Method for Simultaneous Epicardial and Endocardial Mapping of In Vivo Canine Heart: Application to Atrial Conduction Properties and Arrhythmia Mechanisms

Derakhchan, Kathy; Li, Danshi; Courtemanche, Marc; Smith, Benjamin M.; Brouillette, Judith; Pagé, Pierre; Nattel, Stanley

doi:10.1046/j.1540-8167.2001.00548.x

Cited by 76 publications

(51 citation statements)

References 17 publications

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“…30 and 31). Lewis' mother wave concept has recently received support from a range of experimental observations that point to single dominant rotors underlying AF in a variety of experimental paradigms (4,5,14,24,45).…”

Section: Discussionmentioning

confidence: 99%

Substrate size as a determinant of fibrillatory activity maintenance in a mathematical model of canine atrium

Zou¹,

Kneller²,

Leon³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Nattel. Substrate size as a determinant of fibrillatory activity maintenance in a mathematical model of canine atrium. Am J Physiol Heart Circ Physiol 289: H1002-H1012, 2005. First published April 22, 2005; doi:10.1152/ajpheart.00252.2005.-Tissue size has been considered an important determinant of atrial fibrillation (AF), but recent work has questioned the critical size hypothesis. Here, we use a previously developed mathematical model of the two-dimensional canine atrium with realistic action potential, ionic, and conduction properties to address substrate size effects on the maintenance of fibrillatory activity. Cholinergic AF was simulated at different acetylcholine (ACh) concentrations ([ACh]) and distributions, with substrate area varied 11.1-fold. Automated phase singularity detection was used to facilitate the analysis of arrhythmic activity. The duration of activity induced by a single extrastimulus increased with increasing substrate dimensions. Two general mechanisms underlying activity were observed and were differentially affected by substrate size. For large mean [ACh], single primary rotors anchored in low-[ACh] zones maintained activity and substrate dimensions were not critical. At lower mean [ACh], extensive spiral wave meander prevented the emergence of single stable rotors. Prolonged activity was favored when substrate size permitted a sufficiently large number of simultaneous longer-lasting rotors that extinction of all was unlikely. Thus either single dominant rotor or multiple reentrant spiral generator mechanisms could maintain fibrillatory activity in this model and were differentially dependent on substrate size. These results speak to recent debates about the role in AF of single driver rotors versus multiple reentrant circuit mechanisms by suggesting that either may maintain fibrillatory atrial activity depending on atrial size and electrophysiological properties.heart arrhythmia mechanisms; phase singularity; spiral waves; bioelectricity computer modeling; cardiac action potential ATRIAL FIBRILLATION (AF) is the most common sustained arrhythmia in humans, is an important contributor to human morbidity and possibly mortality, and presents a variety of therapeutic challenges (29). The mechanisms underlying AF have been a subject of long-standing debate and recent intense investigation (31). Some of the basic properties of fibrillation induced by faradic stimulation were described by MacWilliam (23) in the late 1800s, along with the discoordinating effects of vagal nerve activation on atrial fluttering caused by faradic currents. MacWilliam also showed that ventricular fibrillation could persist in isolated sections of ventricular tissue. Garrey (8) extended MacWilliam's approach and noted that the ability of isolated tissue to fibrillate depends on its mass, introducing the notion of a "critical mass" for fibrillation related to conditions required for multiple circuit reentry. This idea was later incorporated in Moe's "multiple wavelet hypothesis" (26). An alternative conceptual fra...

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Section: Discussionmentioning

confidence: 99%

Substrate size as a determinant of fibrillatory activity maintenance in a mathematical model of canine atrium

Zou¹,

Kneller²,

Leon³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…2,12 CHF produces important atrial fibrosis, which is associated with localized conduction abnormalities that are believed to promote AF by stabilizing reentry. 2,13 However, CHF also produces substantial atrial ionic remodeling. 3 Among other changes, CHF increases expression of I NCX , an important carrier of postrepolarization transient inward currents that cause DADs.…”

Section: Relationship To Previous Studies Of Af Mechanisms In Experimmentioning

confidence: 99%

Dissociation Between Ionic Remodeling and Ability to Sustain Atrial Fibrillation During Recovery From Experimental Congestive Heart Failure

et al. 2004

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Background— Congestive heart failure (CHF) downregulates atrial transient outward ( I to ), slow delayed rectifier ( I Ks ), and L-type Ca 2+ ( I Ca,L ) currents and upregulates Na + -Ca 2+ exchange current ( I NCX ) (ionic remodeling) and causes atrial fibrosis (structural remodeling). The relative importance of ionic versus structural remodeling in CHF-related atrial fibrillation (AF) is controversial. Methods and Results— We measured hemodynamic and echocardiographic parameters, mean duration of burst pacing–induced AF (DAF), and atrial-myocyte ionic currents in dogs with CHF induced by 2-week ventricular tachypacing (240 bpm), CHF dogs allowed to recover without pacing for 4 weeks (REC), and unpaced controls. Left ventricular ejection fraction averaged 58.6±1.2% (control), 36.2±2.3% (CHF, P <0.01), and 57.9±1.6% (REC), indicating full hemodynamic recovery. Similarly, left atrial pressures were 2.2±0.3 (control), 13.1±1.5 (CHF), and 2.4±0.4 (REC) mm Hg. CHF reduced I to density by ≈65% ( P <0.01), decreased I Ca,L density by ≈50% ( P <0.01), and diminished I Ks density by ≈40% ( P <0.01) while increasing I NCX density by ≈110% ( P <0.05). In REC, all ionic current densities returned to control values. DAF increased in CHF (1132±207 versus 14.3±8.8 seconds, control) and remained increased with REC (1014±252 seconds). Atrial fibrous tissue content also increased in CHF (2.1±0.2% for control versus 10.2±0.7% for CHF, P <0.01), with no recovery observed in REC (9.4±0.8%, P <0.01 versus control, P =NS versus CHF). Conclusions— With reversal of CHF, there is complete recovery of ionic remodeling, but the prolonged-AF substrate and structural remodeling remain. This suggests that structural, not ionic, remodeling is the primary contributor to AF maintenance in experimental CHF.

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“…Our inability to map complete circuits may have been a result of endocardial or intramural components. We have previously performed combined atrial endocardial and epicardial mapping in situ 24 ; however, the need for an atriotomy, the limited resolution of the 64-electrode endocardial balloon array, and the hemodynamic effects of prolonged mapping with the system made it unsuitable for the present study. More detailed mapping work will be needed to define the precise mechanisms of prolonged AF during atrial ischemia.…”

Section: Potential Limitationsmentioning

confidence: 99%

Atrial Ischemia Promotes Atrial Fibrillation in Dogs

et al. 2003

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Background-Coronary artery disease is a significant risk factor for atrial fibrillation (AF), but the basis for this association is incompletely understood. The present study evaluated the hypothesis that atrial ischemia can create a substrate for AF maintenance. Methods and Results-Atrial ischemia was induced by occlusion of an atrial arterial branch that did not provide blood flow to the ventricles. Atrial-arterial occlusion increased the duration of AF induced by burst pacing from 57Ϯ32 seconds (control) to 803Ϯ214 seconds (PϽ0.001) after 0.5 hour of occlusion and to 887Ϯ209 seconds (PϽ0.001) after 3 hours of occlusion. Prolonged AF (Ͼ20 minutes) was induced in 0 of 16 dogs (0%) under control conditions, 7 of 16 (44%, PϽ0.01) at 0.5 to 3 hours, and 5 of 13 (38%, PϽ0.01) 3 to 5 hours after occlusion. Atrial conduction was slowed substantially within the ischemic zone: eg, conduction delay was 8Ϯ1 ms at a cycle length of 200 ms, control, versus 22Ϯ5 ms (PϽ0.01) after 0.5 hours and 27Ϯ5 ms (PϽ0.001) after 3 hours of ischemia. Refractoriness was initially unaffected but was prolonged 5 hours after occlusion. Phase-delay analysis and high-density mapping confirmed severe conduction slowing in the ischemic zone. Histological examination confirmed the location of ischemic regions and revealed extensive ischemia-induced necrosis at sites of conduction delay. Conclusions-Experimental atrial ischemia creates a substrate for AF maintenance, apparently by causing local conduction slowing that promotes reentry. These results suggest that atrial ischemia may significantly promote AF, and may be relevant to AF mechanisms in association with coronary artery disease.

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Method for Simultaneous Epicardial and Endocardial Mapping of In Vivo Canine Heart: Application to Atrial Conduction Properties and Arrhythmia Mechanisms

Abstract: We conclude that activation mapping using simultaneous recording from both epicardial and endocardial surfaces provides potentially important insights into the mechanisms of atrial conduction and arrhythmogenesis.

Cited by 76 publications

References 17 publications

Substrate size as a determinant of fibrillatory activity maintenance in a mathematical model of canine atrium

Substrate size as a determinant of fibrillatory activity maintenance in a mathematical model of canine atrium

Dissociation Between Ionic Remodeling and Ability to Sustain Atrial Fibrillation During Recovery From Experimental Congestive Heart Failure

Atrial Ischemia Promotes Atrial Fibrillation in Dogs

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