Steady-state and nonsteady-state action potentials in fibrillating canine atrium: abnormal rate adaptation and its possible mechanisms

Hara, Motoki; Shvilkin, Alexei; Rosen, Michael R.; Danilo, Peter; Boyden, Penelope A.

doi:10.1016/s0008-6363(99)00044-9

Cited by 62 publications

(60 citation statements)

References 43 publications

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“…Mechanistically, AF-related APD maladaptation may be associated with reduced mRNA expression for the ␣-subunit of the L-Ca 2ϩ channel, 13 may reflect cytosolic Ca 2ϩ overload, 16 and is attenuated by ryanodine. 12 Although these calcium-dependent mechanisms may be inhibited by L-Ca 2ϩ antagonists, our non-AF-inducible patients (without maladaptation at these rates; Figure 1) did not have higher rates of use of such medications (Table).…”

Section: Nonuniformity and Rate Maladaptation Of Atrial Apdmentioning

confidence: 71%

“…Indeed, studies in canine atria emphasize that factors including spatial nonuniformity, rather than cellular electrophysiology, influence the stability of AF. 12 Although the repolarization dynamics of the isthmus are poorly described, atrial effective refractory period (ERP) in post-AF cardioversion patients lengthened paradoxically at shorter CLs in the LRA than the HRA, coronary sinus, or control patients. 17 It is unclear whether the isthmus was included with LRA in that study.…”

Section: Nonuniformity and Rate Maladaptation Of Atrial Apdmentioning

confidence: 99%

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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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Section: Nonuniformity and Rate Maladaptation Of Atrial Apdmentioning

confidence: 71%

Section: Nonuniformity and Rate Maladaptation Of Atrial Apdmentioning

confidence: 99%

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

et al. 2002

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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%

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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“…IKr or IKs may or may not be altered [5,36]. Several studies have reported increased background inward-rectifier current, attributed to IK 1 , in AF [36,37,38] that may contribute to the reduced action potential duration [39]. Atrial remodeling in experimental heart failure is distinctly different from atrial tachycardia remodeling [39].…”

Section: Remodeling Of Atrial Myocardium In Af; Sarcolemmal Ion Channelsmentioning

confidence: 99%

Is there a role for remodeled connexins in AF? No simple answers

Duffy¹,

Wit²

2008

Journal of Molecular and Cellular Cardiology

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Steady-state and nonsteady-state action potentials in fibrillating canine atrium: abnormal rate adaptation and its possible mechanisms

Cited by 62 publications

References 43 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

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

Is there a role for remodeled connexins in AF? No simple answers

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