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European Journal of Heart Failure 2003 5(2):179-186; doi:10.1016/S1388-9842(02)00245-3
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© 2002 European Society of Cardiology

Regional myocardial perfusion during chronic biventricular pacing and after acute change of the pacing mode in patients with congestive heart failure and bundle branch block treated with an atrioventricular sequential biventricular pacemaker

Jens Cosedis Nielsen*, Morten Bøttcher, Henrik Kjærulf Jensen, Torsten Toftegaard Nielsen, Anders Kirstein Pedersen and Peter Thomas Mortensen

Department of Cardiology, Skejby Sygehus, Aarhus University Hospital Brendstrupgaardsvej, DK-8200 Aarhus N, Denmark

* Corresponding author. Fax: +45-89-49-60-09 E-mail address: cosedis{at}dadlnet.dk


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
Background: Biventricular (BiV) pacing has been found to improve systolic function and exercise tolerance in patients with severe congestive heart failure and bundle branch block. The mechanisms behind this beneficial effect is still not sufficiently clarified.

Aim: To evaluate the regional myocardial perfusion (MP) during BiV pacing and after acute change of the pacing mode to conventional dual chamber (DDD) pacing, and single chamber atrial (AAI) pacing in patients with severe congestive heart failure and prolonged QRS width treated with chronic BiV pacing.

Methods and Results: Fourteen patients (age 63±7 years, 13 male) were evaluated 13±7 months after implantation of a triple-chamber biventricular pacemaker. MP was quantified with 13N-labeled ammonia positron emission tomography during BiV pacing, DDD pacing, and AAI pacing. MP was assessed in the anterior, lateral, inferior, and septal regions, and the global mean MP was calculated. Clinical assessment was performed before pacemaker implantation and after at least 3 months of BiV pacing including a 6-min walk test (WT), New York Heart Association (NYHA) class functional score and echocardiography. Global mean MP (BiV: 0.65±0.20 vs. DDD: 0.65±0.21 vs. AAI: 0.65±0.18 mlg–1min–1) and MP in each of the four regions did not differ between the three pacing modes. The patients improved clinically during BiV pacing; 6 min WT increased (338±59 vs. 415±73 m, P<0.001), NYHA class score improved (class I/II/III/IV: 0/0/11/3 vs. 1/9/2/0, P<0.001), and left ventricular ejection fraction increased (21±5 vs. 29±8%, P=0.004).

Conclusion: No differences in regional MP are detectable after chronic BiV pacing when the pacing mode is changed acutely in patients with severe congestive heart failure and bundle branch block. This finding indicates, that the clinical improvement caused by BiV pacing is not associated with any increase in the MP and thereby oxygen demand.

Key Words: Perfusion • Regional blood flow • Pacing • Heart failure

Received January 15, 2002; Revised August 16, 2002; Accepted September 17, 2002


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
Biventricular (BiV) pacing has been introduced as additive treatment in patients with severe congestive heart failure and prolonged QRS width [1,2]. Results from uncontrolled studies indicates that BiV pacing is beneficial for selected heart failure patients [2–6]. In the largest of these studies, the InSync study, comprising 68 patients, BiV pacing was associated with significant improvements in New York Heart Association (NYHA) functional class, 6-min walk distance, and quality of life when comparing follow-up at 3, 6 and 12 months with baseline [2]. Recently, BiV pacing was reported to improve exercise tolerance, functional class and quality of life score and decrease hospitalisations because of heart failure in both a randomised, controlled cross-over study [7] and a randomised controlled trial [8]. The physiological effects of BiV pacing are to correct the non-uniformity of ventricular activation, contraction, and relaxation sequences [6,9]. Furthermore, atrioventricular (AV) sequential BiV pacing may be beneficial in shortening a prolonged AV conduction [10], in prolonging diastole [11] and in reducing mitral regurgitation [12,13]. Recently, it was estimated that approximately 10% of heart failure patients would be candidates for BiV pacing [14]. It has recently been shown, that dual chamber pacing (DDD) causes a decrease in the inferior, septal and global mean myocardial perfusion (MP) as compared with single chamber atrial pacing (AAI) in patients with sick sinus syndrome [15]. This change in regional MP is probably caused by changes in the regional myocardial workload [16,17]. BiV pacing changes the myocardial activation and contraction sequences, and therefore could change also the regional myocardial blood flow. The aim of the present study was to evaluate the regional MP during chronic BiV pacing and after acute change of the pacing mode to conventional dual chamber pacing (DDD) and AAI pacing in patients with severe congestive heart failure and prolonged QRS width treated with chronic AV sequential BiV pacing.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 5. Conclusions
 References
 
2.1. Population
During the period from 1997 to May 2000, 52 selected patients with severe congestive heart failure were treated with AV sequential BiV pacing at Aarhus University Hospital (Skejby Hospital). At the time of pacemaker implantation the patients were in NYHA functional class III–IV despite optimal medical treatment, had bundle branch block with a QRS duration of at least 120 ms, their left ventricular end-diastolic diameter exceeded 5.5 cm, their left ventricular ejection fraction (LVEF) was 35% or lower, and they did not have chronic atrial fibrillation. Several of our patients who were treated with BiV pacing early during this period were included in the international multicenter InSync or InSync Registry studies, the later of which required QRS width >=120 ms for inclusion. Consecutive patients who were clinically stable and at least 3 months after the pacemaker implantation were considered candidates for the present study. A total of 14 of these patients agreed to participate in the present study, and MP study was performed 13±7 months (range 3.9–23.8 months) after pacemaker implantation. Data from these patients at the time of pacemaker implantation and after at least 3 months of BiV pacing are presented in Table 1. Their mean height was 176±10 cm and mean weight was 75±16 kg. Five of the patients suffered from diabetes, 5 patients were smokers, and all 7 patients with coronary artery disease had one or more prior myocardial infarctions. At the time of MP study, the patients were stable on anticongestive medication: diuretics (n=14), ACE-inhibitors (n=12), beta-blockers (n=6), digoxin (n=11), long-acting nitrates (n=4), and 7 were on amiodarone.


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  		Table 1 Baseline and follow-up characteristics for the study population

 
2.2. PET and quantification of myocardial perfusion
MP was quantified using 13N-labeled ammonia and dynamic PET imaging (Model EXACT HR 961, Siemens/CTI, Knoxville, TN). A 20 min attenuation scan was performed ‘on the fly’ to correct for photon attenuation. The image acquisition (12 frames of 10 s each) started simultaneously with the intravenous injection of 13N-labeled ammonia (740 MBq in 20 ml saline; 30 s bolus injection). Following this dynamic sequence two 30-s, one 60-s and one 900-s static non-gated image frames were acquired to obtain high resolution images for the assignment of regions of interest (ROIs).

The transaxially acquired images were reoriented to obtain 12 short-axis images of the left ventricle as described previously [18]. Three mid-ventricular short-axis planes of the static images were selected to assign four ROIs referring to the three major coronary vascular territories (anterior: left anterior descending artery (LAD), lateral: left circumflex artery (LCX), and inferior: right coronary artery (RCA)) and the interventricular septum. The ROIs were subsequently copied to the dynamic image sequence. This allowed us to obtain myocardial tissue time-activity curves for 13N-labeled ammonia [19]. The arterial input function was obtained from a small ROI in the centre of the left ventricular blood pool on the static frame and copying this ROI to the serially acquired blood pool images [20]. The myocardial time-activity curves were corrected for partial volume effects by assuming a uniform left ventricular wall thickness of 1 cm which yields a recovery coefficient of 0.78 [21]. Corrections were also made for physical decay of 13N-labeled ammonia activity on both the blood pool and myocardial time-activity curves. MP was quantified by fitting the corrected tissue and blood pool time-activity curves to a validated two compartment model for 13N-labeled ammonia [18]. This model corrects for spillover activity from the left ventricular blood pool to the left ventricular myocardium [21,22]. MP was calculated in each ROI. The global mean MP was calculated as the average MP in the four ROIs. In patients with prior MI, regions with scar were avoided when defining ROIs for obtaining time-activity curves as described by Czernin et al. [23]. Resting MP is closely related to rate-pressure product (RPP), defined as systolic blood pressure x heart rate [19], and therefore MP values normalized to the RPP were also calculated (corrected MP=(MP/RPP)x10.000).

2.3. Study protocol
In all patients, MP was measured at three different pacing modes; AV sequential BiV pacing, dual chamber DDD pacing with capture of the ventricles from the right ventricular lead (DDD), and single chamber atrial pacing (AAI). The order of the three measurements was randomised. DDD pacing was established by reducing the output below the level causing left ventricular capture but still higher than the threshold in the right ventricle. In each patient, the three MP measurements were performed at the same heart rate. All MP measurements were performed in the same scanning session on 1 day in each patient. Alterations in pacing mode was done 5 min before injection of 13N-labeled ammonia and reverted to the usual lower rate and usual mode after completion of the dynamic image acquisition (120 s after start of the 13N-labeled ammonia infusion). The first MP study was performed after each patient had rested in the supine position for at least 30 min. The 12-lead ECG was monitored continuously throughout each study. Heart rate and blood pressure were measured twice immediately after each 13N-labeled ammonia injection with an automatic blood pressure device. The average value of these two measurements is reported.

2.4. Clinical assessment
Before pacemaker implantation and again during chronic BiV pacing at least 3 months after pacemaker implantation, LVEF was assessed by two-dimensional echocardiography. Six-minute walk test (WT) and NYHA-class scoring were performed before pacemaker implantation and again during follow-up after at least 3 months of BiV pacing. Before pacemaker implantation, the patients did a training test to confirm that they were able to complete the 6 min WT before obtaining the ‘baseline’ 6 min WT. Twelve lead ECG was obtained before pacemaker implantation, immediately after BiV pacing was initiated, and during each of the three pacing modes at time of MP study.

2.5. Pacemaker implantation and programming
AV sequential biventricular pacemakers (Medtronic InSync®, Minneapolis, USA) [2] were implanted in all patients. The pacemaker was connected to one bipolar atrial lead implanted in the upper parts of the right atrial free wall and two ventricular leads, one bipolar lead implanted in the right ventricular apex and one unipolar lead implanted transvenously through the coronary sinus to pace and sense the left ventricle [24]. The coronary sinus lead was implanted in the lateral or posterior cardiac vein. The two ventricular leads were connected to the same channel within the pacemaker for pacing and sensing. The pacemaker was programmed in DDD mode with an AV delay ensuring complete biventricular capture in the ECG. Echocardiography was used to select the optimal AV delay [25]. Lower and upper rates as well as rate-adaptive function were programmed individually.

2.6. Statistics
In a prior study of 15 patients with DDD pacemakers we observed a highly significant 15% increase in global mean MP associated with change in pacing mode from DDD to AAI [15]. Therefore, a total of 14 patients was decided to be sufficient in the present study to detect any important differences in MP between pacing modes using paired statistics.

Continuous variables are reported as mean±S.D. The paired t-test or the nonparametric Wilcoxon signed rank test was utilised to compare blood flow, hemodynamic measurements and echocardiographic findings during different pacing modes. {chi}2-test was used to compare discrete variables. SPSS 10.0 for Windows was used for statistics. All probability values are two-tailed; P<0.05 was considered statistically significant.

2.7. Ethics
The study was approved by the Local Ethical Committee and was conducted in accordance with the Helsinki II declaration. Each patient gave written informed consent.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 5. Conclusions
 References
 
3.1. Myocardial perfusion
As indicated by Table 2 and Figs. 1 and 2, there were no significant differences in MP in any of the four regions or in global mean MP between the three pacing modes. Graphically, there seemed to be a trend towards lower MP during DDD pacing than during the other two pacing modes in the RCA region (Fig. 2) (DDD vs. AAI, P=0.16, DDD vs. BiV, P=0.06). None of the other three regions showed any obvious trend indicating a minor change in regional MP associated with change in pacing mode (Fig. 2). As shown in Figs. 1 and 2 MP could not be measured in all regions in all patients. In one patient, MP was not measured in the AAI mode because of second degree AV block during AAI pacing. In another patient, the threshold on the left ventricle was lower than on the right ventricle, and reducing ventricular output caused AV synchronous left ventricular pacing and not standard DDD pacing. The MP data obtained in the AV synchronous left ventricular pacing mode for this patient have been excluded. In other patients, MP could not be measured in one or more regions because of scar areas after prior myocardial infarctions. In 7 patients, MP could be measured in all four ROI's, whereas 6 and 1 patients contributed with data from three and two ROI's, respectively. RPP did not differ between pacing modes. MP corrected for RPP did not differ between pacing modes.


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  		Table 2 Myocardial perfusion and hemodynamics

 


Figure 1
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  		Fig. 1 Individual global mean MP during single chamber atrial (AAI) pacing mode, conventional dual chamber DDD pacing with capture of the ventricles from the right ventricular lead (DDD), and AV sequential BiV pacing. For statistical comparisons see Table 2.

 


Figure 2
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  		Fig. 2 Individual regional MP during single chamber atrial (AAI) pacing mode, conventional dual chamber DDD pacing with capture of the ventricles from the right ventricular lead (DDD), and AV sequential BiV pacing. LAD, LCX, and RCA indicate the three major coronary vascular territories; left anterior descending artery, left circumflex artery, and right coronary artery. For statistical comparisons see Table 2.

 
Analysing separately the 7 patients without coronary artery disease, who had a more uniform reduction in left ventricular function and no scar areas after prior myocardial infarctions, the results were similar with no significant differences in regional or mean MP (Global mean MP: AAI: 0.68±0.20 vs. DDD: 0.65±0.23 vs. BiV: 0.67±0.27 ml g–1 min–1, P=ns).

3.2. Clinical parameters before pacemaker implantation and during chronic biventricular pacing
During chronic BiV pacing the NYHA functional class had improved as compared with assessment before pacemaker implantation (P<0.001, {chi}2-test). Distance walked at 6-min WT increased on average 23% during BiV pacing as compared with the pre-implantation distance (338±59 vs. 415±73 m, P<0.001, paired t-test) (Table 1). LVEF increased from 21±5 to 29±8% (P=0.004, paired t-test) when comparing pre-implantation and BiV pacing at time of MBF study.

In the ECG, the QRS width decreased when BiV pacing was initiated (before: 164±21 ms vs. after: 151±24 ms, P=ns). At the time of the MP study, the QRS width was 165±23 ms during BiV pacing, 172±21 ms during AAI pacing, and 206±21 ms during DDD pacing. In all patients, electrocardiographic signs of so-called cardiac memory [26] were observed during AAI pacing mode at the time of the MP study.


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
5. Conclusions
 References
 
The present study documents, that no differences in regional MP are detectable after chronic BiV pacing when the pacing mode is changed acutely in patients with severe congestive heart failure and bundle branch block. This finding indicates, that the clinical improvement caused by BiV pacing is not associated with any increase in the MP and thereby oxygen demand.

To our knowledge, the present study is the first study measuring quantitatively the regional MP during BiV pacing. The mean MP observed is slightly lower than reported in prior studies of patients with congestive heart failure (0.75–0.88 ml g–1 min–1) [27] and normal controls (0.82 ml g–1 min–1) [28]. The finding of an unchanged regional and global mean MP during BiV pacing indicates, that regionally the myocardial contractile work load and the myocardial oxygen consumption is unaltered during BiV pacing [16,17]. This assumption can be made because the oxygen extraction in the myocardium is very high and particularly in the ischemic myocardium, the contractile work can only be increased by increasing perfusion. Our results therefore support, that the beneficial effects of BiV pacing on the left ventricular performance are caused by mechanisms, which are not associated with any increased myocardial work in the single contracting segments. Such mechanisms may include a better coordination of the left ventricular segmental contraction—a resynchronisation, a prolongation of diastole [11], a reduction in the severity of mitral regurgitation [12,13], and a better AV synchrony [10].

Recently the first study on changes in coronary blood flow during acute BiV pacing in patients with dilated cardiomyopathy was reported by Nelson et al. [29]. In that study, coronary blood flow was assessed using an intracoronary Doppler catheter in the left main coronary artery and the arterial-coronary sinus oxygen saturation difference was determined by hemoximeter. The flow in the RCA and the actual perfusion were not measured. During BiV pacing, the myocardial oxygen consumption declined approximately 10% because of a fall in the transcardiac oxygen gradient despite an improvement in the left ventricular systolic function. The left main coronary artery flow did not change significantly. It was concluded, that BiV pacing improves cardiac function at diminished energy cost. The present findings support the findings by Nelson et al. [29], that BiV pacing does not increase overall myocardial energy cost or global mean MP. However, we furthermore have documented that the regional perfusion, reflecting the regional myocardial energy cost is unchanged during BiV pacing.

In the present study we did not obtain precise invasive parameters of left ventricular function, and we therefore cannot calculate the myocardial energy cost and workload. The improvement in left ventricular function during BiV pacing has, however, been documented in previous studies [6,29–31], and the beneficial effects of BiV pacing in the present study was indicated by the clinical improvement—increased 6-min walking distance and LVEF and decreased NYHA functional class—observed during BiV pacing.

The MP study was done during chronic BiV pacing, and does not necessarily reflect the acute situation when BiV pacing is initiated. In the present study, 6 min WT and echocardiography were done before pacemaker implantation and again after several months of BiV pacing, at a time point when chronic BiV pacing may have induced myocardial remodelling [32]. Therefore, the improvements observed in exercise capacity and left ventricular function are not necessarily explained alone by differences in pacing mode. Myocardial remodelling could be partially responsible for the changes observed. At present, it is not known whether chronic BiV pacing also improves myocardial contractility. After a mean of 13 months of BiV pacing, the so-called cardiac memory effect is expected to last for weeks [26], and in fact, electrocardiographic patterns of cardiac memory were observed in all patients in the present study during temporary AAI pacing. Therefore it cannot be excluded, that this phenomenon may have influenced the MP measured during temporary AAI and DDD pacing. In the present study, MP was measured only after several months of BiV pacing. The study therefore does not show whether BiV pacing could improve perfusion over time. To evaluate that question, serial MP studies must be done over time in a group of patients treated with BiV pacing.

In a prior study, we reported that ventricular pacing in the DDD mode reduced significantly the inferior, septal, and global mean MBF as compared with temporary AAI pacing in patients with sick sinus syndrome, no bundle branch block, and normal left ventricular function [15]. Similarly, Tse et al. reported inferior MP defects associated with right ventricular pacing [33]. In the present study we found no significant differences in regional or global mean MBF between AAI and DDD pacing modes, which seems to be in contrast to the prior findings. However, although the difference was insignificant, there was a trend towards lower MP in the inferior region during DDD pacing than during AAI pacing, which is in accordance with the prior results. The reason why the difference was not significant probably is the low number of patients (n=8–9) in whom MP could be measured in the inferior region, where the largest difference was expected. Furthermore, in the prior study on patients with sick sinus syndrome, QRS width was in mean 85 ms during AAI pacing and 164 ms during DDD pacing, indicating a profound change in the ventricular activation pattern [15], whereas the change in QRS width was substantially less (from 172 to 206 ms) in the present study, indicating a lower impact on ventricular activation pattern of DDD pacing in patients who have a pre-existing broad QRS complex. Lastly, it is not known whether the myocardium in the failing heart has the same potential for changing regional work load and MP as the myocardium of a heart with normal left ventricular function. In contrast to most prior studies [2,6], we observed no significant reduction in QRS width during BiV pacing. However, when BiV pacing was initiated, QRS width shortened, and at the time of the MP study, QRS width was shortest during BiV pacing and longest during DDD pacing, indicating, that BiV pacing was associated with a reduced contraction asynchrony—a resynchronisation in the present study. The QRS width reduction in the present study was slightly lower than the median 20 ms reduction observed in the randomised MIRACLE (Multicenter InSync Randomized Clinical Evaluation) trial [8], which may be due to our relative small population.

4.1. Limitations
Small changes in MP between pacing modes may have been missed because of the relative limited number of patients. The patients in the present study were treated with drugs, which could potentially influence the global mean MP. The MP study, however, was done on one day and drug treatment therefore was identical in the three pacing modes for each patient. In some of the patients, medication might have changed slightly from pre-implantation to clinical assessment during chronic BiV pacing or MP study, which may have influenced the comparisons of LVEF, NYHA-class, and 6 min WT at the two time points. However, at the time of pacemaker implantation, the patients were in heart failure class III or IV despite optimal anticongestive medication, and therefore it is unlikely that changes in medication are responsible for the considerable clinical improvements observed during chronic BiV pacing. The clinical assessment in the present study was not done blinded, and therefore placebo effect and investigators bias cannot be excluded. The 23% increased distance at 6-min WT is, however, identical to the finding in the randomised, single-blind MUSTIC trial [7], indicating a realistic clinical effect of BiV pacing in the present study. Some of our patients had prior myocardial infarctions and probably regional differences in contractility. Regional wall motion was not analysed in the present study. Therefore we cannot rule out, that changes in regional wall motion may have influenced comparisons of MP during different pacing modes.


   5. Conclusions
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusions
References
 
The present study documents, that no differences in regional MP are detectable after chronic BiV pacing when the pacing mode is changed acutely in patients with severe congestive heart failure and bundle branch block. This finding indicates, that the clinical improvement caused by BiV pacing is not associated with any increase in the MP and thereby oxygen demand.


   Acknowledgements
 
We greatly appreciate the technical support of all staff involved in scanning and production of radiotracers at the PET centre, Aarhus University Hospital. The authors thank Karin Boisen for her invaluable assistance in acquisition and analysis of data.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 

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