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PubMed1995

[The QTc interval and its dispersion in hypertrophic myocardiopathy--its relation to complex ventricular arrhythmias and the effect of anti-arrhythmia agents].

UNLABELLED: The aim of the present study was to evaluate, in patients with hypertrophic cardiomyopathy (HCM): 1. The relation of rate corrected QT interval (QTc) and of QTc interlead variability (QTc dispersion) to complex ventricular arrhythmias (CVA); 2. The effects of amiodarone (Am), beta-blockers (beta B) and calcium antagonists (CA) on QTc and on QTc dispersion. Surface 12 leads ECG was analysed in 55 patients with HCM (39 +/- 12 years, 32 males). All patients were in sinus rhythm, without bundle branch block. Maximum (max), minimum (min) and mean QTc values were considered. QTc dispersion was calculated as: a) max QTc - min QTc (max-min); b) dispersion index (DI) = standard deviation of QTc/mean QTcx100. Patients groups were defined accordingly to: 1--the absence (group A1-35 patients) or the presence (group A2-20 patients) of CVA on 24 hours Holter monitoring; II--absence of cardioactive medication (group B1-20 patients) versus monotherapy with Am (group B3-10 patients), or beta B (group B4-15 patients), or CA (group B5-10 patients). Age, gender, type of HCM (asymmetric versus concentric) and echocardiographic fractional shortening were not different in the studied groups. RESULTS: [table: see text] CONCLUSIONS: 1. Maximum QTc interlead QTc dispersion are increased in patients with HCM that show CVA on Holter monitoring; 2. Amiodarone prolongs QTc but reduces QTc dispersion, while beta-blockers and calcium antagonists do not significantly change neither the duration nor the dispersion of ventricular repolarization.

Adrenergic beta-Antagonists↗

PubMed2001

Loratadine and terfenadine interaction with nefazodone: Both antihistamines are associated with QTc prolongation.

BACKGROUND AND OBJECTIVE: Nefazodone inhibits CYP3A; therefore coadministration with CYP3A substrates such as terfenadine or loratadine may result in increased exposure to these drugs. A potential pharmacodynamic consequence is electrocardiographic QTc prolongation, which has been associated with torsade de pointes cardiac arrhythmia. Therefore a clinical pharmacokinetic-pharmacodynamic evaluation of this potential interaction was conducted. METHODS: A randomized, double-blind, double-dummy, parallel group, multiple-dose design was used. Healthy men and women who were given doses of 60 mg of terfenadine every 12 hours, 20 mg of loratadine once daily, and 300 mg of nefazodone every 12 hours were studied. Descriptive pharmacokinetics (time to maximum concentration, maximum concentration, and area under the plasma concentration-time curve) were used for the examination of interactions among the respective parent drugs and metabolites. QTc prolongation (mean value over the dosing interval) was the pharmacodynamic parameter measured. Kinetic and dynamic analysis was used for the examination of pooled concentration and QTc data with the use of a linear model. RESULTS: Concomitant nefazodone treatment markedly increased the dose interval area under the plasma concentration-time curve of both terfenadine (mean value, 17.3 +/- 8.5 ng. mL/h versus 97.4 +/- 48.9 ng. mL/h; P <.001) and carboxyterfenadine (mean value, 1.69 +/- 0.48 microg. h/mL versus 2.88 +/- 0.53 microg. h/mL; P <.001) and moderately increased the dose interval area under the plasma concentration-time curve of both loratadine (mean value, 31.5 +/- 27.9 ng. h/mL versus 43.7 +/- 25.9 ng. h/mL; P <.014) and descarboethoxyloratadine (mean value, 73.4 +/- 54.9 ng. h/mL versus 81.9 +/- 26.2 ng. h/mL; P <.002). The mean QTc was unchanged with terfenadine alone; however, it was markedly prolonged with concomitant nefazodone and terfenadine (mean [90% confidence interval] prolongation 42.4 ms [34.2, 50.6 ms]; P <.05). Similarly, the mean QTc was unchanged with loratadine alone; however, it was prolonged with concomitant nefazodone and loratadine (21.6 ms [13.7, 29.4 ms]; P <.05). Nefazodone alone did not change mean QTc. QTc was positively correlated with terfenadine plasma concentration (r (2) = 0.21; P =.0001). Similarly, QTc was positively correlated with loratadine plasma concentration (r (2) = 0.056; P =.0008) but with a flatter slope. There was no relationship between QTc and nefazodone plasma concentration during treatment with nefazodone alone (r (2) = 0.002, not significant). CONCLUSIONS: In healthy men and women, concomitant nefazodone treatment at a therapeutic dose increases exposure to both terfenadine and carboxyterfenadine. This increased exposure is associated with marked QTc prolongation, which is correlated with terfenadine plasma concentration. A similar interaction occurs with loratadine, although it is of lesser magnitude. Concomitant administration of nefazodone with terfenadine may have predisposed individuals to the arrhythmia associated with QTc prolongation, torsade de pointes, when terfenadine was available for clinical use. However, a new finding is that in the context of higher than clinically recommended daily doses (20 mg) of loratadine concomitant administration with a metabolic inhibitor such as nefazodone can also result in QTc prolongation.

Adult↗

PubMed1995

Three-lead measurement of QTc dispersion.

INTRODUCTION: QTc dispersion has traditionally been calculated from all 12 leads of a standard electrocardiogram (ECG). It is possible that alternative, quicker methods using fewer than 12 leads could be used to provide the same information. METHODS AND RESULTS: We have previously shown a difference in QTc dispersion from ECGs recorded at least 1 month after myocardial infarction between patients who subsequently died and long-term survivors. In the current study, we recalculated QTc dispersion in these ECGs using different methods to determine if the observed difference in QTc dispersion measurements between the two groups, as calculated from 12-lead ECGs, persisted when using smaller sets of leads. QTc dispersion was recalculated by four methods: (1) with the two extreme QTc intervals excluded; (2) from the six precordial leads; (3) from the three leads most likely to contribute to QTc dispersion (aVF, V1, V4); and (4) from the three quasi-orthogonal leads (aVF, I, V2). For each of the 270 12-lead ECGs examined, a mean of 9.9 leads (SD 1.5 leads) had a QT interval analyzed; the QT interval could not be accurately measured in the remaining leads. Using the standard 12-lead measurement of QTc dispersion, there was a difference in the fall in QTc dispersion from early to late ECG between the groups: 9.1 (SD 60.8) msec for deaths versus 34.4 (55.2) msec for survivors (P = 0.016). This difference in QTc dispersion between early and late ECGs was maintained using either three-lead method (quasi-orthogonal leads: -2.6 [56.2] msec for deaths vs 26.9 [54.3] msec for survivors [P = 0.003]; "likeliest" leads: 8.6 [64.9] msec vs 29.5 [50.2] msec [P = 0.05]), but not when using the other two methods (precordial leads: 19.1 [55.5] msec vs 22 [50.8] msec [P = 0.76]; extreme leads removed: 9.2 [50.1] msec vs 21.8 [42] msec [P = 0.13]). CONCLUSION: QTc dispersion calculated from three leads may be as useful a measurement as QTc dispersion calculated from all leads of a standard ECG. Its advantages over the standard measurement are its simplicity and the lack of problems with lead adjustment.

Case-Control Studies↗

PubMed2004

Utility of a simplified lidocaine and potassium infusion in diagnosing long QT syndrome among patients with borderline QTc interval prolongation.

BACKGROUND: Congenital long QT syndrome (LQTS) is caused by mutations in the cardiac Na+ or K+ channels that result in a prolonged QTc interval and increased QT dispersion. Na+ channel blockers and K+ can reverse the repolarization abnormalities in the Na+ channel variant (LQT3) and K+ channel variant (LQT1, LQT2), respectively. The phenotype of LQTS can be difficult to recognize, especially when the QTc interval is mildly prolonged. Additional noninvasive testing methods are needed to enhance the diagnosis of LQTS. This study compared the response of the QTc interval and QT dispersion to a sequential lidocaine/K+ infusion in LQTS patients with borderline QTc interval prolongation and control patients as a means of diagnosing LQTS. METHODS: In this study, eight LQTS patients with borderline QTc, defined as QTc < 470 ms, and 10 healthy controls received sequential lidocaine/K+ infusion. RESULTS: At baseline, LQTS patients had a longer QTc (446 +/- 29 vs 416 +/- 28 ms, P < 0.05) but similar QT dispersion (43 +/- 14 vs 29 +/- 10 ms) compared to controls. After lidocaine administration, baseline QTc and QT dispersion did not change in either LQTS or controls. One LQTS patient had a 54 ms (12%) reduction in his QTc but no change in QT dispersion. Following K+ infusion, baseline QTc and QT dispersion decreased by 9% (P < 0.005) and 45% (P < 0.005), respectively in LQTS. No effect was seen in control patients, where QTc and QT dispersion shortened by 1% (5 +/- 14 ms) and 20% (6 +/- 7 ms), respectively, compared to baseline. The combined lidocaine/K+ infusion had a sensitivity, specificity, and accuracy of 88%, 100%, and 94%, respectively, in diagnosing LQTS. CONCLUSIONS: A simplified sequential lidocaine/K+ challenge is accurate in diagnosing LQTS among patients with borderline QTc prolongation.

Adult↗

PubMed1999

Long-term treatment with antipsychotic drugs in conventional doses prolonged QTc dispersion, but did not increase ventricular tachyarrhythmias in patients with schizophrenia in the absence of cardiac disease.

OBJECTIVE: The aim of this study was to examine the hypothesis that long-term treatment with antipsychotic drugs in conventional doses prolongs QTc dispersion and increases ventricular tachyarrhythmias in patients with schizophrenia in the absence of cardiac disease. METHODS: We measured QTc and QTc dispersion and ventricular tachyarrhythmias in 64 patients with schizophrenia, including 59 patients who received psychiatric medications, and five patients who did not receive psychiatric medications, and 45 healthy volunteers. None of the subjects had a history of cardiac disease or showed any abnormality in chest radiograph and transthoracic echocardiographic studies. None of the subjects had electrolyte abnormality. None of the subjects were taking drugs known to influence the QT interval, other than psychiatric medications. RESULTS: QTc and QTc dispersion were significantly (P < 0.017) increased in patients who received psychiatric medications compared with patients who did not receive psychiatric medications, or with healthy volunteers [QTc: 0.442 (0.029), 0.418 (0.029), 0.417 (0.028) s, QTc dispersion: 0.054 (0.013), 0.038 (0.017), 0.038 (0.009) s]. Daily ventricular premature beats were 183 (689), 77 (23), and 86 (149), respectively. No ventricular tachycardia was observed. There were no correlation between QTc and QTc dispersion and ventricular premature beats. CONCLUSION: Long-term treatment with antipsychotic drugs in conventional doses prolonged both QTc and QTc dispersion in patients with schizophrenia, but did not increase ventricular tachyarrhythmias in patients with schizophrenia in the absence of cardiac disease. However, despite the negative findings, ventricular tachyarrhythmias may occur as a rare side-effect of antipsychotic drugs, particularly if a patient has additional risk factors.

Adult↗

PubMed2006

QTc interval and survival in 75-year-old men and women from the general population.

AIMS: The study concerns the relationship of the corrected QT (QTc) interval to 6.4 years of survival and to measures of cardiac function, such as echocardiographic variables and plasma levels of brain natriuretic peptide (BNP), in 75-year-old people. METHODS AND RESULTS: QTc was measured in a 12-lead electrocardiogram (ECG) in 210 men and 223 women, comprising a randomly selected sample from the general population (70% participation rate). The Sicard 440/740 computer-analysis program, with Hodges' formula for heart rate-based QT correction, was used. The optimal cut-off point for predicting survival according to the receiver operating characteristic curve was found between 429 and 430 ms. Individuals with a QTc interval of > or =430 ms (n = 115) had decreased survival when compared with those with shorter QTc interval (n = 318); the relative risk was 2.4 (95% confidence interval 1.5-3.7). The predictive ability of QTc reflects an association between QTc and the following variables: BNP, left ventricular mass, and left ventricular ejection fraction (but not diastolic filling patterns). Both Hodges' and Bazett's formulae for heart rate correction of the QT interval were useful for predicting survival. The median QTc was 415 ms using Hodges' formula and 430 ms with Bazett's formula. The QRS component of QTc predicted survival better than the rest of the QTc interval and was approximately as useful as the QTc interval itself. CONCLUSION: The computer-derived QTc obtained from the ordinary 12-lead ECG identifies high-risk individuals among elderly people from the general population.

Aged↗

PubMed2005

Impact of haemodialysis on QTc dispersion in children.

BACKGROUND: The purpose of the present paper was to investigate the corrected QT (QTc) interval and QTc dispersion value, and the impact of haemodialysis on these parameters in children with chronic renal failure. METHODS: Nineteen patients with chronic renal failure receiving haemodialysis were included in the present study. Electrocardiography (ECG), echocardiography and serum biochemistry were performed in all patients. Serum electrolyte levels were measured before and after haemodialysis, at the time of the ECG. Nineteen healthy age- and sex-matched children served as the control group. RESULTS: Patients with chronic renal failure had greater QTc interval and QTc dispersion compared to control subjects. The patients' sex, age and presence of hypertension or left ventricular hypertrophy (LVH) were not related to QTc interval/dispersion. However, the patients with left ventricular (LV) systolic dysfunction had significantly greater QTc dispersion value. After haemodialysis session, both QTc interval and QTc dispersion values significantly increased. Serum potassium levels significantly decreased, whereas the calcium level significantly increased after the haemodialysis session. The changes in electrolyte values were not associated with the changes in both QTc interval and QTc dispersion. CONCLUSION: Children receiving haemodialysis may be at greater risk of ventricular arrhythmia and sudden death because QTc dispersion reflects heterogeneous recovery of ventricular excitability.

Adolescent↗

PubMed2003

Prolonged QTc interval and high B-type natriuretic peptide levels together predict mortality in patients with advanced heart failure.

BACKGROUND: The role of QTc interval prolongation in heart failure remains poorly defined. To better understand it, we analyzed the QTc interval duration in patients with heart failure with high B-type natriuretic peptide (BNP) levels and analyzed the combined prognostic impact of prolonged QTc and elevated BNP. METHODS AND RESULTS: QTc intervals were measured in 241 patients with heart failure who had BNP levels >400 pg/mL. QT interval duration was determined by averaging 3 consecutive beats through leads II and V4 on a standard 12-lead ECG and corrected by using the Bazett formula. QTc intervals were prolonged (>440 ms) in 122 (51%) patients and normal in 119 (49%). The BNP levels in these 2 groups were not significantly different (786+/-321 pg/mL in the prolonged QTc group versus 733+/-274 pg/mL in the normal QTc group, P=0.13). During 6 months of follow-up, 46 patients died, 9 underwent transplantation, and 17 underwent left ventricular assist device implantation. The deaths were attributed to pump failure (n=24, 52%), sudden cardiac death (n=18, 39%), or noncardiac causes (n=4, 9%). Kaplan-Meier survival rates were 3 times higher in the normal QTc group than in the prolonged QTc group (P<0.0001). On multivariate analysis, prolonged QTc interval was an independent predictor of all-cause death (P=0.0001), cardiac death (P=0.0001), sudden cardiac death (P=0.004), and pump failure death (P=0.0006). CONCLUSIONS: Prolonged QTc interval is a strong, independent predictor of adverse outcome in patients with heart failure with BNP levels >400 pg/mL.

Aged↗

PubMed2001

QTc dispersion measurement for risk of syncope in patients with aortic stenosis.

The purposes of this study are to evaluate the clinical usefulness of maximum QTc and QTc dispersion determination in aortic stenosis, and to compare the effects of maximum QTc and QTc dispersion on the risk of syncope in aortic stenosis. The QT interval dispersion has long been known to be a marker of dispersion of ventricular repolarization and, hence, electrical instability. Additionally, it has been shown that these patients have a propensity to ventricular tachyarrhythmic syncope. The study included 86 patients with aortic stenosis who underwent left-heart catheterization and coronary angiography during investigation of syncope and 30 healthy subjects. The patients were characterized with regard to the presence or absence of a history of syncope and the severity of aortic stenosis (the degree of peak transvalvular gradient). In addition, QT max and QT dispersion measurements were corrected for heart rate according to Bazett's formula. The QTc max and QTc dispersion were greater in patients with aortic stenosis than in the healthy subjects (477 +/- 49 ms vs 370 +/- 22 ms, p < 0.001; 60 +/- 13 ms vs 38 +/- 1 ms, p < 0.001). Similarly, the QTc max and QTc dispersion were greater in the patients with a history of syncope than in the patients with no history of syncope (493 +/- 48 ms vs 459 +/- 4 ms, p < 0.001; 68 +/- 12 ms vs 53 +/- 10 ms, p < 0.001). In addition, both parameters were greater in the patients with a high transvalvular gradient than in the patients with a low transvalvular gradient (489 +/- 49 ms vs 451 +/- 39 ms, p < 0.001; 65 +/- 12 ms vs 50 +/- 9 ms, p < 0.001). Multivariate logistic regression analysis showed that only a increased QTc dispersion had significant value for the risk of syncope in aortic stenosis. An increased QTc dispersion caused a 10.4% increase in the occurrence of syncope in aortic stenosis. These results suggest that high values of QTc dispersion are sensitive noninvasive markers to determine the risk for syncope in aortic stenosis.

Adult↗

PubMed2002

Antipsychotic-related QTc prolongation, torsade de pointes and sudden death.

Sudden unexpected deaths have been reported with antipsychotic use since the early 1960s. In some cases the antipsychotic may be unrelated to death, but in others it appears to be a causal factor. Antipsychotics can cause sudden death by several mechanisms, but particular interest has centred on torsade de pointes (TdP), a polymorphic ventricular arrhythmia that can progress to ventricular fibrillation and sudden death. The QTc interval is a heart rate-corrected value that represents the time between the onset of electrical depolarisation of the ventricles and the end of repolarisation. Prolongation of the QTc interval is a surrogate marker for the ability of a drug to cause TdP. In individual patients an absolute QTc interval of >500 msec or an increase of 60 msec from baseline is regarded as indicating an increased risk of TdP. However, TdP can occur with lower QTc values or changes. Concern about a relationship between QTc prolongation, TdP and sudden death applies to a wide range of drugs and has led to the withdrawal or restricted labelling of several. Among antipsychotics available in the UK, sertindole was voluntarily suspended, droperidol was withdrawn, and restricted labelling introduced for thioridazine and pimozide. The degree of QTc prolongation is dose dependent and varies between antipsychotics reflecting their different capacity to block cardiac ion channels. Significant prolongation is not a class effect. Among currently available agents, thioridazine and ziprasidone are associated with the greatest QTc prolongation. Virtually all drugs known to cause TdP block the rapidly activating component of the delayed rectifier potassium current (I(kr)). Arrhythmias are more likely to occur if drug-induced QTc prolongation coexists with other risk factors, such as individual susceptibility, presence of congenital long QT syndromes, heart failure, bradycardia, electrolyte imbalance, overdose of a QTc prolonging drug, female sex, restraint, old age, hepatic or renal impairment, and slow metaboliser status. Pharmacodynamic and pharmacokinetic interactions can also increase the risk of arrhythmias. Further research is needed to quantify the risk of sudden death with antipsychotics. The risk should be viewed in the context of the overall risks and benefits of antipsychotic treatment. It seems prudent, where possible, to select antipsychotics that are not associated with marked QTc prolongation. If use of a QTc-prolonging drug is warranted, then measures to reduce the risk should be adopted.

Antipsychotic Agents↗

PubMed2001

Analysis of the QTc interval during olanzapine treatment of patients with schizophrenia and related psychosis.

BACKGROUND: There may be a temporal association between some antipsychotics and prolongation of the heart-rate-corrected QT interval (QTc) representing a delay in ventricular repolarization. QTc prolongation significantly exceeding normal intra-individual and interindividual variation may increase the risk of ventricular tachydysrhythmias, especially torsade de pointes, and therefore, sudden cardiac death. METHOD: Electrocardiogram recordings obtained as part of the safety assessment of olanzapine in 4 controlled, randomized clinical trials (N = 2,700) were analyzed. These analyses were conducted to characterize any change in QTc temporally associated with olanzapine, compared with placebo, haloperidol, and risperidone, in acutely psychotic patients (DSM-III-R and DSM-IV) and to characterize variability and temporal course of the QTc in this patient population. Changes from baseline to minimum and maximum QTc were tested for significance, and baseline to acute-phase endpoint change in mean QTc was tested for significance within treatments and for differences between olanzapine and comparators. The possibility of a linear relationship between dose of olanzapine and mean change in QTc, as well as incidence of treatment-emergent prolongation of QTc (change from < 430 msec at baseline to > or =430 msec at endpoint), was tested. RESULTS: The incidence of maximum QTc > or = 450 msec during treatment was approximately equal to the incidence of QTc > or =450 msec at baseline. CONCLUSION: Results of these analyses suggest that olanzapine, as therapeutically administered to patients with schizophrenia and related psychoses, does not contribute to QTc prolongation resulting in potentially fatal ventricular arrhythmias.

Acute Disease↗

PubMed2002

QTc interval in children with chronic renal failure and with renal transplants.

Prolongation of the QTc interval, a risk factor for cardiac arrhythmias, has been observed in adult hemodialysis patients; there are few data on the QTc interval in children with chronic renal failure (CRF) and following renal transplantation (Tx). The purpose of our study was to determine the QTc interval in children with CRF and post renal Tx. Twenty children with CRF and 16 children with renal Tx who were followed at the University of California, Davis, underwent prospective EKG monitoring. The mean QTc interval in the CRF and post-Tx cohorts was normal at 407.9 ms and 408.2 ms, respectively. None of the children with CRF had QTc prolongation. Two Tx recipients had QTc prolongation; both had cardiac dilatation on echocardiography (ECHO). There was no correlation between the QTc interval and the creatinine clearance in either group. However, a significant correlation was noted between QTc prolongation and cardiac dilatation on ECHO in the Tx group (P=0.02, Fisher's exact test). In conclusion, QTc prolongation is uncommon in children with CRF and following Tx, in the absence of cardiac dilatation. However, caution is still needed before prescribing medications known to cause QTc prolongation.

Adolescent↗

PubMed1986

Transient prolongation of the QTc interval after balloon valvuloplasty and angioplasty in children.

QTc-interval changes were evaluated in 39 children who had undergone balloon dilation procedures. In 30 children who had undergone balloon pulmonary valvuloplasty (BPV), QTc intervals were measured on standard electrocardiograms recorded before and 16 to 24 hours after the procedure and at follow-up during the next 1 to 15 months (mean 7). The QTc interval increased from 0.380 +/- 0.027 second before BPV to 0.429 +/- 0.027 second after BPV (p less than 0.002) and returned to 0.377 +/- 0.026 second at follow-up. To determine when during the catheterization-dilation procedure the QTc interval increased, QTc intervals were measured on monitor electrocardiograms recorded during cardiac catheterization. The baseline QTc was 0.382 +/- 0.041 second, was unchanged after angiography and increased to 0.427 +/- 0.043 second after BPV (p less than 0.002). A similar prolongation occurred in 3 of 4 children who had undergone balloon aortic valvuloplasty and in 4 of 5 who had undergone coarctation angioplasty. In control children, who had undergone catheterization without dilation, QTc was unchanged. Thus, transient increases in QTc interval occur after semilunar valvuloplasty and coarctation angioplasty. These dilation procedures are a cause of QTc prolongation; however, the mechanism is unknown. It is possible that the sudden unilateral increase in afterload affects the myocardium or myocardial sympathetic receptors. Because QTc prolongation may predispose children to the R-on-T phenomenon, postprocedure monitoring appears to be warranted.

Adolescent↗

PubMedDate not supplied

QTc interval and scintigraphically assessed myocardial perfusion in newly diagnosed and long-term type 1 diabetes mellitus.

In diabetes mellitus, heart rate corrected QT interval (QTc) has been suggested to be related to ischemic heart disease and increased risk of sudden cardiac death. The aim of the study was to analyze the length of QTc interval with regard to global and regional myocardial perfusion in type 1 diabetic patients. Myocardial perfusion was investigated in 20 newly diagnosed and 40 long-term type 1 diabetic patients without clinical evidence for coronary artery disease by means of Tc-99-methoxyisobutylisonitrile (Tc-99m-MIBI)-scintigraphy (myocardial uptake (MU) score: 1-6). Five consecutive RR and QT intervals of resting electrocardiogram (ECG) tracing were measured and corrected for the previous cycle length. ECG-based cardiac autonomic neuropathy (CAN) was assessed with five cardiac reflex tests. Length of QTc interval was 423+/-29 ms in newly diagnosed and 433+/-26 ms in long-term type 1 diabetic patients. Nine (45%) newly diagnosed and 18 (45%) long-term diabetic patients demonstrated a prolonged QTc interval (>440 ms). Both newly diagnosed and long-term diabetic patients did not display significant global or regional myocardial perfusion defects (mean MU scores<3). In newly diagnosed diabetic patients, the length of QTc interval was related to global, posterior and septal Tc-99m-MIBI uptake (p<0.05, respectively). In long-term diabetic patients, the length of QTc interval was associated with apical Tc-99m-MIBI uptake (p<0.05). Two (10%) newly diagnosed and 19 (48%) long-term type 1 diabetic patients demonstrated ECG-based CAN. In long-term type 1 diabetic patients, global myocardial Tc-99m-MIBI uptake did not differ significantly between patients with and without CAN. QTc interval was not significantly different between diabetic patients with and without ECG-based CAN (433+/-19 ms vs. 428+/-17 ms). Long-term diabetic patients, of whom 10 (25%) patients had microalbuminuria and seven (18%) patients had macroalbuminuria, demonstrated an association between QTc interval and albuminuria (p<0.05). The results somewhat suggest an association between QTc interval and vascular factors in type 1 diabetes mellitus. Future investigations are required to analyze the role of QTc interval in the pathogenesis of abnormalities of myocardial perfusion.

Adult↗

PubMed2002

QTc interval in the assessment of cardiac risk.

In the United States alone 300,000-400,000 people die of sudden cardiac death every year. Much of this mortality is assumed to be caused by ventricular tachyarrhythmias. Prolonged QTc reflect cardiac repolarization prolongation and/or increased repolarization inhomogenity known to be associated with increased risk of arrhythmias. The paper gives a review of the possibilities to assess the risk of ventricular arrhythmia and/or cardiac death from QTc. Prolonged QTc may hold independent prognostic importance for mortality in common diseases as ischemic heart disease and diabetes mellitus where as the prognostic importance in heart failure and arterial hypertension is more uncertain. In more rare diseases as the inborn long QT syndrome the QT interval gives not only important hint to the diagnosis but the magnitude also provides information on prognosis. QTc has probably no independent prognostic importance in hypertrophic cardiomyopathy or in the arrhythmogenic right ventricular disease. The degree of QTc prolonging during treatment with QTc prolonging drugs is prognostic for the risk of ventricular arrhythmia in form of torsade de pointes and QTc prolonging drugs should probably not be prescribed for patients with a QTc greater than 460 ms and withdrawn if QTc exceeds 500 ms during treatment. Data from the DIAMOND study suggest that QTc can be used to point out those heart failure patients who will benefit from antiarrhythmic therapy.

Cardiovascular Diseases↗

PubMed1999

QTc dispersion and complex ventricular arrhythmias in untreated newly presenting hypertensive patients.

Increased dispersion of ventricular repolarisation (increased QT dispersion) is believed to predispose to arrhythmias associated with sudden death in certain cardiac diseases. Hypertension is also associated with increased risk of sudden death, particularly in those with left ventricular hypertrophy (LVH). Therefore, the first aim of this study is to look into the possible pathogenic role of QT dispersion on the ventricular arrhythmias occurring in a group of never-treated hypertensive patients. The second aim is to look at other possible determinants of QT dispersion (ie, level of blood pressure, hypokalaemia, electrocardiographic LVH and presence or absence of strain pattern) in hypertensive patients, and their relevance to complex ventricular arrhythmias. QTc (corrected QT) was measured in 70 newly presenting (never-treated) hypertensive patients (47 male, 23 female, mean age 51.9 +/- 12.5 years) from a standard 12-lead surface electrocardiogram (ECG). Blood pressure measurements and 24-h ECG holter recordings were performed in all patients. Serum potassium level was measured in 51 of the patients. Ventricular arrhythmias were classified using a modified Lown's scoring system. Maximum QTc, minimum QTc and QTc dispersion for all patients were 442 +/- 30.3 ms, 380 +/- 26.7 ms and 61.5 +/- 21.6 ms respectively. High grade ventricular arrhythmias (Lown's score >/=3) were found in 43% of the patients. The QTc dispersion was strongly correlated with the Lown's classification of arrhythmia and the age of the patients. Patients with more severe ectopy (Lown's score >/=3) were significantly older (57.4 +/- 10.3 years) compared to those with score </=2 (48.3 +/- 12.6 years) (P = 0.0067) and had a significantly greater QTc dispersion (69.9 +/- 22.5 ms vs55.2 +/- 18. 8 ms; P = 0.002). Presence of electrocardiographic strain did not affect the severity of arrhythmia, as 29% of the patients with LVH and strain had grade >/=3 Lown's score compared to 39% in the group with LVH but without strain. In the presence of relative hypokalaemia, hypertensive patients with LVH showed more QTc dispersion (85.7 +/- 15.5 ms) and a greater tendency for complex ventricular arrhythmias (100% grade >/=3 Lown's score) compared to those with LVH and normal serum potassium levels (64.1 +/- 22.6 ms and 35%, QTc dispersion and Lown's score >/=3, respectively P = 0. 05). The level of blood pressure had no effect on either the QTc dispersion or the prevalence of complex ventricular arrhythmias. Prevalence of complex ventricular arrhythmias in hypertensive patients is strongly correlated with QTc dispersion and age. When hypertensive patients with LVH have low potassium levels the risk of developing complex ventricular arrhythmias is significantly increased.

Aging↗

PubMed2002

QTc interval in infants receiving cisapride.

OBJECTIVE: To examine the effect of cisapride on the corrected QT (QTc) interval in infants over a 14-day period. STUDY DESIGN: A prospective cohort study of infants receiving cisapride (0.8 mg/kg per day). Twelve-lead electrocardiograms were obtained before and 3, 5, 7, and 14 days after cisapride initiation. RESULTS: Fifty infants completed the study; none had arrhythmias. Fifteen of 50 infants (30%) developed QTc interval > or =450 msec; QTc interval normalized in 13 of 15 infants. Infants with QTc interval on day 3 > or =2 standard deviations above the mean baseline QTc interval (401+40 msec) were more likely to develop prolonged QTc interval (p<0.0001). CONCLUSION: QTc interval prolongation was noted in 30% of infants. Subsequently, the majority of those infants had QTc interval normalization by day 14 of cisapride therapy. QTc interval 3 days following cisapride initiation may identify infants at risk for transient QTc interval prolongation. With appropriate monitoring, hospitalized infants receiving cisapride may have improved gastrointestinal motility without cardiac morbidity.

Analysis of Variance↗

PubMed2000

QTc interval length and QT dispersion as predictors of mortality in patients with non-insulin-dependent diabetes.

Patients with non-insulin-dependent diabetes (NIDDM) are at independent risk of cardiovascular death. The reason is only partially understood. The aim of our study was therefore to evaluate the impact of corrected QT interval length (QTc) and QT dispersion (QT-disp) on mortality in a cohort of 324 Caucasian NIDDM patients. A resting 12-lead ECG was recorded at baseline. Maximum (QT-max) and minimum QT (QT-min) intervals were measured, and QT-max was corrected for heart rate (QTc-max). QT-disp was defined as the difference between QT-max and QT-min. QTc-max was 454 (376-671) ms(1/2) (median (range)) and QT-disp 61 (0-240) ms. Prolonged QTc interval (PQTc), defined as QTc-max > 440 ms(1/2), was present in 67% of the patients and prolonged QT-disp (PQT-disp), defined as QT-disp > 50 ms, was present in 51%. During the 9-year follow-up period, 100 patients died (52 from cardiovascular diseases). Thirty-seven percent of the patients with PQTc died compared with 17% with normal QTc interval (p<0.001). The Cox proportional hazard model, including putative risk factors at baseline, revealed the following independent predictors of all cause mortality; QTc-max (p<0.05), age (p<0.0001), albuminuria (p<0.01), retinopathy (p<0.01), HbA1c (p<0.05), insulin treatment (p<0.01), total cholesterol (p<0.01), serum creatinine (p<0.05) and presence of cardiac heart disease based on Minnesota coded ECG (p<0.001). Whereas QT-disp was not a predictor, QTc-max interval was an independent predictor of cardiovascular mortality. Our study showed a high prevalence of QTc and QT-disp abnormalities and indicated that QTc-max but not QT-disp is an independent predictor of all cause and cardiovascular mortality in NIDDM patients.

Albuminuria↗