Effect of atrioventricular interval during pacing or reciprocating tachycardia on atrial size, pressure, and refractory period. Contraction-excitation feedback in human atrium.

Klein, Lawrence S.; Miles, William M.; Zipes, Douglas P.

doi:10.1161/01.cir.82.1.60

Cited by 113 publications

(56 citation statements)

References 13 publications

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“…27 However, atrial pressure elevation caused by AV interval manipulation has been associated with either an increase or no change in atrial ERPs. 9,10 Our findings of nonuniform prolongation of atrial ERPs, increased PWD, and impairment of sinus node function after long-term loss of AV synchrony are consistent with those from prior human studies of short-term atrial dilatation and animal studies of long-term atrial dilatation. 5,9,18,20,21 Persistence of ERP adaptation to rate contrasts with animal studies of electrical remodeling that show loss of rate adaptation.…”

Section: Electrical Remodeling Associated With Atrial Dilatationsupporting

confidence: 87%

“…Human data have, thus far, been limited to short-term pacing studies; here, too, conflicting data exist. 9,10 An emerging body of evidence suggests that long-term asynchronous ventricular pacing (VVI) is associated with an increased incidence of AF; ongoing multicenter trials are addressing this issue. [11][12][13][14] The mechanism underlying this observation is unknown.…”

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confidence: 99%

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Electrical Remodeling of the Atria Following Loss of Atrioventricular Synchrony

et al. 1999

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Background-Evidence suggests that an increased incidence of atrial fibrillation occurs in patients undergoing single-chamber ventricular pacing (VVI) when compared with those undergoing single-chamber atrial pacing (AAI) or those having dual-chamber atrioventricular pacing (DDD). The mechanism for this is unknown. We hypothesized that long-term loss of atrioventricular (AV) synchrony leads to atrial electrical remodeling: a potential explanation for this difference. Methods and Results-The study was a prospective, randomized comparison between 18 patients paced in VVI mode and 12 patients paced in DDD mode for 3 months. Under autonomic blockade, effective refractory periods (ERPs) from the lateral right atrium (RA), RA appendage, RA septum, and coronary sinus-corrected sinus node recovery times (cSNRTs), as well as P-wave duration (PWD), and biatrial diameters were measured at baseline and 3 months. The VVI group was then programmed to DDD pacing and reevaluated after a further 3 months. After long-term VVI pacing, ERPs at all 4 atrial sites increased significantly in a nonuniform fashion in association with biatrial dilatation. PWD and cSNRTs also prolonged significantly. With the reestablishment of AV synchrony, ERPs, PWD, cSNRTs, and biatrial dimensions returned to baseline levels. In the 12 patients who underwent long-term DDD pacing from baseline, no significant changes in atrial electrophysiology or biatrial dimensions were demonstrated. Conclusions-Long-term loss of AV synchrony induced by VVI pacing is associated with atrial electrical remodeling, which is reversible after the reestablishment of AV synchrony with DDD pacing. This process may be partly responsible for the higher incidence of atrial fibrillation in patients undergoing VVI pacing compared with AV sequential pacing.

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Section: Electrical Remodeling Associated With Atrial Dilatationsupporting

confidence: 87%

mentioning

confidence: 99%

Electrical Remodeling of the Atria Following Loss of Atrioventricular Synchrony

et al. 1999

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“…This model mimics heart failure-related AF associated with regional atrial conduction slowing due to increased collagen turnover and interstitial fibrosis (16). However, it also results in substantial interanimal variability in AF production and in overt congestive heart failure, occasionally leading to premature death (prior to completion of the protocol) (11).An ideal AF model should be simple, clinically relevant (i.e., simulate human disease), and allow for reliable sustained AF production and thereby sensitivity to intervention (25).Based on these considerations and inspired by observations made in humans that a very short ventriculoatrial interval (during reciprocating tachycardia) can cause a marked increase in atrial pressure by inducing atrial contractions during mitral valve closure (18,20,31), we developed a fast simultaneous atrioventricular pacing (SAVP) model. This new model was designed to produce hemodynamic consequences that have been shown to lead to atrial electrical and structural remodeling and AF vulnerability (15).…”

mentioning

confidence: 99%

“…Based on these considerations and inspired by observations made in humans that a very short ventriculoatrial interval (during reciprocating tachycardia) can cause a marked increase in atrial pressure by inducing atrial contractions during mitral valve closure (18,20,31), we developed a fast simultaneous atrioventricular pacing (SAVP) model. This new model was designed to produce hemodynamic consequences that have been shown to lead to atrial electrical and structural remodeling and AF vulnerability (15).…”

mentioning

confidence: 99%

Experimental studies of atrial fibrillation: a comparison of two pacing models

Laurent¹,

Moe²,

Hu³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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is a well-established animal model of atrial fibrillation (AF). However, this model is limited by a high mortality rate and severe heart failure. The purpose of our study was to assess a new canine model of inducible AF. We performed acute, short-term, simultaneous atrioventricular pacing (SAVP) and RVP (in random order) in 14 dogs for 30 s. SAVP produced more echocardiographic pulmonary venous flow reversal, a greater increase in mean pulmonary capillary wedge pressure, and a significantly greater decrease in left atrial emptying function (Ϫ84.4 Ϯ 38.6% vs. Ϫ23.7 Ϯ 27.1%, P Ͻ 0.05) than RVP. Thirty dogs were randomized to three, longer-term, study groups: eight dogs in the control group (no pacing), eight dogs in the RVP group (2 wk at 240 beats/min followed by 3 wk at 220 beats/min), and fourteen dogs in the SAVP group (2 wk at 220 beats/min). SAVP induced less left ventricular dysfunction but more left atrial dysfunction than RVP. SAVP dogs had similar atrial effective refractory periods as RVP dogs but more heterogeneity in conduction and more AF inducibility (83% vs. 40%, P Ͻ 0.05) and maintenance (median 1,660 vs. 710 s, P Ͻ 0.05) than RVP dogs. SAVP induced more collagen turnover and was associated with a significantly greater increase in type III collagen in the atria compared with RVP dogs (6.9 Ϯ 1.5 vs. 4.8 Ϯ 1.6, respectively, P Ͻ 0.05 vs. 1.1 Ϯ 0.7 in unpaced control dogs). In conclusion, the SAVP model induced profound mechanical and substrate atrial remodeling and reproducible sustained AF. This new model is clinically relevant and may be useful for testing AF interventions. experimental atrial arrhythmia; extracellular matrix; remodeling ATRIAL FIBRILLATION (AF) is the most common sustained cardiac arrhythmia and frequently causes cardiovascular morbidity and mortality. Although AF can occur in patients with normal hearts (lone AF), the majority of patients with AF have coexisting structural heart disease, most commonly hypertension or heart failure (1). To better understand the relationship between the atrial substrate and AF vulnerability and to evaluate therapies for AF, multiple animal models of AF have been developed. They include sterile pericarditis, acute atrial ischemia, atrial volume overload, mitral regurgitation, pacemakerinduced atrial tachycardia, and ventricular pacing-induced heart failure (25).One of the most commonly used models employs rapid atrial pacing (RAP) at 400 beats/min with control of the ventricular response (atrioventricular node ablation) (24). This model helps to understand the mechanisms underlying the tendency of paroxysmal AF to become persistent but does not relate closely to the most frequent clinical conditions associated with AF, in which the left atrium (LA) dilates and is fibrosed, exhibiting conduction slowing (14, 21). The other commonly used model is rapid ventricular pacing (RVP) to induce heart failure (240 -280 beats/min for 3-8 wk), sometimes combined with RAP (RVP at 240 beats/min for 2 wk combined with additional RAP at 400 beats/min during the sec...

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“…Unfortunately, the clinical data are less clear. Whereas Klein et al 44 reported a marked increase in atrial effective refractory period in association with increased atrial pressures mediated by a short AV interval, Calkins et al 45 found no meaningful change in a similar experiment. Thus, whereas AF certainly is more prevalent in patients with dilated left atria, atrial dilatation may be due to many factors, including anatomic remodeling and scarring due to chronic increases in pressures, ischemia, or neurohormonal alterations.…”

Section: Atrial Fibrillationmentioning

confidence: 94%