Short atrioventricular delay dual-chamber pacing early after coronary artery bypass grafting in patients with poor left ventricular function

Short Atrioventricular Delay Dual-Chamber Pacing Early After Coronary Artery Bypass Grafting in Patients With Poor Left Ventricular Function Andreas Liebold, MD, Gabriele R6dig, MD, Johannes Merk, MD, and Dietrich E. Birnbaum, MD Objective: To investigate the effect of short atrioventricular (AV) delay dual-chamber pacing on mean arterial pressure (MAP) and stroke volume index (SVI) in patients with poor left ventricular (LV) function after cardiac surgery. Design: A prospective study. Setting: A university hospital, single-center study. Participants: The study group consisted of 20 patients aged 63 ~- 9 years with a left ventricular ejection fraction (LVEF) less than 30%. The control group consisted of 20 patients aged 61 +- 10 years, with an LVEF greater than 50%. Interventions: Immediately after routine coronary artery bypass grafting (CABG) the AV delay was shortened from 160 to 40 milliseconds in atrial-paced (DDD) mode and from 100 to 40 milliseconds in atrial-sensed ventricular stimulation (VDD) mode. MAP was on-line monitored and SVI was calculated by thermodilution. In one patient with an LVEF of 18% (case study), transmitral flow velocity and LV isovolumetric relaxation time were assessed using Doppler echocardiography during VDD pacing at 40-, 80-, and 120-millisecond AV delay. Results: Short-AV delay DDD pacing decreased MAP in

the control group (84.3 +- 9 v 75.7 +- 9 mmHg; p < 0.05) and SVI in both groups (study group, 35.9 -+ 7 v31.7 -+ 7 mL/m2; control group, 35.3 -+ 6 v31.O _+ 6 mL/m2;p < 0.05). Shortening the AV delay had no influence on MAP and SVI during VDD pacing. During the echocardiographic case study, AV delay shortening distinctly modified ventricular filling patterns. Optimal LV filling and transmittal flow were achieved with an intermediate AV delay of 80 milliseconds. Conclusion: Dual-chamber pacing with nonphysiologic short AV delay failed to improve acute hemodynamics in patients with poor LV function after CABG. Short AV delay VDD pacing was superior to DDD pacing in both normal and impaired LV function. The use of Doppler echocardiography enabled optimization of the AV delay on the basis of LV filling patterns.

EMPORARY CARDIAC PACING immediately after disconnection of cardiopulmonary bypass and during the early postoperative course is required in patients with chronotropic incompetence. Further indications are overdrive suppression of arrhythmias and increase of cardiac output (CO). The need for temporary pacing is poorly defined and is mostly influenced by the anesthesiologist's experience. Discord exists about the optimal pacing mode, especially in patients with severely depressed left ventricular (LV) function. 1-3 Dualchamber pacing with nonphysiologically short atrioventricular (AV) delay has recently been proposed to be beneficial in end-stage cardiomyopathy. 4-7 The aim of this study was to assess the effects of shortening the AV interval on acute hemodynamics after myocardial revascularization in patients with globally impaired left ventricular function. Shortening the AV delay can be performed either with conventional DDD pacing or with atrial-sensed ventricular stimulation (VDD) pacing, which provides atrioventricular synchronization without altering the intra-atrial conduction. Therefore, both pacing modes were compared with respect to the potential beneficial effects of VDD pacing.

enter into the study. Patients with a history of atrial tachyan-hythmias, atrial fibrillation or flutter, ventricular ectopia, emergency procedures, coexistent valve lesions, and mechanical circulatory support were excluded. Demographic and hemodynamic data, as well as basic sinus node rate and spontaneous AV delay, obtained preoperatively, are listed in Table 1. All patients gave written informed consent preoperatively, and the study was approved by the hospital's ethical committee. Anesthesia was induced intravenously with fentanyl, etomidate, and pancuronium, and was maintained with isoflurane supplemented with fentanyl and pancuronium bolus doses throughout the procedure. The patients underwent surgery in a standardized manner using extracorporeal circulation (ECC) with cold Bretschneiders' crystalloid cardioplegia and mild hypothermia (33 ° to 34°C). Temporary bipolar epicardial pacing wires (TME 63-ZS; Sulzer Osypka lnc, Ktln, Germany) were placed as part of the cardiac surgical routine. The atrial wire was attached to the upper part of the right atrial lateral wall in the proximity of the sinus node. The ventricular lead was placed apically at the right ventricular anterior wall. After threshold testing, the leads were connected to an external dual-chamber pacemaker (EDP 30/A; Biotronik, Berlin, Germany). Measurements were initially obtained 2 hours after termination of ECC to avoid hemodynamic disturbances because of volume imbalances and arrhythmias during the early postoperative course. Measurements were performed in the intensive care unit with the patients receiving mild sedation (propofol, 1 to 4 mg/kg]h) and continuing mechanical ventilation. Administration of propofol was determined by the patient's ability to react to verbal stimuli, thus avoiding cardiodepressant effects. Inotropic support and volume supply were continued without dose corrections during the study period. Mean arterial pressure (MAP) was monitored with an indwelling radial arterial catheter. An intraoperatively placed pulmonary artery catheter (93A-931; Baxter Healthcare, Irvine, CA) was used to intermittently measure CO by thermodilution. Stroke volume index (SVI) was calculated using the Sirecust 1281 (Siemens Medical Electronics; Danvers, MA). The protocol included SR and four different pacing modes (Table 2): Dual-chamber pacing was performed either in DDD or VDD mode. Because right atrial pacing delays left atrial contraction due to the interatrial conduction time, the authors chose as "long AV delay" a paced AV delay of 160 milliseconds (DDD mode) and a sensed AV

T

PATIENTS A N D METHODS

Twenty patients with left ventricular ejection fraction (LVEF) less than 30%, assessed preoperatively by LV angiography and scheduled for selective myocardial revascularization, were enrolled into the study group. Twenty consecutive patients with normal LV function (EF > 50%) served as control group. A stable sinus rhythm (SR) was necessary to

From the Department of Cardiothoracic Surgery and Anesthesiology, University of Regensburg, Regensburg, Germany. Address reprint requests to Andreas Liebold, MD, Klinik fiir Herz-, Thorax- und herznahe GefgiJ3chirurgie, Klinikum der Universitiit Regensburg, Franz-Josef-Strauss-Allee 11, 93042 Regensburg, Germany. Copyright © 1998 by W.B. Saunters Company 1053-0770/98/1203-000858.00/0 284

Copyright© I998by W.B, Saunders Company KEY WORDS: temporary cardiac pacing, short atrioventricular delay, poor left ventricular function, coronary artery bypass grafting

Journal of Cardiothoracic and Vascular Anesthesia, Vol 12, No 3 (June), 1998: pp 284-287

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Table 1. Demographic and Preoperative Hemodynamic Data

No. of patients Male/female Age (yr) NYHA CAD MI (%) LVEF (%) LVEDVI (mL/m 2) LVEDP (mmHg) HR (beats/min) PR (msec)

Study Group

Control Group

20 12/8 63 -- 9 3.1 ± 0.5 2.5 ± 0.8 75* 21.2 -+ 6* 141 _+ 38* 26.3 ± 8* 81 ± 13 135 _+ 33

20 13/7 61 _+ 10 2.9 ± 0.4 2.6 ± 0.6 33 69.2 ± 9 86.2 _+ 24 12.2 ± 4 78 ± 9 144 _+ 21

Abbreviations: NYHA, New York Heart Association functional class; CAD, number of diseased coronary arteries; MI, history of myocardial infarction; LVEF, left ventricular ejection fraction; LVEDVI, left ventricular end-diastolic volume index; LVEDP, left ventricular end-diastolic pressure; HR, baseline heart rate; PR, PR interval. *p < 0.05.

delay of 100 milliseconds (VDD mode). Interestingly, all patients, including those who had a spontaneous AV delay shorter than 160 milliseconds, could be paced with the long AV delay in DDD mode without tile occurrence of fusion beats. This may be because the pacing wires were attached to the flee lateral atrial wall apart from the sinus node, thus adding the spike-to-P-wave time to the electrical AV delay. The "short AV delay" was 40 milliseconds in both conditions because of the shortest programmable AV delay with the equipment used. In DDD mode, the pacer was set at a stimulation rate 5 beats/min greater than the spontaneous sinus rate, thus avoiding changes in CO caused by an elevated heart rate. After an equilibration time of at least 2 minutes for SR, pacing mode measurements and calculations for each mode were repeated three times. Average MAP mad SVI were used to compare the pacing modes. In a 64-year-old man with an LVEF of 18% who underwent triple bypass surgery, an aortic dissection was suspected postoperatively. Thus, a transesophageal echocardiogram and Doppler examination using a phased array imaging system (HP Sonos 2000, Hewlett Packard, Andower, MA) were performed. The following parameters were obtained: (1) isovolumetric relaxation time (IVRT) sampling between the aortic outflow and the mitral inflow, obtained from the aortic valve closure to the opening of the mitral valve on the Doppler signal, (2) early diastolic peak velocity (E), (3) end-diastolic peak velocity (A), and (4) mean transmittal flow velocity during VDD pacing with various AV intervals (120, 80, and 40 milliseconds). Based on the velocity parameters, the E/A ratio was calculated for each AV delay. Values given in the text or tables are expressed as mean _+ standard deviation. Groups were checked for normal distribution by means of the Kolmogoroff-Smimoff test. The differences in hemodynamic parameters obtained during various pacing modes were analyzed by paired Student's t-test. Student's unpaired t-test was used for intergroup comparison. The significance level assumed was p less than 0.05.

AV Delay (msec)

Sinus rhythm

Variable

There was no difference between groups with respect to age, sex, number of diseased coronaries, preoperative New York Heart Association functional class, resting sinus node rate, and PR interval. Significant differences existed for history of myocardial infarction, preoperative LVEF, end-diastolic volume index, and end-diastolic pressure (Table 1). In addition, the number of patients in Canadian Cardiovascular Society (CCS) angina score III and IV was significantly higher in the control group than in the study group (12/20 v 5/20; p < 0.05). The number of coronary anastamoses was similar between groups (2.9 ± 1.1 v 3.4 ± 0.8; p = not significant [NS] ), as was the mean ECC time (101.9 ± 2l rain v 105.1 ± 19 min; p = NS) and aortic cross-clamp time (48.1 + 17 min v 53.2 ± 18 min; p = NS). M A P during SR was 81.9 + 6.9 mmHg in the study group and 82.7 ± 9.5 mmHg in the control group. Shortening the AV delay during DDD pacing caused a significant drop in M A P in the control group (84.3 ± 9.4 v 75.7 ± 9.0 mmHg; p < 0.05), whereas M A P remained stable in the study group (78.1 ± 7.1 v 71.4 ± 9.4 rnmHg; p = NS). During VDD pacing, shortening the AV delay had no influence on M A P in both groups (study group; 80.8 ± 8.2 v77.8 ± 8.9 mmI-tg; control group, 81.2 ± 8.8 v 79.3 ± 8.4 mmHg; p = NS) (Fig 1). There was no difference comparing SR with the best pacing mode in both groups. SVI during SR was 37.4 ± 6.1 mL/m 2 in the study group and 33.6 ± 5.5 mL/m 2 in the control group. As shown in Figure 2, short-AV delay pacing produced a significant decrease in SVI during DDD pacing in both groups (study group; 35.9 ± 6.5 v

90 85 ...... ,. ..............

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80 75

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70 65 60 Long

AV Delay

Shorl

VDD

mmHg

90

85

Original Recording*

75

~

70

DDD long

160

-L~

65

DDD short

40

~L~

60

VDD long

100

VDD short

40

*Original electrocardiogram recording.

DDD

mmHg

80

Table 2. Pacing Protocol Rhythm

RESULTS

Long

AV Delay

Short

Fig 1. MAP at dual-chamber pacing with long and short AM delay. II, study group; A, control group, *p < 0.05.

LIEBOLD ET AL

286

Table 3. Echocardiographic Parameters of Transmittal Flow and LV Filling Obtained During VDD Pacing With Various AV Delays

DDD

mL/m2 42 40 38 36 34

AV Delay (msec)

E/A ratio

Vm (cm/sec)

[VRT (msec)

120 80 40

0.89 0.97 0.83

23.1 33.2 30.6

105 50 85

32 Note. Patient is 64 years old, with an LVEF of 18%, who underwent three grafts. Abbreviations: AV delay, atrioventricular delay; E, early-diastolic peak velocity; A, end-diastolic peak velocity; Vm, mean transmitral flow velocity; IVRT, left ventricular isovolumetric relaxation time.

30 28 26

I

24 Long

Short

AV Delay

VDD

mL/m2 4240

ris

38 36 34

ns

32 30 28 26 24 Long

AV Delay

Short

Fig 2, SVI at dual-chamber pacing w i t h " l o n g " and "short" AM delay. II, study group; ~, control group. *p < 0,05.

31.7 _+ 6,6 mL/m2; control group, 35.3 _+ 6.2 v 31.0 +_ 6.2 mL/m2; p < 0.05). SVI remained stable during short AV delay VDD pacing (study group, 37.6 _+ 3.7 v 37.1 _+ 4.2 mL/m2; control group, 34.4 _+ 6.6 v 33.6 +_ 7.9 mLImZ,p = NS). Again, there was no statistically significant difference between SR and the best pacing mode in both groups. In one study group patient, echocardiographic Doppler data were obtained when the AV delay was modified. Transmittal flow showed different patterns during VDD pacing and SR (Fig 3). The calculated parameters of transmitral flow and diastolic left ventricular function are listed in Table 3. Accordingly, the optimal AV delay in this particular patient was 80 milliseconds. DISCUSSION

Several recent articles on symptomatic and clinical improvement in patients with dilated cardiomyopathy and end-stage

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Fig 3. Doppler tracing of mitral valve inflow velocity and simultaneous electrocardiograph recording in a patient with an EF of 18%. E, early diastolic inflow caused by ventricular relaxation; A, enddiastolic inflow caused by atrial contraction. (Left) Sinus rhythm. Inversed E/A ratio indicates ventricular relaxation disturbance. (Right) VDD pacing with 80- millisecond AV delay. Normalization of the E/A ratio.

heart failure after dual-chamber pacing with short-AV delays suggest that this nontraditional treatment may have considerable benefit.l,3-6In those patients, ventricular filling time may be so short as to limit stroke volume, especially when the PR interval is long. Short AV delay pacing may improve the relation between atrial and ventricular systole by prolonging the ventricular filling time and by eliminating the presystolic component of AV valve regurgitation. 8-1°The literature principally focused on long-term effects of short AV delay pacing and little is known about acute hemodynamic changes using this electrical therapy. In addition, there is a lack of information about the acute response to short AV delay pacing in patients with end-stage coronary artery disease undergoing myocardial revascularization. Encouraged by the results of Brecker et al,7 who showed an increased CO in eight patients with dilated cardiomyopathy, the authors conducted a study on post-CABG patients with poor LV function. Brecker used AV delays of 6 to 31 milliseconds and found the shortest AV delay to be best in all cases. In contrast, the authors could not show any beneficial effect of shortening the AV delay in both normal and impaired LV function. On the contrary, a deterioration of LV function was observed when atrium and ventricle were paced with the nonphysiologic short delay of 40 milliseconds. These data confirmed a report of Shinbane et a111 on nine patients with refractory heart failure who were studied at AV delays of 200, 150, 100, and 50 milliseconds. The authors found no hemodynamic benefit during right heart catheterization. Others have reported improved CO with "optimal" AV pacing intervals. Mehta et als used Doppler-estimated CO determinations in patients with chronic implanted dual-chamber pacers and showed that the "optimal" interval at rest was longer (140 to 150 milliseconds) than during treadmill exercise (75 to 80 milliseconds). Using similar techniques in their study, Modena et al3 identified an "optimal" AV delay of 100 milliseconds in 13 patients. Both studies dealt with normal LV function and permanent pacemakers. The effects of varying lead placement was not mentioned. According to the authors' echocardiographic case study, short AV delay pacing appears to influence ventricular filling in dilated heart failure. Modena et ai3 defined a pattern of abnormal LV relaxation in patients with IVRT greater than 100 milliseconds and E/A ratio less than 1. A delay in LV contraction results in a relative shortening of LV diastole that may cause a prolongation of IVRT with a delayed opening of the mitral valve. One patient also presented with prolonged IVRT and inverse E/A ratio. Shortening the AV delay improved ventricular performance by shifting ventricular contraction toward the

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287

atrial systole. Thus, optimal LV filling was achieved with an AV delay of 80 milliseconds. Further AV-delay shortening caused the reverse effect. This finding supports the theory that a subset of patients with severe ventricular disease may benefit from short AV delay pacing. Individual AV delay optimizing by means of Doppler echocardiography therefore is essential. Nishimura et all2 have recently shown in patients with severe LV dysfunction that the AV interval required to maximize CO varies from patient to patient, mainly depending on the ability to correctly resynchronize the left atrium and LV, thus achieving improved filling. Comparing sensed versus paced AV delay, there was a clear advantage with VDD mode in this study. Pacing the atrium resulted in increased interatrial conduction time. The major clinical impact of slowed interatrial conduction was a decrease in left heart AV delay. Right atrial and fight ventricular pacing (DDD) delayed LV contraction because of the interatrial and interventricular conduction time. Therefore, DDD pacing could result in a highly nonphysiologic mechanical delay between left atrium and LV, when the interatrial

conduction time was considerably shorter than the pathologically extended interventricular conduction time. This condition may be present in dilated heart failure. When the right atrium was sensed (VDD), the left-side mechanical delay depended only on the AV delay and interventricular conduction time. In fact, pacing in DDD mode showed a considerably greater deterioration of MAP and stroke volume than was evident during VDD pacing. Therefore, if dual-chamber pacing is required, VDD pacing with a physiologic AV delay is preferable. From the authors' data, it is concluded that dual-chamber pacing with nonphysiologically short AV delay generally failed to improve acute hemodynamics in patients with severe LV dysfunction who underwent myocardial revasculafization. This type of pacing should be optimized on the basis of ventricular filling patterns and applies only to patients with diastolic relaxation disturbance. In case of postoperative AV conduction disorder, VDD pacing with normal AV delay should be preferred.

REFERENCES

1. Auricchio A, Sommariva L, Salo RW, et al: Improvement of cardiac function in patients with severe congestive heart failure and coronary artery disease by dual-chamber pacing with shortened AV delay. PACE 16:2034-2043, 1993 2. Innes D, Leitch JW, Fletcher PJ: VDD pacing at short atrioventricular intervals does not improve cardiac output in patients with dilated heart failure. PACE 17:959-965, 1994 3. Modena MG, Rossi R, Carcagni A, et al: The importance of different atrioventricular delay for left ventricutar filling in sequential pacing: Clinical implications. PACE 19:1595-1604, 1996 4. Hochleitner M, H6rtnagl H, H6rtnagl H, et al: Long-term efficacy of physiologic dual-chamber pacing in the treatment of end-stage idiopathic dilated cardiomyopathy. Am J Cardiol 70:13201325, 1992 5. Hochleitner M, H6rtnagl H, Ng CK, et al: Usefulness of physiologic dual-chamber pacing in drug-resistant idiopathic dilated cardiomyopathy. Am J Cardio166:198-202, 1990 6. Ronaszeki A, Ector H, Denef B: Effect of short atrioventricular delay on cardiac output. PACE 13:1728-1731, 1990

7. Brecker SJ, Xiao HB, Sparrow J, et al: Effects of dual-chamber pacing with short atrioventricular delay in dilated cardiomyopathy. Lancet 340:1308-1312, 1992 8. Mehta D, Gilmour S, Ward DE, et al: Optimal atrioventricular delay at rest and during exercise in patients with dual-chamber pacemakers: A noninvasive assessment by continous wave Doppler. Br Heart J 61:161-166, 1989 9. Ng KSK, Gibson DG: Impairment of diastolic function by shortened filling period in severe left ventricular disease. Br Heart J 62:246-252, 1989 10. Ng KSK, Gibson DG: Relation of filling pattern to diastolic function in severe left ventricular disease. Br Heart J 63:209-214, 1990 11. Shinbane JS, Chu E, DeMarco T, et al: Does dual chamber pacing with short AV delay acutely improve cardiac performance in refractory heart failure? J Heart Lung Transpl 15:40A, 1996 12. Nishimura RA, Hayes DL, Homes DR: Mechanism of hemodynamic improvement by dual-chamber pacing for severe left ventricular dysfunction: An acute Doppler and catheterization hemodynamic study. J Am Coll Cardio125:281-288, 1995