Atrial contractile performance after cessation of atrial fibrillation

Leistad, E.; Christensen, Geir; Ilebekk, Arnfinn

doi:10.1152/ajpheart.1993.264.1.h104

Cited by 17 publications

(20 citation statements)

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“…Cumulative evidence suggests that changes in the [Ca 2+ ] i homeostasis may initiate electrical remodeling during atrial fibrillation, which is characterized by a marked shortening of the action potential plateau phase [55], [56], [57]. In future studies, the presented model, which is based on an atrial-specific description of Ca 2+ signaling, has thus great potential in elucidating the function of the remodeled cells with altered Ca 2+ homeostasis and SL ion currents.…”

Section: Discussionmentioning

confidence: 99%

Impact of Sarcoplasmic Reticulum Calcium Release on Calcium Dynamics and Action Potential Morphology in Human Atrial Myocytes: A Computational Study

2011

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Electrophysiological studies of the human heart face the fundamental challenge that experimental data can be acquired only from patients with underlying heart disease. Regarding human atria, there exist sizable gaps in the understanding of the functional role of cellular Ca2+ dynamics, which differ crucially from that of ventricular cells, in the modulation of excitation-contraction coupling. Accordingly, the objective of this study was to develop a mathematical model of the human atrial myocyte that, in addition to the sarcolemmal (SL) ion currents, accounts for the heterogeneity of intracellular Ca2+ dynamics emerging from a structurally detailed sarcoplasmic reticulum (SR). Based on the simulation results, our model convincingly reproduces the principal characteristics of Ca2+ dynamics: 1) the biphasic increment during the upstroke of the Ca2+ transient resulting from the delay between the peripheral and central SR Ca2+ release, and 2) the relative contribution of SL Ca2+ current and SR Ca2+ release to the Ca2+ transient. In line with experimental findings, the model also replicates the strong impact of intracellular Ca2+ dynamics on the shape of the action potential. The simulation results suggest that the peripheral SR Ca2+ release sites define the interface between Ca2+ and AP, whereas the central release sites are important for the fire-diffuse-fire propagation of Ca2+ diffusion. Furthermore, our analysis predicts that the modulation of the action potential duration due to increasing heart rate is largely mediated by changes in the intracellular Na+ concentration. Finally, the results indicate that the SR Ca2+ release is a strong modulator of AP duration and, consequently, myocyte refractoriness/excitability. We conclude that the developed model is robust and reproduces many fundamental aspects of the tight coupling between SL ion currents and intracellular Ca2+ signaling. Thus, the model provides a useful framework for future studies of excitation-contraction coupling in human atrial myocytes.

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Section: Discussionmentioning

confidence: 99%

Impact of Sarcoplasmic Reticulum Calcium Release on Calcium Dynamics and Action Potential Morphology in Human Atrial Myocytes: A Computational Study

2011

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“…26,27 In 2 studies, this atrial contractile dysfunction caused by short-term AF was ameliorated by pretreatment with verapamil. 7,8 However, those studies had major limitations characterized by poorly defined AF duration and absence of any assessment of atrial function before the onset of AF.…”

Section: Effects Of Verapamil On Mechanical Remodelingmentioning

confidence: 98%

Oral Verapamil Attenuates the Progression of Pacing-Induced Electrical and Mechanical Remodeling of the Atrium

Kinebuchi

Mitamura

Shiroshita-Takeshita

et al. 2004

Circ J

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apid atrial excitation, as seen during atrial fibrillation (AF), modifies the electrophysiological and mechanical functions of the chamber, thereby promoting the perpetuation of arrhythmias and clot formation. Even brief periods of atrial tachycardia can shorten the atrial effective refractory period (ERP), with loss of rate adaptation 1-6 and development of contractile abnormalities. 7,8 Several experimental and clinical studies have suggested that Ca overload plays a major role in the electrical and mechanical remodeling caused by prolonged rapid atrial excitation. [9][10][11][12][13] Other studies have demonstrated that AF-induced electrical and mechanical dysfunction can be reduced by pretreatment with a Ca blocker, verapamil; 14-17 however, the long-term effects of verapamil on both electrical and mechanical remodeling remain controversial. We recently reported that atrial electrical remodeling is, to at least some degree, positively correlated with mechanical remodeling in a canine rapid atrial pacing model 18 and the purpose of the present study was to demonstrate whether verapamil can prevent both electrical and mechanical atrial remodeling in a canine rapid pacing model. Methods Animal PreparationThe study protocol was approved by the institutional scientific review committee. For this study, we used 16 adult mongrel dogs of either sex weighing 9-15 kg (average, 12 kg). The dogs were anesthetized with an intravenous injection of pentobarbital sodium (20 mg/kg iv) and ketamine chloride (15 mg/kg iv), then intubated and placed on mechanical ventilation with a volume-cycled ventilator (Model 607 Ventilator Harvard Apparatus). The heart was exposed via a right fifth intercostal thoracotomy and suspended in a pericardial cradle with continuous surface electrocardiographic (ECG) monitoring. A custom-designed set of electrodes, comprising a pair of electrodes with a distal hook for pacing and 2 pairs of electrodes with an interelectrode distance of 15 mm aligned proximally serving for recording, was sutured to the epicardial surface of the ridge of the right atrial appendage (RAA). Each pair of electrodes was positioned with interpolar distance of 2 mm. After closure of the thorax, the distal ends of these electrode leads were tunneled subcutaneously and exposed at the back, and then connected to a pacemaker (Nihon Kohden, output of 5 V with 0.7 ms pulse duration) in the jacket. The pacemaker was programmed to provide rapid atrial pacing at 400 ppm. This rate was maintained except for a brief period for measurement of electrophysiological and mechanical parameters. Following the surgical procedure, all dogs were administered oral antibiotics during the 5-day recovery period.

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“…15 Indeed, a transient period of hypercontractility has been shown to occur immediately after termination of relatively short (Յ30 minutes) but not after long periods of AF in porcine atria in vivo. 16 Vagotonic AF is believed to be uncommon in clinical practice 11 ; accordingly, due caution must be exercised in extrapolating to humans the mechanism of reinduction of AF observed in presence of ACh in isolated canine right atria. This cautionary stance notwithstanding, the effect of ACh to abbreviate atrial repolarization may be pertinent in that it mimics the abbreviation of atrial APD and refractoriness resulting from electrical remodeling of the atria during the initial hours and days of AF.…”

Section: Study Limitationsmentioning

confidence: 99%

Reinduction of Atrial Fibrillation Immediately After Termination of the Arrhythmia Is Mediated by Late Phase 3 Early Afterdepolarization–Induced Triggered Activity

2003

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Background-Atrial fibrillation (AF) at times recurs immediately after termination of the arrhythmia. The mechanism (s) responsible for the extrasystole that reinduces AF is largely unknown. We hypothesized that abbreviation of action potential duration (APD) would permit very rapid rates of excitation, known to induce intracellular calcium loading, which in turn could promote delayed and/or early afterdepolarizations (EADs). Methods and Results-Acetylcholine (ACh, 1 mol/L) was used to abbreviate atrial APD and permit rapid-pacing induction of AF in isolated coronary-perfused canine right atria. Transmembrane action potentials, pseudo-ECG, and tension development were recorded. AF or rapid pacing was associated with an increase in tonic tension. Termination of AF or rapid pacing (cycle length, 150 to 80 ms) resulted in a dramatic rise of phasic tension, prolongation of repolarization of the initial beats at the regular rate (cycle length, 700 ms), and the development of late phase 3 EADs and extrasystoles. These extrasystoles initiated AF in 15 cases (involving 9 right atria) within the first 11 seconds after termination of AF or rapid pacing. This novel EAD mechanism is observed only in association with marked APD abbreviation. The calcium channel blocker nifedipine reduced, and the sarcoplasmic reticulum calcium release blocker ryanodine eliminated, the post-rapid pacing-induced increase in phasic tension, late phase 3 EADs, and extrasystoles that initiate AF. Conclusions-These data suggest that calcium overload conditions present after termination of vagally mediated AF contribute to the development of late phase 3 EAD-induced triggered activity and that this mechanism may be responsible for the extrasystolic activity that reinitiates AF. Key Words: action potentials Ⅲ fibrillation Ⅲ calcium Ⅲ triggered activity A number of studies have documented the reinitiation of atrial fibrillation (AF) by an atrial extrasystole arising soon after termination of the arrhythmia. [1][2][3][4] Although a reentrant mechanism is thought to underlie the maintenance of the arrhythmia, the mechanism(s) responsible for the premature beat(s) that reinduce AF is largely unknown. Immediate recurrence of AF (IRAF) was found to be unexpectedly high in patients with implanted atrial defibrillators, occurring after 27% of successful shocks. 5 Patients who experience early AF recurrence after cardioversion have been shown to display briefer mean AF cycle lengths (CLs) than those who do not. 6 In addition, acute treatment with the calcium channel blocker verapamil has been shown to reduce IRAF after electrical cardioversion in the clinic. 4 These observations highlight the importance of rapid rates and calcium homeostasis in the early reinitiation of AF.Like electrical remodeling, 7 vagal influences are known to cause a marked abbreviation of atrial action potential duration (APD), permitting activation of atrial cells at much higher frequencies than otherwise possible. We hypothesized that immediately after termination of these rapid ra...

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Atrial contractile performance after cessation of atrial fibrillation

Cited by 17 publications

References 0 publications

Impact of Sarcoplasmic Reticulum Calcium Release on Calcium Dynamics and Action Potential Morphology in Human Atrial Myocytes: A Computational Study

Impact of Sarcoplasmic Reticulum Calcium Release on Calcium Dynamics and Action Potential Morphology in Human Atrial Myocytes: A Computational Study

Oral Verapamil Attenuates the Progression of Pacing-Induced Electrical and Mechanical Remodeling of the Atrium

Reinduction of Atrial Fibrillation Immediately After Termination of the Arrhythmia Is Mediated by Late Phase 3 Early Afterdepolarization–Induced Triggered Activity

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