Action potential duration restitution kinetics in human atrial fibrillation

Kim, Byung Soo; Kim, Young Hoon; Hwang, Gyo Seung; Pak, Hui Nam; Lee, Sang Chil; Shim, Wan Joo; Oh, Dong Joo; Ro, Young Moo

doi:10.1016/s0735-1097(02)01760-6

Cited by 107 publications

(105 citation statements)

References 27 publications

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“…This hypothesis was inspired by several observations. First, elevated heart rates may lead to alternans of the T wave, 2 ventricular APD, 3 and, in preliminary reports from our laboratory and others, 4 atrial APD. Second, numeric simulations have elegantly described mechanisms through which rate-related APD alternans, indicating temporal heterogeneity in repolarization, may lead to reentry.…”

mentioning

confidence: 83%

Alternans of Atrial Action Potentials During Atrial Flutter as a Precursor to Atrial Fibrillation

et al. 2002

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Background-The mechanisms underlying the transition of typical atrial flutter (Afl) to fibrillation (AF) remain unclear.We set out to test the hypothesis that Afl disorganizes to AF via alternans of atrial action potentials. Methods and Results-In 38 patients with Afl, monophasic action potentials (MAPs) were recorded at the isthmus and either high or low right atrium (HRA, LRA) during overdrive pacing to 160 ms or to the initiation of AF, whichever came first. MAP duration measured at 90% repolarization was longer at the isthmus in all patients, and failed to shorten with rate, compared with the HRA (nϭ38) or LRA (nϭ5). In 20 patients who developed AF, progressive pacing first caused alternans of isthmus MAP duration and amplitude at mean cycle length of 219Ϯ45 ms, followed by AF at a mean onset cycle length of 184Ϯ38 ms. Subsets of this group showed spontaneous action potential duration alternans at the isthmus (11 of 20 patients) and 2:1 isthmus conduction block immediately preceding AF (4 of 20 patients). In the 18 patients who did not develop AF, MAP alternans was less common (9 of 18 patients; PϽ0.0003), and occurred only at faster pacing (cycle lengthϭ169Ϯ25 ms; PϽ0.05). Conclusions-In patients with typical Afl, action potential duration rate maladaptation at the isthmus may lead to action potential duration alternans and conduction block preceding the transition to AF. These isthmus characteristics may enable the spontaneous initiation of AF through wavefront fractionation and may explain the benefits of isthmus ablation in preventing AF recurrence.

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confidence: 83%

Alternans of Atrial Action Potentials During Atrial Flutter as a Precursor to Atrial Fibrillation

et al. 2002

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“…In some cases, more significant rate adaptation can be observed at the shortest CLs (Kim et al, 2002;Dobrev and Ravens, 2003). Similar alterations to those given by Courtemanche et al (1999) have been observed in other experiments as well (Dobrev and Ravens, 2003), including substantial reductions in I Ca,L (Bosch et al, 1999;Van Wagoner et al, 1999;Skasa et al, 2001;Workman et al, 2001) and I to (Van Wagoner et al, 1997;Bosch et al, 1999;Brandt et al, 2000;Grammer et al, 2000;Workman et al, 2001).…”

Section: Atrial Fibrillation-induced Changes In Rate Dependence and Mmentioning

confidence: 99%

Dynamics of human atrial cell models: Restitution, memory, and intracellular calcium dynamics in single cells

Cherry

Hastings

Evans

2008

Progress in Biophysics and Molecular Biology

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Mathematical models of cardiac cells have become important tools for investigating the electrophysiological properties and behavior of the heart. As the number of published models increases, it becomes more difficult to choose a model appropriate for the conditions to be studied, especially when multiple models describing the species and region of the heart of interest are available. In this paper, we will review and compare two detailed ionic models of human atrial myocytes, the Nygren et al. model (NM) and the Courtemanche et al. model (CM). Although both models include the same transmembrane currents and are largely based on the same experimental data from human atrial cells, the two models exhibit vastly different properties, especially in their dynamical behavior, including restitution and memory effects. The CM produces pronounced rate adaptation of action potential duration (APD) with limited memory effects, while the NM exhibits strong rate dependence of resting membrane potential (RMP), limited APD restitution, and stronger memory, as well as delayed afterdepolarizations and auto-oscillatory behavior upon cessation of rapid pacing. Channel conductance modifications based on experimentally measured changes during atrial fibrillation modify rate adaptation and memory in both models, but do not change the primary rate-dependent properties of APD and RMP for the CM and NM, respectively. Two sets of proposed changes to the NM that yield a spike-and-dome action potential morphology qualitatively similar to the CM at slow pacing rates similarly do not change the underlying dynamics of the model. Moreover, interchanging the formulations of all transmembrane currents between the two models while leaving calcium handling and ionic concentrations intact indicates that the currents strongly influence memory and the rate adaptation of RMP, while intracellular calcium dynamics primarily determine APD rate adaptation. Our results suggest that differences in intracellular calcium handling between the two human atrial myocyte models are responsible for marked dynamical differences and may prevent reconciliation between the models by straightforward channel conductance modifications.

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“…The time course of restitution obtained by S 1 S 2 was fitted using a monoexponential equation and Origin 7.0 software (OriginLab Corp., Northampton, MA, USA), and the maximum slope of the APDR curve (slopemax) was obtained by the maximum value of the first derivative of the monoexponential equation fitting curve. [21][22][23][24] (Tables II and III). Electrophysiologic study: There was no significant difference between the groups in terms of the AH interval or the HV interval (Table IV).…”

Section: Construction Of the Action Potential Duration Restitution (Amentioning

confidence: 99%

“…Thus, we included male and female RA MAPD 80 in the control group. We did not compare the IACT and APD restitution characteristics between Brugada patients and control AF patients, but Kim, et al 22) compared the APD restitution curve between patients with chronic AF, paroxysmal AF, and control patients. Although the method of calculating slopemax was slightly different, they reported the slopemax was 1.4 ± 0.3 in chronic AF patients, 1.1 ± 0.4 in paroxysmal AF patients, and 0.5 ± 0.3 in control patients.…”

Section: Study Limitationsmentioning

confidence: 99%

Abnormal Atrial Repolarization and Depolarization Contribute to the Inducibility of Atrial Fibrillation in Brugada Syndrome

et al. 2010

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SummaryBrugada syndrome is often accompanied by atrial tachyarrhythmia, such as atrial fibrillation (AF). The aim of this study was to examine atrial vulnerability in patients with Brugada syndrome. Two groups of patients were compared: 18 patients with Brugada syndrome (Brugada syndrome group) and 11 age-matched patients with neither organic heart disease nor AF episodes (control group). Programmed electrical stimulation was performed from the right atrium (RA), and the effective refractory period of the right atrium (ERP-RA), interatrial conduction time (IACT), monophasic action potentials (MAPs) at the high RA, and the inducibility of AF lasting > 30 seconds were studied. MAP duration at 80% repolarization (MAPD 80 ) was calculated. AF was induced with a single extrastimulus or double extrastimuli in all patients with Brugada syndrome but in none of the control patients. The ERP-RA did not differ between the groups. IACT at the shortest diastolic interval was significantly increased in the Brugada syndrome group compared to that in the control group. The maximum slope of the MAPD 80 restitution curve was significantly steeper in the Brugada syndrome group than in the control group (2.4 ± 2.0 versus 0.82 ± 0.36, P < 0.02). Ventricular fibrillation was induced with ventricular programmed stimulation in all Brugada syndrome patients. Both abnormal interatrial conduction and steep restitution of action potential duration may contribute to the atrial arrhythmogenicity in Brugada syndrome. (Int Heart J 2010; 51: 159-165)

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Action potential duration restitution kinetics in human atrial fibrillation

Cited by 107 publications

References 27 publications

Alternans of Atrial Action Potentials During Atrial Flutter as a Precursor to Atrial Fibrillation

Alternans of Atrial Action Potentials During Atrial Flutter as a Precursor to Atrial Fibrillation

Dynamics of human atrial cell models: Restitution, memory, and intracellular calcium dynamics in single cells

Abnormal Atrial Repolarization and Depolarization Contribute to the Inducibility of Atrial Fibrillation in Brugada Syndrome

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