|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
,Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio 44195
| |
ABSTRACT |
|---|
|
|
|---|
Atrial fibrillation (AF) is characterized by short and irregular ventricular cycle lengths (VCL). While the beneficial effects of heart rate slowing (i.e., the prolongation of VCL) in AF are well recognized, little is known about the impact of irregularity. In 10 anesthetized dogs, R-R intervals, left ventricular (LV) pressure, and aortic flow were collected for >500 beats during fast AF and when the average VCL was prolonged to 75%, 100%, and 125% of the intrinsic sinus cycle length by selective atrioventricular (AV) nodal vagal stimulation. We used the ratio of the preceding and prepreceding R-R intervals (RRp/RRpp) as an index of cycle length irregularity and assessed its effects on the maximum LV power, the minimum of the first derivative of LV pressure, and the time constant of relaxation by using nonlinear fitting with monoexponential functions. During prolongation of VCL, there was a pronounced decrease in curvature with the formation of a plateau, indicating a lesser dependence on RRp/RRpp. We conclude that prolongation of the VCL during AF reduces the sensitivity of the LV performance parameters to irregularity.
vagus; relaxation; hemodynamics; atrial fibrillation
| |
INTRODUCTION |
|---|
|
|
|---|
THE WORSENING OF LEFT VENTRICULAR (LV) performance during atrial fibrillation (AF) is due to an increase of both the ventricular rate and the ventricular rate irregularity (5, 6, 32). Our previous work (29, 32) has shown that ventricular rate slowing during AF improves ventricular performance, although it is still associated with substantial irregularity.
The randomly timed beats during AF result in a complex hemodynamic sequence of events. Contractility during AF changes on a beat-by-beat basis and its exact evaluation remains debatable (3, 4, 28). Previous computational models, as well as experimental data, have shown that beat-to-beat contractility in AF may be reasonably estimated from the ratio of preceding and prepreceding R-R intervals (RRp/RRpp) (26) that determine mechanical restitution and potentiation (26, 27, 31). However, these studies used a simple linear model, whereas the relationship between contractility and RRp/RRpp (26) is intrinsically nonlinear. Moreover, the effects of the underlying average ventricular rate on the shape of the contractility-to-RRp/RRpp relationship have never been assessed. Finally, whereas mechanical restitution also affects LV relaxation (18), the relaxation to RRp/RRpp relationship in AF was not investigated.
The major aim of this study was to assess the role of the cycle length
irregularity on ventricular performance during AF by studying the
relationships between several hemodynamic parameters [maximal LV
(LVmax) power, the minimum of the first derivative of LV
pressure (dP/dtmin), and the time constant of
isovolumic pressure decay (
)] and the ratio
RRp/RRpp during various underlying average ventricular rates. We applied nonlinear estimation
methods to determine the LV performance-interval relationships.
| |
METHODS |
|---|
|
|
|---|
The study was approved by the Institutional Animal Research Committee and is in compliance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals.
Terminology. The ventricular cycle length (VCL) is the time interval between two consecutive ventricular depolarizations. It can be measured between the QRS complexes of the surface ECG or by the use of electrical signals recorded directly from the ventricles. In this study, an individual VCL was determined as the R-R interval between two consecutive right ventricular electrograms.
During regular rhythm there is a simple relationship between the constant VCL and the heart rate (HR), namely, HR (beats/min) = 60,000/VCL (ms). However, because the VCL changes from beat to beat (especially during AF), only an average HR can be determined based on the average VCL of a large number of beats. According to the above equation, a prolongation of the average VCL is equivalent to a slowing of the average HR. In the following text, we will quantify the changes in the HR by using the parameter (average) VCL. Accordingly, its irregularity will be measured as a ratio of two consecutive R-R cycle lengths (see subsequent text).Surgical preparation. The study procedures have been previously described (29, 32). The study was performed using 10 healthy open-chest dogs. Briefly, anesthesia was maintained with 1-2% isoflurane, with monitoring of volume status, arterial blood gases, and body temperature. Subcutaneous needle electrodes obtained a standard ECG. Custom-made quadripolar Ag-AgCl plate electrodes were sutured to the high right atrium and right ventricular apex for recording local electrical activity. Similar bipolar plate electrodes were sutured to two epicardial fat pads that contain parasympathetic (vagal) neural pathways selectively innervating the sinus node and the AV node (23). A Millar catheter was inserted through the left carotid artery and advanced into the left ventricle for pressure measurements. A flowmeter probe (model 16A/20A, HT 207, Transonic Systems; Ithaca, NY) was placed around the ascending aorta. All signals were amplified, displayed, and stored on a dedicated recording system (CardioLab, GE Marquette Medical Systems).
Study protocol. After the recording of the hemodynamics at normal sinus rhythm, AF was induced by rapid right atrial pacing (20 Hz, 1 ms) and was further maintained by subthreshold stimulation (20 Hz, 50 µs) of the sinus node fat pad located near the right upper pulmonary vein-atrial junction (23). In several cases, AF was maintained simply by continuing the rapid right atrial pacing.
The following four steps were then performed in each experiment. In step 1, after the hemodynamics stabilized for a minimum of 15 min, data were recorded during "fast" AF. The term fast is used to stress that this was the step with the fastest ventricular rate (or the shortest VCL) in each animal, which was observed before any modifications of the rate were attempted. In steps 2-4, while the atria continued to fibrillate, three longer average VCLs were achieved by graded AV nodal vagal stimulation. For quantitative purposes, these VCLs were expressed as a percentage from the spontaneous sinus cycle length (SCL) in each animal. Because the average VCL observed during fast AF was only 58 ± 5% of SCL, the three longer VCL were chosen as 75%, 100%, and 125% of the SCL (29). The computer-controlled vagal stimulation consisted of brief bursts of current impulses synchronized with the ECG (Fig. 1) and was applied onto the fat pad located at the left atrium-inferior vena cava junction (23). This epicardial structure contains vagal pathways to the AV node and its activation produces selective dromotropic effects and a slowing of the ventricular rate (22, 23). The role of the computer was the following: 1) to determine the duration of each VCL on a beat-to-beat basis, 2) to compare the measured value with the predetermined target level (75%, 100%, or 125% of SCL), and 3) to adjust instantaneously the amplitude of the vagal stimulation so that the error between the measured VCL and the target is minimized (32).
|
Data analysis. Electrograms and hemodynamic data were digitized at 1 kHz per channel for up to 1,000 ventricular beats in each AF period. The beats numbered 200-700 were analyzed by customized software.
We used three parameters to assess LV performance. First, mechanical performance was characterized by LVmax power calculated as a product of the peak aortic flow and peak LV pressure and expressed in watts (2). Second, peak relaxation was characterized by dP/dtmin. Finally, the time course of relaxation was characterized by
. It was calculated by fitting the
pressure-time data (from the point of dP/dtmin
to LV pressure 5 mmHg higher than next LV end-diastolic pressure) to
the equation (24)
|
.
We measured the duration of each VCL electronically by using the
electrograms recorded at the right ventricular apex, as the time
interval R-R (in ms) between the upstrokes (maximum first derivative)
of two consecutive responses. The VCL irregularity was expressed as a
ratio of two consecutive R-R intervals. As shown in Fig. 1, for each
ventricular beat (e.g., current LV response in Fig. 1) two
characteristic cycle lengths were determined. RRp is
the cycle length immediately preceding the analyzed beat.
RRpp is the prepreceding one. The ratio
RRp/RRpp was used in subsequent calculations related to the analyzed beat (see below).
The parameter RRp/RRpp has been
previously used to estimate the average values of hemodynamic
parameters during AF. However, only linear regressions have been
considered (26, 27). In the present study, the
relationship between LVmax power or
(dP/dtmin) and
RRp/RRpp was modeled by the following
nonlinear equation
|
(1) |
|
and
RRp/RRpp was fitted to the equation
|
(2) |
max is maximum
,
min is
minimum
(plateau of the relationship), and
RRp/RRppmin is the
minimum RRp/RRpp at which
could
be determined.
Comparison of LVmax power and contractility index Emax. Because LVmax power is preload dependent (11) and therefore is not an optimal contractility index, we compared it to the theoretical normalized maximal elastance (Emax; the slope of LV end-systolic pressure volume relationships) to evaluate how close the two indexes were correlated in the framework of the present experimental model. We used the equation derived by Yue et al. (31) that has been previously validated in a numerical simulation of contractility in AF (26) and calculated the normalized Emax from actual RRp and RRpp intervals in six randomly picked data sets. The normalized Emax was then compared by linear regression to the LVmax power measured in the same data sets.
We also determined the relationship between the normalized Emax and RRp/RRpp during fast AF and when the VCL was prolonged to 125% SCL.Statistical analysis.
Data are represented as means ± SD. The presence of nonlinear
components in LV performance
RRp/RRpp relationships was confirmed in six randomly chosen data sets. For this purpose, after initial simple linear regression analysis, a fourth-order polynomial equation was fitted to the residuals.
) was compared by
two-way repeated-measures ANOVA, followed by contrast analysis. A
P value of <0.05 was considered significant.
| |
RESULTS |
|---|
|
|
|---|
Comparison of theoretical normalized Emax and
LVmax power.
The coefficients of correlation between the normalized
Emax and the LVmax power in six
evaluated data sets ranged from 0.86 to 0.92 (P < 0.0001 for all). However, as shown in Fig.
2, the LVmax power
underestimated the normalized Emax when
Emax values were <0.75.
|
|
Global characterization of LV performance parameters during AF at
various average VCL.
The parameters characterizing the ventricular rate and its variance in
the studied animals are shown in Table 1.
The average VCL during fast AF (285 ± 54 ms) was 58% of the
intrinsic SCL (489 ± 81 ms). During vagally induced slowing,
average VCL was prolonged to 371 ± 62 ms (75% SCL), 486 ± 81 ms (100% SCL), and 601 ± 91 ms (125% SCL), respectively. In
an average animal, the standard deviation of both the VCL and the ratio
RRp/RRpp showed a
tendency to increase during vagal nerve stimulation.
|
. Quantitatively, this
resulted in a smaller scattering index S for longer VCL
(8). Second, the scatterogram mean (red dots) indicated
that with longer VCL there was an increase in LVmax power
and dP/dtmin, whereas
decreased. For
example, the proportion of the beats with LVmax power <1
dropped from 50.4% (during fast AF) to 5.3% (at VCL = 125%
SCL).
|
Nonlinear relationship between LV performance parameters and
RRp/RRpp at various average VCL.
The above scatterograms do not permit quantification of the role of the
cycle length irregularity. For that purpose, we determined the
nonlinear relationships between LV performance parameters (LVmax power, dP/dtmin, and
) and
RRp/RRpp. Figure
5 illustrates the results obtained in one
representative experiment. The regression lines for each level of VCL
are shown along with the raw data points. Figure 5, E,
J, and O, contain the four superimposed
regression lines for each parameter, respectively.
|
|
|
,
during VCL prolongation the plateau and the C did not change
(Table 4, P = 0.08 and
0.1, respectively). However,
at
RRp/RRpp = 1 still decreased, i.e.,
the relaxation improved (Table 4, P < 0.0001). This
was due to a leftward shift of
RRp/RRpp relations at longer VCL (Fig. 5O).
|
(P = 0.003 for both vs. LV maximal power).
| |
DISCUSSION |
|---|
|
|
|---|
Major findings. These data demonstrate that during AF the relationship between VCL irregularity (expressed as the ratio of two subsequent coupling intervals, RRp/RRpp) and LV performance parameters is curvilinear and that this curvilinearity increases as the average VCL is prolonged. For this reason, during fast AF, both LVmax power and relaxation are more dependent on RRp/RRpp, whereas this dependence is attenuated at slower ventricular rates (longer average VCL).
Previous studies have established that cardiac contractility is not constant during AF (3) and that mechanistically its beat-to-beat irregularity is governed in part by the effects of restitution and potentiation (26). While both of these effects depend nonlinearly on the RRp and RRpp coupling intervals (31), a unique linear relationship has been described between contractility and the RRp/RRpp (26). In fact, we have proposed a similar linear relationship as a tool for evaluation not only of contractility but also for assessment of a broader selection of hemodynamic parameters during AF (27). The present study extends previous observations by elucidating the role of the prevailing average ventricular rate (or average VCL) during AF and by defining the relaxation-interval relationships during AF. In particular, we established that nonlinear dependence on the RRp/RRpp better describes ventricular performance, especially during longer average VCL, and thus provided a more comprehensive explanation for the benefits of the slowed ventricular rate during AF.Assessment of LV mechanical performance and relaxation during AF. Evaluating cardiac contractility during AF is still problematic in view of the absence of a standard approach. The maximum rate of change of the LV pressure (+dP/dtmax) has been frequently used to evaluate cardiac contractility during AF (28), although its usefulness is limited by beat-to-beat variations in preload. The LV maximal elastance (Emax, the slope of end-systolic pressure-volume relationships) is frequently referred to as the "gold standard" measure of cardiac contractility (12). This parameter is preload independent, but its determination requires the generation of a family of stable pressure-volume loops while varying the diastolic filling. The determination of an accurate Emax during AF is therefore associated with significant difficulties (30) and a model-derived theoretical normalized Emax (26, 31), has been proposed as an approximation.
In this study, we found a good correlation between LVmax power and the normalized Emax calculated as a function of the RRp and RRpp intervals, using the equation derived by Suzuki et al. (26) and Yue et al. (31). As shown in Fig. 2, these two variables were closely and positively correlated. Furthermore, we also demonstrated that both the experimentally measured LVmax power (Fig. 5) and the calculated normalized Emax (Fig. 3) exhibit a nonlinear dependence on the ratio RRp/RRpp. Despite these similarities, however, the present data establish only the LVmax power as a practically convenient index of LV mechanical performance during AF, rather than as a surrogate of Emax. In accordance with previous studies by Prabhu and Freeman (18-20), we used both
and
dP/dtmin as relaxation parameters. While both
parameters showed nonlinear behavior with a "plateau" (Fig. 5), the
latter was more pronounced for
. A possible explanation for this
observation is that values for this parameter had a distribution that
was highly skewed to the left.
Irregularity ratio RRp/RRpp as predictor of cardiac performance during AF. It has been well established that the varying contractile function during AF depends on the complex interaction of mechanisms that are triggered by changes in both volume and interval. The former refers to the Frank-Starling relationship (14), which predicts that increased venous return (and thus end-diastolic volume) would produce greater stroke volume during the next heart cycle. However, the precise molecular mechanisms governing the Frank-Starling relationship (17) and its involvement during AF remain unclear (7, 9).
On the other hand, cardiac performance in a given beat during AF depends also on the particular time sequence of several preceding beats (30). However, a good approximation is achieved by taking into account just the RRp and the RRpp intervals underlying the mechanisms of mechanical restitution and potentiation, respectively (31). Both canine (30) and human (3) studies found that RRp and RRpp were the predominant predictors of contractility in AF. Recently, several investigators (26, 30) noted that, in addition to RRp and RRpp, the ratio RRp/RRpp is a strong predictor of LV performance during AF. In particular, a linear relationship between LV systolic parameters and the ratio RRp/RRpp has been reported. Moreover, it was demonstrated that values at RRp/RRpp = 1 in the linear regression lines can estimate the average values of various parameters (Doppler stroke volume, ejection fraction, peak aortic flow rate, and +dP/dtmax) during AF (27).Nonlinear relationship between ventricular performance and RRp/RRpp ratio during AF. In view of the nonlinear dependence of both the restitution and the potentiation on the RRp and RRpp intervals, respectively, the previously reported existence of a linear relationship between a number of systolic left ventricular performance parameters during AF and the ratio RRp/RRpp appears somewhat surprising (26, 27, 30). However, our mathematical modeling (Fig. 3) and careful inspection of the data by Yue et al. (31) suggest that this linearity holds true only for a certain range of average VCL during AF. The simple linear equation used for description of the force-interval relations during fast AF may be inadequate if the average R-R interval during AF is prolonged. Such prolongation, of course, is not just an experimental utility. It is a major therapeutic goal during treatment of patients with AF (15).
Our experimental data showed that the normalized theoretical Emax (31), as well as all measured LV performance parameters deviated from linear dependency on RRp/RRpp with prolongation of the VCL (Fig. 5). The curvilinear effects were less noticeable during fast AF (Fig. 5, A, F, and K), and were progressively accentuated as the cycle length was prolonged to 75% (Fig. 5, B, G, and L), 100% (Fig. 5, C, H, and M), and 125% (Fig. 5, D, I, and N) of the spontaneous SCL. Our data also showed that all hemodynamic parameters estimated at RRp/RRpp = 1 exhibited an improvement when the VCL was prolonged (Fig. 5, E, J, and O). This resulted from the combined effect of the VCL prolongation on the plateau, C, and position of the studied relationships (Tables 2-4). Finally, the relaxation-interval relationships were more curvilinear than the LVmax power-interval relationship (Tables 1 and 4, Fig. 5). This confirms previous observations that extrasystolic relaxation restitution is faster (more curvilinear) than the mechanical one (18).Clinical implications and limitations.
Our findings suggest that in patients with AF and controlled slower
average ventricular rates (e.g., by appropriate pharmacological agents,
such as
-blockers, Ca2+ channel blockers, or adenosine),
the clinical benefit of AF conversion with subsequent regularization of
the rate may be relatively small. Such a speculation is further
supported by recent clinical studies that found that rate control is
more important than rhythm regularization for improving quality of life
and exercise capacity in patients with permanent AF (15).
We should stress, however, that our experiments were performed on
anesthetized open-chest dogs, which precludes direct clinical extrapolation.
| |
ACKNOWLEDGEMENTS |
|---|
We thank Dr. Stan Dannemiller for guidance in the care and well- being of the animals and William J. Kowalewski for expert help during the surgical preparation and assistance in the experiments. We also acknowledge technical support from St. Jude Medical (St. Paul, MN) and Medtronic (Minneapolis, MN) for leads and pacing equipment.
| |
FOOTNOTES |
|---|
This study was supported in part by National Heart, Lung, and Blood Institute Grant RO1-HL-60833.
Address for reprint requests and other correspondence: T. N. Mazgalev, Research Institute FF1-02, The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195 (E-mail: mazgalt{at}ccf.org).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
August 22, 2002;10.1152/ajpheart.00571.2002
Received 12 July 2002; accepted in final form 14 August 2002.
| |
REFERENCES |
|---|
|
|
|---|
1.
Anan, T,
Sunagawa K,
Araki H,
and
Nakamura M.
Arrhythmia analysis by successive RR plotting.
J Electrocardiol
23:
243-248,
1990[Web of Science][Medline].
2.
Armstrong, GP,
Carlier SG,
Fukamachi K,
Thomas JD,
and
Marwick TH.
Estimation of cardiac reserve by peak power: validation and initial application of a simplified index.
Heart
82:
357-364,
1999
3.
Brookes, CIO,
White PA,
Staples M,
Oldershaw PJ,
Redington AN,
Collins PD,
and
Noble MIM
Myocardial contractility is not constant during spontaneous atrial fibrillation in patients.
Circulation
98:
1762-1768,
1998
4.
Chen, CH,
Fetics B,
Nevo E,
Rochitte CE,
Chiou KR,
Ding PA,
Kawaguchi M,
and
Kass DA.
Noninvasive single-beat determination of left ventricular end-systolic elastance in humans.
J Am Coll Cardiol
38:
2028-2034,
2001
5.
Clark, DM,
Plumb VJ,
Epstein AE,
and
Kay GN.
Hemodynamic effects of an irregular sequence of ventricular cycle lengths during atrial fibrillation.
J Am Coll Cardiol
30:
1039-1045,
1997[Abstract].
6.
Daoud, EG,
Weiss R,
Bahu M,
Knight BP,
Bogun F,
Goyal R,
Harvey M,
Strickberger SA,
Man KC,
and
Morady F.
Effect of an irregular ventricular rhythm on cardiac output.
Am J Cardiol
78:
1433-1436,
1996[Web of Science][Medline].
7.
Edmands, RE,
Greenspan K,
and
Fisch C.
The role of inotropic variation in ventricular function during atrial fibrillation.
J Clin Invest
49:
738-746,
1970[Web of Science][Medline].
8.
Garrigue, S,
Tchou PJ,
and
Mazgalev TN.
Role of the differential bombardment of atrial inputs to the atrioventricular node as a factor influencing ventricular rate during high atrial rate.
Cardiovasc Res
44:
344-355,
1999
9.
Gosselink, AT,
Blanksma PK,
Crijns HJ,
Van Gelder IC,
De Kam PJ,
Hillege HL,
Niemeijer MG,
Lie KI,
and
Meijler FL.
Left ventricular beat-to-beat performance in atrial fibrillation: contribution of Frank-Starling mechanism after short rather than long RR intervals.
J Am Coll Cardiol
26:
1516-1521,
1995[Abstract].
10.
Hayano, J,
Sakata S,
Okada A,
Mukai S,
and
Fujinami T.
Circadian rhythms of atrioventricular conduction properties in chronic atrial fibrillation with and without heart failure.
J Am Coll Cardiol
31:
158-166,
1998
11.
Kass, DA,
and
Beyar R.
Evaluation of contractile state by maximal ventricular power divided by the square of end-diastolic volume.
Circulation
84:
1698-1708,
1991
12.
Kass, DA,
and
Maughan WL.
From "Emax" to pressure-volume relations: a broader view.
Circulation
77:
1203-1212,
1988
13.
Kjorstad, KE,
Korvald C,
and
Myrmel T.
Pressure-volume-based single-beat estimations cannot predict left ventricular contractility in vivo.
Am J Physiol Heart Circ Physiol
282:
H1739-H1750,
2002
14.
Lakatta, EG.
Length modulation of muscle performance: Frank-Starling law of the heart.
In: The Heart and Cardiovascular System, edited by Fozzard HA.. New York: Raven, 1992, p. 1325-1351.
15.
Levy, T,
Walker S,
Mason M,
Spurrell P,
Rex S,
Brant S,
and
Paul V.
Importance of rate control or rate regulation for improving exercise capacity and quality of life in patients with permanent atrial fibrillation and normal left ventricular function: a randomised controlled study.
Heart
85:
171-178,
2001
16.
Lorenz, EN.
Deterministic nonperiodic flow.
J Atmospher Sci
10:
130-138,
1963.
17.
Moss, RL,
and
Fitzsimons DP.
Frank-Starling relationship: long on importance, short on mechanism.
Circ Res
90:
11-13,
2002
18.
Prabhu, SD,
and
Freeman GL.
Kinetics of restitution of left ventricular relaxation.
Circ Res
70:
29-38,
1992
19.
Prabhu, SD,
and
Freeman GL.
Effect of tachycardia heart failure on the restitution of left ventricular function in closed-chest dogs.
Circulation
91:
176-185,
1995
20.
Prabhu, SD,
and
Freeman GL.
Postextrasystolic mechanical restitution in closed-chest dogs. Effect of heart failure.
Circulation
92:
2652-2659,
1995
21.
Prabhu, SD,
and
Freeman GL.
Altered LV inotropic reserve and mechanoenergetics early in the development of heart failure.
Am J Physiol Heart Circ Physiol
278:
H698-H705,
2000
22.
Randall, WC,
Ardell JL,
Calderwood D,
Miloslavljevic M,
and
Goyal SC.
Parasympathetic ganglia innervating the canine atrioventricular nodal region.
J Auton Nerv Syst
16:
311-323,
1986[Web of Science][Medline].
23.
Randall, WC,
Ardell JL,
O'Toole MF,
and
Wurster RD.
Differential autonomic control of SAN and AVN regions of the canine heart: structure and function.
Prog Clin Biol Res
275:
15-31,
1988[Medline].
24.
Senzaki, H,
Fetics B,
Chen CH,
and
Kass DA.
Comparison of ventricular pressure relaxation assessments in human heart failure: quantitative influence on load and drug sensitivity analysis.
J Am Coll Cardiol
34:
1529-1536,
1999
25.
Shishido, T,
Sugimachi M,
Kawaguchi O,
Miyano H,
Kawada T,
Matsuura W,
Ikeda Y,
Sato T,
Alexander J, Jr,
and
Sunagawa K.
A new method to measure regional myocardial time-varying elastance using minute vibration.
Am J Physiol Heart Circ Physiol
274:
H1404-H1415,
1998
26.
Suzuki, S,
Araki J,
Morita T,
Mohri S,
Mikane T,
Yamaguchi H,
Sano S,
Ohe T,
Hirakawa M,
and
Suga H.
Ventricular contractility in atrial fibrillation is predictable by mechanical restitution and potentiation.
Am J Physiol Heart Circ Physiol
275:
H1513-H1519,
1998
27.
Tabata, T,
Grimm RA,
Greenberg NL,
Agler DA,
Mowrey KA,
Wallick DW,
Zhang Y,
Zhuang S,
Mazgalev TN,
and
Thomas JD.
Assessment of LV systolic function in atrial fibrillation using an index of preceding cardiac cycles.
Am J Physiol Heart Circ Physiol
281:
H573-H580,
2001
28.
Takagaki, M,
McCarthy PM,
Chung M,
Connor J,
Dessoffy R,
Ochiai Y,
Howard M,
Doi K,
Kopcak M,
Mazgalev TN,
and
Fukamachi K.
Preload-adjusted maximal power: a novel index of left ventricular contractility in atrial fibrillation.
Heart
88:
170-176,
2002
29.
Wallick, DW,
Zhang Y,
Tabata T,
Zhuang S,
Mowrey KA,
Watanabe J,
Greenberg NL,
Grimm RA,
and
Mazgalev TN.
Selective AV nodal vagal stimulation improves hemodynamics during acute atrial fibrillation in dogs.
Am J Physiol Heart Circ Physiol
281:
H1490-H1497,
2001
30.
Yamaguchi, H,
Takaki M,
Ito H,
Tachibana H,
Lee S,
and
Suga H.
Pressure-interval relationship characterizes left ventricular irregular beat contractilities and their mean level during atrial fibrillation.
Jpn J Physiol
47:
101-110,
1997[Web of Science][Medline].
31.
Yue, DT,
Burkhoff D,
Franz MR,
Hunter WC,
and
Sagawa K.
Postextrasystolic potentiation of the isolated canine left ventricle. Relationship to mechanical restitution.
Circ Res
56:
340-350,
1985
32.
Zhang, Y,
Mowrey KA,
Zhuang S,
Wallick DW,
Popovic ZB,
and
Mazgalev TN.
Optimal ventricular rate slowing during atrial fibrillation by feedback AV nodal-selective vagal stimulation.
Am J Physiol Heart Circ Physiol
282:
H1102-H1110,
2002
This article has been cited by other articles:
![]() |
Y. Notomi, Z. B. Popovic, H. Yamada, D. W. Wallick, M. G. Martin, S. J. Oryszak, T. Shiota, N. L. Greenberg, and J. D. Thomas Ventricular untwisting: a temporal link between left ventricular relaxation and suction Am J Physiol Heart Circ Physiol, January 1, 2008; 294(1): H505 - H513. [Abstract] [Full Text] [PDF] |
||||
![]() |
V. Melenovsky, I. Hay, B. J. Fetics, B. A. Borlaug, A. Kramer, J. M. Pastore, R. Berger, and D. A. Kass Functional impact of rate irregularity in patients with heart failure and atrial fibrillation receiving cardiac resynchronization therapy Eur. Heart J., April 1, 2005; 26(7): 705 - 711. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Tabata, R. A. Grimm, J. Asada, Z. B. Popovic, H. Yamada, N. L. Greenberg, D. W. Wallick, Y. Zhang, S. Zhuang, K. A. Mowrey, et al. Determinants of LV diastolic function during atrial fibrillation: beat-to-beat analysis in acute dog experiments Am J Physiol Heart Circ Physiol, January 1, 2004; 286(1): H145 - H152. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Yamada, D. O. Martin, K. A. Mowrey, N. L. Greenberg, and D. W. Wallick Effects of coupled pacing on cardiac performance during acute atrial tachycardia and fibrillation: an old therapy revisited for a new reason Am J Physiol Heart Circ Physiol, December 1, 2003; 285(6): H2630 - H2638. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |