The QT and Tp-e intervals in left and right chest leads: comparison between patients with systemic and pulmonary hypertension

Hlaing, Thinn; Guo, Dan; Zhao, Xiaojing; DiMino, Tara; Greenspon, Lee; Kowey, Peter R.; Yan, Gan‐Xin

doi:10.1016/j.jelectrocard.2005.06.028

Cited by 31 publications

(23 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The electrophysiology of rodents is distinct from that of humans, and its applicability can be questioned. However, alterations in the ECG ventricular gradient and QT interval in response to MCT (22,37,47) were similar to changes seen in humans with pulmonary hypertension (23,26,27); therefore, understanding the mechanisms causing these changes may be relevant to the clinical setting (10,63).…”

Section: Discussionmentioning

confidence: 85%

“…This includes pulmonary hypertension, where RV failure is the major cause of death in patients (6). Pulmonary hypertension is associated with RV electrical remodeling (23,26,27) and a higher risk of arrhythmias (17). Sudden death occurs in 30 -40% of sufferers (10,63), and lethal arrhythmias are thought to be one cause, in addition to other mechanisms, such as pulmonary embolism and pulmonary artery dissection.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Cardiac arrhythmia mechanisms in rats with heart failure induced by pulmonary hypertension

Benoist

Stones

Drinkhill

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Pulmonary hypertension provokes right heart failure and arrhythmias. Better understanding of the mechanisms underlying these arrhythmias is needed to facilitate new therapeutic approaches for the hypertensive, failing right ventricle (RV). The aim of our study was to identify the mechanisms generating arrhythmias in a model of RV failure induced by pulmonary hypertension. Rats were injected with monocrotaline to induce either RV hypertrophy or failure or with saline (control). ECGs were measured in conscious, unrestrained animals by telemetry. In isolated hearts, electrical activity was measured by optical mapping and myofiber orientation by diffusion tensor-MRI. Sarcoplasmic reticular Ca(2+) handling was studied in single myocytes. Compared with control animals, the T-wave of the ECG was prolonged and in three of seven heart failure animals, prominent T-wave alternans occurred. Discordant action potential (AP) alternans occurred in isolated failing hearts and Ca(2+) transient alternans in failing myocytes. In failing hearts, AP duration and dispersion were increased; conduction velocity and AP restitution were steeper. The latter was intrinsic to failing single myocytes. Failing hearts had greater fiber angle disarray; this correlated with AP duration. Failing myocytes had reduced sarco(endo)plasmic reticular Ca(2+)-ATPase activity, increased sarcoplasmic reticular Ca(2+)-release fraction, and increased Ca(2+) spark leak. In hypertrophied hearts and myocytes, dysfunctional adaptation had begun, but alternans did not develop. We conclude that increased electrical and structural heterogeneity and dysfunctional sarcoplasmic reticular Ca(2+) handling increased the probability of alternans, a proarrhythmic predictor of sudden cardiac death. These mechanisms are potential therapeutic targets for the correction of arrhythmias in hypertensive, failing RVs.

show abstract

Section: Discussionmentioning

confidence: 85%

mentioning

confidence: 99%

Cardiac arrhythmia mechanisms in rats with heart failure induced by pulmonary hypertension

Benoist

Stones

Drinkhill

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…40 It is a useful index in the assessment of arrhythmic risk, as an amplifi cation of the transmural dispersion of repolarization may facilitate propagation of early aft erdepolarizations (R-on-T phenomenon) and lead to functional transmural reentry and development of polymorphic ventricular tachycardia and fi brillation. 41 Further, an increase of the transmural dispersion of repolarization under conditions of QT prolongation serves as a functional reentrant substrate for the maintenance of torsade de pointes.…”

Section: P Value By Wilcoxon Matched-pairs Test For Comparisons Betwementioning

confidence: 99%

Effect of Oxygen and Acetazolamide on Nocturnal Cardiac Conduction, Repolarization, and Arrhythmias in Precapillary Pulmonary Hypertension and Sleep-Disturbed Breathing

Schumacher

Müller-Mottet

Hasler

et al. 2014

Chest

View full text Add to dashboard Cite

“…This is associated with decreased K ϩ channel activity, although studies disagree precisely which channels (26,27,32,41). Interestingly, the changes in ventricular gradient and QT interval seen in human PAH (17,19,20) are also seen in the MCT model (16,27,32). These observations would predict that the MCT model is proarrhythmic, but this has not previously been directly investigated.…”

mentioning

confidence: 97%

“…In humans, pulmonary artery hypertension (PAH) is a disease that can be unstable and RV failure is a common outcome (4,13,38). The QT interval and QT dispersion of the ECG have been reported to be increased (19,20), and the shift in ECG derived ventricular gradient [reflecting action potential duration (APD) dispersion] has been related to increased RV load (17). Such changes in electrical activity have been linked to arrhythmias (1,39), and PAH is associated with arrhythmias in patients (11).…”

mentioning

confidence: 99%

Arrhythmogenic substrate in hearts of rats with monocrotaline-induced pulmonary hypertension and right ventricular hypertrophy

Benoist

Stones

Drinkhill

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Benoist D, Stones R, Drinkhill M, Bernus O, White E. Arrhythmogenic substrate in hearts of rats with monocrotaline-induced pulmonary hypertension and right ventricular hypertrophy. Am J Physiol Heart Circ Physiol 300: H2230 -H2237, 2011. First published March 11, 2011 doi:10.1152/ajpheart.01226.2010.-Mechanisms associated with right ventricular (RV) hypertension and arrhythmias are less understood than those in the left ventricle (LV). The aim of our study was to investigate whether and by what mechanisms a proarrhythmic substrate exists in a rat model of RV hypertension and hypertrophy. Rats were injected with monocrotaline (MCT; 60 mg/kg) to induce pulmonary artery hypertension or with saline (CON). Myocardial levels of mRNA for genes expressing ion channels were measured by real-time RT-PCR. Monophasic action potential duration (MAPD) was recorded in isolated Langendorff-perfused hearts. MAPD restitution was measured, and arrhythmias were induced by burst stimulation. Twenty-two to twenty-six days after treatment, MCT animals had RV hypertension, hypertrophy, and decreased ejection fractions compared with CON. A greater proportion of MCT hearts developed sustained ventricular tachycardias/fibrillation (0.83 MCT vs. 0.14 CON). MAPD was prolonged in RV and less so in the LV of MCT hearts. There were decreased levels of mRNA for K ϩ channels. Restitution curves of MCT RV were steeper than CON RV or either LV. Dispersion of MAPD was greater in MCT hearts and was dependent on stimulation frequency. Computer simulations based on ion channel gene expression closely predicted experimental changes in MAPD and restitution. We have identified a proarrhythmic substrate in the hearts of MCT-treated rats. We conclude that steeper RV electrical restitution and rate-dependant RV-LV action potential duration dispersion may be contributing mechanisms and be implicated in the generation of arrhythmias associated with in RV hypertension and hypertrophy. electrical restitution; fibrillation; action potentials INCREASED PULMONARY ARTERIAL pressure increases loading on the right ventricle (RV), which can lead to electrical, mechanical, and structural remodeling. In humans, pulmonary artery hypertension (PAH) is a disease that can be unstable and RV failure is a common outcome (4, 13, 38). The QT interval and QT dispersion of the ECG have been reported to be increased (19,20), and the shift in ECG derived ventricular gradient [reflecting action potential duration (APD) dispersion] has been related to increased RV load (17). Such changes in electrical activity have been linked to arrhythmias (1, 39), and PAH is associated with arrhythmias in patients (11). RV pathophysiology is in general understudied compared with the left ventricle (LV; Ref. 38), and the mechanisms that underlie RV changes in electrical activity in response to hypertension are not well understood.The monocrotaline (MCT)-induced model of pulmonary arterial hypertension and RV hypertrophy is well established (e.g., Refs. 14, 23). MCT is a pyrrolizidine alkaloid from...

show abstract

The QT and Tp-e intervals in left and right chest leads: comparison between patients with systemic and pulmonary hypertension

Cited by 31 publications

References 18 publications

Cardiac arrhythmia mechanisms in rats with heart failure induced by pulmonary hypertension

Cardiac arrhythmia mechanisms in rats with heart failure induced by pulmonary hypertension

Effect of Oxygen and Acetazolamide on Nocturnal Cardiac Conduction, Repolarization, and Arrhythmias in Precapillary Pulmonary Hypertension and Sleep-Disturbed Breathing

Arrhythmogenic substrate in hearts of rats with monocrotaline-induced pulmonary hypertension and right ventricular hypertrophy

Contact Info

Product

Resources

About