The Relation of QT Dispersion and Localized QT Difference to Coronary Pathology in a Population with Unstable Coronary Artery Disease

Kesek, Milos; Englund, Anders; Jernberg, Tomas; Lagerqvist, Bo; Lindahl, Bertil

doi:10.1046/j.1542-474x.2003.08105.x

Cited by 3 publications

(1 citation statement)

References 38 publications

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“…In this study, they reported that although some patients had myocardial perfusion abnormalities, none of the patients had obstructive epicardial coronary disease, supporting the suggestion of microvascular abnormalities. Previous studies concerning QT dispersion in coronary artery disease have shown that QT dispersion increased in case of myocardial ischemia [27, 28]. So, SCD-associated myocardial ischemia may also cause an increase in QT dispersion.…”

Section: Discussionmentioning

confidence: 96%

Increased QT Dispersion in Sickle Cell Disease: Effect of Pulmonary Hypertension

et al. 2007

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Background: QT dispersion has been proposed to be a predictor of adverse outcomes in a variety of cardiac disease states. The objective of this study was to examine QT dispersion in patients with sickle cell disease (SCD) and to assess the effect of pulmonary hypertension (PHT) on QT dispersion. Methods: We performed Doppler echocardiographic assessments of pulmonary artery systolic pressure in 73 (mean age 18.5 ± 8.0 years) steady-state SCD patients and 25 (mean age 19.6 ± 7.2 years) healthy subjects. Resting 12-lead electrocardiogram was recorded and QT dispersion was calculated as the difference between maximum and minimum QT intervals. Bazett’s formula was used to obtain a rate-corrected value of the QT interval (QTc). Results: Maximum QTc, minimum QTc and QTc dispersion were significantly increased in SCD patients compared to the control subjects (p < 0.0001, p < 0.05, p < 0.0001, respectively). Among SCD patients, patients with PHT had higher maximum QTc and QTc dispersion than patients without PHT (p < 0.0001). However, minimum QTc showed no significant differences between the two patient groups. Conclusion: QTc dispersion is significantly increased in SCD patients, especially those with PHT indicating regional inhomogeneity of ventricular repolarization.

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Section: Discussionmentioning

confidence: 96%

Increased QT Dispersion in Sickle Cell Disease: Effect of Pulmonary Hypertension

et al. 2007

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Structural Barrier Increases QT-peak Dispersion in Swine Left Ventricle in Vivo

Shen

Gong²,

Iwai³

et al. 2006

2006 International Conference of the IEEE Engineering in Medicine and Biology Society

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QT dispersion (QTD) is thought to represent the regional nonuniformity of ventricular repolarization and can serve as a prognostic marker for vulnerability to ventricular arrhythmias and risk for sudden cardiac death (SCD). In this study, we used an in vivo swine model to investigate the change of QT-peak dispersion before and after the introduction of a left-ventricular (LV) free-wall structural barrier (SB). Baseline and post-ablation pacing were delivered to: (i) the epicardial LV base, (ii) the epicardial LV apex, and (iii) the right ventricular (RV) endocardium. Four unipolar electrograms were measured from LV free wall epicardial sites referenced to an intrathorax electrode. An SB (approximately 4 x 1 x 1 cm (length, width, depth)) was created by cryoablation in the middle of the two electrode pairs. QTD was computed as the difference between QT-peak intervals for each beat from two electrodes across the SB region from one another. A significant increase of QTD occurred (p<0.05) after the introduction of the SB in all six animals. These results may reflect the accentuation of anatomical repolarization heterogeneity due to SB disruption of electrotonic coupling. Given the link between dispersion of repolarization and initiation of reentry, these findings are consistent with the increased arrhythmia risk of structural heart disease.

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Admission N-terminal pro-brain natriuretic peptide and its interaction with admission troponin T and ST segment resolution for early risk stratification in ST elevation myocardial infarction

Björklund

Jernberg²,

Johanson³

et al. 2005

Heart

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Objective: To assess the long term prognostic value of N-terminal pro-brain natriuretic peptide (NTproBNP) on admission and its prognostic interaction with both admission troponin T (TnT) concentrations and resolution of ST segment elevation in fibrinolytic treated ST elevation myocardial infarction (STEMI). Design and setting: Substudy of the ASSENT (assessment of the safety and efficacy of a new thrombolytic) -2 and ASSENT-PLUS trials. Patients: NT-proBNP and TnT concentrations were determined on admission in 782 patients. According to NT-proBNP concentrations, patients were divided into three groups: normal concentration (for patients ( 65 years, ( 184 ng/l and ( 268 ng/l and for those . 65 years, ( 269 ng/l and ( 391 ng/l in men and women, respectively); higher than normal but less than the median concentration (742 ng/l); and above the median concentration. For TnT, a cut off of 0.1 mg/l was used. Of the 782 patients, 456 had ST segment resolution (, 50% or > 50%) at 60 minutes calculated from ST monitoring. Main outcome measures: All cause one year mortality. Results: One year mortality increased stepwise according to increasing concentrations of NT-proBNP (3.4%, 6.5%, and 23.5%, respectively, p , 0.001). In receiver operating characteristic analysis, NTproBNP strongly trended to be associated more with mortality than TnT and time to 50% ST resolution (area under the curve 0.81, 95% confidence interval (CI) 0.72 to 0.9, 0.67, 95% CI 0.56 to 0.79, and 0.66, 95% CI 0.56 to 0.77, respectively). In a multivariable analysis adjusted for baseline risk factors and TnT, both raised NT-proBNP and ST resolution , 50% were independently associated with higher one year mortality, whereas raised TnT contributed independently only before information on ST resolution was added to the model. Conclusion: Admission NT-proBNP is a strong independent predictor of mortality and gives, together with 50% ST resolution at 60 minutes, important prognostic information even after adjustment for TnT and baseline characteristics in STEMI.

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The Relation of QT Dispersion and Localized QT Difference to Coronary Pathology in a Population with Unstable Coronary Artery Disease

Abstract: QTd in ischemia seems to be increased by a mechanism unrelated to localization and severity of coronary disease.

Cited by 3 publications

References 38 publications

Increased QT Dispersion in Sickle Cell Disease: Effect of Pulmonary Hypertension

Increased QT Dispersion in Sickle Cell Disease: Effect of Pulmonary Hypertension

Structural Barrier Increases QT-peak Dispersion in Swine Left Ventricle in Vivo

Admission N-terminal pro-brain natriuretic peptide and its interaction with admission troponin T and ST segment resolution for early risk stratification in ST elevation myocardial infarction

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