QT Interval Dispersion In Patients Research Articles

CHARACTERISTICS OF HEART RHYTHM DISORDERS ACCORDING TO THE DATA OF HOLTER ECG MONITORING IN PATIENTS WITH HEART FAILURE AND ATRIAL FIBRILLATION

Chronic heart failure (CHF) is one of the most significant medical, economic and social problems of the 21st century and remains the main cause of morbidity and mortality worldwide.The purpose. To study the indicators of Holter ECG monitoring, the dynamics of ischemic changes, heart rate, indicators of heart rhythm variability and blood pressure in patients with heart failure and atrial fibrillation.Material and methods. 150 patients aged 45-65 were examined. All patients were divided into groups: Group I – patients with HF with sinus rhythm or atrial fibrillation (AF) (permanent or persistent form), (n=75). Group II – patients without HF with AF, (n=75). Group III – control group: 36 practically healthy people. All patients underwent a clinical examination, ECG, echocardiography (ECHOKG), Holter ECG monitoring (HM ECG) and daily BP monitoring (DMAT).Research results. The analysis of the ECG of the examined patients indicates the presence of heart rhythm disorders, which is an important risk factor and progression of CHF. The results of XM ECG indicate the presence of ventricular arrhythmias of various gradations along with AF. There was a probable difference in the direction of an increase in the number of ventricular extrasystoles (VAS), both single and, most importantly, extrasystoles of high gradations, in patients with CHF and AF compared with healthy subjects. In addition, the number of SHEs in patients with CHF and AF was likely lower than in patients with CHF with sinus rhythm. Indicators of maximum heart rate, ST segment depression and QT interval dispersion in patients with CHF and AF were significantly higher (p<0.05) than similar parameters in patients without CHF with AF.Conclusions: Ventricular heart rhythm disturbances were detected in the examined patients, which is a predictor of an unfavorable prognosis in patients with chronic heart failure. There was a probable difference in the direction of increased levels of maximum heart rate, maximum depression, ST segment elevation, dispersion of the QT interval, QTc, an increase in the total duration of episodes of myocardial ischemia, in patients with chronic heart failure and atrial fibrillation in comparison with healthy subjects.

QT interval dispersion in patients with Q‑wave myocardial infarction

QT interval dispersion in patients with Q‑wave myocardial infarction

Decreased risk of ventricular arrhythmias with treatment of nebivolol in patients with coronary slow flow

Coronary slow-flow (CSF) is an angiographic phenomenon characterised by delayed opacification of vessels in the absence of any evidence of obstructive epicardial coronary disease. QT interval dispersion (QTD) reflects regional variations in ventricular repolarisation and cardiac electrical instability and has been reported to be longer in patients with CSF. To examine QT duration and dispersion in patients with CSF and the effects of nebivolol on these parameters. The study population included 67 patients with angiographically proven normal coronary arteries and CSF, and 38 patients with angiographically proven normal coronary arteries without associated CSF. The patients were evaluated with 12-lead electrocardiography, and echocardiography before and three months after treatment with nebivolol. Compared to the control group QTcmax and QTcD were significantly longer in patients with CSF (p = 0.036, p = 0.019, respectively). QTcD significantly correlated with the presence of CSF (r = 0.496, p < 0.001). QTcmax (p = 0.027), QTcD (p = 0.002), blood pressure (p = 0.001), and heart rate (p < 0.001) values significantly decreased after treatment with nebivolol. Coronary slow flow is associated with increased QTD. Nebivolol reduced increased QTD in patients with CSF after three months.

Coronary Revascularization Improves QT Dispersion in Patients with Chronic Coronary Artery Total Occlusion.

As an important parameter of cardiac functions, QT interval is usually irregular in patients with chronic coronary artery total occlusion (CTO). We sought to determine the effect of coronary revascularization (CRV) on QT interval dispersion in patients with CTO. To this end, we used electrocardiogram of 12 leads to record changes in the QT interval dispersion in 22 patients with CTO treated with percutaneous coronary intervention (PCI) and 24 patients treated with coronary artery bypass grafting (CABG). Our data showed that QTd and QTcd diminished markedly (P < 0.01) after PCI or CABG. No significant difference was observed between the postoperative groups (P > 0.05) or between PCI and CABG groups. We concluded that CRV could diminish QTd and QTcd in patients with CTO with no distinguishable differences with PCI and CABG procedures. Therefore, CRV can revitalize the existing functional myocardium and resume the myocardial electrophysiological functions in patients with CTO.

Taurine effects on the occurrence of cardiac arrhythmias and QT interval dispersion in patients with postinfarction cardiosclerosis and chronic heart failure: a comparative randomised study

Aim. To study the effects of taurine therapy on the occurrence of cardiac arrhythmias and QT interval dispersion (dQT) among patients with postinfarction cardiosclerosis (PICS) and subsequent chronic heart failure (CHF). Material and methods. The study included 40 patients with previous myocardial infarction (MI), left ventricular ejection fraction (LVEF) &lt;45 %, and Functional Class (FC) II-III CHF (NYHA). The participants were randomised into two groups: the main group (MG) included 20 patients receiving standard CHF treatment and taurine, while the control group (CG; n=20) was administered standard CHF treatment only. Both groups were comparable by the main clinical and anamnestic parameters. The therapy phase lasted 3 months. The analysis of taurine effects on the occurrence of cardiac arrhythmias and dQT was performed in the subgroups defined according to the CHF FC. dQT was assessed by 12-lead electrocardiography (ECG), while the arrhythmia occurrence was assessed by Holter ECG monitoring. The examined parameters were measured at baseline and after 3 months of the therapy. Results. In PICS patients with CHF, taurine demonstrated beneficial effects on the dynamics of dQT and cardiac arrhythmia occurrence. Conclusion. Taurine could be included in the complex treatment of PICS patients with FC II-III CHF.

Effect of Transient Myocardial Ischemia on QT Interval Dispersion Among Patients with Unstable Angina

Objective : Our aim was to examine the effect of transient myocardial ischemia on QT interval and QT interval dispersion in patients presenting with unstable angina. Methods : We studied 31 patients (mean age 64±10, 22 men, 16 with an old myocardial infarction, 6 with previous coronary bypass surgery) admitted with unstable angina manifestations. Patients with a history of complex ventricular ectopy, malignant ventricular arrhythmias, advanced congestive heart failure or antiarrhythmic drug therapy were excluded. The uncorrected and corrected QT interval and QT dispersion were measured during angina as well as after the relief of pain. Results: The RR intervals were not significantly changed by the ischemic event (879±121 ms at rest to 877±173 ms during angina). However, both the uncorrected and corrected QT intervals were significantly increased during angina (from 410±45 ms and 440±41 ms at rest to 425±53 ms and 460±42 ms during angina respectively, p<0.05 for both). Similarly, both the uncorrected (QTd) and the corrected (QTcd) QT dispersion values were significantly prolonged during ischemia (QTd: 58±23 ms at rest to 83±33 ms during ischemia, p<0.001, QTcd: 63±26 ms at rest to 95±36 ms during ischemia, p<0.001). The observed increment in the QTd and QTcd provoked by ischemia was not different among the unstable angina patients with and without old myocardial infarction. Conclusion: Transient myocardial ischemia besides an increase in the QT and QTc intervals provokes an increase in both the corrected and uncorrected QT interval dispersion. Under certain circumstances, this may contribute to the genesis of serious reentry ventricular arrhythmias.

Effect of primary percutaneous coronary intervention on myocardial repolarization

We aimed to investigate the effect of coronary perfusion on QT interval dispersion in patients with acute myocardial infarction (MI). Seventy-seven consecutive patients who had undergone primary percutaneous coronary intervention (PCI) for a first ST segment elevation MI during the first 12 h of symptom onset were included in the study. After achievement of thrombolysis in MI (TIMI) 3 flow of the infarct-related artery, corrected TIMI frame count (cTFC) and TIMI myocardial perfusion grade (TMPG) were measured. ECGs were performed in the following manner: at baseline, within 1 h after completion of the procedure, 24 h after the procedure and 48 h after the procedure. The corrected QT dispersion (QTd) and ST segment resolution (STR) were calculated. There was a difference between the durations of corrected QTd (cQTd) before PCI and cQTd just after PCI. On the first day, cQTd before PCI was significantly more prolonged (52.3 ± 80 vs. 41.5 ± 49, P = 0.05) than cQTd on second day (52.3 ± 80 vs. 37 ± 50, P = 0.001). In the correlation analysis conducted among the durations of cQTd, cTFC and TMPG, no significant association was established. STR was, however, inversely correlated with duration of cQTd. Our study results demonstrated that primary percutaneous coronary intervention leads to progressive shortening of QT dispersion in successful reperfusion, even in reduced cTFC.

QT dispersion in patients with rheumatic mitral stenosis and its relation with echocardiographic findings and serum NT-proBNP levels

We evaluated the value of QT interval dispersion in patients with rheumatic mitral stenosis (MS) in association with echocardiographic parameters and serum N-terminal pro brain natriuretic peptide (NT-proBNP) levels. The study consisted of 46 patients (39 women, 7 men; mean age 46.9±9.7 years) with moderate-to-severe rheumatic MS. All patients underwent echocardiographic examination. Blood samples for NT-proBNP were collected immediately after ECG recording. QT interval and QRS complex were measured manually on standard 12-lead surface ECGs. Electrocardiographic and echocardiographic findings and serum NT-proBNP levels were compared with those of a control group consisting of 30 healthy subjects (26 women, 4 men; mean age 46.1±7.3 years). Compared to controls, serum NT-proBNP levels were significantly higher in MS patients (284.6±206.5 vs. 70.2±9.3 pg/ml, p<0.001). The mean QT interval, QTc interval, and QT dispersion were significantly prolonged in MS patients compared to controls (378±25 vs. 349±21, 420±22 vs. 401±19, and 61±21 vs. 38±15 msec, respectively; p<0.005). QT and QTc dispersions were negatively correlated with mitral valve area (QT: r=-0.311, p=0.03; QTc: r=-0.327, p=0.02), and positively correlated with serum NT-proBNP level (QT: r=0.583, p<0.001; QTc: r=0.637, p<0.001). QTc dispersion was also an independent predictor of serum NT-proBNP level in regression analysis (β=0.330, p=0.03). Our results indicate that QT dispersion is related to the echocardiographic degree of rheumatic mitral valve disease and serum NT-proBNP levels in rheumatic MS. Being a noninvasive, easy, and inexpensive method, QT dispersion may be used as a complementary tool to the clinical and echocardiographic evaluation of patients with rheumatic MS.

Flow mediated dilatation and QT interval dispersion in patients with coronary artery disease with or without myocardial infarction

Objectives: To evaluate the changes in flow mediated dilatation (FMD) and QT interval dispersion (QTd) in stable coronary artery disease (CAD) patients with or without myocardial infarction (MI). Results: 152 patients participated in the study 64 patients with MI. MI patients showed a significantly lower FMD (3.58 ± 4.45 versus 5.16 ± 4.80, p = 0.040) and higher QTd (62 ± 36 versus 56 ± 32, p = 0.036 for QTd1; 19.45 ± 11 versus 16.25 ± 10, p = 0.021 for QTd2) compared to no-MI patients. There wasn't a significant difference in FMD and QTd according to coronary artery occlusion within MI patients. In the group of no-MI patients, those with coronary occlusion showed significantly lower FMD than patients without occlusion, whereas QTd values didn't differ significantly according to the occlusion status. Conclusion: MI patients have significantly lower FMD and higher QTd compared to no-MI patients. Low FMD in no-MI patients may be an index of chronic coronary occlusion.

QT interval dispersion in patients with chronic heart failure secondary to Chagas' cardiomyopathy: correlation with clinical variables of prognostic significance

Background QTc interval dispersion has rarely been studied in patients with chronic heart failure (CHF) secondary to Chagas' cardiomyopathy. One study has demonstrated an association between QT interval dispersion and sudden cardiac death. No data exist regarding the association of clinical variables and QT interval dispersion in patients with this condition. Methods Sixty three patients with CHF due to Chagas' cardiomyopathy, 34 Chagas' disease patients with no systolic dysfunction on echocardiography, and 36 individuals with no previous cardiac history, matched by sex and a 10-year age interval, were included in the investigation. The QTc interval dispersion was defined as the difference between maximum and minimum QTc. Results The mean QTc interval dispersion was 74±30.3 ms in surviving and 87±30.6 ms in nonsurviving patients ( P=.13). Mean QTc dispersion was 95.20±28.46 ms in patients who died from pump failure, 73.33±29.61 ms in patients who died suddenly, and 74.46±30.27 in survivors ( P=.07). Mean QTc dispersion value was higher in patients in the Class III or IV ( P=.01).). Mean QTc interval dispersion was 67.2±22.7 ms in patients with and 85.5±33.5 ms in patients without premature ventricular contractions ( P=.01), and 67.5±29.8 ms in patients with and 84.7±31.8 ms in patients without left ventricular apical aneurysm ( P=.03). A correlation could be observed in QTc interval dispersion and left atrium dimension ( r=.32; P=.009) Thus, QTc interval dispersion is associated to some prognostic indicators in patients with CHF secondary to Chagas' cardiomyopathy.

Effect of epirubicin-based chemotherapy and dexrazoxane supplementation on QT dispersion in non-Hodgkin lymphoma patients

Background and objective. – Aim of the present study was to assess the effect of epirubicin-based chemotherapy on QT interval dispersion in patients with aggressive non-Hodgkin lymphoma (NHL), and the effect of dexrazoxane supplementation. Prolongation of QT dispersion may not only represent a sensitive tool in identifying the first sign of anthracycline-induced cardiotoxicity, but it may serve also in identifying patients who are at risk of arrhythmic events. Methods. – Twenty untreated patients, ≤60 years of age with newly-diagnosed aggressive NHL, eligible for a treatment with epirubicin-based chemotherapy were selected for the study. The patients were randomly allocated in two subgroups ( N = 10) to receive or not dexrazoxane hydrochloride (400 mg/m 2) after epirubicin infusion. The patients underwent 12-lead electrocardiogram (ECG) before and after epirubicin infusion and after dexrazoxane supplementation. QT dispersion was defined as the difference between the maximum and the minimum QT interval occurring in any of the 12 ECG leads, corrected (QTc) for heart rate. Results. – All the 20 patients showed increased QT dispersion (44.3 ± 8.4 vs. 68.4 ± 11.4 ms, P < 0.001) and QTc dispersion (46.2 ± 6.2 vs. 72.2 ± 8.4, P < 0.001) after chemotherapy infusion. The 10 patients who underwent supplementation with dexrazoxane exhibited a significant reduction of QT dispersion (67.4 ± 8.1 vs. 49.5 ± 4.2 ms, P < 0.001) and QTc dispersion (71.2 ± .7 vs. 51.4 ± 4.3 ms, P < 0.001), while the 10 patients not supplemented with dexrazoxane did not (QT dispersion: 69.3 ± 7.6 vs. 64.2 ± 6.9 ms; QTc dispersion: 72.8 ± 8.1 vs. 67.3 ± 7.2 ms, ns). Conclusions. – Epirubicin-based chemotherapy causes an early increase of the QT and QTc dispersion, which is attenuated by dexrazoxane supplementation. Therefore, dexrazoxane can reduce the arrhythmic risk in patients treated with epirubicin.

QT Interval Dispersion in Patients with Heart Failure and Preserved Left Ventricle Systolic Function

QT Interval Dispersion in Patients with Heart Failure and Preserved Left Ventricle Systolic Function

A11-1 Prognostic value of corrected QT-interval dispersion in patients with acute coronary syndromes without st-segment elevation

A11-1 Prognostic value of corrected QT-interval dispersion in patients with acute coronary syndromes without st-segment elevation

A11-11 Prognostic value of corrected qt-interval dispersion in patients with acute coronary syndromes without st-segment elevation

A11-11 Prognostic value of corrected qt-interval dispersion in patients with acute coronary syndromes without st-segment elevation

Impact of carvedilol on QT interval dispersion in patients with chronic heart failure

Background: The role of QT interval dispersion (QTD) in heart failure (HF) remains poorly defined and controversial. Our objective was to evaluate the impact of QTD in the clinical evolution of chronic HF patients under control due to the use of carvedilol (CVD). Methods: We selected 108 patients (22-82 years), 65.7% were male, 72.2% caucasians, with stable chronic HF and NYHA functional class (FC) II, III and IV on optimized treatment, with an left ventricle ejection fraction (LVEF) of ≤0.40 for therapy with CVD.

Relation Between QT Dispersion and the Extent of Myocardial Ischemia in Patients With Three-Vessel Coronary Artery Disease

The aim of the study was to examine the relation between the extent of myocardial ischemia and changes in QT interval dispersion in patients with obstructive coronary artery disease and in patients with normal coronary arteries. QT interval dispersion reflects regional variations in ventricular repolarization and cardiac electrical instability. Previous studies showed QT interval dispersion changes during episodes of myocardial ischemia in patients with coronary artery disease, but no data on the relation between extent of myocardial ischemia and degree of QT interval dispersion changes are available. To assess the effects of myocardial ischemia on myocardial repolarization by analyzing the change in QT dispersion during incremental atrial pacing, we studied 33 patients (7 women and 26 men, mean age 60.1 ± 5.1 years, 18 patients with normal coronary arteries, 15 patients with coronary 3-vessel disease). QT dispersion was measured at baseline, after each pacing period, within 30 seconds after cessation of pacing (“peak ischemic stress”), and at 1-minute intervals for up to 5 minutes. Paired blood samples for determination of serum lactate were withdrawn from the coronary sinus and radial artery to determine the cardiac lactate extraction ratio at each point of electrocardiographic registration. In patients with coronary artery disease, QT dispersion increased from a baseline value of 39 ± 7 ms to a peak ischemic stress value of 63 ± 10 ms (p <0.0001). Patients with normal coronary arteries showed almost unchanged values of QT dispersion (41 ± 9 vs 42 ± 7 ms). There was a significant relation between the pacing-induced change in QT dispersion and the induced change in myocardial lactate extraction ratio (r = 0.76, p <0.0001). The change in QT dispersion (baseline vs peak pacing stress) was related to the extent of the cardiac lactate extraction ratio (r = −0.79, p <0.0001). These data indicate that the severity or extent of induced myocardial ischemia was related to the degree of induced changes of the variability in the timing of the ventricular recovery pattern.

Antiarrhythmic Drug Effects on QT Interval Dispersion in Patients Undergoing Electropharmacologic Testing for Ventricular Tachycardia and Fibrillation

The effects of antiarrhythmic drugs on QT interval dispersion as a predictor of antiarrhythmic drug therapy has not been rigorously assessed. This study was performed to determine whether the effects of antiarrhythmic drugs on QT interval dispersion predict antiarrhythmic drug response in patients undergoing electropharmacologic testing for ventricular tachycardiarrythmias. Precordial QT intervals and QT interval dispersions were measured at baseline and during steady-state antiarrhythmic drug therapy in 72 consecutive patients with documented coronary artery disease and remote myocardial infarction presenting with spontaneous sustained ventricular tachyarrhythmias who underwent electropharmacologic studies to assess arrhythmia suppression. QT interval dispersion was similar at baseline in drug responders (42 ± 21 ms) and drug nonresponders (46 ± 21 ms), whereas during antiarrhythmic therapy QT interval dispersion was shorter in drug responders (33 ± 15 ms) than in drug nonresponders (55 ± 29 ms, p <0.001). QT interval dispersion was shorter in 7 drug responders during their effective drug trials (27 ± 14 ms) than during their ineffective drug trials (47 ± 24 ms, n = 9, p <0.05). QT dispersion ≤50 ms (p <0.002) and a patent infarct-related artery (p <0.003) were independent predictors of antiarrhythmic therapy. The positive and negative predictive value of QT interval dispersion during drug therapy to predict a successful drug response was 32% and 96%, respectively. QT interval dispersion predicted the outcome of electropharmacologic studies independent of infarct-related artery patency. QT interval dispersion >50 ms during drug therapy was associated with ineffective drug therapy.

Influence of early coronary reperfusion on QT interval dispersion after acute myocardial infarction.

We studied the influence of early coronary reperfusion on QT interval dispersion in patients with acute myocardial infarction (MI). There were 54 males and 18 females with a mean age of 60 +/- 10 years. Of the 51 patients with recanalization of the infarct related vessel in the recovery phase, 28 (group A) had early coronary reperfusion (5.5 +/- 2.7 hours), 23 other patients (group B) were not confirmed with early coronary reperfusion. Twenty-one patients (group C) did not undergo recanalization of the infarct related vessel in the recovery phase. Corrected QT (QTc) maximum, QTc minimum, and QTc dispersion calculated as the difference between the maximum and minimum QTc intervals, were compared among these three groups at both acute and recovery phase. At the acute phase after MI, there were no significant differences in the QTc maximum, QTc minimum, QT dispersion, and QTc dispersion among these three groups. At the recovery phase after MI, there were also no significant differences in the QTc maximum and QTc minimum. However, there were significant differences in the QT dispersion (0.035 +/- 0.010 in group A, 0.049 +/- 0.015 in group B, and 0.061 +/- 0.031 s in group C, respectively; P = 0.0001), and QTc dispersion (0.038 +/- 0.012 in group A, 0.050 +/- 0.015 in group B, and 0.063 +/- 0.032 s in group C, respectively; P = 0.0003) among the three groups. Comparison of QTc dispersion between acute and recovery phase revealed significant reduction from acute to recovery phase in group A. The number of premature ventricular contraction was lower in group A and B than group C. In summary, early coronary reperfusion may reduce electrophysiological instability by reducing QT dispersion in the recovery phase after acute MI.