Methods: Eighteen consecutive patients (13 males, 5 females; mean age 66.2±12.4; range 47 to 77 years) undergoing coronary artery bypass grafting who were candidates for a pacemaker placement postoperatively were included in the study. Temporary epicardial pacing wires were intraoperatively placed both on the right ventricle (RV) and on the left ventricle (LV) in all patients. The epicardial wires were placed on the RV to the outflow tract and on the LV to the apex. On the fifth postoperative day echocardiography (Vivid 5, Vingmed, General Electric Healthcare) was performed and tissue Doppler measurements were taken during basal, RV pacing and LV pacing. During RV and LV pacing, the heart rate was increased above the basal rate. During the analysis, at least three cardiac cycles were recorded in the tissue velocity imaging mode. The recorded images were analyzed by EchoPAC (EchoPAC 6.3, Vingmed-General Electric Healthcare). In the images that were collected for tissue synchronization LV septal and lateral segments were marked and were subsequently analyzed for delay in the septo-lateral segment. The results were shown in mean ± standard deviation and statistical analysis was performed using the Wilcoxon signed rank test (p<0.05).
Results: In all patients, during RV pacing significant intraventricular delay was documented between the septum and the lateral wall (52.9±20.7 ms versus 20.6±14.6 ms, p<0.001). During LV pacing in all patients intraventricular delay was measured shorter than the basal value (12.7±12.1 ms versus 20.6±14.6 ms, p=0.001). No complications were observed in all patients during the placement of intraoperative pacemaker wire, in the postoperative period when asynchrony measurements were performed and after the removal of the wires.
Conclusion: In patients undergoing coronary artery bypass grafting surgery the temporary epicardial pacing wires should be placed on the left ventricle instead of the right ventricle.
The study protocol
Temporary epicardial pacing wires were intraoperatively
placed both on the right ventricle (RV) and LV in
all patients. The epicardial wires were placed on the RV
to the outflow tract and on the LV to the apex. On the
fifth postoperative day echocardiography was performed
and tissue Doppler measurements taken during basal,
RV pacing and LV pacing. During RV and LV pacing,
the heart rate was increased above the basal rate. During
the analysis, at least three cardiac cycles were recorded
in the tissue velocity imaging (TVI) mode. The recorded
images were analyzed by EchoPAC (EchoPAC 6.3,
Vingmed-General Electric Healthcare). In the images
that were collected for tissue synchronization LV septal
and lateral segments were marked and were subsequently
analyzed for delay in the septo-lateral segment.
Conventional transthorasic echocardiographic TVI
evaluation
Transthoracic echocardiographic studies were performed,
with the patient in the left lateral position, using GE Vingmed Vivid 5 system (Vingmed Ltd,
General Electric Healthcare) in accordance with recommendations
proposed by the American Society of
Echocardiography.[7] Tissue Doppler sampled at the mitral
and tricuspid annulus in the apical four-chamber
view was used to derive peak tricuspid annular systolic
velocity.
Color-coded tissue Doppler cine loops were obtained as routinely performed in our echocardiography laboratory from three beats obtained in the apical four-chamber view at the depths of 14±2 cm with pulse repetition frequency set at 1 kHz, Nyquist velocity range ±16 cm/second and frame rates 99±9 Hz. Initial length for longitudinal strain assessment was set at 12 mm and regions of interest (20±2 mm by 7±1 mm) were placed in the basal segments of the interventricular septum, and left ventricular lateral wall (Fig. 1). Left ventricular lateral wall dyssynchrony was determined as the difference in time to peak strain between the left ventricular lateral wall and the septum.
Fig 1: The color-coded tissue Doppler image belongs to one patient.
Statistical analysis
The statistical analysis was performed using the SPSS
for Windows version 11.0 (SPSS Inc., Chicago, Illinois,
USA). The results were shown in mean ± standard deviation
and differences between two pacing sites were
assessed using the Wilcoxon signed rank test. A p<0.05
was considered statistically significant.
During normal LV activation LV segments contract simultaneously.[12] All the ventricular segments must contract in a time period of up to 40 ms. If the segments do not contract simultaneously than the LV systolic performance deteriorates because of the asynchronous movements. The segments that contract late cause an increase in wall tension of the early contracted segments, an increase in end systolic pressure and a decrease in relaxation. While the regions that contract early cannot provide pressure to start an ejection; the regions that contract late due to an increase in pressure earlier, contract against this increased pressure and this event causes a paradoxical increase in tension in the regions that have already completed their contraction. A delay in LV lateral wall activation and a delay in the posteromedial papillary muscle contraction contribute to the development of mitral insufficiency.
Breithardt et al.[13] found that the delay in the septum lateral wall is an important predictor of the interventricular asynchrony in echocardiographic evaluations. By the use of the tissue Doppler echocardiographic studies, different myocardial segment peak systolic or diastolic velocities are determined as compared to the beginning of the QRS. The evaluation of asynchrony is based on the time difference between the peak myocardial velocities. The time difference between the two different segment velocities are measured in ms and the values that are calculated are used to demonstrate the asynchrony. The difference between the earliest and the latest peak velocities must be greater than 60 ms to be considered as asynchrony.
The RV pacing has disadvantages that it may cause LV dysfunction that can not be converted. Right ventricular apical pacing may especially cause different levels of preload in different myocardial segments. Compared to the segment that is further away from the place that is paced there is less use of oxygen and glucose and the result is the formation of weaker contractions. In the studies of DAVID (dual chamber and VVI implantable defibrillator) and MADIT II (multicenter automatic defibrillator implantation trial) in patients having chronic RV pacing there is a detection of more cases of new or worsened heart failure, increase in hospitalization secondary to heart failure and death.[14,15] Chronic RV pacing causes LV wall tension, distraction in homogeneity of the myocardium, disorganization of the myocardial fibers, and all these result in injury of the LV myocardial cells.[16-19] Inferolateral myocardial perfusion defect due to right ventricular pacing have been reported.[20]
The results of Blanc et al.[21] are similar to our findings. A delay in intraventricular conduction is observed in 27 patients and if patients received LV pacing or biventricular pacing the return of the acute hemodynamic parameters to basal values was statistically significant when compared to the patients that received RV pacing that showed no significant improvement.[22]
In our study the main finding is the demonstration of the intraventricular delay between the septum and the lateral wall compared to the basal values during RV pacing. Contrary to this finding, all patients who had LV pacing had shorter intraventricular delay values compared to the basal values. As a result of all of these observations, in patients with possible need for a pacemaker in the postoperative period, the temporary pacing wires should be placed on the LV.
Declaration of conflicting interests
The authors declared no conflicts of interest with respect
to the authorship and/or publication of this article.
Funding
The authors received no financial support for the
research and/or authorship of this article.
1) Bax JJ, Molhoek SG, van Erven L, Voogd PJ, Somer S,
Boersma E, et al. Usefulness of myocardial tissue Doppler
echocardiography to evaluate left ventricular dyssynchrony
before and after biventricular pacing in patients with idiopathic
dilated cardiomyopathy. Am J Cardiol 2003;91:94-7.
2) Bax JJ, Marwick TH, Molhoek SG, Bleeker GB, van Erven
L, Boersma E, et al. Left ventricular dyssynchrony predicts
benefit of cardiac resynchronization therapy in patients with
end-stage heart failure before pacemaker implantation. Am J
Cardiol 2003;92:1238-40.
3) Ghio S, Constantin C, Klersy C, Serio A, Fontana A,
Campana C, et al. Interventricular and intraventricular dyssynchrony
are common in heart failure patients, regardless of
QRS duration. Eur Heart J 2004;25:571-8.
4) Heyndrickx GR, Vantrimpont PJ, Rousseau MF, Pouleur
H. Effects of asynchrony on myocardial relaxation at rest
and during exercise in conscious dogs. Am J Physiol
1988;254:817-22.
5) Unverferth DV, Magorien RD, Moeschberger ML, Baker PB,
Fetters JK, Leier CV. Factors influencing the one-year mortality
of dilated cardiomyopathy. Am J Cardiol 1984;54:147-52.
6) Bader H, Garrigue S, Lafitte S, Reuter S, Jaïs P, Haïssaguerre
M, et al. Intra-left ventricular electromechanical asynchrony.
A new independent predictor of severe cardiac events in heart
failure patients. J Am Coll Cardiol 2004;43:248-56.
7) Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendations
regarding quantitation in M-mode echocardiography: results
of a survey of echocardiographic measurements. Circulation
1978;58:1072-83.
8) Goldman BS, Hill TJ, Weisel RD, Scully HE, Mickleborough
LL, Pym J, et al. Permanent cardiac pacing after open-heart
surgery: acquired heart disease. Pacing Clin Electrophysiol
1984;7:367-71.
9) Gordon RS, Ivanov J, Cohen G, Ralph-Edwards AL.
Permanent cardiac pacing after a cardiac operation: predicting
the use of permanent pacemakers. Ann Thorac Surg
1998;66:1698-704.
10) Baerman JM, Kirsh MM, de Buitleir M, Hyatt L, Juni JE,
Pitt B, et al. Natural history and determinants of conduction
defects following coronary artery bypass surgery. Ann
Thorac Surg 1987;44:150-3.
11) Lewis JW Jr, Webb CR, Pickard SD, Lehman J, Jacobsen G.
The increased need for a permanent pacemaker after reoperative
cardiac surgery. J Thorac Cardiovasc Surg 1998;116:74-81.
12) Park RC, Little WC, O’Rourke RA. Effect of alteration of left
ventricular activation sequence on the left ventricular endsystolic
pressure-volume relation in closed-chest dogs. Circ
Res 1985;57:706-17.
13) Breithardt OA, Stellbrink C, Kramer AP, Sinha AM, Franke
A, Salo R, et al. Echocardiographic quantification of left
ventricular asynchrony predicts an acute hemodynamic benefit
of cardiac resynchronization therapy. J Am Coll Cardiol
2002;40:536-45.
14) Wilkoff BL, Cook JR, Epstein AE, Greene HL, Hallstrom
AP, Hsia H, et al. Dual-chamber pacing or ventricular backup
pacing in patients with an implantable defibrillator: the Dual
Chamber and VVI Implantable Defibrillator (DAVID) Trial.
JAMA 2002;288:3115-23.
15) Steinberg JS, Fischer A, Wang P, Schuger C, Daubert J,
McNitt S, et al. The clinical implications of cumulative right
ventricular pacing in the multicenter automatic defibrillator
trial II. J Cardiovasc Electrophysiol 2005;16:359-65.
16) Prinzen FW, Augustijn CH, Arts T, Allessie MA, Reneman
RS. Redistribution of myocardial fiber strain and blood flow
by asynchronous activation. Am J Physiol 1990;259:H300-8.
17) Adomian GE, Beazell J. Myofibrillar disarray produced
in normal hearts by chronic electrical pacing. Am Heart J
1986;112:79-83.
18) Tse HF, Lau CP. Long-term effect of right ventricular pacing on myocardial perfusion and function. J Am Coll Cardiol
1997;29:744-9.
19) Altın T, Karaoğuz R. Konvansiyonel sağ ventrikül apikal
pacing: Olası zararlı etkileri ve bu etkilerin önlenmesi. MN
kardiyoloji 2007;14:415-23.
20) Erdogan O, Altun A, Durmus-Altun G, Ozbay G. Inferolateral
myocardial perfusion defect caused by right ventricular outflow
tract pacing. Pacing Clin Electrophysiol 2004;27:808-11.