Human ventricular repolarization and T wave genesis

Franz, Michael R.; Bargheer, Klaus; Costard‐Jäckle, Angelika; Miller, D. Craig; Lichtlen, Paul R.

doi:10.1016/0033-0620(91)90003-5

Cited by 59 publications

(22 citation statements)

References 77 publications

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“…[6][7][8][9] In the present study, the plateau phase of MAPMid diminished rapidly after the beginning of ischemia and the average difference in MAPD90 and ERP between the midlayer and other 2 layers was approximately 80 ms and 20 ms, respectively, during the 5-30 min after CO. These marked transmural gradients of MAPD and ERP that appear in the ventricular wall under ischemia conditions may represent the substrate of functional reentry, 8,11 and are in agreement with previous reports in isolated cells from the 3 layers of the ventricular wall in which acute MI shortened the APD. [12][13][14][15] In this study, although the MAPD and ERP were shortened proportionately in the epicardium and endocardium after MI, they separated and PRR was observed in the M cells during the 5-30 min after CO.…”

Section: Discussionsupporting

confidence: 92%

Differences in the Changing Trends of Monophasic Action Potential Duration and Effective Refractory Period of the Ventricular Myocardium After Myocardial Infarction in Vivo

Huang

Bao

Jiang

et al. 2004

Circ J

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growing body of evidence suggests that heterogeneity of electrophysiological characteristics is an important property of the ventricular myocardium. 1,2 Importantly, a subpopulation of cells, called midmyocardial cells (M cells), have been described in the ventricular wall of the guinea pig, 3 canine 1 and human. 2 The M cells display a longer action potential duration (APD) and a steeper dependence of APD on rate than epicardial or endocardial cells. This electrophysiological difference between M cells and the other cell types is the main source of the heterogeneity observed in the normal heart.Transmural and regional heterogeneities in the electrical properties of cardiac cells contribute to the normal function of the heart. They are susceptible to many pathological factors, such as ischemia, hypertrophy, or heart failure, and any significant alternation in these electrical heterogeneities can lead to the development of life-threatening cardiac arrhythmias and sudden death. The heterogeneity of the ventricular electrical properties is reflected in aspects such as APD, effective refractory period (ERP) and conduction velocity, and is more marked in vitro than in the intact heart. 4 In the setting of ischemia, hypertrophy, or heart failure, the altered electrophysiological heterogeneity of the Circulation Journal Vol.68, December 2004ventricle may have significance in the development of ventricular arrhythmias, but the dynamic variations of the electrophysiological characteristics of the ventricle under pathological conditions are poorly understood.Myocardial infarction (MI) can create abnormal electrophysiological substrates that trigger ventricular arrhythmias and at different stages of MI, the mechanism underlying the ventricular arrhythmias vary. The study by Anyukhovsky et al suggested that myocardial injury may in fact permit dispersion of repolarization to be manifested transmurally in vivo, and in the setting of Ca 2+ overload the transmural electrophysiological dispersion of ventricle wall may be further exaggerated. 4 Consequently, the aims of the present study were twofold. First, to investigate the effects of MI on transmural electrophysiological characteristics in the rabbit heart in vivo and second, to compare the changing trends of the monophasic APD (MAPD) and ERP of the endocardial, M and epicardial cells after MI in vivo. Methods Animal PreparationForty New Zealand white rabbits, including both male and female, weighing 2-2.5 kg, were randomized into either a sham operation (SO) group (n=10) or MI group (n=30). All rabbits were anesthetized with sodium pentobarbital (30 mg/kg iv). Additional smaller doses were given as needed to maintain deep anesthesia. Under controlled ventilation, a thoracotomy through a left parasternal inciCirc J 2004; 68: 1205 -1209 (Received March 22, 2004; revised manuscript received August 26, 2004; accepted August 30, 2004

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Section: Discussionsupporting

confidence: 92%

Differences in the Changing Trends of Monophasic Action Potential Duration and Effective Refractory Period of the Ventricular Myocardium After Myocardial Infarction in Vivo

Huang

Bao

Jiang

et al. 2004

Circ J

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“…6,7 In the ECG, QRS duration is a measure of differences in activation times. 29 The observed prognostic value of QRS duration in the present study may be related in part to the fact that delayed conduction per se is one of the factors increasing susceptibility to reentrant ventricular arrhythmias. In addition, prolonged QRS duration may be a marker of cellular uncoupling, and even small changes in cellular coupling may have profound effects on repolarization gradients at the myocardial level.…”

Section: Qrs Duration Qt Intervals and Mortality In Patients With Lvhmentioning

confidence: 79%

QRS Duration and QT Interval Predict Mortality in Hypertensive Patients With Left Ventricular Hypertrophy

et al. 2004

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Abstract-Left ventricular hypertrophy is a risk factor for cardiovascular mortality, including sudden cardiac death.Experimentally, left ventricular hypertrophy delays ventricular conduction and prolongs action potential duration. Electrocardiographic QRS duration and QT interval measures reflect these changes, but whether these measures can further stratify risk in patients with electrocardiographic left ventricular hypertrophy is unknown. We measured the QRS duration and QT intervals from the baseline 12-lead electrocardiograms in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) study, which included hypertensive patients with electrocardiographic evidence of left ventricular hypertrophy randomized to either losartan-based or atenolol-based treatment to lower blood pressure. In the present study, we related study baseline electrocardiographic measures to cardiovascular and all-cause mortality. There were 5429 patients (male 45.8%; mean age 66Ϯ7 years) included in the present analyses. After a mean follow-up of 4.9Ϯ0.8 years, there were 417 deaths from all causes, including 214 cardiovascular deaths. In separate univariate Cox regression analyses, QRS duration and several QT measures were significant predictors of cardiovascular mortality and all-cause mortality. However, in multivariate Cox analyses including all electrocardiographic measures and adjusting for other risk factors as well as treatment strategy, only QRS duration and maximum rate-adjusted QT apex interval remained as significant independent predictors of cardiovascular (Pϭ0.022 and Pϭ0.037, respectively) and all-cause mortality (Pϭ0.038 and Pϭ0.002, respectively). In conclusion, in a hypertensive risk population identified by electrocardiographic left ventricular hypertrophy, increased QRS duration and maximum QT apex interval can further stratify mortality risk even in the setting of effective blood pressure-lowering treatment. Key Words: electrocardiography Ⅲ hypertension Ⅲ mortality Ⅲ hypertrophy L eft ventricular hypertrophy (LVH) is an important indicator of target organ damage in chronic arterial hypertension. Electrocardiographically and echocardiographically detected LVH independently predict increased morbidity and mortality, 1,2 including sudden cardiac death, 3,4 and the relative risk of these events increases with increasing LV mass. The impact of LVH on outcome may in part be mediated by adverse changes in LV mechanical function. However, LVH also induces potentially arrhythmogenic changes in LV electrophysiology. Experimental evidence shows that LVH alters ventricular conduction and repolarization. [5][6][7][8][9][10][11][12][13][14] In the 12-lead ECG, these changes may prolong the QRS and QT interval duration, respectively, and affect T-wave morphology. [15][16][17] In hypertensive patients with ECG LVH, increase in LV mass was associated with prolonged QRS and QT interval duration and measures of QT dispersion. 18 However, it is unknown if these ECG measures can further stratify risk in patients with LVH. T...

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“…This underscores that intrinsic characteristics are important. AT-ARI relationships are less steep in diseased hearts, 33,44 which therefore will display more dispersion in repolarization time. One other implication of a relatively steep relation between activation times and ARIs is that areas where dispersion in action potential duration is largest 45 are not necessarily areas where dispersion in repolarization time is also largest.…”

Section: Quantitative Aspects Of Dispersion In Repolarization: Activamentioning

confidence: 99%

Is there a significant transmural gradient in repolarization time in the intact heart?

Opthof

Coronel

Janse

2009

Circ: Arrhythmia and Electrophysiology

107

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Human ventricular repolarization and T wave genesis

Cited by 59 publications

References 77 publications

Differences in the Changing Trends of Monophasic Action Potential Duration and Effective Refractory Period of the Ventricular Myocardium After Myocardial Infarction in Vivo

Differences in the Changing Trends of Monophasic Action Potential Duration and Effective Refractory Period of the Ventricular Myocardium After Myocardial Infarction in Vivo

QRS Duration and QT Interval Predict Mortality in Hypertensive Patients With Left Ventricular Hypertrophy

Is there a significant transmural gradient in repolarization time in the intact heart?

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