 192 subjects, 132 (68.8%) were women and 60 (31.2%) were men. The mean age (+/-S.D.) was 56.6+/-12.9 years (range: 23-84, median: 58.0 years). Women had longer QTc interval compared to men (0.402+/-0.030 s vs. 0.387+/-0.026 s, P<0.01). Of the 192 subjects, 18 women and two men had prolonged QTc interval (QTc >0.433 s). Women with prolonged QTc interval have a 2.8-fold greater rate of cardiovascular disease as compared to those with normal QTc interval (38.9% vs. 14.0%, P<0.05). Using multiple regression analysis (stepwise) to assess the relationship with QTc interval with age, sex, body mass index, waist-hip ratio, blood pressure, fasting plasma glucose, glycated haemoglobin, lipid profiles, smoking and duration of diabetes as independent variables (R(2)=0.146, F=8.88, P<0.001), systolic blood pressure (beta=0.198, P=0.017), age (beta=0. 189, P=0.023) and female gender (beta=0.157, P=0.037) were found to be independently associated with QTc interval. In conclusion, we have shown a significant association between prolonged QTc interval, ischaemic heart disease and cardiovascular disease in Chinese type 2 diabetic women. Age, systolic blood pressure and female gender are independently correlated to QTc interval.

Adult↗

QTc interval prolongation associated with intravenous methadone.

Numerous medications prolong the rate-corrected QT (QTc) interval and induce arrhythmias by blocking ionic current through cardiac potassium channels composed of subunits expressed by the human ether-a-go-go-related gene (HERG). Recent reports suggest that high doses of methadone cause torsades de pointes. To date, no controlled study has described an association between methadone and QTc prolongation. The only commercial formulation of parenteral methadone available in the United States contains the preservative chlorobutanol. The objectives of this study are to determine: (1) whether the administration of intravenous (i.v.) methadone causes QTc prolongation in humans; (2) whether methadone and/or chlorobutanol block cardiac HERG potassium currents (IHERG) in vitro. Over 20 months, we identified every inpatient with at least one electrocardiogram (ECG) performed on i.v. methadone. For each patient, we measured QTc intervals for every available ECG performed on and off i.v. methadone. Concurrent methadone doses were also recorded. Similar data were collected for a separate group of inpatients treated with i.v. morphine. In a separate set of experiments IHERG was evaluated in transfected human embryonic kidney cells exposed to increasing concentrations of methadone, chlorobutanol, and the two in combination. Mean difference (+/- standard error) per patient in QTc intervals on and off methadone was 41.7 (+/- 7.8)ms, p<0.0001. Mean difference in QTc intervals on and off morphine was 9.0 (+/- 6.1)ms, p=0.15. The approximately linear relationship between QTc measurements and log-dose of methadone was significant (p<0.0001). Methadone and chlorobutanol independently block IHERG in a concentration-dependent manner with IC50 values of 20 +/- 2 microM and 4.4 +/- 0.3 mM, respectively. Chlorobutanol potentiates methadone's ability to block IHERG. Methadone in combination with chlorobutanol is associated with QTc interval prolongation. Our data strongly suggest that methadone in combination with chlorobutanol is associated with QTc interval prolongation.

Cell Line↗

Effect of metoprolol on QTc intervals after acute myocardial infarction.

The effect of metoprolol on corrected QT interval (QTc) was studied retrospectively in 111 survivors of AMI below 70 years of age. Prior to discharge the patients were stratified by age, infarction size and ventricular arrhythmias and randomized. Metoprolol, 100 mg b.i.d., or placebo were given double-blindly to 59 and 52 patients, respectively. QTc intervals were measured four times prior to randomization and three times during the follow-up year. The highest QTc mean was registered on the second day in the CCU. QTc intervals subsequently decreased significantly in both groups between discharge and the three-month control (p < 0.001). Patients on metoprolol had significantly shorter QTc intervals during the follow-up year than those on placebo (0.394 +/- 0.028 vs. 0.406 +/- 0.034 sec, p < 0.001). The QTc-shortening effect of beta-receptor blockade was most marked in patients with prolonged QTc intervals at discharge. Patients who died suddenly had prolonged QTc intervals prior to discharge. In this group the proposed beneficial effect of beta-receptor blockade on QTc interval cannot be evaluated as most of these patients had died before the first control.

Adult↗

Dispersion of QT and QTc interval in healthy children, and effects of sinus arrhythmia on QT dispersion.

OBJECTIVE: To determine the normal values of QT and QTc dispersion and the effects of sinus arrhythmia on QT dispersion in healthy children. PATIENTS AND SETTING: The study was carried out in a university hospital on 372 local schoolchildren (200 male, 172 female), aged seven to 18 years. METHODS: The QT and preceding RR intervals of at least one sinus beat were measured manually in a range of nine to 12 leads on standard 12 lead surface ECGs. The corrected QT interval was computed by the method of Bazett. Dispersion of QT and QTc were defined as (1) the difference between the maximum and minimum QT and QTc intervals occurring in any of the 12 leads (QTD and QTcD), (2) the standard deviation of the QT and QTc interval in the measurable leads (QT-SD and QTc-SD). RESULTS: There was no significant difference in QT, QTc, and RR dispersion between girls and boys. Overall 53% of children had sinus arrhythmia. Although QTD and QT-SD were not affected by sinus arrhythmia, both QTcD and QTc-SD were significantly greater in children with sinus arrhythmia than in those without (QTcD: 52.9 (17.4) v 40.9 (13.1); QTc-SD: 17.5 (5.9) v 13.2 (4.0); p < 0.001). CONCLUSIONS: As calculation of QTc dispersion is affected by sinus arrhythmia, which is common in childhood, we suggest that QT dispersion should not be corrected for heart rate in children.

Adolescent↗

Effect of direct stent implantation on QTc dispersion.

The aim of this study was to evaluate whether direct stenting is superior to conventional stent implantation technique with respect to QTc dispersion in prospectively selected patients with simple lesion morphology and class II stable angina undergoing elective coronary stenting. One hundred thirty-four consecutive patients were divided into 2 groups based on the stenting technique used: the direct stenting without predilation group, group I (n = 64), and the stenting with predilation group, group II (n = 70). All patients had single-vessel disease. The primary end point of the study was the QTc dispersion at the 24th hour and at the first month after the procedure and the secondary end point of the study was the major clinical events (MCEs) rate in the hospital period and up to 1 month. Baseline maximum QTc, minimum QTc, and QTc dispersion were not different between the 2 groups. QTc dispersion decreased from 47+/-8 msec before stent implantation to 41+/-11 msec at 24 hours and 37+/-7 msec 1 month after angioplasty in group I (p < 0.006 and p < 0.01, respectively), whereas QTc dispersion decreased from 49+/-9 msec before stent implantation to 46+/-8 msec at 24 hours and 42+/-10 msec 1 month after angioplasty in group II (p < 0.03 and p < 0.01, respectively). Compared with group II, the decrease in QTc dispersion was significantly greater at the 24th hour and at the first month after the procedure in group I (p < 0.003 and p < 0.001, respectively). There was a decreased trend toward MCE rate in group I in relation to that of group II, but the statistical difference was not significant. Direct stenting is a feasible and safe technique. It is superior to conventional stenting technique in decreasing the QTc dispersion at the 24th hour and at the first month after the procedure, whereas it is equivalent to single-vessel conventional stent implantation technique with respect to MCEs rate in the short-term period.

Adult↗

QTc interval measurement and metabolic parameters in psychiatric patients taking typical or atypical antipsychotic drugs: a preliminary study.

BACKGROUND: Antipsychotic drugs have been associated with prolongation of the QTc interval on the electrocardiogram, and QTc prolongation is, in turn, associated with an increased risk of cardiac arrhythmias and sudden death. Antipsychotic polypharmacy has been implicated in reduced survival, possibly secondary to cardiotoxic effects of antipsychotic medication. Abnormalities of glucose homeostasis, which may be more common in individuals with major mood disorders and schizophrenia, also affect the QTc interval. METHOD: We performed detailed assessment of metabolic parameters in 103 psychiatric out-patients, from across the diagnostic spectrum, who had been taking antipsychotic medication (typical, atypical, or a combination thereof) for a minimum of 6 months. We measured the QTc interval in a subset of these patients (N = 65). RESULTS: Only 2 patients (3%) had a prolonged QTc interval. There was a statistical trend (p = .08) toward a lower QTc interval in patients receiving antipsychotic polypharmacy. QTc interval was associated with age (p = .04) but not with any metabolic parameter. CONCLUSION: QTc prolongation in this population is uncommon. There was a significant association between increasing age and QTc interval, but cardiac repolarization was not related to any metabolic parameter. Further large prospective studies of similar patients are needed to confirm these findings.

Alcohol Drinking↗

QTc interval prolongation predicts postoperative mortality in heart failure patients undergoing surgical revascularization.

QTc interval prolongation is associated with increased mortality rates in patients with advanced heart failure. We investigated the predictive value of prolonged QTc interval in 567 patients with heart failure who were undergoing coronary artery bypass graft surgery The patients were in New York Heart Association class III or IV, with left ventricular ejection fractions of 0.40 or less. Before surgery, the QT interval duration was measured in leads II and V4 of the standard electrocardiogram and corrected by use of the Bazett formula. The QTc interval was prolonged (>440 msec) in 243 patients (43%) and normal in 324 (57%). The 2 study groups--prolonged QTc versus normal QTc--did not differ in terms of age (62 +/- 11 years vs 64 +/- 10 years, P=0.65), sex (80% male vs 76% male, P=0.31), ejection fraction (0.29 +/- 0.08 vs 0.29 +/- 0.09, P=0.72), hypertension (82% vs 78%, P=0.34), or diabetes (11% vs 7%, P=0.10). Within 1 month after coronary artery bypass grafting, 22 of 243 patients (9.1%) in the prolonged QTc group died, compared with 5 of 324 in the normal QTc group (1.5%) (P=0.0001). QTc interval prolongation was the only independent predictor of postoperative mortality on multivariate analysis (P=0.002). We conclude that patients with heart failure and preoperative QTc interval prolongation have increased mortality rates after coronary artery bypass grafting.

Coronary Artery Bypass↗

Heart rate-independent prolongation of QTc interval in women with syndrome X.

BACKGROUND: Cardiac syndrome X is usually diagnosed in the presence of typical exertional chest pain, a positive response to exercise testing, and normal coronary angiograms. The underlying pathogenic mechanisms are speculative, but myocardial ischemia and increased sympathetic activity have been implicated. HYPOTHESIS: The present study examined whether QTc interval is prolonged in women with syndrome X when confounding factors such as heart rate, gender, and environmental conditions are accounted for. METHODS: Maximum QTc interval and its relationship to clinical and exercise variables were evaluated in 32 women with syndrome X (exertional chest pain, positive exercise testing, and completely normal coronary arteries) and 34 normal controls. RESULTS: Patients with syndrome X had significantly longer QTc interval (440 +/- 24 ms) than normal subjects (410 +/- 26 ms, p < 0.004). However, this QTc prolongation appears to be heart rate-independent as patients with syndrome X showed longer QT and QTc intervals than controls despite an identical heart rate. No relation was found between QTc prolongation and clinical or exercise test variables in patients with syndrome X. CONCLUSION: Although increased sympathetic drive is present in syndrome X, and this variable is likely to modulate QTc duration, the mechanism and clinical implications of QTc interval prolongation in syndrome X remain speculative.

Case-Control Studies↗