Enhanced parasympathetic tone shortens atrial refractoriness in man

Prystowsky, Eric N.; Naccarelli, Gerald V.; Jackman, Warren M.; Rinkenberger, Robert L.; Heger, James J.; Zipes, Douglas P.

doi:10.1016/s0002-9149(83)80018-6

Cited by 82 publications

(32 citation statements)

References 17 publications

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Section: Discussionmentioning

confidence: 99%

“…Because the signal transduction pathways activated by adenosine and acetylcholine converge on the same potassium channels to produce similar electrophysiologic effects in the atrial myocardium, adenosine induced and vagus nerve-dependent AF are mechanistically similar. Both adenosine and vagus nerve activation cause spatially and temporally heterogeneous shortening of atrial refractoriness [10].Some authors reported also a dangerous increase of the ventricular rate in atrial flutter patients following the administration of adenosine, with conduction increasing from 2:1 to 1:1 after a brief period of high grade atrioventricular block [11][12][13]. Three of these five reported cases required electrical cardioversion.…”

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confidence: 99%

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Unusual Side Effect of Adenosine Infusion

Russo¹

2013

Anat Physiol

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A 22 year old man was referred to our observation for recurrent palpitations at rest which subside after few minutes. The medical history was negative for familiar sudden death, dizziness or syncope. His body weight was 75 kg and his height was 170 cm. Physical examination revealed a blood pressure of 130/70 mmHg, clear lungs and normal heart sounds. Hematological examination, urinary analysis and thyroid function were all normal. He had no past medical history and denied taking alcohol, tobacco or any medications. Electrocardiographic (ECG) examination showed sinus rhythm of 75 beats/minute, normal atrioventricular conduction (PR: 120 ms), mild slurred QRS upstroke in leads V3-V4, no ST segment or T wave changes (Figure 1). Neither chest x-ray or color-doppler echocardiography revealed any cardiac structural or functional abnormalities. 24 hours ECG Holter monitoring and treadmill stress test did not show arrhythmias. He underwent transesophageal electrophysiological evaluation: the atrioventricular node refractory period was 240 msec. During the test it was not used any anesthesia. The patient was conscious during the entire test and its O 2 saturation, measured at pulse oximeter, was consistently 98-99%. Programmed atrial stimulation up to two extrastimuli did not induce supraventricular arrhythmias. Intravenous adenosine (12 mg) was performed for slowing of AV conduction and unmasking unapparent pathways. After a single-bolus, rapidly followed by saline flush, a sinus tachycardia at a frequency of 145 beats/min was induced. It was self-terminated in approximately 50 seconds, without change in QRS morphology (Figure 2). At the second adenosine bolus, carried out about 5 minutes later, similar effect was induced. Patient remained conscious and asymptomatic during the tachycardia. DiscussionAdenosine is an endogenous nucleoside whose actions were first investigated by Drury and Szent-Gyorgyi [1]. They described a slowing of sinus rate and a reduction of conduction through the atrioventricular node in the hearts of laboratory mammals. The adenosine test seems to have good sensitivity for unmasking pre-excitation about 76-100% in small series [2,3], because it extends the atrioventricular node refractory period favoring anterograde conduction through an accessory pathway. The electrophysiologic effects of adenosine on a specific AV bypass tract depend on the type of cell that the tract consists: nodal type cells (with decremental conduction) or atrial myocytes. In sinoatrial nodal cells, the activation of a potassium outward current results in a reduced rate of phase IV depolarization, thereby slowing sinoatrial node automaticity.In the AV node, adenosine prolongs postrepolarization refractoriness and suppresses excitability of cells in the N region of the node, resulting in AV nodal conduction block of variable degrees.Some authors reported serious adverse events related to the adenosine infusion, including supraventricular and life threatening ventricular arrhythmias [4,5]. To date, while the association betwee...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Unusual Side Effect of Adenosine Infusion

Russo¹

2013

Anat Physiol

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“…It shortens atrial myocyte action potential duration (APD) and reduces atrial effective refractory period (ERP), 67 thereby shortening the atrial re-entrant wavelength (the product of ERP and conduction velocity) enhancing the possibility of re-entry. 68,69 It also depresses intra-atrial conduction, and can induce re-entrant atrial arrhythmias.…”

Section: Vagal Stimulation Vagal Stimulation and Atrial Electrophysiomentioning

confidence: 99%

Device-Based Approaches to Modulate the Autonomic Nervous System and Cardiac Electrophysiology

Hucker

Singh

Parks

et al. 2014

Arrhythm Electrophysiol Rev

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The interplay between the central nervous system and cardiac electrophysiology is fundamental, and becomes obvious each time one's pulse quickens in response to stress. Normally, cardiac neurohormonal regulation is accomplished through the balanced effects of sympathetic and parasympathetic autonomic stimulation, along with the hormonal regulation of the renin-angiotensinaldosterone system (RAAS). Autonomic and hormonal input modulate multiple facets of cellular electrophysiology -action potential duration, ion channel kinetics and intracellular calcium dynamics (just to name a few) -which translate into macroscopic manifestations of autonomic modulation such as heart rate variability, atrioventricular (AV) conduction time and QT interval variability.1 Therefore, it is no surprise that neurohormonal regulation of cardiac electrophysiology is an area of active investigation for its potential antiarrhythmic effects. Recent reviews have focused on the efficacy of neurohormonal modulation, via non-pharmacological methods, to enhance heart failure treatment. 2,3 This review will attempt to provide a state-of-the-art on the potential antiarrhythmic efficacy of renal artery denervation, spinal cord stimulation and direct vagal stimulation. Neurohormonal Control in the Normal and Failing HeartAutonomic control of cardiac physiology is often conceptualised as parasympathetic (cholinergic) and sympathetic (adrenergic) innervation existing in a 'yin and yang' balance under normal circumstances; however, this concept may be over-simplified. 4 In reality, the intrinsic cardiac nervous system, composed of several ganglia located primarily posterior to the atria, likely acts as a 'little brain' of the heart -it provides efferent input to the myocardium, collects afferent signals on a beat-to-beat basis and performs some integrative functions on its own, all under the tonic modulation of extrinsic sympathetic and parasympathetic input (see Figure 1). 4-8The ganglia are predominantly composed of cholinergic neurons; however, sympathetic efferent neurons are also present. Due to the complex interconnectivity between the ganglia, afferent mechanosensory, nociceptive and chemosensory signals from all four chambers of the heart may be processed within a single ganglion. 4 Such interconnectivity implies that predicting the effect of stimulation or ablation of a particular ganglion may be difficult, because each ganglion performs multiple functions. 7,9Abstract Alterations in resting autonomic tone can be pathogenic in many cardiovascular disease states, such as heart failure and hypertension.Indeed, autonomic modulation by way of beta-blockade is a standard treatment of these conditions. There is a significant interest in developing non-pharmacological methods of autonomic modulation as well. For instance, clinical trials of vagal stimulation and spinal cord stimulation in the treatment of heart failure are currently underway, and renal denervation has been studied recently in the treatment of resistant hypertension. Notably, autonom...

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“…Since pyridostigmine is a cholinomimetic drug, it is expected to reduce sinusal automatism (22) and chronotropic and dromotropic function (23), increasing the cardiac excitability threshold (24) and the refractory period of sinusal and atrioventricular nodes, but reducing the atrial refractory period (25,26). Therefore, the purpose of the present study was to determine the cardiac electrophysiologic consequences of a single oral dose of pyridostigmine bromide in man.…”

Section: Introductionmentioning

confidence: 99%