Competing autonomic mechanisms precedethe onset of postoperative atrial fibrillation

Amar, David; Zhang, Hao; Miodownik, Saul; Kadish, Alan H.

doi:10.1016/s0735-1097(03)00955-0

Cited by 190 publications

(137 citation statements)

References 32 publications

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“…Coumel et al 53 in 1978 first reported that cardiac autonomic activities might predispose patients to develop paroxysmal atrial arrhythmias. Subsequent studies [54][55][56] with heart rate variability analysis indicate that, rather than being triggered by either vagal or sympathetic activity, the onset of AF can be associated with simultaneous discharge of both limbs, leading to an imbalance between these 2 arms of cardiac ANS. With implanted radiotransmitters, spontaneous simultaneous sympathetic (from LSG) and parasympathetic (from thoracic vagus nerve) nerve activity was observed to precede the onset of paroxysmal AF in ambulatory dogs with rapid atrial pacing ( Figure 3A) 48 and HF.…”

Section: Atrial Fibrillationmentioning

confidence: 99%

Role of the Autonomic Nervous System in Modulating Cardiac Arrhythmias

Shen

Zipes

2014

Circulation Research

687

543

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I n 1628, William Harvey hinted at a link between the brain and the heart when he wrote, "For every affection of the mind that is attended with either pain or pleasure, hope or fear, is the cause of an agitation whose influence extends to the heart."1 For the past half century, numerous anatomic and physiological studies of cardiac autonomic nervous system (ANS) 2-6 have investigated this link and found it to be very complex. Autonomic activation alters not only heart rate, conduction, and hemodynamics, but also cellular and subcellular properties of individual myocytes. The characterization of extrinsic cardiac ANS and intrinsic cardiac ANS ranges from the recognition of anatomic relationships at the gross level to discovery of chemoreceptors, mechanoreceptors, and intracardiac ganglia lining specific regions along the cardiac chambers and great vessels. Moreover, studies beginning >80 years ago [7][8][9] have demonstrated the critical role of cardiac ANS in cardiac arrhythmogenesis. This topic has garnered much recent interest because of mounting evidence showing that neural modulation either by ablation or stimulation can effectively control a wide spectrum of cardiac arrhythmias. [10][11][12][13] In this review, we will briefly discuss the anatomic aspects of cardiac ANS, focusing on how autonomic activities influence cardiac electrophysiology. We will also discuss specific autonomic triggers of various cardiac arrhythmias, including atrial fibrillation (AF), ventricular arrhythmias, and inherited arrhythmia syndromes. Lastly, we will discuss the latest avenues of research and clinical trials regarding the application of neural modulation in the treatment of specific cardiac arrhythmias.

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Section: Atrial Fibrillationmentioning

confidence: 99%

Role of the Autonomic Nervous System in Modulating Cardiac Arrhythmias

Shen

Zipes

2014

Circulation Research

687

543

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“…11 Neurotransmitters released by postganglionic axons of one limb can readily act on nerve terminals of the other, and activation of peripheral components of one elicits activity in the other (reciprocal activation and accentuated antagonism) 11,12 ; it is, thus, difficult to imagine isolated and independent adrenergic or vagal effects in complex arrhythmias, like AF. Supporting evidence for potential clinical implications of these notions comes from several experimental and clinical studies, indicating that a primary increase in adrenergic tone followed by a marked modulation toward vagal predominance precedes episodes of paroxysmal AF, 10,[13][14][15][16] both in patients with lone paroxysmal AF and in those with structural heart disease. 15 This knowledge, mainly formulated by studies conducted during the past decade, is important for potential therapeutic modalities aimed at modulation of the autonomic system: inhibition of the sympathetic limb can be expected (at least in principle) to have an effect not only in the small subset of AF patients with predominantly adrenergic AF but also in the majority of patients with paroxysmal AF.…”

Section: Discussionmentioning

confidence: 98%

Central Sympathetic Inhibition to Reduce Postablation Atrial Fibrillation Recurrences in Hypertensive Patients

et al. 2014

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The objective of this prospective, randomized, controlled study was to test the hypothesis that central sympathetic inhibition, using the centrally acting agent moxonidine, can lead to reduced postablation recurrence risk in patients with hypertension who are undergoing pulmonary vein isolation for drug-refractory paroxysmal AF.Background-The autonomic system is an important determinant of atrial arrhythmogenesis. Current evidence indicates that a combined sympathovagal drive is most commonly responsible for eliciting atrial fibrillation (AF) episodes. The purpose of this study was to test whether moxonidine, a centrally acting sympathoinhibitory agent, can lead to a reduction in postablation AF recurrence. Methods and Results-This was a prospective, double-blinded, randomized study of 291 hypertensive patients with symptomatic paroxysmal AF who were scheduled to undergo pulmonary vein isolation. Patients were randomly assigned to receive either moxonidine (0.2-0.4 mg daily) or placebo, along with standard antihypertensive treatment. No significant differences in blood pressure levels were observed between the 2 groups. In the primary outcome analysis, mean recurrence-free survival was 467 days (95% CI, 445-489 days) in the moxonidine group as compared with 409 days (95% CI, 381-437 days) in control subjects (log rank test, P=0.006). The calculated 12-month recurrence rate estimates were 36.9% in the control group and 20.0% in the moxonidine group (P=0.007). Moxonidine treatment was associated with lower recurrence risk after adjustment for age, body mass index, number of AF episodes in the previous year, and left atrial diameter (adjusted hazard ratio, 0.35 [95% CI, 0.22-0.55]; P<0.001). Conclusions-Treatment with moxonidine is associated with less AF recurrences after ablation treatment for drugrefractory AF in patients with hypertension. The observed effect does not appear to depend on the antihypertensive action of this agent. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01791699.

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“…Rapidly firing foci initiating paroxysmal AF arise most commonly from the atrial myocardial sleeves that extend into pulmonary veins. (11) Although the pulmonary veins are the most common sites for ectopic focal triggers, they can also arise SIGNA VITAE 2017; 13(2): [14][15][16][17][18][19] elsewhere, including the posterior LA (left atrium), ligament of Marshall, coronary sinus, venae cavae, septum, and appendages. Atrial myocardial fibers are oriented in disparate directions, and possess unique anatomical and electrophysiological features for their arrhythmogenic nature.…”

Section: Pathophysiology Of Afmentioning

confidence: 99%

Do we need an individual approach to atrial fibrillation and adrenergic overload in the critically ill?

2017

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Despite catecholamines being lifesaving drugs, they can also be harmful. Adrenergic overload is one of the major causes of supra-and ventricular arrhythmias, which induce haemodynamic instability of critically ill patients. In this paper we will focus on the pathophysiology of atrial fibrillation (AF), the importance of adrenergic overload for triggering AF, the importance of the autonomic nervous system and we will challenge the importance of decreasing adrenergic load with selective and nonselective β-blockers, which have different effects on the metabolism of the severely ill. We will also emphasize the importance of an individual approach due to pharmacogenetic differences in β-adrenergic signalling.

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Competing autonomic mechanisms precedethe onset of postoperative atrial fibrillation

Cited by 190 publications

References 32 publications

Role of the Autonomic Nervous System in Modulating Cardiac Arrhythmias

Role of the Autonomic Nervous System in Modulating Cardiac Arrhythmias

Central Sympathetic Inhibition to Reduce Postablation Atrial Fibrillation Recurrences in Hypertensive Patients

Do we need an individual approach to atrial fibrillation and adrenergic overload in the critically ill?

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