(Circulation. 1997;96:4050-4056.)
© 1997 American Heart Association, Inc.
Articles |
Electrophysiological Effects of Acute Dilatation in the Isolated Rabbit Heart
Cycle Length–Dependent Effects on Ventricular Refractoriness and Conduction Velocity
From the Department of Physiology (Z.Z., C.J.H.K., MA.A.), Maastricht University, The Netherlands; and the Department of Medicine (M.J.R., M.L.), University of Colorado Health Sciences Center, Denver, Colo.
Correspondence to Michael J. Reiter, MD, PhD, Division of Cardiology, Box B-130, University of Colorado Health Sciences Center, 4200 E 9th Ave, Denver, CO 80262. E-mail Michael.Reiter{at}UCHSC.edu
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background Acute ventricular dilatation has important electrophysiological effects: Dilatation shortens action potential duration and refractoriness without an apparent effect on conduction velocity. These effects have been implicated as a potential mechanism of arrhythmias in patients with congestive failure. Because the influence of cycle length on these phenomena has not been studied, we examined the effects of dilatation during ventricular pacing at cycle lengths from 1000 to 150 ms.
Methods and Results Thin epicardial layers were created in isolated, perfused rabbit left ventricles (n=7). A fluid filled latex balloon was secured in the left ventricle to dilate the left ventricle. Mapping was performed with 248 epicardial electrodes. Longitudinal conduction velocity (76±1 cm/s; mean±SEM) and transverse conduction velocity (26±1 cm/s) were not influenced by dilatation at any cycle length. In contrast, the effects of dilatation in decreasing left ventricular effective refractory period (ERP) were significantly greater at shorter drive cycle lengths: The decrease in ERP was 2±2 ms (a 1% change) at a drive cycle length of 1000 ms and 18±4 ms (a 20% change) at a drive cycle length of 150 ms. In 10 additional intact, isolated perfused rabbit hearts, dilatation decreased ERP to a greater degree during 250 ms drive cycle length pacing than during pacing at 400 ms (25±4 versus 16±3 ms; P=.01).
Conclusions Acute dilatation exaggerates the normal rate-dependent shortening of refractoriness but does not influence transverse or longitudinal conduction velocity. This observation suggests that the electrophysiological effects of acute dilatation may be greater during tachycardia than at slower cycle lengths. This may have implications for arrhythmias in patients with congestive heart failure.
Key Words: heart failure • conduction • reentry • refractoriness • arrhythmias
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Electrophysiological changes that occur as a result of alterations in myocardial loading conditions have been referred to as "mechano-electrical feedback" or "contraction excitation feedback"1–3 and have been implicated as a potential arrhythmogenic factor in patients with congestive heart failure.4–6 A shortening of action potential duration3,7–9 and myocardial refractoriness3,10–12 in response to an acute sustained dilatation has been observed in a variety of preparations, including humans.13–16 However, the influence of heart rate on the shortening of refractoriness observed with acute dilatation has not been previously studied. Stretching of cardiac muscle has also been reported to decrease conduction velocity.17,18 However, in the intact heart,10 no change in conduction time between two epicardial electrodes was observed after dilatation, although, due to the three-dimensional nature of the preparation, conduction velocity could not be directly measured.
The purpose of the present study was to study the influence of cycle length on the change in effective refractory period and the directly measured conduction velocity in response to acute dilatation of the left ventricle.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Preparation: Thin Left Ventricular Epicardial Layer
Seven Flemish rabbits of either sex weighing between 3.3 to 4.0 kg were sedated with Hypnorm (Phillips-Duphar B.V; fentanyl 0.2 mg/ml and fluanisone 10 mg/ml; 0.5 mL/kg). After heparinization (1000 IU IV), animals were killed by cervical dislocation. The thorax was rapidly opened by midsternal incision, and the heart was removed and placed in cold (10OC) perfusion fluid. The aorta was cannulated and the heart retrogradely perfused at a pressure of 50 mm Hg and a temperature of 36.8° to 37.2°C with Tyrode's solution. The millimolar composition of the perfusion fluid was NaCl 130, NaHCO3 20.1, KCl 4.0, CaCl2 2.2, MgCl2 0.6, Na2HPO4 1.2, and glucose 12. The perfusion fluid was equilibrated with a mixture of 95% O2–5% CO2 and had a pH of 7.35. Coronary flow was determined in triplicate by timed collection of coronary effluent.
The right ventricle, septum, and endocardial and intramural layers of
the left ventricle were destroyed by freezing with a technique
previously described.19 Briefly, a cryoprobe was
inserted through the pulmonary artery into the right ventricle
and filled with liquid nitrogen, destroying the right ventricle. The
cryoprobe was subsequently repositioned in the right ventricle through
the right atrium, and freezing was repeated to ensure complete
destruction. The cryoprobe was then inserted into the left
ventricular cavity through the left atrium and the heart
immersed in a tissue bath of Tyrode's solution maintained at
30OC. The coronary circulation was
temporarily interrupted and the cryoprobe was filled with liquid
nitrogen. After 7 minutes, the cryoprobe was removed, coronary
circulation was restored, and the heart removed from the bath. These
procedures created a preparation consisting of a thin (
1 mm)
layer of normal left ventricular epicardium. In this
surviving epicardial layer,
electrophysiological properties are normal
and stable for hours. The left ventricle was then vented and a
fluid-filled latex balloon was secured in the left
ventricular cavity with a purse string suture through the
mitral apparatus. The initial balloon volume was adjusted
to a volume equivalent to an end-diastolic pressure of
0 mm Hg. This volume (estimated at 0.1 to 0.3 mL) was
defined as the starting volume. The left ventricle could then be
dilated by adding up to 1 mL to the balloon. Cryoablation of the
endocardial and intramural layers influenced wall compliance, making
assessment of the degree of dilatation achieved at the epicardial layer
less accurate: however, in previous
experiments10,20 the addition of 1.0 mL to the
left ventricular balloon raised end-diastolic
pressure to 25 mm Hg.
Preparation: Intact Langendorff-Perfused Hearts
Adult New Zealand White rabbits (n=10) of either sex, weighing
2.5 to 3.5 kg, were killed after sedation and the hearts prepared and
perfused by methods similar to those described above, with the
exception that no cryodestruction was performed. The left atrium was
cannulated and perfused with oxygenated Tyrode's solution.
The atrioventricular valve apparatus was
left intact. Ventricular pressure was measured through an
18-gauge trocar inserted directly through the left
ventricular wall, by a pressure transducer (P23Db, Statham)
connected to a pressure amplifier (model 13-4615-58, Gould). To dilate
the left ventricle,20 the perfusion pressure of
the left atrium was increased to give left ventricular
end-diastolic pressures of 0 and 25 mm Hg, in
random order.
Electrophysiological Measurements
Activation mapping was accomplished in the left
ventricular epicardial layer with a spoon-shaped electrode
array consisting of 248 silver electrodes (0.3 mm diameter)
2.25 mm apart designed to enclose completely the left
ventricular epicardial surface. The electrode matrix was
connected to a custom-made,21 computerized
mapping system. Individual unipolar electrograms were amplified,
filtered (low pass, 1 Hz; high pass, 400 Hz), multiplexed (sampling
rate, 1 kHz), and AD converted. All data were recorded for
subsequent review and analysis. Local activation was determined
by a computerized algorithm that detected intrinsic negative
deflections in each of the electrograms, which were manually reviewed
and edited as necessary.
Bipolar pacing used two adjacent electrodes in the array situated in
the upper left-hand portion of the preparation. Bipolar pacing was
performed at various cycle lengths from 1000 to 150 ms with square wave
pulses of 2 ms pulse width and an amplitude twice diastolic
threshold. Activation maps were plotted and isochrones were drawn
by hand at 10-ms intervals. An ellipsoid wave front, with slow
conduction transverse to fiber direction and fast conduction parallel
to fiber direction, was recorded.19 The
longitudinal and transverse axes of conduction were determined from the
ellipsoidal shape of the isochrones. Conduction velocity was
defined as the distance traveled per unit of time normal to the
isochrones (Fig 1
) and the
longitudinal and transverse conduction velocity at each drive cycle
length and left ventricular balloon volume was calculated,
in each experiment, as the average of two values obtained for each
axis.
|
The effective refractory period (ERP) was determined during pacing at various cycle lengths. Pacing was initiated at a drive cycle length of 1000 ms. After 2 minutes of pacing for equilibration, the effective refractory period was determined with the extrastimulus technique. After every 20 paced beats, a single extrastimulus was introduced starting at a closely spaced coupling interval. A pause of 250 ms was introduced between successive trains. The coupling interval was increased in 5-ms intervals until capture was achieved, then was decreased in 1-ms decrements until capture was lost on two successive trains at the same coupling interval. This value was defined as the ERP. After determining the ERP at 1000 ms, the drive cycle length was decreased, the pacing threshold redetermined, and pacing at the new cycle length initiated at twice diastolic threshold. After 2 minutes of pacing at the new cycle length, the ERP was again determined. After measurement of the ERPs at all six cycle lengths at a given volume, the balloon volume was changed and the ERPs determined at all cycle lengths at the new volume. Volumes of 0, 0.25, 0.5, 0.75, and 1.0 mL were studied in random order. In the intact ejecting hearts, ERP was determined during continuous pacing (at twice diastolic threshold) at drive cycle lengths of either 400 or 250 ms at each volume.
Statistical Analysis
All data, which were normally distributed, are presented
as mean±SEM unless otherwise noted. The influence of
ventricular volume and cycle length on flow rate, pacing
threshold, longitudinal and transverse conduction velocity, and ERP was
assessed with an ANCOVA and the Student-Newman-Keuls multiple
comparison test.22 To examine the effect of cycle
length on the relation between ERP and left ventricular
volume, we performed linear regression analysis and obtained a
slope for this relationship for each heart at a specific cycle length.
We compared mean data for slopes, undilated ERP, and change in ERP
after dilatation from 0.0 to 1.0 mL with the use of a t
test. In the intact hearts, the difference in ERP between nondilated
and dilated preparations at the two cycle lengths (400 and 250 ms) were
compared with the use of a paired t test. A value of
P<.05 was considered statistically significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Conduction Velocity
Coronary flow rate was not influenced by ventricular volume or drive cycle length. Pacing threshold was uninfluenced by drive cycle length except for a small but statistically significant increase only at the shortest paced cycle length. Threshold was slightly but consistently higher at a ventricular volume of 1.0 mL compared with 0.0 mL. In the anisotropic epicardial preparation, fiber direction is different in different regions of the preparation.23 Because of the essentially two-dimensional nature of the preparation, mapping of the activation wave allowed accurate measurement of conduction velocity (Fig 1
). Longitudinal conduction velocity averaged 76±1 cm/s
in seven preparations (Table 1) and was
not influenced by either dilatation or basic pacing cycle length (Fig 2A). Transverse conduction velocity
averaged 26±1 cm/s and was also not influenced by either dilatation or
basic pacing cycle (Fig 2B).
|
|
Effective Refractory Period
In contrast to the independence of conduction velocity on
pacing cycle length and left ventricular volume, the
refractory period was influenced by both cycle length and balloon
volume. Fig 3 shows the results of a
typical experiment. In the undilated preparation, as drive cycle length
shortens (Fig 3A), ERP decreases. This simply reflects the rate
adaptation of refractoriness. After the addition of 0.5 mL into the
left ventricular balloon, the ERP at cycle lengths 
350 ms
was not different than the undilated ERP at the same cycle length.
However, at shorter drive cycle lengths the ERP was clearly decreased
when the preparation is dilated. This effect was exaggerated with
additional left ventricular dilatation (ie, 1.0 mL) since
the ERP is shortened compared with the undilated state now at drive
cycle lengths 
500 ms. Fig 3B illustrates data from the same
preparation in a different format. Dilatation has no effect on
refractoriness determined at a drive cycle length of 1000 ms but caused
a progressively greater decrease in ERP at shorter drive cycle lengths.
This phenomenon was consistently observed. In Table 2, the mean slopes of the ERP versus
volume relationship are given as a function of basic drive cycle
length, demonstrating a progressively greater effect of increasing left
ventricular volume on ERP as the cycle length decreases in
each of the seven preparations. As the drive cycle length shortens from
1000 to 150 ms, in the undilated ventricle the ERP decreases from
195±8 to 88±4 ms. The effects of dilatation on ERP are greater at
shorter cycle lengths whether assessed by an absolute decrease in ERP
or as a relative change. At a drive cycle length of 1000 ms, a 1.0-mL
increase in left ventricular balloon volume has a trivial
(and statistically insignificant) effect on ERP. In contrast, at a
drive cycle length of 250 ms, a similar balloon volume decreases
epicardial ERP an average of 22 ms, a decrease of 21% compared with
the undilated ERP.
|
|
ERP)
To determine whether the cycle length–dependent effect of dilatation
on refractoriness was unique to the thin epicardial layer, ERP was also
determined in contracting, ejecting hearts at drive cycle lengths of
400 and 250 ms. In this different preparation, it was again observed
that an acute increase in left ventricular
end-diastolic pressure decreases ERP to a greater degree at
shorter cycle lengths (Fig 4). Thus it
appears that dilatation, rather than shortening effective refractory
period equally at all drive cycle lengths, exaggerates the
physiological rate-dependent shortening of ERP.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
We have shown that acute dilatation, to a degree that increases left ventricular diastolic pressure in a clinically relevant range, does not influence epicardial conduction velocity but shortens the effective refractory period in a rate-dependent manner. These observations may have clinically important implications.
Effects of Dilatation on Conduction Velocity
Several previous observations have suggested that stretch of
myocardial tissue decreases conduction velocity. Penefsky and
Hoffman17 measured the conduction time between
two carbon particles positioned on cat papillary muscle preparations
from which they calculated conduction velocity before and after
stretch. Conduction velocity was constant with mild stretch but
decreased when the muscle was stretched above its optimal length (the
length at which maximal contractile tension was recorded; 125%
of its initial length). The degree of stretch required to influence
conduction velocity in the papillary muscle preparations probably
exceeds the physiologically important range of
cardiac muscle length. In contrast, the degree of stretch produced by
the addition of 1 mL to the left ventricular balloon in the
present experiment probably increases muscle length by <10%.
Circumferential interelectrode distance is not measurably changed by
this degree of dilatation in the isolated rabbit
heart.24 Because of the stiffening of the left
ventricular wall by the cryoprocedure, in the present
experiments it was not possible to measure the increase in left
ventricular end-diastolic pressure resulting
from the addition of 1 mL in the thin epicardial layer. However, in
previous experiments,10,20 it was shown that this
volume resulted in left ventricular
end-diastolic pressures between 25 and 30 mm Hg.
Moreover, the ERP shortening in the thin epicardial layer observed with
the addition of 1 mL was comparable to the change in ERP observed when
the end-diastolic pressure is increased to 25
mm Hg in the intact hearts (25±8 versus 22±4 ms).
Zabel et al18 used the time between pacing
stimulus and the upstroke of a monophasic action potential as a measure
of conduction velocity in isolated rabbit hearts. Dilatation, by the
addition of 1 mL of left ventricular volume, increased the
activation time 12%, which suggests either a decrease in conduction
velocity or an increase in conduction path length. However, these
results were not consistent with results of earlier studies in
a similar preparation.10,24 Conduction velocity
in a three-dimensional structure (ie, the intact heart) is difficult to
measure when the exact path followed by the impulse cannot be
accurately determined. In experiments with a ring of
Langendorff-perfused anisotropic rabbit
epicardium,25 ventricular dilatation
did not appear to influence conduction velocity because the cycle
length of ventricular tachycardia due to
continuous reentrant propagation around the ring did not change.
However, divergent effects of dilatation on transverse and longitudinal
conduction around the ring could conceivably have resulted in an
unchanged ventricular tachycardia cycle
length.
The current experiments were designed to measure directly the conduction velocity in a two-dimensional preparation with the use of previously validated methodology.26 These experiments, which represent the first direct measurement of conduction velocity, demonstrate that dilatation within a physiological range does not influence either transverse and longitudinal velocity.
Effects of Dilatation on ERP
While the effect of ventricular dilatation on action
potential duration and myocardial refractoriness has been well
documented in a variety of
preparations,1–3,6–16 the role of heart rate on
this effect of dilatation has not been adequately studied. In earlier
experiments, we determined action potential duration and ERP before and
during persistent left ventricular dilatation at a cycle
length of 250 ms10,20,24 or during
ventricular
tachycardia.25 At these cycle lengths
a significant decrease in refractoriness was observed with left
ventricular dilatation. In the present experiments, a
consistent cycle length–dependent effect of
ventricular dilatation was observed, with the slope of ERP
versus volume increasing as cycle length shortened in all seven
preparations.
A recent study by Horner et al27 examined the effect of aortic occlusion on action potential duration in the anesthetized pig. These authors observed that there was more shortening of action potential duration during increased loading at longer cycle lengths (600 ms) compared with shorter cycle lengths (400 ms), in contrast to our observations. While the discrepancies between this study and our data remain unexplained, there are several important differences in the experimental conditions of the two studies. The preparation used by Horner et al is characterized by an intact autonomic nervous system, a confounding variable, since hemodynamics and thus autonomic tone is expected to be affected by paced cycle length. The effects of anesthesia and the open chest nature of the preparation used by Horner et al are unclear. We measured ERP, which is not necessarily equivalent to action potential duration at 70% of repolarization as measured by Horner et al. We examined the effects of cycle lengths from 1000 to 150 ms, whereas Horner et al studied the effects of cycle lengths only from 300 to 600 ms. Finally, aortic occlusion primarily increases systolic wall stress and is fundamentally different than an increase in diastolic wall stress, the primary determinant of action potential duration shortening20 in the isolated rabbit heart. Increases in diastolic wall stress are probably a more accurate mimic of acute ventricular dilatation in clinically decompensated congestive heart failure.
The observation that dilatation has a cycle length–dependent effect on refractoriness has important implications. First, the effects of dilatation on refractoriness may be minor (and possibly undetectable) when measured during sinus rhythm or at long cycle lengths. This may explain some of the discrepant results obtained in different laboratories.11,28 Second, the effects of dilatation, while minor in sinus rhythm, may be clinically important at shorter cycle lengths or during tachycardia. A decrease in refractoriness and the corresponding decrease in myocardial wavelength has important arrhythmogenic effects.24,29,30 When a tachyarrhythmia develops, there is a shortening of action potential duration and refractoriness due to the rate adaptation of action potential duration. If a ventricular tachycardia develops in a dilated ventricle (or leads to ventricular dilatation) then there is, in addition, a synergistic effect of mechanoelectrical feedback in shortening refractoriness, an effect that is exaggerated at shorter cycle lengths.
Finally, these observations have mechanistic implications. A nonspecific cation channel opened by mechanical stretch, with a reversal potential of -30 to -40 mV, has been described in mammalian myocardium.31,32 Opening of this channel during diastole may account for the diastolic depolarization and ventricular extrasystoles observed with acute transient stretch.33 Because this channel does not demonstrate fatigue, it has also been suggested34 that its activation during the action potential plateau might account for shortening of refractoriness caused by sustained dilatation. The current results, we believe, make this unlikely. While opening of this channel could conceivably cause an outward current accelerating repolarization, this effect should be apparent even at slow cycle lengths and should not exhibit cycle length dependency. We can, at this juncture, only speculate on the ionic mechanism responsible for a rate-dependent decrease in refractoriness with ventricular dilatation. It is, however, interesting to note that Jurkiewicz and Sanginetti35 have shown that the slow component of the delayed rectifier current (iKs) may contribute to rate-dependent action potential abbreviation and that this current is increased by cell distention and mechanical stretch.36
Limitations
In these experiments we measured ERP during continuous pacing by
the extrastimulus technique. Action potential duration was not directly
measured. However, in previous experiments we24
and others3,11 have shown that the decrease in
epicardial ERP caused by ventricular dilatation is
completely accounted for by a shortening of action potential duration
as assessed by a monophasic action potential catheter. These effects
may be specific for rabbit epicardium. At this time, we cannot
generalize to other species or human myocardium. However,
it is important to point out that the effects of dilatation in the
rabbit myocardium have been, heretofore, very similar to
phenomena observed in humans.
The results observed in this study are not believed to be due to
ischemia resulting from rapid pacing at dilated volumes.
Although tissue oxygen saturation and effluent lactate was not measured
in these experiments, in previous experiments10
there was no decrease in coronary sinus effluent
PO2 in intact isolated rabbit hearts
when ventricular volume was increased and coronary
sinus lactate was undetectable during dilatation at paced cycle lengths
of both 450 and 250 ms. Additionally, decreases in left
ventricular ERP were independent of coronary
perfusion pressures between 73 to 88 mm Hg. In the current
experiments, coronary flow rate, which averaged 66±18 mL/min
(mean±SD) in the intact heart before cryodestruction, decreased 24%
(to 50±19 mL/min) after the cryoprocedure. The cryoprocedure resulted
in complete destruction of the right ventricle,
intraventricular septum, and 80% of the
endocardial and intramural left ventricular free
wall.19 Since only an estimated 10% (1
g) of functional myocardium remains after the
cryodestruction, ischemia seems less likely in this preparation
than in the intact isolated heart. This is especially true because of
the preferential perfusion of the surviving epicardial layer. The
constancy of conduction velocity also argues against
ischemia.
While it is possible that the observed electrophysiological changes are specific to acute dilatation (and different electrophysiological effects may be seen with chronic dilatation37), they may have important clinical consequences. Ischemia, mitral valve prolapse, decompensation of congestive heart failure, acute hemodynamic abnormalities (eg, septal rupture, acute mitral regurgitation) can produce acute changes in global and regional wall stress. Furthermore, the development of a supraventricular or ventricular tachyarrhythmia could lead to chamber dilatation with subsequent and important electrophysiological effects secondary to mechanoelectrical feedback, perhaps even leading to degeneration of an initially stable tachycardia.
Conclusions
Acute ventricular dilatation shortens myocardial
refractoriness in a rate-dependent fashion in Langendorff-perfused
rabbit hearts but does not change conduction velocity. These
electrophysiological consequences of
dilatation may have important arrhythmogenic effects.
Received June 16, 1997; revision received August 24, 1997; accepted August 24, 1997.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
-
Lab MJ. Mechanically dependent changes in action
potentials recorded from the intact frog ventricle.
Circ Res. 1978;42:519–528.
[Abstract/Free Full Text]
-
Lab MJ. Contraction-excitation feedback in
myocardium: physiological basis and
clinical relevance. Circ Res. 1982;50:757–766.
[Free Full Text]
-
Lerman BB, Burkhoff D, Yue DT, Franz MR, Sagawa K.
Mechanoelectrical feedback: independent role of preload and
contractility in modulation of canine
ventricular excitability. J Clin Invest. 1985;76:1843–1850.
-
Reiter MJ. Pathophysiology of
ventricular arrhythmias in patients with congestive
heart failure. Heart Failure. 1989;5:155–166.
-
Dean JW, Lab MJ. Arrhythmia in heart failure:
role of mechanically induced changes in electrophysiology.
Lancet. 1989;10:1309–1311.
-
Taggart P, Sutton P, Lab M. Interaction between
ventricular loading and repolarization: relevance to
arrhythmogenesis. Brit Heart J. 1992;67:213–215.
[Free Full Text]
-
Hansen DE. Mechanoelectrical feedback effects of
altering preload, afterload, and ventricular shortening.
Am J Physiol. 1993;264 (Heart Circ Physiol
33):H423–H432.
-
Dean JW, Lab MJ. Effect of changes in load on
monophasic action potential and segment length of pig heart in situ.
Cardiovasc Res. 1989;23:887–896.[Medline]
[Order article via Infotrieve]
-
Kaufmann RL, Lab MJ, Hennekes R, Krause H. Feedback
interaction of mechanical and electrical events in the isolated
mammalian ventricular myocardium (cat papillary
muscle). Pfluegers Arch. 1970;324:100–123.
-
Reiter MJ, Synhorst DP, Mann DE. Electrophysiologic
effects of acute ventricular dilatation in the isolated
rabbit heart. Circ Res. 1988;62:554–562.
[Abstract/Free Full Text]
-
Calkins H, Maughan WL, Kass DA, Sagawa K, Levine JH.
Electrophysiological effects of volume load in
isolated canine hearts. Am J Physiol. 1989;256:H1697–H1706.
[Abstract/Free Full Text]
-
Franz MR, Burkhoff D, Yue DT, Sagawa K. Mechanically
induced action potential changes and arrhythmia in isolated and
in situ canine heats. Cardiovasc Res. 1989;23:213–223.[Medline]
[Order article via Infotrieve]
-
Levine JH, Guarnieri T, Kadish AH, White RI, Calkins H,
Kan JS. Changes in myocardial repolarization in patients undergoing
balloon valvuloplasty for congenital pulmonary
stenosis: evidence for contraction-excitation feedback in
humans. Circulation. 1988;77:70–77.
[Abstract/Free Full Text]
-
Taggart P, Sutton PMI, Treasure T, Lab M, O'Brien W,
Runnalls M, Swanton RH, Emanual RW. Monophasic action potentials at
discontinuation of cardiopulmonary bypass: evidence for
contraction-excitation feedback in man. Circulation. 1988;77:1266–1275.
[Abstract/Free Full Text]
-
Taggart P, Sutton P, Lab M, Runnalls M, O'Brien W,
Treasure T. Effect of abrupt changes in ventricular loading
on repolarization induced by transient aortic occlusion in humans.
Amer J Physiol. 1992;263 (Heart Circ Physiol
32):H816–H823.
-
Bashir Y, Sneddon JF, O'Nunain S, Paul VE, Gibson S,
Ward DE, Camm AJ. Comparative
electrophysiological effects of captopril
or hydralazine combined with nitrate in patients with left
ventricular dysfunction and inducible
ventricular tachycardia. Brit Heart
J. 1992;67:355–360.
[Abstract/Free Full Text]
-
Penefsky ZJ, Hoffman BF. Effects of stretch on
mechanical and electrical properties of cardiac muscle. Am J
Physiol. 1963;204:433–438.
-
Zabel M, Portnoy S, Franz MR. Effects of sustained load
on electrophysiologic parameters during steady state,
pacing, and premature electrical stimulation in the isolated intact
rabbit heart. J Am Coll Cardiol. 1994;327A. Abstract.
-
Schalij MJ, Lammers WJEP, Rensma PL, Allessie MA.
Anisotropic conduction and reentry in perfused epicardium of rabbit
left ventricle. Am J Physiol. 1992;263:H1466–H1478.
[Abstract/Free Full Text]
-
Halperin BD, Adler SW, Mann DE, Reiter MJ. Mechanical
correlates of contraction- excitation feedback during acute
ventricular dilatation. Cardiovasc Res. 1993;27:1084–1087.
[Abstract/Free Full Text]
-
Hoeks APG, Schmitz GML, Allessie MA, Jas H, Hollen SJ,
Reneman RS. Multichannnel storage and display system to record the
electrical activity of the heart. Med Biol Eng Comput. 1988;26:434–438.[Medline]
[Order article via Infotrieve]
-
Steel RGD, Torrie JH. Principles and Procedures
of Statistics. New York, NY: McGraw-Hill Book Co; 1960;110–112,
366–387.
-
Brugada J, Boersma L, Kirchhof C, Brugada P, Havenith
M, Wellens HJ, Allessie M. Double-wave reentry as a mechanism of
acceleration of ventricular tachycardia.
Circulation. 1990;81:1633–1643.
[Abstract/Free Full Text]
-
Reiter MJ, Mann DE, Williams GR. Interaction of
hypokalemia and ventricular dilatation in the isolated
rabbit heart: a potential model of arrhythmias in congestive
heart failure. Am J Physiol. 1993;265 (Heart Circ
Physiol 34):H1544–H1550.
-
Reiter MJ, Zetelaki Z, Kirchoff CJH, Boersma L,
Allessie MA. Acute ventricular dilatation decreases the
class III effects of d-sotalol during sustained reentrant
ventricular tachycardia around a fixed
obstacle. Circulation. 1994;89:423–431.
[Abstract/Free Full Text]
-
Boersma L, Brugada J, Schalij MJ, Kirchhof C, Allessie
M. The effects of K+ on anisotropic conduction in
sheets of perfused rabbit ventricular epicardium.
J Cardiovasc Electrophysiol. 1991;2:492–502.
-
Horner SM, Dick DJ, Murphy CF, Lab MJ. Cycle length
dependence of the electrophysiological
effects of increased load on the myocardium.
Circulation. 1996;94:1131–1136.
[Abstract/Free Full Text]
-
Kadish AH, Kou WH, Schmaltz S, Morady F. Effect of
atrioventricular relationship on
ventricular refractoriness in humans. Am J
Physiol. 1990;259:H1463–H1470.
[Abstract/Free Full Text]
-
Smeets JLRM, Allessie MA, Lammers WJEP, Bonke FI,
Hollen J. The wavelength of the cardiac impulse and reentrant
arrhythmias in isolated rabbit atria: the role of heart rate,
autonomic transmitters, temperature, and potassium. Circ
Res. 1986;58:96–108.
[Abstract/Free Full Text]
-
Rensma PL, Allessie MA, Lammers WJEP, Bonke FI, Schalij
MJ. Length of the excitation wave and susceptibility to reentrant
atrial arrhythmias in normal conscious dogs. Circ
Res. 1988;62:395–410.
[Abstract/Free Full Text]
-
Rukknudin A, Sachs F, Bustamante JO.
Stretch-activated ion channels in tissue-cultured chick heart.
Am J Physiol. 1993;264:H960–H972.
[Abstract/Free Full Text]
-
Craelius W, Chen V, El-Sherif N. Stretch
activated ion channels in ventricular myocytes.
Biosci Rep. 1988;8:407–414.[Medline]
[Order article via Infotrieve]
-
Hansen DE, Borganelli M, Stacy G, Taylor LK.
Dose-dependent inhibition of stretch-induced arrhythmias by
gadolinium in isolated cainine ventricles: evidence for a unique mode
of antiarrhythmic action. Circ Res. 1991;69:820–831.
[Abstract/Free Full Text]
-
Zabel M, Koller B, Franz MR. Amplitude and polarity of
stretch-induced systolic and diastolic voltage
changes depend on the timing of stretch: a means to characterize
stretch-activated channels in the intact heart.
PACE. 1993;16:886. Abstract.
-
Jurkiewicz NK, Sanguinetti MC. Rate-dependent
prolongation of cardiac action potentials by a methanesulfonanilide
class III antiarrhythmic agent: specific block of rapidly activating
delayed rectifier K+ current by dofetilide.
Circ Res. 1993;72:75–83.
[Abstract/Free Full Text]
-
Wang Z, Mitsuiye T, Noma A. Cell distention-induced
increase of the delayed rectifier K+ current in
guinea pig ventricular myocytes. Circ Res. 1996;78:466–474.
[Abstract/Free Full Text]
-
Kääb S, Nuss B, Chiamvimonvat N, O'Rourke
B, Pak PH, Kass DA, Marban E, Tomaselli GF. Ionic mechanism of action
potential prolongation in ventricular myocytes from dogs
with pacing-induced heart failure. Circ Res. 1996;78:262–273.
[Abstract/Free Full Text]
This article has been cited by other articles:
 |
|
 |
|
  S. Y. Hayashi, A. Seeberger, B. Lind, J. Nowak, M. M. do Nascimento, B. Lindholm, and L.-A. Brodin A single session of haemodialysis improves left ventricular synchronicity in patients with end-stage renal disease: a pilot tissue synchronization imaging study Nephrol. Dial. Transplant., June 13, 2008; (2008) gfn311v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. Narayan, D. D. Drinan, R. P. Lackey, and C. F. Edman Acute volume overload elevates T-wave alternans magnitude J Appl Physiol, April 1, 2007; 102(4): 1462 - 1468. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. M. Pedrotty, J. Koh, B. H. Davis, D. A. Taylor, P. Wolf, and L. E. Niklason Engineering skeletal myoblasts: roles of three-dimensional culture and electrical stimulation Am J Physiol Heart Circ Physiol, April 1, 2005; 288(4): H1620 - H1626. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. D. Harding, V. Piacentino III, J. P. Gaughan, S. R. Houser, and K. B. Margulies Electrophysiological Alterations After Mechanical Circulatory Support in Patients With Advanced Cardiac Failure Circulation, September 11, 2001; 104(11): 1241 - 1247. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. L Burton and S. M Cobbe Dispersion of ventricular repolarization and refractory period Cardiovasc Res, April 1, 2001; 50(1): 10 - 23. [Full Text] [PDF]
|
|
|
|
|
|
G. L. Pierpont, S. S. Chugh, J. A. Hauck, and C. C. Gornick Endocardial activation during ventricular fibrillation in normal and failing canine hearts Am J Physiol Heart Circ Physiol, October 1, 2000; 279(4): H1737 - H1747. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. C. Baker, B. London, B.-R. Choi, G. Koren, and G. Salama Enhanced Dispersion of Repolarization and Refractoriness in Transgenic Mouse Hearts Promotes Reentrant Ventricular Tachycardia Circ. Res., March 3, 2000; 86(4): 396 - 407. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||