Cumulative effects of cycle length on ventricularrefractoriness in man

Brownstein, Sheldon L.; Blackwell, William; Welch, William J.; Bauernfeind, Robert A.

doi:10.1016/s0002-8703(05)80023-7

Cited by 8 publications

(5 citation statements)

References 22 publications

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“…16 It also depends on whether the cycle change is from short to long or vice versa. 17,18 The present study has shown that in the epicardial border of the ischemic zone the lengthening of ERP associated with a single long cycle ranged from 44% to 79% of the total increase in ERP after a series of eight long cycles. Epicardial sites closer to the center of the ischemic zone that showed more electrophysiological abnormality as suggested by their longer ERP showed greater dependence on the immediately preceding cycle compared with more normal sites located close to the border of the ischemic zone.…”

Section: Effects Of Sudden Change In Cycle Length On Ventricular Refrmentioning

confidence: 56%

Reentrant ventricular arrhythmias in the late myocardial infarction period: mechanism by which a short-long-short cardiac sequence facilitates the induction of reentry.

1991

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The electrophysiological mechanism by which a short-long-short stimulated cardiac sequence facilitates the induction of ventricular tachyarrhythmia was investigated in dogs 4 days after ligation of the left anterior descending coronary artery. In these dogs, reentry develops in the surviving electrophysiologically abnormal epicardial layer that overlies the infarct zone when premature stimulation results in a critically long arc of functional conduction block. The activation wavefront circulates around both ends of the arc, coalesces, and conducts slowly distal to the arc before reactivating sites proximal to the arc to initiate a figure-eight reentrant circuit. Epicardial isochronal activation maps and effective refractory periods (ERPs) were determined during three different stimulation protocols: A, a basic train of eight beats at a cycle length of 300 msec followed by a single premature stimulus (S2); B, a basic train of eight beats at a cycle length of 300 msec with abrupt lengthening of the last cycle of the train before S2 to 600 msec; C, a basic train of eight beats at a cycle length of 600 msec followed by S2. Protocol B was found to result in a differential lengthening of ERP at adjacent sites within the border of the epicardial ischemic zone, whereas protocols A and C induced, respectively, comparable shortening and lengthening of ERPs at the same sites. The differential lengthening of ERPs at adjacent sites resulted in an increased dispersion of refractoriness so that a premature stimulus induced functional conduction block between those sites. The development of a longer arc of conduction block and, hence, a longer reentrant pathway as well as slower conduction of the circulating wavefront during protocol B allowed more time for refractoriness to expire proximal to the arc and for the circulating wavefront to reexcite those sites to initiate reentry. The lengthening of ERP, associated with a single long cycle (protocol B), ranged from 44% to 79% of the total increase in ERP after a series of eight long cycles (protocol C). Epicardial sites with longer ERPs located close to the center of the ischemic zone showed more lengthening of refractoriness during protocol B compared with more normal sites near the border of the ischemic zone. This strongly suggests that the increased dispersion of refractoriness during protocol B is caused by the shorter memory of ischemic myocardium to the cumulative effects of preceding cycle lengths.

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Section: Effects Of Sudden Change In Cycle Length On Ventricular Refrmentioning

confidence: 56%

Reentrant ventricular arrhythmias in the late myocardial infarction period: mechanism by which a short-long-short cardiac sequence facilitates the induction of reentry.

1991

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“…However, the increase in pressure was associated with slowing of the sinus rate before the initiation of the eight-stimuli pacing run; the sinus bradycardia in turn, before the pacing run, could statistically account for the lengthening of refractoriness. Some kind of 'repolarization memory' has been described by Brownstein et al [20] . For this reason, in these experiments continuous drive of the atria was applied at a constant rate, while administering a premature stimulus after each eight driving stimulus.…”

Section: Discussionmentioning

confidence: 96%

Some observations on the mechanism of pressure related atrial fibrillation

Sideris

Toumanidis

Thodorakis

et al. 1994

European Heart Journal

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In order to investigate the effect of atrial pressure on the propensity of the atria to fibrillate and the mechanism of this association, the right atrial pressure was changed acutely by transfusion-bleeding in 12 anaesthetized open-chest dogs. Under various atrial pressures the conduction time was measured between two pairs of hook electrodes positioned on the two atrial appendages respectively. The effective refractory period was measured by continuous pacing of the right atrium at a 250 ms cycle length at double threshold intensity and interpolating a progressively earlier stimulus after each eighth paced beat. The propensity of fibrillation was studied by rapid (450 min-1) pacing of the atria at double threshold intensity for 10 s at different atrial pressures. At a high (> or = 14 mmHg) atrial pressure the conduction time (45.7 +/- 14.2 ms) was significantly (P < 0.01) longer, the effective refractory period (157.9 +/- 15.2 ms) significantly (P < 0.01) longer and the atrial fibrillation (11/19 or 57.9%) significantly (chi 2 = 9.95, P < 0.001) more common than at a low (< or = 10 mmHg) pressure (35.2 +/- 11.6, 146.2 +/- 12.4, 3/24 or 12.5%, respectively). Analysis of variance showed that the probability of atrial fibrillation was significantly affected by the atrial pressure but not by either the conduction time or the effective refractory period. The findings suggest that an increase in right atrial pressure by acute volume overload prolongs the inter-atrial conduction time and right atrial refractoriness and increases the propensity of the atria to fibrillate by rapid atrial stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…variation, three dogs (3,4, and 8) were tested twice and one dog (9) was tested three times (nine experiments) ( Table II). The time interval hetween consecutive experiments in the same dog was at least 1 week.…”

Section: Methodsmentioning

confidence: 99%

“…In each dog a single experiment was performed to test the interindividual variation (Table I) At 800 and 350 msec PCL (VERPgoo and VERP350), the difference between VERPBOO and VERP350 (Jtof), the change in VERP after an abrupt change in PCL from 800 from 350 msec after 3 and 20 beats {A3 and J20) expressed in msec and in % of Jtot RR interval of idioventricular rate. variation, three dogs (3,4, and 8) were tested twice and one dog (9) was tested three times (nine experiments) ( Table II). The time interval hetween consecutive experiments in the same dog was at least 1 week.…”

Section: Methodsmentioning

confidence: 99%

Inter‐ and Intraindividual Variations in Shortening of Ventricular Effective Refractory Period After an Abrupt Decrease in Pacing Cycle Length

Leerssen

Vos

Dulk

et al. 1994

Pacing Clinical Electrophis

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After an abrupt decrease in pacing cycle length (PCL), the ventricular effective refractory period (VERP) shortens. The pacing protocol needed to determine accurate and reproducible values for the VERP during this process is elaborate and time consuming. In this study, steady-state values of VERP at 800 and 350 msec PCL and dynamic values of VERP due to an abrupt change in PCL from 800 to 350 msec were determined. This was done for 11 different dogs to test the interindividual variation and repetitively in the same dog to test the intraindividual variation. The results for steady-state and dynamic values of the VERP show a wide range for both groups. This means that accurate prediction of steady-state and dynamic values of VERP based on previous measurements is not possible.

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Cumulative effects of cycle length on ventricularrefractoriness in man

Cited by 8 publications

References 22 publications

Reentrant ventricular arrhythmias in the late myocardial infarction period: mechanism by which a short-long-short cardiac sequence facilitates the induction of reentry.

Reentrant ventricular arrhythmias in the late myocardial infarction period: mechanism by which a short-long-short cardiac sequence facilitates the induction of reentry.

Some observations on the mechanism of pressure related atrial fibrillation

Inter‐ and Intraindividual Variations in Shortening of Ventricular Effective Refractory Period After an Abrupt Decrease in Pacing Cycle Length

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