The significance of ventriculoatrial conduction in pathogenesis of pacemaker syndrome and the intervenient study of Amiodarone
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《中华医药杂志》英文版
【Abstract】 Objectives The mechanism of pacemaker syndrome (PMS)is failed to understand and the present ways in which to deal with PMS are not very effective. The present study aims to search for the significance of ventriculoatrial conduction(VAC) in pathogenesis of PMS and determine the act of amiodarone on VAC, thereby looking for methods for cure PMS.Methods The sixteen patients with VVI pacemaker complicated by PMS, as well as showed VAC on their surface electrocardiogram(ECG),were selected into our study. The authors measured cardiac output(CO) and pulmonary capillary wedge pressure(PCWP)by Swan-Ganz catheter before and after using Amiodarone intravenously (300mg) in all of 16 patients and thereby prescribed Amiodarone 200mg t.i.d for a week followed by 200mg q.d for 6 months. Meanwhile monitoring their ECG and conscious symptoms. Results In this study the PMS patients with VAC had a lower CO (3.36±0.30L/min) and a higher PCWP(18.41±0.71mmHg).However, their COs go up (3.71±0.26L/min,P<0.001) and PCWPs go down(17.07±0.78mmHg,P<0.05) after Amiodarone injection, Patients symptoms, together with the VACs on the ECG, disappeared after Amiodarone administrated.Conclusion Since VAC result in a higher left atrial pressure and a lower CO in patients with VVI pacemaker, VAC gave rise to a series clinical symptoms in these patients. The present study suggested that VAC play a key role in pathogenesis of PMS and Amiodarone may be applied to treat PMS by blocking VAC. Theoretically, Amiodarone also may be applied to treat pacemaker-mediated tachycardia (PMT) resulting from VAC in patients with DDD pacemaker.
【Key wards】 pacemaker syndrome; ventriculoatrial conduction; amiodarone
INTRODUCTION
Pacemaker syndrome (PMS) is the constellation of symptoms and signs due to inappropriate timing of the atrial and ventricular contractions. The underlying mechanism is the coincidence of the atrial and ventricular contractions, whereby atrial contract against closed atrioventricular valves and their content retrogresses to the venae. This phenomenon occurs mainly during ventricular pacing (VVI mode) whenever ventriculoatrial conduction (VAC) is maintained, and ventricular systole is rapidly followed by the atrial one before the onset of the ventricular relaxation[1-4]. The present study aims to investigate the haemodynamic effects of the VAC on the cardiac output (CO) and pulmonary capillary wedge pressure (PCWP) in patients with VVI pacemaker and their changes after using Amiodarone. For this purpose, the patients with the surface electrocardiogram (ECG), proved retrograde VAC, were selected so that the requirements for the reproduction of the typical haemodynamic conditions of PMS may be fulfilled.
CLINICAL DATA
We studied a total of sixteen patients aged 52~78 years (mean 61 years, 11 males and 5 females). All patients had a permanent pacemaker of VVI type and had a normal ventricular function. The reasons for the implantation of a permanent pacemaker were sick sinus syndrome (SSS) in 13 patients, among whom were 8 patients with atrial fibrillation, and high grade atrial ventricular block in 3 patients. All patients had symptoms of PMS and presented with retrograde VAC on their surface ECG after VVI pacemaker implantation.
By method of the right cardiac catheter technique and fixed the pacing rate at 70 bpm, CO and PCWP were measured by Swan-Ganz catheter. After this process, Amiodarone were intravenously used (150mg intravenously injection for 5 minutes and 150mg intravenously drop within 30 minutes),then CO and PCWP were repeatedly measured.Therefore, Amiodarone were adminstrated orally 200mg tid for a week followed by qd. for 6 months. Meanwhile the surface ECG and conscious symptoms were monitored within 6-month follow-up.
Statistical evaluation of the observed changes was carried out using parametric methods-Students pair test.
RESULTS
The results are presented in details in the following table 1.
The results showed the patients with PMS existing VAC on surface ECG have lower COs and higher PCWPs, however, COs go up (P<0.001,Figure 1 See Cover 3) and their PCWPs go down (P<0.05,Figure 2 See Cover 3) after using intravenously Amiodarone. Following-up 6 months, the symptoms, together with the retrograde VAC on their surface ECGs,disappeared in 14 of 16 patients after Amiodarone administration and the other 2 patients relieved obviously.
DISCUSSION
Considerable evidence supports a relationship between AV asynchrony and PMS. The haemodynamic consequences of AV asynchrony include a reduction of stroke volume, functional mitral regurgitation, and atrial cannon waves[5-9]. The changes in arterial blood pressure during VVI pacing have been previously described[10,11]. For a better understanding of the physiopathology of PMS, we studied the changes of CO and PCWP by Swan-Ganz catheter under VVI pacing conditions in selected patients with electrophysiologically proved VAC. The results showed these patients have a lower CO (3.36±0.30L/min) and a higher PCWP(18.41±0.71mmHg), but after using Amiodarone, their COs increased significantly (3.71±0.26L/min, P<0.001) and PCWPs decreased significantly (17.07±0.78mmHg, P<0.05). The patients symptoms,as well as VAC on their ECG, disappeared. The results suggest that VAC increases the atrial pressure and decreases cardiac outcome during VVI pacing mode. The resultant oscillations in left atrial pressure cause inappropriate over-activation of atrial stretch receptors, leading to vasodilatation. Ours results also testified antiarrhythmia drug Amiodarone may block the retrograde VAC so as to make AV synchrony improving and atrial pressure descending.
In addition, the vascular response to ventricular pacing may take part in physiopathological process of PMS[12]. PMS may occur in patients with DDD pacemaker under the states of existing retrograde VA conduction. Theoretically, Amiodarone also may be applied to treat pacemaker-mediated tachycardia (PMT) resulting from VAC in the patients with DDD pacemaker.
REFERENCES
1 Barold SS. Cardiac pacing haemodynamics: the pacemaker syndrome. Cardiology,1991,8:36-51.
2 Travil CM, Sutton R. Pacemaker syndrome: an iatrogenic condition. Br Heart J,1992,68:163-166.
3 Lee TM, Su SF, Lin YJ, et al. Role of transesophageal echocardiography in the evaluation of patients with clinical pacemaker syndrome. Am Heart J,1998,135(4):634-640.
4 Kashani A, Mehdirad A, Fredman C,et al. A case of pacemaker and pacemaker-like syndrome. J Interv Card Electrophysiol,2003,9(3):361-364.
5 Ausubel K, Furman S. The pacemaker syndrome. Ann Int Med,1985,103:420-429.
6 Theodorakis GN, Panou F, Markianos M, et al. Left atrial function and atrial natriuretic factor/cyclic guanosine changes in DDD and VVI pacing modes. Am J Cardiol,1997,79(3):366-370.
7 Lamas GA, Orav EJ, Stambler BS, et al. Quality of life and clinical outcomes in elderly patients treated with ventricular pacing as compared with dual-chamber pacing. Pacemaker Selection in the Elderly Investigators. N Engl J Med,1998,338(16):1097-1104.
8 Buckingham TA, Janosik DL, Pearson AC. Pacemaker haemodynamics: clinical implications. Prog Cardiovasc Dis,1992,34:347-366.
9 Dennis MJ, Sparks PB. Pacemaker mediated tachycardia as a complication of the autointrinsic conduction search function.Pacing Clin Electrophysiol,2004,27(6 Pt 1):824-826.
10 Channon KM, Hargreaves MR, Gardner M, et al. Noninvasive beat-to-beat arterial blood pressure measurement during VVI and DDD pacing: relationship to symptomatic benefit from DDD pacing. Pace,1997,20(part 1):25-33.
11 Papadopoules CL, Kakkas BA, Sakadamis GC, et al.ANP concentrations during interchanging DDD-VVI pacing modes in patients with retrograde ventriculo-atrial conduction. Acta Cardiologica,1997,52(1):37-47.
12 Ellenbogen KA, Gilligan DM, Wood MA, et al.The pacemaker syndrome-a matter of definition. Am J Cardiol,1997,79:1226-1229.
1. Heart Center, Beijing Chaoyang Hospital, Beijing 100020,China
2. Department of Cardiology, The Second Hospital of Peking University, Beijing 100044, P. R. China
3. Department of Cardiology, the First Hospital of Xinjiang Medical University, Urumuqi,Xinjiang 830054, China
Correspondence to Dr. Zou Yangchun, the Heart Center, Beijing Chaoyang Hospital, Beijing 100020,China
Tel,Fax: 86-10-65951064
(Editor Guo Hui-ling)(ZOU Yang-chun，YANG Xin-ch)
【Key wards】 pacemaker syndrome; ventriculoatrial conduction; amiodarone
INTRODUCTION
Pacemaker syndrome (PMS) is the constellation of symptoms and signs due to inappropriate timing of the atrial and ventricular contractions. The underlying mechanism is the coincidence of the atrial and ventricular contractions, whereby atrial contract against closed atrioventricular valves and their content retrogresses to the venae. This phenomenon occurs mainly during ventricular pacing (VVI mode) whenever ventriculoatrial conduction (VAC) is maintained, and ventricular systole is rapidly followed by the atrial one before the onset of the ventricular relaxation[1-4]. The present study aims to investigate the haemodynamic effects of the VAC on the cardiac output (CO) and pulmonary capillary wedge pressure (PCWP) in patients with VVI pacemaker and their changes after using Amiodarone. For this purpose, the patients with the surface electrocardiogram (ECG), proved retrograde VAC, were selected so that the requirements for the reproduction of the typical haemodynamic conditions of PMS may be fulfilled.
CLINICAL DATA
We studied a total of sixteen patients aged 52~78 years (mean 61 years, 11 males and 5 females). All patients had a permanent pacemaker of VVI type and had a normal ventricular function. The reasons for the implantation of a permanent pacemaker were sick sinus syndrome (SSS) in 13 patients, among whom were 8 patients with atrial fibrillation, and high grade atrial ventricular block in 3 patients. All patients had symptoms of PMS and presented with retrograde VAC on their surface ECG after VVI pacemaker implantation.
By method of the right cardiac catheter technique and fixed the pacing rate at 70 bpm, CO and PCWP were measured by Swan-Ganz catheter. After this process, Amiodarone were intravenously used (150mg intravenously injection for 5 minutes and 150mg intravenously drop within 30 minutes),then CO and PCWP were repeatedly measured.Therefore, Amiodarone were adminstrated orally 200mg tid for a week followed by qd. for 6 months. Meanwhile the surface ECG and conscious symptoms were monitored within 6-month follow-up.
Statistical evaluation of the observed changes was carried out using parametric methods-Students pair test.
RESULTS
The results are presented in details in the following table 1.
The results showed the patients with PMS existing VAC on surface ECG have lower COs and higher PCWPs, however, COs go up (P<0.001,Figure 1 See Cover 3) and their PCWPs go down (P<0.05,Figure 2 See Cover 3) after using intravenously Amiodarone. Following-up 6 months, the symptoms, together with the retrograde VAC on their surface ECGs,disappeared in 14 of 16 patients after Amiodarone administration and the other 2 patients relieved obviously.
DISCUSSION
Considerable evidence supports a relationship between AV asynchrony and PMS. The haemodynamic consequences of AV asynchrony include a reduction of stroke volume, functional mitral regurgitation, and atrial cannon waves[5-9]. The changes in arterial blood pressure during VVI pacing have been previously described[10,11]. For a better understanding of the physiopathology of PMS, we studied the changes of CO and PCWP by Swan-Ganz catheter under VVI pacing conditions in selected patients with electrophysiologically proved VAC. The results showed these patients have a lower CO (3.36±0.30L/min) and a higher PCWP(18.41±0.71mmHg), but after using Amiodarone, their COs increased significantly (3.71±0.26L/min, P<0.001) and PCWPs decreased significantly (17.07±0.78mmHg, P<0.05). The patients symptoms,as well as VAC on their ECG, disappeared. The results suggest that VAC increases the atrial pressure and decreases cardiac outcome during VVI pacing mode. The resultant oscillations in left atrial pressure cause inappropriate over-activation of atrial stretch receptors, leading to vasodilatation. Ours results also testified antiarrhythmia drug Amiodarone may block the retrograde VAC so as to make AV synchrony improving and atrial pressure descending.
In addition, the vascular response to ventricular pacing may take part in physiopathological process of PMS[12]. PMS may occur in patients with DDD pacemaker under the states of existing retrograde VA conduction. Theoretically, Amiodarone also may be applied to treat pacemaker-mediated tachycardia (PMT) resulting from VAC in the patients with DDD pacemaker.
REFERENCES
1 Barold SS. Cardiac pacing haemodynamics: the pacemaker syndrome. Cardiology,1991,8:36-51.
2 Travil CM, Sutton R. Pacemaker syndrome: an iatrogenic condition. Br Heart J,1992,68:163-166.
3 Lee TM, Su SF, Lin YJ, et al. Role of transesophageal echocardiography in the evaluation of patients with clinical pacemaker syndrome. Am Heart J,1998,135(4):634-640.
4 Kashani A, Mehdirad A, Fredman C,et al. A case of pacemaker and pacemaker-like syndrome. J Interv Card Electrophysiol,2003,9(3):361-364.
5 Ausubel K, Furman S. The pacemaker syndrome. Ann Int Med,1985,103:420-429.
6 Theodorakis GN, Panou F, Markianos M, et al. Left atrial function and atrial natriuretic factor/cyclic guanosine changes in DDD and VVI pacing modes. Am J Cardiol,1997,79(3):366-370.
7 Lamas GA, Orav EJ, Stambler BS, et al. Quality of life and clinical outcomes in elderly patients treated with ventricular pacing as compared with dual-chamber pacing. Pacemaker Selection in the Elderly Investigators. N Engl J Med,1998,338(16):1097-1104.
8 Buckingham TA, Janosik DL, Pearson AC. Pacemaker haemodynamics: clinical implications. Prog Cardiovasc Dis,1992,34:347-366.
9 Dennis MJ, Sparks PB. Pacemaker mediated tachycardia as a complication of the autointrinsic conduction search function.Pacing Clin Electrophysiol,2004,27(6 Pt 1):824-826.
10 Channon KM, Hargreaves MR, Gardner M, et al. Noninvasive beat-to-beat arterial blood pressure measurement during VVI and DDD pacing: relationship to symptomatic benefit from DDD pacing. Pace,1997,20(part 1):25-33.
11 Papadopoules CL, Kakkas BA, Sakadamis GC, et al.ANP concentrations during interchanging DDD-VVI pacing modes in patients with retrograde ventriculo-atrial conduction. Acta Cardiologica,1997,52(1):37-47.
12 Ellenbogen KA, Gilligan DM, Wood MA, et al.The pacemaker syndrome-a matter of definition. Am J Cardiol,1997,79:1226-1229.
1. Heart Center, Beijing Chaoyang Hospital, Beijing 100020,China
2. Department of Cardiology, The Second Hospital of Peking University, Beijing 100044, P. R. China
3. Department of Cardiology, the First Hospital of Xinjiang Medical University, Urumuqi,Xinjiang 830054, China
Correspondence to Dr. Zou Yangchun, the Heart Center, Beijing Chaoyang Hospital, Beijing 100020,China
Tel,Fax: 86-10-65951064
(Editor Guo Hui-ling)(ZOU Yang-chun，YANG Xin-ch)