Cell Biochem Biophys (2014) 69:225–228 DOI 10.1007/s12013-013-9786-2
ORIGINAL PAPER
Ventricular Pacing on the Prognosis of Patients with Pacemaker Implantation Liuying Zheng • Xinping Du
Published online: 16 November 2013 Springer Science+Business Media New York 2013
Abstract Excessive right ventricular apex pacing has significant adverse effects on the cardiac function and hence, it is necessary to clinically optimize pacing parameters and advocate suitable physiological pacing to safeguard the cardiac function after pacemaker implant. Minimizing ventricular pacing is an atrioventricular node priority function, to encourage ventricular self conduction and to reduce unnecessary right ventricular pacing. Minimized ventricular pacing reduces ventricular pacing by encouraging self atrioventricular conduction function and extending the AV interval. This study is a prospective cohort study to evaluate the changes of cardiac function in patients and serum amino-terminal natriuretic peptide (NTproBNP) before and after pacing, and the risk of atrial fibrillation with different CUM% VP. The study has shown that the cardiac function will deteriorate with an increase in pacing rate. Keywords CUM%VP Ventricular Pacing NTProBNP Atrial fibrillation Minimized ventricular pacing
Introduction Dual-chamber pacemakers (DDD) are pacemakers whose wire leads are placed in two chambers of the heart. One lead paces the atrium and one paces the ventricle. Since this function more closely resembles the natural pacing of the heart by assisting the heart in coordinating the function
between the atria and ventricles, it is considered an ideal pacemaker. But, the evidence-based medical literature do not support this view and the search evidences from CTOPP, MOST, UKPACE, and the SAVE PACE [1–4] based on long-term follow-up studies comparing VVI pacemaker, and the DDD pacemakers have confirmed that the DDD pacemakers neither improve long-term survival of patients nor they reduce the incidence of cardiovascular events, heart failure, and rate of hospitalization. This is because of the fact that DDD are still not the absolute physiological pacing solution and a high percentage pacing at the apex of right ventricle offsets the benefits of the atrioventricular synchronous pacing. This pacing method further changes the normal sequence of atrioventricular activation, and causes the left and right ventricular systolic desynchronization leading to cardiac adverse events and heart failure [5–7]. The relationship between the cumulative ventricular pacing percentage (CUM% VP), defined as the percentage of paced rate of total heart rate and the risk of heart failure as well as the atrial fibrillation after pacing demands further research. This study is a prospective cohort study to evaluate the changes in cardiac functions and serum amino-terminal natriuretic peptide level (NTproBNP) in patients before and after pacing, as well as the risk of atrial fibrillation with different CUM% VP values recorded.
Materials and Methods The Objective
L. Zheng X. Du (&) The Fifth Central Hospital of Tianjin, No.41 Zhejiang Road, Tanggu District, Tianjin, China e-mail: [email protected]
A cohort of 192 permanent pacemaker implantation patients was selected for the study from XYZ hospital in the period 2006–2011. Of the 192 cases, 82 cases were
123
226
Cell Biochem Biophys (2014) 69:225–228
male and 110 were female. Of the total, 125 were Sick Sinus Syndrome cases, 24 II degree Atrial Ventricular Block cases and 43 III degree Atrial Ventricular Block cases. All the surgeries were done through the subclavian vein path and by the buried pacemaker implantation method. The pacemaker was DDD type (Medtronic or Shengyou Da), and the pacing site was right atrial appendage, right ventricular apex. Criteria of Patients’ Entry • • • • •
Symptomatic slow type arrhythmia (pacemaker implantation indications) Age [18 years old QRS wave duration \120 ms Without a history of atrial fibrillation for in the last 6 months Expected survival life [2 years.
Methods Grouping Ventricular cumulative pacing (CumVP%) for all the patients was recorded by a pacemaker programmer during the 12 months period after operation, and then patients were divided into 2 groups according to the CumVP% value. 102 cases had CumVP% \40 % and 90 cases had CumVP% [40 %. Patients with normal preoperative cardiac function, valvular disease, and cardiomyopathy were excluded. Blood pressure, blood sugar, and blood lipids were effectively controlled preoperative and postoperatively in all cases included.
Observation The E/A ratio, left ventricular ejection fraction (LVEF), left and right atrial diameter, and left and right end ventricular diastolic volume tracked by cardiac ultrasound preoperative and postoperatively for 12 months period.
Incidence of Atrial Fibrillation All the patients were tested for the incidence of Atrial Fibrillation by a pacemaker programmer postoperative in the 12-months study period. Statistical Analysis All data were analyzed by SPSS16.0 statistical analysis software. The measurement data were expressed as mean ± standard, and analyzed between two groups by T test, taking the value P \ 0.05 as statistically significant.
Results Changes of Echocardiographic Indexes of the Two Groups of Patients All the patients exhibited a LVEF of [ 50 % preoperative and in the CumVP% B40 % group, the changes of LVEF, LV, and E/A ratio before and after operation were not different significantly. In the CumVP% [40 % group, LVEF was significantly lower and E/A ratio decreased (P \ 0.05) in the postoperative 12-month period indicating a reduced cardiac function (Table 1). Changes of NT-ProBNP of the Two Groups of Patients In the CumVP% B40 % group, the NT-proBNP were not different significantly before and after operation, in the CumVP% [40 % group, NT-proBNP levels were found increased and the value statistically significant (P \ 0.05) in the postoperative 12-months period (Table 2). The Incidence of Atrial Fibrillation of the Two Groups of Patients Postoperative 12 Months In the CumVP% B40 % group the incidence of atrial fibrillation was 3.9 %, and in the CumVP % [40 % group Table 1 The comparison of echocardiographic indexes preoperative and postoperative between two groups
Blood NT-proBNP Testing NT-proBNP was detected preoperative and postoperative 12 months for all the patients. Whole blood samples were drawn by non-anticoagulant vacuum blood collection tubes under calm breath in the morning during fasting and then the serum taken for detecting NT-proBNP testing using electrochemical immunoluminescence technique after centrifugation.
123
CumVP% B40 % (102)
CumVP% [40 % (90)
Preoperative
Preoperative
Postoperative
Postoperative
LA
31.9 ± 1.3
32.3 ± 1.0
29.3 ± 0.9
30.2 ± 1.1
LV
44.3 ± 1.4
43.2 ± 1.2
46.7 ± 1.5
50.2 ± 0.9
RA
29.6 ± 0.9
28.3 ± 0.7
27.7 ± 1.1
28.5 ± 1.3
RV
30.8 ± 1.2
30.1 ± 1.3
28.9 ± 0.6
28.1 ± 0.7
EF %
61 ± 4
62 ± 2
58 ± 4
52 ± 3
E/A
1.1 ± 0.1
1.1 ± 0.2
1.2 ± 0.1
0.9 ± 0.05
Cell Biochem Biophys (2014) 69:225–228
227
Table 2 The comparison of NT-ProBNP preoperative and postoperative between two groups (Pg/Ml) CumVP% [40 % (90)
CumVP% B40 % (102)
NT-proBNP
Preoperative
Postoperative
Preoperative
Postoperative
80.6 ± 9.3
74.0 ± 8.9
90.3 ± 8.8
256.3 ± 12.7
Table 3 The comparison of incidence of atrial fibrillation preoperative and postoperative between two groups
AF %
CumVP% B40 % (102)
CumVP% [40 %(90)
Preoperative
Postoperative
Preoperative
Postoperative
0
3.9
0
11.1
the incidence of atrial fibrillation was 11.1 %. The difference in incidence value was statistically significant (P \ 0.05) (Table 3).
Discussion At present, the right ventricular apex is the most commonly utilized pacing site for permanent pacemaker implantation. Recent studies have shown that a long-term right ventricular apex pacing can cause left ventricular abnormal depolarization, leading to left Ventricular Mechanical Asynchrony. Ventricular Mechanical Asynchrony, in turn can cause long-term adverse hemodynamic abnormalities including abnormal contraction and diastolic function of left ventricle and also bring about structural changes in the myocardium [3]. Sweeney et al. [8] have showed that the risk of heart failure has a linear positive correlation with the CUM% VP, when the CUM% VP is 0–80 %. Further, studies have also shown that when the CUM% VP is [80 %, the relative risk of heart failure will increase by 96 % for every increase in 10 % CUM% VP. Steinberg et.al [9] have also found similar results in his study with 567 patients with Implantable Cardioverter Defibrillator. The study has shown that in CUM% VP [50 % patient group the proportion of freshly reported heart failure or death was 25 % higher than in CUM% VP \50 % group. Previous studies have also confirmed that the right ventricular apex pacing technique causes adverse hemodynamic effects like change in the activation sequence of the normal heart and cause disturbed coordination of left ventricular systolic and diastolic functions. Long-term and frequent right ventricular apex pacing can also change the local myocardial perfusion, cellular structure, and myocardial fiber arrangement [10–12]. These pathophysiological changes can lead to various heart dysfunctions, including atrial fibrillation. In this study, the cardiac structure and functions were recorded by echocardiography. In the CumVP%
[40 % group, LVEF and E/A ratios were found to be decreased. Whereas, in the CumVP% B40 % group, there was no significant change preoperatively and postoperatively in LVEF and LVEDV values. This takes us to the conclusion that the cardiac function will deteriorate with an increase in pacing rate. In CumVP%[40 % group, the atrial diameter has been found to be increased postoperatively. The incidence of atrial fibrillation in CumVP%[40 % group has also been found to be increased than in CumVP% B40 % group. This also takes us to the conclusion that a long-term and frequent right ventricular apex pacing can result in atrial structural disturbances and increase the incidence of atrial fibrillation. Although NT-proBNP is not being used in the routine cardiac testing, several clinical studies have indicated that it could be used as one of the indicators for prediction, diagnosis, and risk stratification of a variety of cardiovascular disease [3–15]. The myocardial cells first synthesize BNP with a 108 amino acid sequence called the pro-BNP (BNP precursor). Pro-BNP is then cleaved into NT-proBNP (amino-terminal—proBNP or N-terminal—proBNP). The half-life of BNP is 22 min, while that of the NTproBNP is 120 min. NT-proBNP in vitro is relatively stable, and studies have shown that NT-proBNP has the similar diagnostic accuracy with BNP when screening heart failure from dyspnoeic population, and its sensitivity and specificity are each more than 92 and 93 %, respectively [16]. The present study has further confirmed the adverse effects of right ventricular apex pacing on cardiac function and its relationship with the CUM%VP.
Conclusion Excessive right ventricular apex pacing has significant adverse effects on cardiac functions. It is thus important to clinically optimize pacing parameters and location and advocate appropriate physiological pacing, in order to safeguard cardiac function after a pacemaker intervention. For Sick Sinus Syndrome patients with normal atrioventricular conduction, it is recommended to minimize unnecessary right ventricular pacing and advocate appropriate ventricular pacing. Minimized ventricular pacing is an atrioventricular node priority function that encourages ventricular self conduction and reduces unnecessary right
123
228
ventricular pacing. Minimized ventricular pacing reduces ventricular pacing by encouraging self atrioventricular conduction function and extending the AV interval. This includes fixed lag of the atrioventricular interval, the automatic search of the atrioventricular interval, and the fixation time search of atrioventricular interval.
References 1. Connolly, S. J., Kerr, C. R., Gent, M., et al. (2000). Effects of physiologic pacing versus ventricular pacing on the risk of stroke and death due to cardiovascular causes. The Canadian Trial of Physiologic Pacing Investigators. New England Journal of Medicine, 342(19), 1385–1391. 2. Lamas, G. A., Lee, K. L., Sweeney, M. O., et al. (2002). Ventricular pacing or dualchamberpacing for sinus-node dysfunction. New England Journal of Medicine, 346(24), 1854–1862. 3. Lamas, G. A., Lee, K. L., Sweeney, M. O., et al. (2000). The mode selection trial (MOST) in sinus node dysfunction design, rationale and baseline characteristics of the first 1000 patients. American Heart Journal, 140(4), 541–551. 4. Toff, W. D., Camm, A. J., & Skehan, J. D. (2005). United Kingdom pacing and cardiovascular events trial investigation. Single-chamber versus dualchamberpacing for high-grade atrioventricular block. New England Journal of Medicine, 353(2), 115–155. 5. Stambler, B. S., Ellenbogen, K. A., Liu, Z., et al. (2005). Serial changes in right ventricular apical pacing lead impedance predict changes in left ventricular ejection fraction and functional class in heart failure patients. Pacing and Clinical Electro Physiology, 28, S50–53. 6. Nielsen, J. C., Andersen, H. R., Thomsen, P. E., et al. (1998). Heart failure and echo cardio graphic changes during long-term follow-up of patients with sick sinus syndrome randomized to single-chamber atrial or ventricular pacing. Circulation, 97, 987–995. 7. Lamas, G. A., Lee, K. L., Sweeney, M. O., et al. (2002). Ventricular pacing or dual chamber pacing for sinus node dysfunction. New England Journal of Medicine, 346, 1854–1862.
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Cell Biochem Biophys (2014) 69:225–228 8. Sweeney, M. O., Hellkamp, A. S., Ellenbogenk, A., et al. (2003). Adverse effect of ventricular pacing on heart failure and atrial fibrillation among patients with normal baseline QRS duration in a clinical trial of pacemaker therapy for sinus node dysfunction. Circulation, 107, 2932–2937. 9. Steinberg, J. S., Fisch, E. R. A., & Wang, P. (2005). The clinical implications of cumulative right ventricular pacing in the multicenter automatic defibrillator trial. Journal of Cardiovascular Electrophysiology, 16, 359–365. 10. Nielsen, J. C., Bottcher, M., Nielsen, T. T., et al. (2000). Regional myocardial blood flow in patient s with sick sinus syndrome randomized to long-term single chamber or dual chamber pacingeffect of pacing mode and r ate. Journal of the American College of Cardiology, 35, 1453–1461. 11. Karpawhich, P. P., Justice, C. D., Cavitt, D. K., et al. (1975). Developmental sequelae of fixed rate ventricular pacing in the immature canine heart: An electrophysiological, hemodynamic and his to pathologic evaluation. American Heart Journal, 119, 1077–1083. 12. Adomian, G., & BEAZELL, J. (1986). Myofibrillar disarray produced in normal hearts by chronic electrical pacing. American Heart Journal, 112, 79–83. 13. Schou, M., Gustafsson, F., Kjaer, A., et al. (2007). Long-term clinical variation of NT-proBNP in stable chronic heart failure patients. European Heart Journal, 28, 177–182. 14. Bibbins-Domingo, K., Gupta, R., et al. (2007). N terminal fragment of the prohormone brain-type natriuretic peptide (NTproBNP), cardiovascular events, and mortality in patients with stable coronary heart disease. JAMA, 297, 169–176. 15. Tang, W. H., Steinhubl, S. R., Van Lente, F., et al. (2007). Risk stratification for patients undergoing non urgent percutaneous coronary intervention using N-terminal pro-B-type natriuretic peptide: a Clopidogrel for the Reduction of Events during Observation (CREDO) substudy. American Heart Journal, 153, 36–41. 16. Sanz, M. P., Borque, L., Rus, A., et al. (2006). Comparison of BNP and NT-ProBNP assays in the approach to the emergency diagnosis of acute Dyspnea. Journal of Clinical Laboratory Analysis, 20, 227–232.
ORIGINAL PAPER
Ventricular Pacing on the Prognosis of Patients with Pacemaker Implantation Liuying Zheng • Xinping Du
Published online: 16 November 2013 Springer Science+Business Media New York 2013
Abstract Excessive right ventricular apex pacing has significant adverse effects on the cardiac function and hence, it is necessary to clinically optimize pacing parameters and advocate suitable physiological pacing to safeguard the cardiac function after pacemaker implant. Minimizing ventricular pacing is an atrioventricular node priority function, to encourage ventricular self conduction and to reduce unnecessary right ventricular pacing. Minimized ventricular pacing reduces ventricular pacing by encouraging self atrioventricular conduction function and extending the AV interval. This study is a prospective cohort study to evaluate the changes of cardiac function in patients and serum amino-terminal natriuretic peptide (NTproBNP) before and after pacing, and the risk of atrial fibrillation with different CUM% VP. The study has shown that the cardiac function will deteriorate with an increase in pacing rate. Keywords CUM%VP Ventricular Pacing NTProBNP Atrial fibrillation Minimized ventricular pacing
Introduction Dual-chamber pacemakers (DDD) are pacemakers whose wire leads are placed in two chambers of the heart. One lead paces the atrium and one paces the ventricle. Since this function more closely resembles the natural pacing of the heart by assisting the heart in coordinating the function
between the atria and ventricles, it is considered an ideal pacemaker. But, the evidence-based medical literature do not support this view and the search evidences from CTOPP, MOST, UKPACE, and the SAVE PACE [1–4] based on long-term follow-up studies comparing VVI pacemaker, and the DDD pacemakers have confirmed that the DDD pacemakers neither improve long-term survival of patients nor they reduce the incidence of cardiovascular events, heart failure, and rate of hospitalization. This is because of the fact that DDD are still not the absolute physiological pacing solution and a high percentage pacing at the apex of right ventricle offsets the benefits of the atrioventricular synchronous pacing. This pacing method further changes the normal sequence of atrioventricular activation, and causes the left and right ventricular systolic desynchronization leading to cardiac adverse events and heart failure [5–7]. The relationship between the cumulative ventricular pacing percentage (CUM% VP), defined as the percentage of paced rate of total heart rate and the risk of heart failure as well as the atrial fibrillation after pacing demands further research. This study is a prospective cohort study to evaluate the changes in cardiac functions and serum amino-terminal natriuretic peptide level (NTproBNP) in patients before and after pacing, as well as the risk of atrial fibrillation with different CUM% VP values recorded.
Materials and Methods The Objective
L. Zheng X. Du (&) The Fifth Central Hospital of Tianjin, No.41 Zhejiang Road, Tanggu District, Tianjin, China e-mail: [email protected]
A cohort of 192 permanent pacemaker implantation patients was selected for the study from XYZ hospital in the period 2006–2011. Of the 192 cases, 82 cases were
123
226
Cell Biochem Biophys (2014) 69:225–228
male and 110 were female. Of the total, 125 were Sick Sinus Syndrome cases, 24 II degree Atrial Ventricular Block cases and 43 III degree Atrial Ventricular Block cases. All the surgeries were done through the subclavian vein path and by the buried pacemaker implantation method. The pacemaker was DDD type (Medtronic or Shengyou Da), and the pacing site was right atrial appendage, right ventricular apex. Criteria of Patients’ Entry • • • • •
Symptomatic slow type arrhythmia (pacemaker implantation indications) Age [18 years old QRS wave duration \120 ms Without a history of atrial fibrillation for in the last 6 months Expected survival life [2 years.
Methods Grouping Ventricular cumulative pacing (CumVP%) for all the patients was recorded by a pacemaker programmer during the 12 months period after operation, and then patients were divided into 2 groups according to the CumVP% value. 102 cases had CumVP% \40 % and 90 cases had CumVP% [40 %. Patients with normal preoperative cardiac function, valvular disease, and cardiomyopathy were excluded. Blood pressure, blood sugar, and blood lipids were effectively controlled preoperative and postoperatively in all cases included.
Observation The E/A ratio, left ventricular ejection fraction (LVEF), left and right atrial diameter, and left and right end ventricular diastolic volume tracked by cardiac ultrasound preoperative and postoperatively for 12 months period.
Incidence of Atrial Fibrillation All the patients were tested for the incidence of Atrial Fibrillation by a pacemaker programmer postoperative in the 12-months study period. Statistical Analysis All data were analyzed by SPSS16.0 statistical analysis software. The measurement data were expressed as mean ± standard, and analyzed between two groups by T test, taking the value P \ 0.05 as statistically significant.
Results Changes of Echocardiographic Indexes of the Two Groups of Patients All the patients exhibited a LVEF of [ 50 % preoperative and in the CumVP% B40 % group, the changes of LVEF, LV, and E/A ratio before and after operation were not different significantly. In the CumVP% [40 % group, LVEF was significantly lower and E/A ratio decreased (P \ 0.05) in the postoperative 12-month period indicating a reduced cardiac function (Table 1). Changes of NT-ProBNP of the Two Groups of Patients In the CumVP% B40 % group, the NT-proBNP were not different significantly before and after operation, in the CumVP% [40 % group, NT-proBNP levels were found increased and the value statistically significant (P \ 0.05) in the postoperative 12-months period (Table 2). The Incidence of Atrial Fibrillation of the Two Groups of Patients Postoperative 12 Months In the CumVP% B40 % group the incidence of atrial fibrillation was 3.9 %, and in the CumVP % [40 % group Table 1 The comparison of echocardiographic indexes preoperative and postoperative between two groups
Blood NT-proBNP Testing NT-proBNP was detected preoperative and postoperative 12 months for all the patients. Whole blood samples were drawn by non-anticoagulant vacuum blood collection tubes under calm breath in the morning during fasting and then the serum taken for detecting NT-proBNP testing using electrochemical immunoluminescence technique after centrifugation.
123
CumVP% B40 % (102)
CumVP% [40 % (90)
Preoperative
Preoperative
Postoperative
Postoperative
LA
31.9 ± 1.3
32.3 ± 1.0
29.3 ± 0.9
30.2 ± 1.1
LV
44.3 ± 1.4
43.2 ± 1.2
46.7 ± 1.5
50.2 ± 0.9
RA
29.6 ± 0.9
28.3 ± 0.7
27.7 ± 1.1
28.5 ± 1.3
RV
30.8 ± 1.2
30.1 ± 1.3
28.9 ± 0.6
28.1 ± 0.7
EF %
61 ± 4
62 ± 2
58 ± 4
52 ± 3
E/A
1.1 ± 0.1
1.1 ± 0.2
1.2 ± 0.1
0.9 ± 0.05
Cell Biochem Biophys (2014) 69:225–228
227
Table 2 The comparison of NT-ProBNP preoperative and postoperative between two groups (Pg/Ml) CumVP% [40 % (90)
CumVP% B40 % (102)
NT-proBNP
Preoperative
Postoperative
Preoperative
Postoperative
80.6 ± 9.3
74.0 ± 8.9
90.3 ± 8.8
256.3 ± 12.7
Table 3 The comparison of incidence of atrial fibrillation preoperative and postoperative between two groups
AF %
CumVP% B40 % (102)
CumVP% [40 %(90)
Preoperative
Postoperative
Preoperative
Postoperative
0
3.9
0
11.1
the incidence of atrial fibrillation was 11.1 %. The difference in incidence value was statistically significant (P \ 0.05) (Table 3).
Discussion At present, the right ventricular apex is the most commonly utilized pacing site for permanent pacemaker implantation. Recent studies have shown that a long-term right ventricular apex pacing can cause left ventricular abnormal depolarization, leading to left Ventricular Mechanical Asynchrony. Ventricular Mechanical Asynchrony, in turn can cause long-term adverse hemodynamic abnormalities including abnormal contraction and diastolic function of left ventricle and also bring about structural changes in the myocardium [3]. Sweeney et al. [8] have showed that the risk of heart failure has a linear positive correlation with the CUM% VP, when the CUM% VP is 0–80 %. Further, studies have also shown that when the CUM% VP is [80 %, the relative risk of heart failure will increase by 96 % for every increase in 10 % CUM% VP. Steinberg et.al [9] have also found similar results in his study with 567 patients with Implantable Cardioverter Defibrillator. The study has shown that in CUM% VP [50 % patient group the proportion of freshly reported heart failure or death was 25 % higher than in CUM% VP \50 % group. Previous studies have also confirmed that the right ventricular apex pacing technique causes adverse hemodynamic effects like change in the activation sequence of the normal heart and cause disturbed coordination of left ventricular systolic and diastolic functions. Long-term and frequent right ventricular apex pacing can also change the local myocardial perfusion, cellular structure, and myocardial fiber arrangement [10–12]. These pathophysiological changes can lead to various heart dysfunctions, including atrial fibrillation. In this study, the cardiac structure and functions were recorded by echocardiography. In the CumVP%
[40 % group, LVEF and E/A ratios were found to be decreased. Whereas, in the CumVP% B40 % group, there was no significant change preoperatively and postoperatively in LVEF and LVEDV values. This takes us to the conclusion that the cardiac function will deteriorate with an increase in pacing rate. In CumVP%[40 % group, the atrial diameter has been found to be increased postoperatively. The incidence of atrial fibrillation in CumVP%[40 % group has also been found to be increased than in CumVP% B40 % group. This also takes us to the conclusion that a long-term and frequent right ventricular apex pacing can result in atrial structural disturbances and increase the incidence of atrial fibrillation. Although NT-proBNP is not being used in the routine cardiac testing, several clinical studies have indicated that it could be used as one of the indicators for prediction, diagnosis, and risk stratification of a variety of cardiovascular disease [3–15]. The myocardial cells first synthesize BNP with a 108 amino acid sequence called the pro-BNP (BNP precursor). Pro-BNP is then cleaved into NT-proBNP (amino-terminal—proBNP or N-terminal—proBNP). The half-life of BNP is 22 min, while that of the NTproBNP is 120 min. NT-proBNP in vitro is relatively stable, and studies have shown that NT-proBNP has the similar diagnostic accuracy with BNP when screening heart failure from dyspnoeic population, and its sensitivity and specificity are each more than 92 and 93 %, respectively [16]. The present study has further confirmed the adverse effects of right ventricular apex pacing on cardiac function and its relationship with the CUM%VP.
Conclusion Excessive right ventricular apex pacing has significant adverse effects on cardiac functions. It is thus important to clinically optimize pacing parameters and location and advocate appropriate physiological pacing, in order to safeguard cardiac function after a pacemaker intervention. For Sick Sinus Syndrome patients with normal atrioventricular conduction, it is recommended to minimize unnecessary right ventricular pacing and advocate appropriate ventricular pacing. Minimized ventricular pacing is an atrioventricular node priority function that encourages ventricular self conduction and reduces unnecessary right
123
228
ventricular pacing. Minimized ventricular pacing reduces ventricular pacing by encouraging self atrioventricular conduction function and extending the AV interval. This includes fixed lag of the atrioventricular interval, the automatic search of the atrioventricular interval, and the fixation time search of atrioventricular interval.
References 1. Connolly, S. J., Kerr, C. R., Gent, M., et al. (2000). Effects of physiologic pacing versus ventricular pacing on the risk of stroke and death due to cardiovascular causes. The Canadian Trial of Physiologic Pacing Investigators. New England Journal of Medicine, 342(19), 1385–1391. 2. Lamas, G. A., Lee, K. L., Sweeney, M. O., et al. (2002). Ventricular pacing or dualchamberpacing for sinus-node dysfunction. New England Journal of Medicine, 346(24), 1854–1862. 3. Lamas, G. A., Lee, K. L., Sweeney, M. O., et al. (2000). The mode selection trial (MOST) in sinus node dysfunction design, rationale and baseline characteristics of the first 1000 patients. American Heart Journal, 140(4), 541–551. 4. Toff, W. D., Camm, A. J., & Skehan, J. D. (2005). United Kingdom pacing and cardiovascular events trial investigation. Single-chamber versus dualchamberpacing for high-grade atrioventricular block. New England Journal of Medicine, 353(2), 115–155. 5. Stambler, B. S., Ellenbogen, K. A., Liu, Z., et al. (2005). Serial changes in right ventricular apical pacing lead impedance predict changes in left ventricular ejection fraction and functional class in heart failure patients. Pacing and Clinical Electro Physiology, 28, S50–53. 6. Nielsen, J. C., Andersen, H. R., Thomsen, P. E., et al. (1998). Heart failure and echo cardio graphic changes during long-term follow-up of patients with sick sinus syndrome randomized to single-chamber atrial or ventricular pacing. Circulation, 97, 987–995. 7. Lamas, G. A., Lee, K. L., Sweeney, M. O., et al. (2002). Ventricular pacing or dual chamber pacing for sinus node dysfunction. New England Journal of Medicine, 346, 1854–1862.
123
Cell Biochem Biophys (2014) 69:225–228 8. Sweeney, M. O., Hellkamp, A. S., Ellenbogenk, A., et al. (2003). Adverse effect of ventricular pacing on heart failure and atrial fibrillation among patients with normal baseline QRS duration in a clinical trial of pacemaker therapy for sinus node dysfunction. Circulation, 107, 2932–2937. 9. Steinberg, J. S., Fisch, E. R. A., & Wang, P. (2005). The clinical implications of cumulative right ventricular pacing in the multicenter automatic defibrillator trial. Journal of Cardiovascular Electrophysiology, 16, 359–365. 10. Nielsen, J. C., Bottcher, M., Nielsen, T. T., et al. (2000). Regional myocardial blood flow in patient s with sick sinus syndrome randomized to long-term single chamber or dual chamber pacingeffect of pacing mode and r ate. Journal of the American College of Cardiology, 35, 1453–1461. 11. Karpawhich, P. P., Justice, C. D., Cavitt, D. K., et al. (1975). Developmental sequelae of fixed rate ventricular pacing in the immature canine heart: An electrophysiological, hemodynamic and his to pathologic evaluation. American Heart Journal, 119, 1077–1083. 12. Adomian, G., & BEAZELL, J. (1986). Myofibrillar disarray produced in normal hearts by chronic electrical pacing. American Heart Journal, 112, 79–83. 13. Schou, M., Gustafsson, F., Kjaer, A., et al. (2007). Long-term clinical variation of NT-proBNP in stable chronic heart failure patients. European Heart Journal, 28, 177–182. 14. Bibbins-Domingo, K., Gupta, R., et al. (2007). N terminal fragment of the prohormone brain-type natriuretic peptide (NTproBNP), cardiovascular events, and mortality in patients with stable coronary heart disease. JAMA, 297, 169–176. 15. Tang, W. H., Steinhubl, S. R., Van Lente, F., et al. (2007). Risk stratification for patients undergoing non urgent percutaneous coronary intervention using N-terminal pro-B-type natriuretic peptide: a Clopidogrel for the Reduction of Events during Observation (CREDO) substudy. American Heart Journal, 153, 36–41. 16. Sanz, M. P., Borque, L., Rus, A., et al. (2006). Comparison of BNP and NT-ProBNP assays in the approach to the emergency diagnosis of acute Dyspnea. Journal of Clinical Laboratory Analysis, 20, 227–232.
