ISSN : 1301-5680
e-ISSN : 2149-8156
Turkish Journal of Thoracic and Cardiovascular Surgery     
Koroner arter bypass greftleme ameliyatı sonrası geçici telin en uygun yerleştirilmesi: Sol ventrikül mü yoksa sağ ventrikül mü daha uygundur?
Onursal Buğra1, Ahmet Şaşmazel1, Ali Fedakar1, Ayşe Baysal2, Fuat Büyükbayrak1, Hasan Erdem1, Mehmet Mustafa Can3, Kürşat Tigen3, Hasan Sunar1
1Department of Cardiovascular Surgery, Koşuyolu Kartal Heart Education and Research Hospital, İstanbul
2Department of Anaesthesiology and Reanimation, Koşuyolu Kartal Heart Education and Research Hospital, İstanbul
3Department of Cardiology, Koşuyolu Kartal Heart Education and Research Hospital, İstanbul

Özet

Background: In this study, the left ventricular asynchrony of pacemakers in patients with possible need for a pacemaker in the postoperative period after coronary artery bypass grafting surgery was investigated.

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.

Intraventricular mechanical asynchrony is the term used for the action that is not performed by simultaneous movements of all the segments of the left ventricle (LV) during systole. The critical value for systolic asynchrony is considered as the difference of 60 ms or of a greater value between the measurements that are collected from septum and basal parts of the lateral segments.[1-3] The asynchronous contractions cause a decrease in the performance of the left ventricular systolic functions.[4] The hemodynamic deterioration that is caused by this event may result in the development of heart failure or deterioration of preexisting heart failure. The delay in conduction inside the LV is demonstrated as a more important factor in determining mortality than mean right atrial pressure, pulmonary capillary wedge pressure, arrythmias that are ventricular in origin and ejection fraction.[5] Bader et al.[6] have found in their study that LV asynchrony is a bad prognostic factor. In our study, our goal was to investigate the LV asynchrony in patients with possible need for a pacemaker in the postoperative period after coronary artery bypass surgery.

Yöntem

Patient population
A total of 18 consecutive patients (13 males, 5 females; mean age 66.2±12.4 years; range 47 to 77 years) undergoing coronary artery bypass grafting who were candidates for a pacemaker placement postoperatively were included in the study. All patients provided written informed consent. Twelve of the patients (66%) had previous myocardial infarction, four patients (22%) had diabetes mellitus, and nine (50%) had hypertension.

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.

Bulgular

In all patients, during RV pacing significant intraventricular delay was documented between the septum and the lateral wall (52.94±20.71 ms versus 20.61±14.63 ms; p<0.001). During LV pacing in all patients intraventricular delay was measured shorter than the basal value (12.72±12.08 ms versus 20.61±14.63 ms; p=0.001) (Table 1). No complications were observed in all patients during the placement of intraoperative pacing wires, in the postoperative period when asynchrony measurements were performed and after the removal of the wires. There was no increase in the drainage volumes. Six patients were excluded from the study because of nonfunctioning RV pacing wires. There were no significant problems in the wires that were placed in the left ventricle.

Table 1: During right ventricle pacing significant intraventricular delay was documented between the septum and the lateral wall. During left ventricle pacing intraventricular delay was measured shorter than the basal value in all patients

Tartışma

In open heart surgery, there is a need for pacemaker postoperatively in 2 to 4% of patients.[8,9] In coronary artery bypass grafting surgery this need is around 4%.[10] In patients that require repetitive surgeries this percentage increases up to 10%.[11] During the use of pacemakers the ventricles are stimulated from a different pathway and the different electrophysiologic characteristics of the structures that form the cardiac system there is a production of nonphysiologic impulse by the generation of pacemaker stimulus. This abnormal activation pattern causes a contraction that is nonhomogenous in the LV, defects in the myocardial perfusion, increase in the sympathetic activation, fibrosis, and as a result of all of these changes a reconstruction occurs in the conduction system of the heart. The effects of RV pacing has been investigated in studies that evaluate the middle and long term effects of this pacing and showed that there are changes in the ejection fractions of the patient’s hearts. These changes have been attributed to the abnormal stimulation of the ventricles that causes interventricular and intraventricular asynchronous activities. Due to the asynchrony there are nonsimultaneous contractions in the myocardial walls that result in entrapment of the volume in the contracted ventricle, not enough increase in ventricular pressure and unsuccessful myocardial contraction that does not provide adequate volume. All these events cause deterioration in ventricular global functions. The regions that are activated early are predisposed to a decrease in their myocardial wall thickness whereas the regions that are activated late are observed to develop hypertrophy.

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.

Kaynaklar

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.

21) Blanc JJ, Etienne Y, Gilard M, Mansourati J, Munier S, Boschat J, et al. Evaluation of different ventricular pacing sites in patients with severe heart failure: results of an acute hemodynamic study. Circulation 1997;96:3273-7.

22) Kass DA, Chen CH, Curry C, Talbot M, Berger R, Fetics B, et al. Improved left ventricular mechanics from acute VDD pacing in patients with dilated cardiomyopathy and ventricular conduction delay. Circulation 1999;99:1567-73.

Anahtar Kelimeler : Yapay kalp pili/yöntem; kardiyomiyopati, dilate/terapi; koroner arter bypass greftleme ameliyatı; ekokardiyografi, Doppler; sol ventrikül; sağ ventrikül
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