Adrenergic Effects on Ventricular Vulnerability

Han, Jaok; Jalón, P. Garcia de; Moe, Gordon K.

doi:10.1161/01.res.14.6.516

Cited by 369 publications

(103 citation statements)

References 19 publications

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“…Imbalance of sympathetic tone to the heart is known to produce ventricular arrhythmias.-8 In the present study, the sham-operated group showed a tendency for a greater frequency of induction of ventricular fibrillation during bilateral stimulation of the ansae subclaviae, but not during the infusion of norepinephrine, consistent with the observation of Han et al 1 The present data also show that sympathetic denervation to some areas of the canine heart produced by phenol make the heart more vulnerable to PVS-induced ventricular fibrillation during increased sympathetic tone, i.e., during stimulation of the ansae subclaviae or infusion of norepinephrine. The greater incidence of ventricular fibrillation during these two interventions in dogs treated with phenol alone equaled that in the ligation infarction group.…”

Section: Discussionsupporting

confidence: 90%

Results of sympathetic denervation in the canine heart: supersensitivity that may be arrhythmogenic.

Inoue

Zipes²

1987

Circulation

242

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Latex-induced transmural myocardial infarction or epicardial application of phenol interrupts sympathetic fibers innervating myocardium apical to the infarction or to the phenol-painted area. These denervated regions subsequently show supersensitive shortening of effective refractory period (ERP) in response to the infusion of norepinephrine (denervation supersensitivity). The purpose of this study was to test the hypothesis that such denervation supersensitivity is arrhythmogenic. Ventricular arrhythmias were elicited by programmed ventricular stimulation (PVS) during a control period, during bilateral stimulation of the ansae subclaviae (4 msec pulses, 4 Hz and 3 mA), and during the infusion of norepinephrine (0.5 gg/kg/min). Study groups consisted of 14 sham-operated dogs, 16 dogs with phenol painted over a diagonal branch, 13 dogs with latex embolization of a diagonal branch that resulted in transmural myocardial infarction, 14 dogs with a one-stage ligation of a diagonal branch producing nontransmural myocardial infarction, and 12 dogs undergoing both phenol painting and onestage ligation of a diagonal branch. Four to 22 days after the first operation, PVS was performed in anesthetized, open-chest dogs after neural decentralization of the heart. Dogs with phenol painting on the epicardium and dogs in which latex was injected into a diagonal branch showed supersensitive shortening of ERP to infused norepinephrine at apical sites. PVS resulted in ventricular fibrillation more often during stimulation of the ansae subclaviae (p < .001) and infusion of norepinephrine (p < .001) than during the control state in dogs treated with phenol alone. The incidence of ventricular fibrillation was highest in dogs with ligation-induced infarction that received phenol compared with all other groups during control (p < .001), stimulation of the ansae subclaviae (p < .002), and the infusion of norepinephrine (p < .01). Propranolol (0.5 mg/kg or 10 mg iv at maximum) attenuated supersensitive shortening of ERP and decreased the incidence of induction of ventricular fibrillation. We conclude that (1) the canine heart with phenol-induced sympathetic supersensitivity, but without myocardial infarction, is more vulnerable to PVS-induced ventricular fibrillation during the infusion of norepinephrine compared with the control group, (2) the canine heart with latex-induced myocardial infarction shows sympathetic supersensitivity, but is not more vulnerable to PVS-induced ventricular fibrillation during stimulation of the ansae subclaviae and infusion of norepinephrine, (3) phenolinduced sympathetic supersensitivity combined with nontransmural myocardial infarction makes the canine heart more vulnerable to PVS-induced ventricular fibrillation than any of the other study conditions. Circulation 75, No. 4, 877-887, 1987

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Section: Discussionsupporting

confidence: 90%

Results of sympathetic denervation in the canine heart: supersensitivity that may be arrhythmogenic.

Inoue

Zipes²

1987

Circulation

242

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“…[59][60][61] Destabilization of ventricular wave fronts leading to degeneration ventricular tachycardia into ventricular fibrillation appears to be related to the restitution properties of action potential duration. 61,62 Restitution is described as the change in APD in response to the preceding diastolic interval, and steeply sloped restitution curves with large changes in APD for relatively small changes in diastolic interval over a wide range of diastolic intervals have been associated with complex unstable dynamic rhythms.…”

Section: Effect Of Sympathetic Stimulation On Action Potential Duratimentioning

confidence: 99%

The Role of the Autonomic Nervous System in Sudden Cardiac Death

Vaseghi

Shivkumar²

2008

Progress in Cardiovascular Diseases

336

233

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The cardiac autonomic nervous system consists of 2 branches-the sympathetic and the parasympathetic systems-that work in a delicately tuned, yet opposing fashion in the heart. This extrinsic control mechanism can dominate intrinsic regulatory mechanisms that modulate heart rate and cardiac output. These branches differ in their neurotransmitters (norepinephrine and acetylcholine) and exert stimulatory or inhibitory effects on target tissue via adrenergic and muscarinic receptors. Stimulation of the sympathetic branch exerts facilitatory effects on function, increasing heart rate and myocardial contractility, whereas the stimulation of the parasympathetic branch exerts inhibitory effects that decrease heart rate and contractility. The interplay between these two branches is complex and susceptible to control at several levels, from centrally mediated baroreceptors and chemoreceptors to local interneuronal interactions.Alterations in autonomic function occur in several interrelated cardiac conditions including sudden cardiac death, congestive heart failure, diabetic neuropathy, and myocardial ischemia. Although the full extent of these changes has not been elucidated, multiple autonomic remodeling mechanisms have been observed at both the neuronal fiber and myocardial cellular level that contribute to an arrhythmogenic substrate. We describe the anatomy of both systems in this review. However, the review will premdominantly focus on the sympathetic system, whose role in the modulation of cardiac arrhythmias is slightly better delineated. Cardiac Autonomic Innervation: NeuroanatomyBoth branches of the autonomic nervous system are composed of both afferent and efferent as well interneuronal fibers (Fig 1). Sympathetic innervation originates mainly in the right and left stellate ganglia. These fibers travel along the epicardial vascular structures of the heart and penetrate into the underlying myocardium similar to coronary vessels and end as sympathetic nerve terminals reaching the endocardium. Based on norepinephrine content studies, a gradient exists in sympathetic innervation from atria to the ventricles and from base to apex of the heart. Therefore, the atria are most densely innervated, but the ventricles are also supplied with a sympathetic network, most densely at the base. 1 Parasympathetic effects are carried by the right and left vagus nerves, originating in the medulla. The vagus nerve further divides into the superior and inferior cardiac nerves, finally merging with the postganglionic sympathetic neurons to form a plexus of nerves at the base of the heart, known as the cardiac plexus. In contrast to sympathetic neurons, after parasympathetic fibers cross the atrioventricular (AV) groove along the surface of the heart,

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“…[1][2][3][4] Several studies have demonstrated an increased susceptibility to complex arrhythmias and ventricular fibrillation as a result of sympathetic stimulation. 1 One mechanism that has been shown to underlie the destabilization of activation wavefronts relates to the restitution properties of action potential duration (APD), which may be described as the change in APD in response to an abrupt change in the preceding diastolic interval. Steeply sloped restitution curves, ie, a large change in APD for a relatively small change in diastolic interval, have been shown to be associated with complex unstable dynamics.…”

mentioning

confidence: 99%

Effect of Adrenergic Stimulation on Action Potential Duration Restitution in Humans

et al. 2003

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Background-Enhanced sympathetic activity facilitates complex ventricular arrhythmias and fibrillation. The restitution properties of action potential duration (APD) are important determinants of electrical stability in the myocardium. Steepening of the slope of APD restitution has been shown to promote wave break and ventricular fibrillation. The effect of adrenergic stimulation on APD restitution in humans is unknown. Methods and Results-Monophasic action potentials were recorded from the right ventricular septum in 18 patients.Standard APD restitution curves were constructed at 3 basic drive cycle lengths (CLs) of 600, 500, and 400 ms under resting conditions and during infusion of isoprenaline (15 patients) or adrenaline (3 patients). The maximum slope of the restitution curves was measured by piecewise linear regression segments of sequential 40-ms ranges of diastolic intervals in steps of 10 ms. Under control conditions, the maximum slope was steeper at longer basic CLs; eg, mean values for the maximum slope were 1.053Ϯ0.092 at CL 600 ms and 0.711Ϯ0.049 at CL 400 ms (ϮSEM). Isoprenaline increased the steepness of the maximum slope of APD restitution, eg, from a maximum slope of 0.923Ϯ0.058 to a maximum slope of 1.202Ϯ0.121 at CL 500 ms. The effect of isoprenaline was greater at the shorter basic CLs. A similar overall effect was observed with adrenaline. Conclusions-The

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Adrenergic Effects on Ventricular Vulnerability

Cited by 369 publications

References 19 publications

Results of sympathetic denervation in the canine heart: supersensitivity that may be arrhythmogenic.

Results of sympathetic denervation in the canine heart: supersensitivity that may be arrhythmogenic.

The Role of the Autonomic Nervous System in Sudden Cardiac Death

Effect of Adrenergic Stimulation on Action Potential Duration Restitution in Humans

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