European Heart Journal (1992) 13 (Supplement E), 99-103
Haemodynamic analysis of atrioventricular tachycardia K. GOHL, S. PERL, A. WORTMANN, AND K. BACHMANN
Department of Cardiology, University of Erlangen-Niimberg, Germany
KEY WORDS: Atrioventricular coupling, cardiac output, conductance catheter, end-diastolic pressure, end-systolic pressure, coronary heart disease, hypertensive, haemodynamics, pacing, tachycardia, ventriculo-atrial interval. The aim of the study was to delineate the influence of the ventriculo-atrial interval (VAI) in tachycardia with regard to the underlying heart disease. Haemodynamic studies were performed by the conductance catheter technique during paced tachycardia with a HR of 140, 160 and 180 beat.min'1 at various VAI in 10 patients; three with coronary heart disease (CHD), three with hypertensive heart disease (HHD) and four serving as controls. The influence of the VAI accounted for an overall change in cardiac index (CI) of 30 ± 14%. Alterations in left ventricular peak systolic pressure (LVPSP) depending on VAI were significantly higher (P < 001) in CHD patients (32 ± 9%) than in other groups (14 ± 9% in the controls and 17 ±8% in HHD patients). The influence of VAI on left ventricular end-diastolic pressure (LVEDP) did not differ between the subgroups and accounted for a mean overall change of 32 114%. Atrial activation during the last third of the cardiac cycle led to the highest values ofCI, LVEDP and LVPSP in the control group, whereas in HHD and CHD groups minimal values ofCI were correlated with maxima of LVEDP and LVPSP. Conversely, with atrial activation during the medium third of the cardiac cycle minima ofCI and LVEDP were observed in the controls, whereas in HHD and CHD patients the highest cardiac index coincided with the lowest LVEDP. Thus tachycardias have different haemodynamic effects depending on the nature of myocardial impairment and the timing of AV coupling. Introduction
\ ~
Haemodynamic tolerance of tachycardia depends on systolic and diastolic ventricular function, loading conditions, valvular function, heart rate, atrioventicular coupling and regulatory mechanisms of the vascular system. The interactions between these factors in atrial, atrioventricular and ventricular tachycardias have been the subject of several studies'1'131. In these investigations haemodynamics have been assessed by cineangiography, thermodilution, radionuclide ventriculography and ultrasound techniques. However, conventional haemodynamic studies on tachycardias have been limited in their assessment of ventricular volume and therefore failed to uncover specific changes in cardiac function due to various influences, such as nature of heart disease, atrioventricular coupling and heart rate. A systematic approach to analysing cardiac performance during tachycardia became possible by the conductance catheter technique, as introduced by Baan and co-workers'14151, which allows simultaneous beat-to-beat measurement of left ventricular pressure and volume The purpose of this study was, therefore, (1) to quantify left ventricular pressure and volume changes due to the timing of atrioventricular coupling during paced tachycardia and (2) to compare patients suffering from coronary heart disease or hypertensive heart disease with control subjects. Methods
invasive and invasive diagnostics the patients were classified into three groups (Table 1). Three patients suffered from coronary heart disease (CHD) with prior myocardial infarction (aged 56 ± 5 years, EF 65 ± 12%) and three from hypertensive heart disease (HHD) with concentric left ventricular hypertrophy (aged 61 ± 9 years, EF 73 ± 11%). Four patients without evidence of cardiac disease served as controls (aged 53 ± 6 years, EF 75 ± 3%). All patients gave informed consent before undergoing any investigation. HAEMODYNAMIC MEASUREMENTS
All patients were studied at rest in the supine position. To obtain pressure-volume signals simultaneously, a highfidelity micromanometer (Microtip catheter transducer, Millar Instruments, Texas, U.S.A.) was inserted in the lumen of a 10 electrode conductance catheter (with pigtail, interelectrode distance 10 mm, Webster Laboratories, Baldwin Park, California, U.S.A.) which was positioned in the left ventricle. Volume signals were processed by a Leycom Sigma-5 signal conditioner-processor (Cardio Dynamics, Rynsburg, Netherlands) and simultaneously recorded together with the pressure signal and an intracardiac electrogram on a personal computer (HewlettPackard) using the Lycom Conduct-PC software package. The same software was used for further processing of the data to obtain left ventricular end-diastolic pressure (LVEDP), left ventricular peak systolic pressure (LVPSP) and cardiac index (CI).
PATIENTS
The study was performed in 10 patients (aged 56 ± 7 years, ejection fraction (EF) 71 ± 9%). According to nonCorrapondencc: Dr K. G6hl, Ostliche Stadtmauerstr. 29, W-8520 Erlangen, Germany. 0195-668X/92/OE0099 + 05 S08.OV0
CARDIAC STIMULATION
Two quadripolar electrode catheters were positioned high in the right atrium and the right ventricular apex. Atrial and ventricular stimulation was performed with a programmable stimulator (Era-S-His, Biotronik, © 1992 The European Society of Cardiology
100
S. Perl et al.
Table 1 Patient
Patient characteristics Age
Sex
EF
LVEDVI
LVESV1
Heart disease
1 2 3
57 58 50
m m in
80 61 55
61 78 98
12 30 44
CHD CHD CHD
4 5 6
61 69
52
m m m
65 86 69
96 57 87
33 8 27
HHD HHD HHD
46 45 52 68
m m f m
74 71 79 74
81 62 48 81
21 17 10 21
CON CON CON CON
7
8 9 10
EF " ejection fraction; LVEDVI = left ventricular end-diastolic volume index; LVESV1 - left ventricular end-systolic volume index; CHD = coronary heart disease, HHD = hypertensive heart disease; CON = control.
Germany). To obtain reference values of the haemodynamic data, atrio-ventricular sequential stimulation was performed at a heart rate (HR) of 100 beat.min"1 and an atrioventricular delay (AVD) of 100 ms. After that, ventricular-atrial sequential stimulation was performed at paced heart rates of 140, 160 and 180 beat.min"1. By increasing the ventriculo-atrial interval (VAI) the entire diastole was scanned (increments of 20 ms) during each pacing frequency. Measurements were carried out under steady state conditions. The intracardiac electrocardiograms of the high right atrium and the right ventricular apex were recorded together with multiple surface leads on a Mingograph 7 recorder (Siemens) to check capture of the stimuli. DATA CALIBRATION
Haemodynamic data obtained during baseline stimulation (HR 100 beat.min"1, AVD 100 ms) was set as 100% and served for reference. All data sampled during stimulated tachycardia was linear, transformed according to these baseline reference values.
STATISTICAL ANALYSIS
Differences between groups were analysed comparing minima and maxima of LVEDP, LVESP and CI due to VA interval changes by means of unpaired Whitney-Mann tests. Results QUANTITATIVE CHANGES
Changing the VA interval during VA sequential stimulation with heart rates of 140, 160 and 180 beat.min"1 revealed minima and maxima of CI, LVPSP and LVEDP as shown in Table 2. The extent of these haemodynamic changes did not vary significantly between the heart rates studied. As regards CI, the difference between minima and maxima, related to the respective maximal values, accounted for 30 ± 14% in controls, CHD and HHD groups without significant differences. Maximum-related VAI-induced changes in LVEDP amounted to 32 ± 14%, and again there was no significant difference between the groups. In an absolute sense, both minima and maxima of LVEDP were strongest in the CHD group and significantly
--t Table 2 VAI induced changes of CI, LVPSP and LVEDP as percentage of normal condition (HR 100beatmin'1 AVD 100ms) Minima (% ± SD)
Maxima (% ± SD)
Max-min (% ± SD)
Max-min/max (% ± SD)
CON CHD HHD
94±25 84 ±22 84 ±41
135 ± 35 111 ±24 131 ±41
41 ±20 27 ±13 47 ±28
30 ±11 24 ± 12 37 ±19
LVPSP CON CHD HHD
82 ±14 72 ± 8 82± 8
9 5 : t 9* 107:t 10*t 9 9 :t 3t
13 ± 10 35 ±11 17 ± 8
14 ± 10* 32 ± 9t§ 17 ± 8§
LVEDP CON CHD HHD
111 ±29 146±38§ 86±16§
171 :t60 206: 138:t 31*
61 ± 44 60 ±27 52 ±21
32 ±19 29± 12 37 ± 8
CI
CI = cardiac index; LVPSP = left ventricular peak-systolic pressure; LVEDP = left ventricular end-diastolic pressure; • < = / > < 005. t =• P < O05, i = P < 0-01, § = /> < 001. CHD •» coronary heart disease, HHD — hypertension heart disease; CON = control.
Haemodynamic analysis of atrioventricular tachycardia
J
180 160 I4O 180 160 140 180 160 140
CHD 1 A I Ct
CHD
+
CHD
|Q|
HHD HHD HHD CON CON CON 0
IO2O3O4OSO6O70B09O0
CHD HHD HHD HHD CON CON CON 0 I0203O4O5O60708O9O0
higher than in the HHD group (P < 001). The relative differences in LVPSP, however, were significantly higher in CHD (32 ± 9%) compared to controls (14 ± 6) and the HHD group (17 ± 8%) (P < 001) because maximum values of LVPSP were significantly (P < 0-05) higher in CHD patients compared to both other groups. The influence of the VA interval on LVPSP was more pronounced in CHD than in controls or HHD patients. CHANGES DURING THE CARDIAC CYCLE
Analysis of the temporal relationship of atrioventricular coupling showed maxima and minima of CI, LVPSP and LVEDP occurring at specific times during the cardiac cycle, influenced by heart rate and underlying heart disease. As shown in Fig. 1, in controls CI maxima appeared during the last third and minima during the medium third of the cardiac cycle. In contrast to controls in CHD and HHD patients, CI minima were recorded with atrial systole during the last third and maxima during the medium third of the cycle length. With increasing heart rate, highest CI values tended to be during longer VA intervals in the CHD group, whereas in HHD patients an opposite trend was noted. With atrial systole in the last third of the cardiac cycle LVPSP reached maximal values in all groups, as depicted in
CHD
180
CHD
160
CHD
140
HHD
180 7 C
HHD
160
HHD
140 I
CON
ISO
CON
160
CON
40 IO2O3O4O9O6O7OS09O
10 2030405060708090 0
VA intervol/CL (%)
Figure 1 Minima (O) and maxima (•) with standard deviation (SD_ ) of cardiac index during the cardiac cycle (displayed as percentage of VA interval in relation to cycle length (CL) at different heart rates (140,160,180 beat.min"1) and underlying heart disease (CON = control, CHD = coronary heart disease, HHD = hypertensive heart disease).
I020JO4O5O6070B0900
BO 160 140 180 160 140 180 160 140
CHD
VA intervol/CL (%)
0
1
CHD
K>2O3O4OS06OTO8090O
101
|
0
VA mterwjl/CL (%)
Figure 2 Minima (O) and maxima (•) with standard deviation (SD ) of left ventricular peak systolic pressure (LVPSP) during the cardiac cycle. Abbreviations as in Fig. 1.
Figure 3 Minima (O) and maxima (•) with standard deviation (SD ) of left ventricular end-diastolic pressure (LVEDP) during the cardiac cycle. Abbreviations as in Fig. 1.
Fig. 2. In patients with CHD, LVPSP minima were found in the first half of the cardiac cycle, in controls and HHD patients the lowest LVPSP was the result of atrial and ventricular systole coinciding. As demonstrated in Fig. 3, atrial contribution during the last third of the cardiac cycle resulted in the highest LVEDP of all groups. The lowest LVEDP appeared with atrial activation during the middle third of the cycle. An increase in heart rate revealed a trend towards a shift to shorter VA intervals for the minimal LVEDP in all groups. In contrast to controls and CHD patients in the HHD group, maximal LVEDP was found earlier during the cardiac cycle with shortening of the cycle length. In general, haemodynamics differed in the control and patient groups. Atrial activation during the last third of the cardiac cycle revealed maximal CI values of LVEDP and LVPSP in the control group whereas in the HHD and CHD groups minimal values of CI were correlated with maxima of LVEDP and LVPSP. Conversely, with atrial activation during the middle third of the cardiac cycle, minima of CI and LVEDP were observed in controls whereas in HHD and CHD patients the highest cardiac index coincided with the lowest LVEDP. Discussion
The aim of the study was to delineate the influence of the ventriculo-atrial interval in tachycardia with regard to the underlying heart disease. This study reports that during tachycardia; (1) atrioventricular coupling is responsible for considerable haemodynamic changes; in CI this influence accounts for 30 ± 14%, in LVPSP for 22 ± 12% and in LVEDP for 32 ± 14%; (2) patients with coronary disease or hypertensive heart disease differ from patients without heart disease with regard to quantitative haemodynamic changes and with regard to the haemodynamic effects of the temporal relationship between atrial and ventricular systole. No method other than the conductance catheter system developed by Baan and colleagues'1415! currently offers the possibility of measuring left ventricular volumes continuously in the clinical setting. There is general agreement that the conductance method can provide a reasonably accurate measurement of left ventricular volumes which are lin-
102 S. Perl et al.
early related to volumes as determined by other methods'14"181. In this study design we considered the major limitation of this method to be the measurement of absolute ventricular volume'18"201. Therefore we determined only changes in left ventricular stroke volume (SV). To provide inter-individual comparability and to exclude haemodynamic effects by cardiac stimulation itself21"231 we related SV data, as well as the pressure measurements, to clearly defined baseline coriditions during atrioventricular stimulation capturing atria and ventricles. Studying paced tachycardias enables a systematic approach to determine the impact of the VAI on haemodynamics, but does not completely reflect the conditions in tachycardias with normal or abnormal excitation of atria and/or ventricles. Previous haemodynamic studies on tachycardias are limited by their non-systematic approach to the haemodynamic influence of atrioventricular coupling. Most of the investigations studying atrial, junctional or ventricular tachycardias are characterized by the analysis of induced tachycardias with obviously fixed AV delays or by widemeshed atrioventricular timing during paced tachycardias'2-9'2"31: the extent of VAI-related haemodynamic changes has never been determined before. In contrast to findings of Mitrovic et a/.'321, which were based on patients without significant left ventricular impairment and only three different AVIs studied, our results in controls demonstrate a higher influence of VAI on CI during tachycardia (10-19% vs 30 ± 11%); for LVPSP, the results are comparable (10-15% vs 14 ± 10%). During paced tachycardia, DiCarlo et a/.'331 found a similar decrease in CI with shortening the AV interval in patients with normal and impaired ventricular function. A recent investigation on supraventricular tachycardia by Sganzerla'91 et al. agreed with our results concluding that AV coupling is a major determinant of haemodynamics during tachycardia. In patients with CHD, LVEDP increased more than in those with HHD, probably due to the greater sensitivity of left ventricular diastolic function to high stimulation rates A drop in LVPSP with coincident atrial and ventricular activation was observed in all subjects and is mainly a result of a decrease in systemic vascular resistance mediated by an atrial reflex as described for the pacemaker syndrome'36-37'. The different temporal relationship of atrioventricular coupling to LVEDP and CI in patients with CHD and HHD compared with controls reflects altered diastolic left ventricular function in these patients; due to the impaired diastolic properties of the left ventricle in HHD and CHD, the atrial booster effect is optimized by an early onset of atrial contraction providing an increase in left ventricular end-diastolic volume and thus cardiac output. Conversely, in controls with normal diastolic function, late atrial activation is sufficient and provides a long passivefillingtime. The pronounced influence of VAI on maximal LVPSP without corresponding changes of CI in CHD could be explained by a different response of regulatory mechanisms and remains to be elucidated. Thus, shortlasting tachycardias cause different haemodynamics depending on the type of myocardial impairment and the timing of AV coupling.
LIMITATIONS
Our investigation focused on three clinically important parameters, which reflect haemodynamic alterations caused by tachycardia; the conductance catheter technique, however, offers additional features for more detailed analysis of left ventricular function not used in this study. The haemodynamic influence of inter-individually varying interatrial conduction delay13*-351 was not determined; it was possibly responsible for the dispersion of the timing of minima and maxima during the cardiac cycle within the groups This pilot study compared only a small number of patients with CHD and HHD to normal subjects; further and larger studies are necessary while other types of heart disease must also be investigated. References [1] Hunt D, Bureshaw JA, Baxley WA. Left ventricular volumes during ventricular tachycardia, first post-tachycardia beat, and subsequent beat in normal rhythm. Br Heart J 1974; 36: 148-56. [2] Goldreyer BN, Kastor JA, Kershbaum KL. The hemodynamic effects of induced supraventricular tachycardia in man. Circulation 1976; 54: 783-92. [3] Thormann J, Schlepper M, Neuss H. Coronary hemodynamics in simulated paroxysms of ventricular tachycardia: Role of myocardial impairment and of extravascular resistance. Cardiology 1982; 69: 326-42. [4] Feldman T, Carroll JD, Munkenbeck F et al. Hemodynamic recovery during simulated ventricular tachycardia: role of adrenergic receptor activation. Am Heart J 1988; 115: 576-87. [5] Tsai RC, Yamaji T, Ishibashi M et al. Atrial natriuretic peptide during supraventricular tachycardia and relation to hemodynamic changes and renal function. Am J Cardiol 1988;61:1260-4. [6] Thormann J. Clinical viewpoints of hemodynamics in cardiac arrhythmias and during anti-arrhythmia treatment. Z Kardiol 1988; 77 (Suppl 5): 121-36. [7] Yusoff K, Tai YT, Campbell RW. Hemodynamic consequences of supraventricular tachycardias and their antiarrhythmic treatment. Z Kardiol 1988; 77 (Suppl 5): 137-42 [8] Luederitz B, Manz M. Hemodynamics in ventricular arrhythmias and in their treatment. Z Kardiol 1988; 77 (Suppl 5): 143-9. [9] Sganzerla P, Fabbiocchi F, Grazi S, Cipolla C, Moruzzi P, Guazzi MD. Electrophysiologic and hemodynamic correlates in supraventricular tachycardia. Eur Heart J 1989; 10: 32-9. [10] Crozier IG, Ikram H, Nicholls MG. Hemodynamic and hormone changes during induced ventricular tachycardia secondary to coronary artery disease. Am J Cardiol 1989; 63: 618-21. [11] Baron SB, Huang SK, Comess KA. Left ventricular function during stable sustained ventricular tachycardia. Hemodynamic and echo-Doppler analysis. Chest 1989; 96: 275-80. [12] Lau CP, Leung WH, Wong CK, Cheng CH. Hemodynamics of induced atrial fibrillation: a comparative assessment with sinus rhythm, atrial and ventricular pacing. Eur Heart J 1990; 11:219-24. [13] Waxman MB, Camron DA. The reflex effects of tachycardias on autonomic tone. Ann NY Acad Sci 1990; 601: 378-93. [14] Baan J, Aouw Jong TT, Kerkhof PLM et al Continuous stroke volume and cardiac output from intraventricular dimensions obtained with impedance catheter. Cardiovasc Res 1981; 328-34. [15] Baan J, Van der Velde ET, De Bruin HG et al Continuous measurement of left ventricular volume in animals and humans by conductance catheter. Circulation 1984; 70:812-23.
Haemodynamic analysis of atrioventricular tachycardia
[16] Mur G, Bann J. Computation of the input impedances of a catheter for cardiac volumetry. IEEE Trans Biomed Eng 1984; BME 31:448-53. [17] Burkhoff D, Van der Velde ET, Kass D, Baan J, Maughan WL, Sagawa K. Accuracy of volume measurement by conductance catheter in isolated, ejecting canine hearts Circulation 1985; 72:440-7. [18] Burkhoff D. The conductance method of left ventricular volume estimation. Methodological shortcomings put into perspective. (Editorial). Circulation 1990; 81: 703-6. [19] Boltwood CM, Appleyard RF, Glantz SA. Left ventricular volume measurement by conductance catheter in intact dogs. Circulation 1989; 80:1360. [20] Applegate RJ, Cheng CP, Little WC Simultaneous conductance catheter and dimension assessment of left ventricular volume in the intact animal. Circulation 1990; 81:628-^*8. [21] Lister VW, Klotz DH, Jomain SK, Stuckey JE, Hoffman BE. Effect of pacemaker site on cardiac output and ventricular activation in dogs with complete heart block. Am J Cardiol 1964; 14: 494. [22] Barold SS, Linhart JW, Hildner FJ, Samet P. Haemodynamic comparison of endocardial pacing of outflow tracts of the right ventricle. Am J Cardiol 1969; 23: 697-701. [23] De Maria AN, Kaiyama T, Peng CL. Alterations of left ventricular function and myocardial contractility indices induced by ventricular asynchrony. Clin Res 1973; 21:414. [24] Grover M, Glantz SA. Endocardial pacing site effects left ventricular end-diastolic volume and performance in the intact anesthesized dog. Circ Res 1983; 53: 72. [25] Askenazi J, Alexander JH, Kocnigsberg DI, Belie N, Lesch M. Alteration of left ventricular performance by left bundle branch block simulated with atrioventricular sequential pacing. Am J Cardiol 1984; 53: 99. [26] Saunders DE, Ord JW. The hemodynamk effects of paroxysmal supraventricular tachycardia in patients with the Wolff-Parkinson-White syndrome. Am J Cardiol 1962; 9:223-36.
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[27] Skinner MS, Mitchell JH, Wallace AG, Sarnoff SJ. Hemodynamic effects of altering the timing of atrial systole. Am J Physiol 1963; 205: 499. [28] Ferrer MI, Harvey RM. Some hemodynamic aspects of cardiac arrhythmias in man. A clinico-physiologic correlation. Am Heart J 1964; 68:153. [29] Mclntosh HD, Kong Y, Morris JJ. Hemodynamic effects of supraventricular arrhythmias. Am J Med 1964; 37: 712. [30] Benchimol A, Ellis JG, Dimond EG, Wu T. Hemodynamic consequences of atrial and ventricular arrhythmias in man. Am Heart J 1965; 70: 775. [31] Samet P. Hemodynamic sequelae of cardiac arrhythmias. Circulation 1973; 47: 399. [32] Mitrovic V, Neuss H, Schlepper M, Thormann J. Hemodynamic significance of the synchronization of atrial and ventricular systole in tachycardia. Z Kardiol 1984; 73: 34-^0 [33] DiCarlo LA, Morady F, Krol RB et al. The hemodynamic effects of ventricular pacing with and without atrioventricular synchrony in patients with normal and diminished left ventricular function. Am Heart J 1987; 114:746-52. [34] Wish M, Fletcher RD, Gottdiener JS, Cohen A l Importance of left atrial timing in the programming of dual-chamber pacemakers. Am J Cardiol 1987; 60: 566-71 [35] Janosik DL, Pearson AC Buckingham TA, Labovitz AJ, Redd RM. The hemodynamic benefit of differential atrioventricular delay intervals for sensed and paced events during physiologic pacing. J Am Coll Cardiol 1989; 14: 499-507. [36] Erlebacher JA, Danner RL, Stelzer PE. Hypotension with ventricular pacing: An atrial vasodepressor reflex in human beings. J Am Coll Cardiol 1984; 4: 550-5. [37] Ausubel K, Furman S. The pacemaker syndrome. Ann Int Med 1985; 103: 420-9.
Haemodynamic analysis of atrioventricular tachycardia K. GOHL, S. PERL, A. WORTMANN, AND K. BACHMANN
Department of Cardiology, University of Erlangen-Niimberg, Germany
KEY WORDS: Atrioventricular coupling, cardiac output, conductance catheter, end-diastolic pressure, end-systolic pressure, coronary heart disease, hypertensive, haemodynamics, pacing, tachycardia, ventriculo-atrial interval. The aim of the study was to delineate the influence of the ventriculo-atrial interval (VAI) in tachycardia with regard to the underlying heart disease. Haemodynamic studies were performed by the conductance catheter technique during paced tachycardia with a HR of 140, 160 and 180 beat.min'1 at various VAI in 10 patients; three with coronary heart disease (CHD), three with hypertensive heart disease (HHD) and four serving as controls. The influence of the VAI accounted for an overall change in cardiac index (CI) of 30 ± 14%. Alterations in left ventricular peak systolic pressure (LVPSP) depending on VAI were significantly higher (P < 001) in CHD patients (32 ± 9%) than in other groups (14 ± 9% in the controls and 17 ±8% in HHD patients). The influence of VAI on left ventricular end-diastolic pressure (LVEDP) did not differ between the subgroups and accounted for a mean overall change of 32 114%. Atrial activation during the last third of the cardiac cycle led to the highest values ofCI, LVEDP and LVPSP in the control group, whereas in HHD and CHD groups minimal values ofCI were correlated with maxima of LVEDP and LVPSP. Conversely, with atrial activation during the medium third of the cardiac cycle minima ofCI and LVEDP were observed in the controls, whereas in HHD and CHD patients the highest cardiac index coincided with the lowest LVEDP. Thus tachycardias have different haemodynamic effects depending on the nature of myocardial impairment and the timing of AV coupling. Introduction
\ ~
Haemodynamic tolerance of tachycardia depends on systolic and diastolic ventricular function, loading conditions, valvular function, heart rate, atrioventicular coupling and regulatory mechanisms of the vascular system. The interactions between these factors in atrial, atrioventricular and ventricular tachycardias have been the subject of several studies'1'131. In these investigations haemodynamics have been assessed by cineangiography, thermodilution, radionuclide ventriculography and ultrasound techniques. However, conventional haemodynamic studies on tachycardias have been limited in their assessment of ventricular volume and therefore failed to uncover specific changes in cardiac function due to various influences, such as nature of heart disease, atrioventricular coupling and heart rate. A systematic approach to analysing cardiac performance during tachycardia became possible by the conductance catheter technique, as introduced by Baan and co-workers'14151, which allows simultaneous beat-to-beat measurement of left ventricular pressure and volume The purpose of this study was, therefore, (1) to quantify left ventricular pressure and volume changes due to the timing of atrioventricular coupling during paced tachycardia and (2) to compare patients suffering from coronary heart disease or hypertensive heart disease with control subjects. Methods
invasive and invasive diagnostics the patients were classified into three groups (Table 1). Three patients suffered from coronary heart disease (CHD) with prior myocardial infarction (aged 56 ± 5 years, EF 65 ± 12%) and three from hypertensive heart disease (HHD) with concentric left ventricular hypertrophy (aged 61 ± 9 years, EF 73 ± 11%). Four patients without evidence of cardiac disease served as controls (aged 53 ± 6 years, EF 75 ± 3%). All patients gave informed consent before undergoing any investigation. HAEMODYNAMIC MEASUREMENTS
All patients were studied at rest in the supine position. To obtain pressure-volume signals simultaneously, a highfidelity micromanometer (Microtip catheter transducer, Millar Instruments, Texas, U.S.A.) was inserted in the lumen of a 10 electrode conductance catheter (with pigtail, interelectrode distance 10 mm, Webster Laboratories, Baldwin Park, California, U.S.A.) which was positioned in the left ventricle. Volume signals were processed by a Leycom Sigma-5 signal conditioner-processor (Cardio Dynamics, Rynsburg, Netherlands) and simultaneously recorded together with the pressure signal and an intracardiac electrogram on a personal computer (HewlettPackard) using the Lycom Conduct-PC software package. The same software was used for further processing of the data to obtain left ventricular end-diastolic pressure (LVEDP), left ventricular peak systolic pressure (LVPSP) and cardiac index (CI).
PATIENTS
The study was performed in 10 patients (aged 56 ± 7 years, ejection fraction (EF) 71 ± 9%). According to nonCorrapondencc: Dr K. G6hl, Ostliche Stadtmauerstr. 29, W-8520 Erlangen, Germany. 0195-668X/92/OE0099 + 05 S08.OV0
CARDIAC STIMULATION
Two quadripolar electrode catheters were positioned high in the right atrium and the right ventricular apex. Atrial and ventricular stimulation was performed with a programmable stimulator (Era-S-His, Biotronik, © 1992 The European Society of Cardiology
100
S. Perl et al.
Table 1 Patient
Patient characteristics Age
Sex
EF
LVEDVI
LVESV1
Heart disease
1 2 3
57 58 50
m m in
80 61 55
61 78 98
12 30 44
CHD CHD CHD
4 5 6
61 69
52
m m m
65 86 69
96 57 87
33 8 27
HHD HHD HHD
46 45 52 68
m m f m
74 71 79 74
81 62 48 81
21 17 10 21
CON CON CON CON
7
8 9 10
EF " ejection fraction; LVEDVI = left ventricular end-diastolic volume index; LVESV1 - left ventricular end-systolic volume index; CHD = coronary heart disease, HHD = hypertensive heart disease; CON = control.
Germany). To obtain reference values of the haemodynamic data, atrio-ventricular sequential stimulation was performed at a heart rate (HR) of 100 beat.min"1 and an atrioventricular delay (AVD) of 100 ms. After that, ventricular-atrial sequential stimulation was performed at paced heart rates of 140, 160 and 180 beat.min"1. By increasing the ventriculo-atrial interval (VAI) the entire diastole was scanned (increments of 20 ms) during each pacing frequency. Measurements were carried out under steady state conditions. The intracardiac electrocardiograms of the high right atrium and the right ventricular apex were recorded together with multiple surface leads on a Mingograph 7 recorder (Siemens) to check capture of the stimuli. DATA CALIBRATION
Haemodynamic data obtained during baseline stimulation (HR 100 beat.min"1, AVD 100 ms) was set as 100% and served for reference. All data sampled during stimulated tachycardia was linear, transformed according to these baseline reference values.
STATISTICAL ANALYSIS
Differences between groups were analysed comparing minima and maxima of LVEDP, LVESP and CI due to VA interval changes by means of unpaired Whitney-Mann tests. Results QUANTITATIVE CHANGES
Changing the VA interval during VA sequential stimulation with heart rates of 140, 160 and 180 beat.min"1 revealed minima and maxima of CI, LVPSP and LVEDP as shown in Table 2. The extent of these haemodynamic changes did not vary significantly between the heart rates studied. As regards CI, the difference between minima and maxima, related to the respective maximal values, accounted for 30 ± 14% in controls, CHD and HHD groups without significant differences. Maximum-related VAI-induced changes in LVEDP amounted to 32 ± 14%, and again there was no significant difference between the groups. In an absolute sense, both minima and maxima of LVEDP were strongest in the CHD group and significantly
--t Table 2 VAI induced changes of CI, LVPSP and LVEDP as percentage of normal condition (HR 100beatmin'1 AVD 100ms) Minima (% ± SD)
Maxima (% ± SD)
Max-min (% ± SD)
Max-min/max (% ± SD)
CON CHD HHD
94±25 84 ±22 84 ±41
135 ± 35 111 ±24 131 ±41
41 ±20 27 ±13 47 ±28
30 ±11 24 ± 12 37 ±19
LVPSP CON CHD HHD
82 ±14 72 ± 8 82± 8
9 5 : t 9* 107:t 10*t 9 9 :t 3t
13 ± 10 35 ±11 17 ± 8
14 ± 10* 32 ± 9t§ 17 ± 8§
LVEDP CON CHD HHD
111 ±29 146±38§ 86±16§
171 :t60 206: 138:t 31*
61 ± 44 60 ±27 52 ±21
32 ±19 29± 12 37 ± 8
CI
CI = cardiac index; LVPSP = left ventricular peak-systolic pressure; LVEDP = left ventricular end-diastolic pressure; • < = / > < 005. t =• P < O05, i = P < 0-01, § = /> < 001. CHD •» coronary heart disease, HHD — hypertension heart disease; CON = control.
Haemodynamic analysis of atrioventricular tachycardia
J
180 160 I4O 180 160 140 180 160 140
CHD 1 A I Ct
CHD
+
CHD
|Q|
HHD HHD HHD CON CON CON 0
IO2O3O4OSO6O70B09O0
CHD HHD HHD HHD CON CON CON 0 I0203O4O5O60708O9O0
higher than in the HHD group (P < 001). The relative differences in LVPSP, however, were significantly higher in CHD (32 ± 9%) compared to controls (14 ± 6) and the HHD group (17 ± 8%) (P < 001) because maximum values of LVPSP were significantly (P < 0-05) higher in CHD patients compared to both other groups. The influence of the VA interval on LVPSP was more pronounced in CHD than in controls or HHD patients. CHANGES DURING THE CARDIAC CYCLE
Analysis of the temporal relationship of atrioventricular coupling showed maxima and minima of CI, LVPSP and LVEDP occurring at specific times during the cardiac cycle, influenced by heart rate and underlying heart disease. As shown in Fig. 1, in controls CI maxima appeared during the last third and minima during the medium third of the cardiac cycle. In contrast to controls in CHD and HHD patients, CI minima were recorded with atrial systole during the last third and maxima during the medium third of the cycle length. With increasing heart rate, highest CI values tended to be during longer VA intervals in the CHD group, whereas in HHD patients an opposite trend was noted. With atrial systole in the last third of the cardiac cycle LVPSP reached maximal values in all groups, as depicted in
CHD
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10 2030405060708090 0
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Figure 1 Minima (O) and maxima (•) with standard deviation (SD_ ) of cardiac index during the cardiac cycle (displayed as percentage of VA interval in relation to cycle length (CL) at different heart rates (140,160,180 beat.min"1) and underlying heart disease (CON = control, CHD = coronary heart disease, HHD = hypertensive heart disease).
I020JO4O5O6070B0900
BO 160 140 180 160 140 180 160 140
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Figure 2 Minima (O) and maxima (•) with standard deviation (SD ) of left ventricular peak systolic pressure (LVPSP) during the cardiac cycle. Abbreviations as in Fig. 1.
Figure 3 Minima (O) and maxima (•) with standard deviation (SD ) of left ventricular end-diastolic pressure (LVEDP) during the cardiac cycle. Abbreviations as in Fig. 1.
Fig. 2. In patients with CHD, LVPSP minima were found in the first half of the cardiac cycle, in controls and HHD patients the lowest LVPSP was the result of atrial and ventricular systole coinciding. As demonstrated in Fig. 3, atrial contribution during the last third of the cardiac cycle resulted in the highest LVEDP of all groups. The lowest LVEDP appeared with atrial activation during the middle third of the cycle. An increase in heart rate revealed a trend towards a shift to shorter VA intervals for the minimal LVEDP in all groups. In contrast to controls and CHD patients in the HHD group, maximal LVEDP was found earlier during the cardiac cycle with shortening of the cycle length. In general, haemodynamics differed in the control and patient groups. Atrial activation during the last third of the cardiac cycle revealed maximal CI values of LVEDP and LVPSP in the control group whereas in the HHD and CHD groups minimal values of CI were correlated with maxima of LVEDP and LVPSP. Conversely, with atrial activation during the middle third of the cardiac cycle, minima of CI and LVEDP were observed in controls whereas in HHD and CHD patients the highest cardiac index coincided with the lowest LVEDP. Discussion
The aim of the study was to delineate the influence of the ventriculo-atrial interval in tachycardia with regard to the underlying heart disease. This study reports that during tachycardia; (1) atrioventricular coupling is responsible for considerable haemodynamic changes; in CI this influence accounts for 30 ± 14%, in LVPSP for 22 ± 12% and in LVEDP for 32 ± 14%; (2) patients with coronary disease or hypertensive heart disease differ from patients without heart disease with regard to quantitative haemodynamic changes and with regard to the haemodynamic effects of the temporal relationship between atrial and ventricular systole. No method other than the conductance catheter system developed by Baan and colleagues'1415! currently offers the possibility of measuring left ventricular volumes continuously in the clinical setting. There is general agreement that the conductance method can provide a reasonably accurate measurement of left ventricular volumes which are lin-
102 S. Perl et al.
early related to volumes as determined by other methods'14"181. In this study design we considered the major limitation of this method to be the measurement of absolute ventricular volume'18"201. Therefore we determined only changes in left ventricular stroke volume (SV). To provide inter-individual comparability and to exclude haemodynamic effects by cardiac stimulation itself21"231 we related SV data, as well as the pressure measurements, to clearly defined baseline coriditions during atrioventricular stimulation capturing atria and ventricles. Studying paced tachycardias enables a systematic approach to determine the impact of the VAI on haemodynamics, but does not completely reflect the conditions in tachycardias with normal or abnormal excitation of atria and/or ventricles. Previous haemodynamic studies on tachycardias are limited by their non-systematic approach to the haemodynamic influence of atrioventricular coupling. Most of the investigations studying atrial, junctional or ventricular tachycardias are characterized by the analysis of induced tachycardias with obviously fixed AV delays or by widemeshed atrioventricular timing during paced tachycardias'2-9'2"31: the extent of VAI-related haemodynamic changes has never been determined before. In contrast to findings of Mitrovic et a/.'321, which were based on patients without significant left ventricular impairment and only three different AVIs studied, our results in controls demonstrate a higher influence of VAI on CI during tachycardia (10-19% vs 30 ± 11%); for LVPSP, the results are comparable (10-15% vs 14 ± 10%). During paced tachycardia, DiCarlo et a/.'331 found a similar decrease in CI with shortening the AV interval in patients with normal and impaired ventricular function. A recent investigation on supraventricular tachycardia by Sganzerla'91 et al. agreed with our results concluding that AV coupling is a major determinant of haemodynamics during tachycardia. In patients with CHD, LVEDP increased more than in those with HHD, probably due to the greater sensitivity of left ventricular diastolic function to high stimulation rates A drop in LVPSP with coincident atrial and ventricular activation was observed in all subjects and is mainly a result of a decrease in systemic vascular resistance mediated by an atrial reflex as described for the pacemaker syndrome'36-37'. The different temporal relationship of atrioventricular coupling to LVEDP and CI in patients with CHD and HHD compared with controls reflects altered diastolic left ventricular function in these patients; due to the impaired diastolic properties of the left ventricle in HHD and CHD, the atrial booster effect is optimized by an early onset of atrial contraction providing an increase in left ventricular end-diastolic volume and thus cardiac output. Conversely, in controls with normal diastolic function, late atrial activation is sufficient and provides a long passivefillingtime. The pronounced influence of VAI on maximal LVPSP without corresponding changes of CI in CHD could be explained by a different response of regulatory mechanisms and remains to be elucidated. Thus, shortlasting tachycardias cause different haemodynamics depending on the type of myocardial impairment and the timing of AV coupling.
LIMITATIONS
Our investigation focused on three clinically important parameters, which reflect haemodynamic alterations caused by tachycardia; the conductance catheter technique, however, offers additional features for more detailed analysis of left ventricular function not used in this study. The haemodynamic influence of inter-individually varying interatrial conduction delay13*-351 was not determined; it was possibly responsible for the dispersion of the timing of minima and maxima during the cardiac cycle within the groups This pilot study compared only a small number of patients with CHD and HHD to normal subjects; further and larger studies are necessary while other types of heart disease must also be investigated. References [1] Hunt D, Bureshaw JA, Baxley WA. Left ventricular volumes during ventricular tachycardia, first post-tachycardia beat, and subsequent beat in normal rhythm. Br Heart J 1974; 36: 148-56. [2] Goldreyer BN, Kastor JA, Kershbaum KL. The hemodynamic effects of induced supraventricular tachycardia in man. Circulation 1976; 54: 783-92. [3] Thormann J, Schlepper M, Neuss H. Coronary hemodynamics in simulated paroxysms of ventricular tachycardia: Role of myocardial impairment and of extravascular resistance. Cardiology 1982; 69: 326-42. [4] Feldman T, Carroll JD, Munkenbeck F et al. Hemodynamic recovery during simulated ventricular tachycardia: role of adrenergic receptor activation. Am Heart J 1988; 115: 576-87. [5] Tsai RC, Yamaji T, Ishibashi M et al. Atrial natriuretic peptide during supraventricular tachycardia and relation to hemodynamic changes and renal function. Am J Cardiol 1988;61:1260-4. [6] Thormann J. Clinical viewpoints of hemodynamics in cardiac arrhythmias and during anti-arrhythmia treatment. Z Kardiol 1988; 77 (Suppl 5): 121-36. [7] Yusoff K, Tai YT, Campbell RW. Hemodynamic consequences of supraventricular tachycardias and their antiarrhythmic treatment. Z Kardiol 1988; 77 (Suppl 5): 137-42 [8] Luederitz B, Manz M. Hemodynamics in ventricular arrhythmias and in their treatment. Z Kardiol 1988; 77 (Suppl 5): 143-9. [9] Sganzerla P, Fabbiocchi F, Grazi S, Cipolla C, Moruzzi P, Guazzi MD. Electrophysiologic and hemodynamic correlates in supraventricular tachycardia. Eur Heart J 1989; 10: 32-9. [10] Crozier IG, Ikram H, Nicholls MG. Hemodynamic and hormone changes during induced ventricular tachycardia secondary to coronary artery disease. Am J Cardiol 1989; 63: 618-21. [11] Baron SB, Huang SK, Comess KA. Left ventricular function during stable sustained ventricular tachycardia. Hemodynamic and echo-Doppler analysis. Chest 1989; 96: 275-80. [12] Lau CP, Leung WH, Wong CK, Cheng CH. Hemodynamics of induced atrial fibrillation: a comparative assessment with sinus rhythm, atrial and ventricular pacing. Eur Heart J 1990; 11:219-24. [13] Waxman MB, Camron DA. The reflex effects of tachycardias on autonomic tone. Ann NY Acad Sci 1990; 601: 378-93. [14] Baan J, Aouw Jong TT, Kerkhof PLM et al Continuous stroke volume and cardiac output from intraventricular dimensions obtained with impedance catheter. Cardiovasc Res 1981; 328-34. [15] Baan J, Van der Velde ET, De Bruin HG et al Continuous measurement of left ventricular volume in animals and humans by conductance catheter. Circulation 1984; 70:812-23.
Haemodynamic analysis of atrioventricular tachycardia
[16] Mur G, Bann J. Computation of the input impedances of a catheter for cardiac volumetry. IEEE Trans Biomed Eng 1984; BME 31:448-53. [17] Burkhoff D, Van der Velde ET, Kass D, Baan J, Maughan WL, Sagawa K. Accuracy of volume measurement by conductance catheter in isolated, ejecting canine hearts Circulation 1985; 72:440-7. [18] Burkhoff D. The conductance method of left ventricular volume estimation. Methodological shortcomings put into perspective. (Editorial). Circulation 1990; 81: 703-6. [19] Boltwood CM, Appleyard RF, Glantz SA. Left ventricular volume measurement by conductance catheter in intact dogs. Circulation 1989; 80:1360. [20] Applegate RJ, Cheng CP, Little WC Simultaneous conductance catheter and dimension assessment of left ventricular volume in the intact animal. Circulation 1990; 81:628-^*8. [21] Lister VW, Klotz DH, Jomain SK, Stuckey JE, Hoffman BE. Effect of pacemaker site on cardiac output and ventricular activation in dogs with complete heart block. Am J Cardiol 1964; 14: 494. [22] Barold SS, Linhart JW, Hildner FJ, Samet P. Haemodynamic comparison of endocardial pacing of outflow tracts of the right ventricle. Am J Cardiol 1969; 23: 697-701. [23] De Maria AN, Kaiyama T, Peng CL. Alterations of left ventricular function and myocardial contractility indices induced by ventricular asynchrony. Clin Res 1973; 21:414. [24] Grover M, Glantz SA. Endocardial pacing site effects left ventricular end-diastolic volume and performance in the intact anesthesized dog. Circ Res 1983; 53: 72. [25] Askenazi J, Alexander JH, Kocnigsberg DI, Belie N, Lesch M. Alteration of left ventricular performance by left bundle branch block simulated with atrioventricular sequential pacing. Am J Cardiol 1984; 53: 99. [26] Saunders DE, Ord JW. The hemodynamk effects of paroxysmal supraventricular tachycardia in patients with the Wolff-Parkinson-White syndrome. Am J Cardiol 1962; 9:223-36.
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[27] Skinner MS, Mitchell JH, Wallace AG, Sarnoff SJ. Hemodynamic effects of altering the timing of atrial systole. Am J Physiol 1963; 205: 499. [28] Ferrer MI, Harvey RM. Some hemodynamic aspects of cardiac arrhythmias in man. A clinico-physiologic correlation. Am Heart J 1964; 68:153. [29] Mclntosh HD, Kong Y, Morris JJ. Hemodynamic effects of supraventricular arrhythmias. Am J Med 1964; 37: 712. [30] Benchimol A, Ellis JG, Dimond EG, Wu T. Hemodynamic consequences of atrial and ventricular arrhythmias in man. Am Heart J 1965; 70: 775. [31] Samet P. Hemodynamic sequelae of cardiac arrhythmias. Circulation 1973; 47: 399. [32] Mitrovic V, Neuss H, Schlepper M, Thormann J. Hemodynamic significance of the synchronization of atrial and ventricular systole in tachycardia. Z Kardiol 1984; 73: 34-^0 [33] DiCarlo LA, Morady F, Krol RB et al. The hemodynamic effects of ventricular pacing with and without atrioventricular synchrony in patients with normal and diminished left ventricular function. Am Heart J 1987; 114:746-52. [34] Wish M, Fletcher RD, Gottdiener JS, Cohen A l Importance of left atrial timing in the programming of dual-chamber pacemakers. Am J Cardiol 1987; 60: 566-71 [35] Janosik DL, Pearson AC Buckingham TA, Labovitz AJ, Redd RM. The hemodynamic benefit of differential atrioventricular delay intervals for sensed and paced events during physiologic pacing. J Am Coll Cardiol 1989; 14: 499-507. [36] Erlebacher JA, Danner RL, Stelzer PE. Hypotension with ventricular pacing: An atrial vasodepressor reflex in human beings. J Am Coll Cardiol 1984; 4: 550-5. [37] Ausubel K, Furman S. The pacemaker syndrome. Ann Int Med 1985; 103: 420-9.
