Ventricular activation during sympathetic imbalance and its computational reconstruction

Nash, Martyn P.; Thornton, J R; Sears, Claire E.; Varghese, Anthony; O’Neill, Mark; Paterson, David J.

doi:10.1152/jappl.2001.90.1.287

Cited by 29 publications

(37 citation statements)

References 19 publications

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“…However, no difference in arrhythmia was observed [20]. Desflurane has been reported to cause ventricular arrhythmia by activating the sympathetic nervous system [21][22][23]. In the present study, we demonstrated a statistically significant increase in ventricular arrhythmia in the desflurane group during the first 24 hours after induction.…”

Section: Discussioncontrasting

confidence: 43%

Comparison of the effect of sevoflurane and desflurane on postoperative arrhythmia and QT dispersion

Gözdemir¹,

Yeter²,

Akçay³

et al. 2010

Open Medicine

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AbstractThe aim of this study was to investigate the effect of sevoflurane and desflurane on cardiac arrhythmias in adult patients who will be anesthetized. A total of 40 patients who were in the ASA I–II group and who were to undergo elective surgery were included in the study. No pre-medication was administered to the patients. They were monitored with the Holter equipment at preoperative 24 hours, and also at postoperative 24 hours on condition that Holter monitoring will begin before induction. Following routine monitoring, the patients were randomly divided into two equal groups; group one was given sevoflurane and group two was given desflurane. In this study, desflurane and sevoflurane resulted in both a significant prolongation of QT and QTc and a significant increase in QT and QTc dispersion when compared with the basal values. In the sevoflurane group, there was no significant increase in postoperative ventricular arrhythmia, compared to that during the preoperative period. However, this increase was significant in the desflurane group (p = 0.009). Sevoflurane and desflurane result in an increase in QT dispersion. Postoperative rhythmic control should carefully be monitored, especially in the desflurane group.

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Section: Discussioncontrasting

confidence: 43%

Comparison of the effect of sevoflurane and desflurane on postoperative arrhythmia and QT dispersion

Gözdemir¹,

Yeter²,

Akçay³

et al. 2010

Open Medicine

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“…Anesthesia, intensive care, and surgical methods have been fully described previously 17 but are briefly summarized here. The investigation conformed to the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health and was performed in accordance with the British Home Office license requirements.…”

Section: Methodsmentioning

confidence: 99%

“…Epicardial activation mapping methods have been fully described previously 17 and are outlined schematically in Supplementary Figure S1. According to Haws and Lux, 21 ventricular epicardial activation times were computed for each epicardial electrogram with the steepest negative intrinsic deflection during the QRS complex (minimum dV/dt; see Figure S1A).…”

Section: Signal Analysis and Mappingmentioning

confidence: 99%

Imaging Electrocardiographic Dispersion of Depolarization and Repolarization During Ischemia

2003

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Background-Myocardial ischemia creates abnormal electrophysiological substrates that result in life-threatening ventricular arrhythmias. Identifying patients at risk of such abnormalities by use of body surface electrical measures is controversial. We investigated the sensitivity of torso measures, recorded simultaneously with epicardial electrograms, to changes in dispersion of depolarization and repolarization during localized ventricular ischemia. Methods and Results-Ventricular epicardial electrograms were recorded from 5 anesthetized pigs with a 127-electrode sock. A controllable suture snare was used to ligate the left anterior descending coronary artery (LAD). The chest was reclosed, and a vest with 256 ECG electrodes was fitted to the torso. Simultaneous arrays of epicardial electrograms and torso ECGs were recorded during LAD occlusion and reperfusion. Activation-recovery intervals (ARIs), QT u and RT u dispersion (where u indicates upstroke), and QRST integrals were calculated, and these data were fitted to anatomically customized computational models of the swine ventricular epicardium and torso. LAD occlusion caused the epicardial ARI dispersion to steadily increase, whereas the location of shortest ARI shifted from the posterobasal ventricular tissue (control) to the anteroapical myocardium, distal to the suture snare. These changes were associated with a steady increase in the torso RT u dispersion as the shortest RT u interval moved from the right shoulder (control) to the sternum. QT u and RT u dispersion determined from the 12-lead ECG did not consistently reflect the myocardial changes. Conclusions-Although changes in myocardial repolarization dispersion resulting from localized ischemia are not reliably reflected in temporal indices derived from the 12-lead ECG, they can be readily identified with high-resolution torso ECG mapping.

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“…It can also directly raise the threshold for induction of ventricular fibrillation (72,73). Conditions associated with high vagal tone [e.g., exercise training (23) and gene transfer of neuronal nitric oxide (NO) synthase (nNOS) (25,71)] protect against mortality (20), while impaired vagal function has been demonstrated in both congestive cardiac failure (53) and hypertensive patients (56).…”

Section: Importance Of Autonomic Balance In Cardiovascular Diseasementioning

confidence: 99%

Peripheral cardiac sympathetic hyperactivity in cardiovascular disease: role of neuropeptides

Shanks

Herring

2013

American Journal of Physiology-Regulatory, Integrative and Comp

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High levels of sympathetic drive in several cardiovascular diseases including postmyocardial infarction, chronic congestive heart failure and hypertension are reinforced through dysregulation of afferent input and central integration of autonomic balance. However, recent evidence suggests that a significant component of sympathetic hyperactivity may also reside peripherally at the level of the postganglionic neuron. This has been studied in depth using the spontaneously hypertensive rat, an animal model of genetic essential hypertension, where larger neuronal calcium transients, increased release and impaired reuptake of norepinephrine in neurons of the stellate ganglia lead to a significant tachycardia even before hypertension has developed. The release of additional sympathetic cotransmitters during high levels of sympathetic drive can also have deleterious consequences for peripheral cardiac parasympathetic neurotransmission even in the presence of β-adrenergic blockade. Stimulation of the cardiac vagus reduces heart rate, lowers myocardial oxygen demand, improves coronary blood flow, and independently raises ventricular fibrillation threshold. Recent data demonstrates a direct action of the sympathetic cotransmitters neuropeptide Y (NPY) and galanin on the ability of the vagus to release acetylcholine and control heart rate. Moreover, there is as a strong correlation between plasma NPY levels and coronary microvascular function in patients with ST-elevation myocardial infarction being treated with primary percutaneous coronary intervention. Antagonists of the NPY receptors Y1 and Y2 may be therapeutically beneficial both acutely during myocardial infarction and also during chronic heart failure and hypertension. Such medications would be expected to act synergistically with β-blockers and implantable vagus nerve stimulators to improve patient outcome.

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Ventricular activation during sympathetic imbalance and its computational reconstruction

Cited by 29 publications

References 19 publications

Comparison of the effect of sevoflurane and desflurane on postoperative arrhythmia and QT dispersion

Comparison of the effect of sevoflurane and desflurane on postoperative arrhythmia and QT dispersion

Imaging Electrocardiographic Dispersion of Depolarization and Repolarization During Ischemia

Peripheral cardiac sympathetic hyperactivity in cardiovascular disease: role of neuropeptides

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