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  • 1
    Electronic Resource
    Electronic Resource
    QT Interval Prolongation with Global T-Wave Inversion: A Novel ECG Finding in Acute Pulmonary Embolism (2004)
    350 Main Street , Malden , MA 02148 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Annals of noninvasive electrocardiology 9 (2004), S. 0 
    Details
    ISSN: 1542-474X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objective: The purpose of this study was to report a novel electrocardiographic (ECG) phenomenon in acute pulmonary embolism characterized by QT interval prolongation with global T-wave inversion. Methods: Among a total of 140 study patients with a confirmed diagnosis of acute pulmonary embolism, patients who fulfilled the inclusion criteria for QT interval prolongation with global T-wave inversion were examined. Each of these patients had undergone a detailed clinical evaluation including testing for myocardial injury and echocardiography. Results: QT interval prolongation with global T-wave inversion was found in five patients (age 51–68 years) with acute pulmonary embolism. Four were women. Acute pulmonary embolism was diagnosed by ventilation-perfusion scan in three patients and by spiral computed tomography in other two patients. None of the patients had any right or left ventricular regional wall motion abnormalities on echocardiography. All patients had changes characteristic of hemodynamically significant pulmonary embolism, including right ventricular stunning or hypokinesis and dilatation in five patients with paradoxical septal motion in four. Acute coronary syndrome was ruled out in each patient by clinical evaluation, serial ECGs and cardiac markers, and lack of regional wall motion abnormalities on echocardiography. Prolongation of QT intervals (QTc 456–521 ms) with global T-wave inversion was noted on presentation. The ECG changes gradually resolved in 1 week in all patients with appropriate treatment of acute pulmonary embolism. One patient died. None of the patients developed torsade de pointes. Conclusions: Acute pulmonary embolism may occasionally result in reversible QT interval prolongation with deep T-wave inversion, and, thus should be considered among the acquired causes of the long QT syndrome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1542-474X.2004.91528.x
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  • 2
    Electronic Resource
    Electronic Resource
    Brugada and Long QT-3 Syndromes: Two Phenotypes of the Sodium Channel Disease (2004)
    350 Main Street , Malden , MA 02148 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Annals of noninvasive electrocardiology 9 (2004), S. 0 
    Details
    ISSN: 1542-474X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Brugada and long QT-3 syndromes are two allelic diseases caused by different mutations in SCN5A gene inherited by an autosomal dominant pattern with variable penetrance. Both of these syndromes are ion channel diseases of the heart manifest on surface electrocardiogram by ST-segment elevation in the right precordial leads and prolonged QTc interval, respectively, with predilection for polymorphic ventricular tachycardia and sudden death, which may be the first manifestation of the disease. Brugada syndrome usually manifests during adulthood with male preponderance, whereas long QT3 syndrome usually manifests in teenage years, although it can also manifest in adulthood. Class IA and IC antiarrhythmic drugs increase ST-segment elevation and predilection for polymorphic ventricular tachycardia and ventricular fibrillation in Brugada syndrome, whereas these agents shorten the repolarization and QTc interval, and thus may be beneficial in long QT-3 syndrome. Beta-blockade also increases the ST-segment elevation in Brugada syndrome but decreases the dispersion of repolarization in long QT-3 syndrome. Mexiletine, a class IB sodium channel blocker decreases QTc interval as well as dispersion of repolarization in long QT-3 syndrome but has no effect on Brugada syndrome. The only effective treatment available at this time for Brugada syndrome is implantable cardioverter defibrillator, although repeated episodes of polymorphic ventricular tachycardia can be treated with isoproterenol. In symptomatic patients of long QT-3 syndrome in whom the torsade de pointes is bradycardia-dependent or pause-dependent, a pacemaker could be used to avoid bradycardia and pauses and an implantable cardioverter defibrillator is indicated where arrhythmia is not controlled with pacemaker and beta-blockade. However, the combination of new devices with pacemaker and cardioverter-defibrillator capabilities appear promising in these patients warranting further study.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1542-474X.2004.93533.x
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  • 3
    Electronic Resource
    Electronic Resource
    Left Bundle Branch Block in Type 2 Diabetes Mellitus: A Sign of Advanced Cardiovascular Involvement (2004)
    350 Main Street , Malden , MA 02148 , USA , and 9600 Garsington Road , Oxford OX4 2XG , UK . : Blackwell Publishing, Inc.
    Annals of noninvasive electrocardiology 9 (2004), S. 0 
    Details
    ISSN: 1542-474X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objective: To evaluate left bundle branch block (LBBB) as an indicator of advanced cardiovascular involvement in diabetic (DM) patients by examining left ventricular systolic function and proteinurea. Methods: Data of 26 diabetic patients with left bundle branch block (DM with LBBB) were compared with data of 31 diabetic patients without left bundle branch block (DM without LBBB) and 18 nondiabetic patients with left bundle branch block (non-DM with LBBB). The inclusion criteria were age 〉45 years, and diabetes mellitus type 2 of 〉5 years. Results: Mean ages of patients in DM with LBBB, DM without LBBB, and non-DM with LBBB groups were 67 ± 8, 68 ± 10, and 65 ± 10 years, respectively (P = NS). Females were 65%, 61%, and 61%, respectively (P = NS). Left ventricular ejection fraction in DM with LBBB was significantly lower than in DM without LBBB and non-DM with LBBB (30 ± 10% vs 49 ± 12% and 47 ± 8%, P 〈 0.01). Left ventricular end-diastolic volume was significantly higher in DM with LBBB than in DM without LBBB and non-DM with LBBB (188.6 ± 16.4 mL vs 147.5 ± 22.3 mL and 165.3 ± 15.2 mL, P 〈 0.03). Similarly, left ventricular end-systolic volume was significantly higher in DM with LBBB than in DM without LBBB and non-DM with LBBB (135.4 ± 14.7 mL vs 83.7 ± 9.5 mL and 96.6 ± 18.4 mL, P 〈 0.02). No statistically significant difference was seen in left atrial size. Proteinurea in DM with LBBB (79.4 ± 18.9 mg/dL) was significantly higher than in DM without LBBB (35.6 ± 8.5 mg/dL, P 〈 0.05) and non-DM with LBBB (12 ± 3.5 mg/dL, P 〈 0.05); however, there was no significant difference in Hb A1c levels in DM with LBBB and DM without LBBB (9.01% vs 7.81%, P = NS). Conclusions: Left bundle branch block in diabetic patients indicates advanced cardiovascular involvement manifesting with more severe left ventricular systolic dysfunction and proteinurea compared to both diabetic patients without left bundle branch block and nondiabetic patients with left bundle branch block.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1542-474X.2004.94577.x
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  • 4
    Electronic Resource
    Electronic Resource
    The Comparative Effects of Drive and Test Stimulus Intensity on Myocardial Excitability and Vulnerability (2000)
    Oxford, UK : Blackwell Publishing Ltd
    Pacing and clinical electrophysiology 23 (2000), S. 0 
    Details
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The number and intensity of stimuli that set basic cycle length in cardiac electrophysiological studies can influence the electrical properties assessed by extrastimuli. The relative contribution of drive (S1) and test (S2) stimulus intensity in defining myocardial excitability and vulnerability has not been reported. The purpose of this investigation was to assess this interaction and to determine whether a trial and ventricular findings differed. The effects of S1 and S2 intensity on a trial and ventricular stimulus-intensity-refractory-period curves were determined in open-chest dogs: comparisons were made between curves with S1 intensity varied between diastolic threshold (DT) and 10 mA and S2 intensity maintained at DT and those with S, intensity maintained at DT and S2 intensity varied between DT and 10 mA. S1-S2 was held constant and S1-S2 varied. The effects of different stimulation sites, cycle length, number of stimulations, and neural blockade were assessed. S3 intensity amplification shifted atrial stimulus-intensity-refractory period curves in the direction of increased excitability and vulnerability; the changes were, more pronounced than those obtained by modulating S2 intensity. The changes produced by increasing S1 intensity were evident at different cycle lengths and were enhanced by an increased number of stimulations, but were not evident when S1 and S2 were delivered at different atrial sites. Although beta-blockade attenuated the effects of increasing S1 intensity somewhat, the addition of cholinergic blockade virtually abolished it. Ventricular refractoriness was also changed by modulation of S1 intensity, but the changes were less striking. In the atrium, modulation of S1 intensity has greater effects of stimulus-intensity-refractory-period relations than modulation ofS2 intensity; in the ventricle, the converse is true.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8159.2000.tb00653.x
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