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European Journal of Heart Failure 2007 9(6-7):637-643; doi:10.1016/j.ejheart.2007.03.002
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© 2007 European Society of Cardiology

Impact of heart rate on mechanical dyssynchrony and left ventricular contractility in patients with heart failure and normal QRS duration

Tairo Kuritaa, Katsuya Onishib,*, Kaoru Dohia, Masaki Tanabea, Naoki Fujimotoa, Takashi Tanigawaa, Morimichi Setsudaa, Naoki Isakaa, Tsutomu Noborib and Masaaki Itoa

a Department of Cardiology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan
b Department of Molecular and Laboratory Medicine, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Japan

* Corresponding author. Tel: +81 59 231 5015; fax: +81 59 231 5201. E-mail address: katsu{at}clin.medic.mie-u.ac.jp


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
 References
 
Aims: The quantification of mechanical dyssynchrony has important diagnostic value and may help to determine optimal therapy in heart failure (HF). We hypothesized that mechanical dyssynchrony may be augmented at increased heart rates in patients with HF and normal QRS duration.

Methods and results: From online segmental conductance catheter signals, we derived indices to quantify temporal and spatial aspects of mechanical dyssynchrony during systole in 20 control subjects, 20 HF patients with normal QRS duration, and 12 HF patients with complete left bundle branch block (CLBBB). Data were collected at baseline, and then following a 40 bpm increase in heart rate induced by right atrial pacing. Mechanical dyssynchrony in HF patients with normal QRS duration or CLBBB was higher than that found in control subjects. In HF patients with normal QRS duration, mechanical dyssynchrony increased from 37.4±4.8% at baseline to 43.2±4.4% with increased heart rate (p<0.01), the resultant degree of mechanical dyssynchrony was similar to that at baseline in the HF patients with CLBBB. Increased heart rate did not affect dyssynchrony in the control patients.

Conclusion: Mechanical dyssynchrony was augmented as heart rate increased by right atrial pacing in patients with HF and normal QRS duration.

Key Words: Mechanical dyssynchrony • Conductance catheter • Internal flow • Heart failure • Patient

Received July 19, 2006; Revised January 11, 2007; Accepted March 6, 2007


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 5. Limitations
 References
 
Left ventricular (LV) dyssynchrony is characteristic of patients with heart failure (HF) who have a wide QRS complex, suggesting electromechanical delay [1,2]. LV dyssynchrony is an important determinant of cardiac dysfunction in HF because of inefficient pump performance and energy expenditure [3,4]. Cardiac resynchronization therapy by biventricular pacing, when added to optimal medical therapy in persistently symptomatic patients, has resulted in significant improvements in patients' perceived quality of life, functional class, and exercise capacity, as well as a reduction in morbidity and mortality [5-8]. The ACC/AHA guidelines strongly recommend cardiac resynchronization therapy (CRT) for patients with low LV ejection fraction, sinus rhythm, cardiac dyssynchrony assessed by QRS duration, and NYHA functional class III or ambulatory class IV symptoms despite optimal medical therapy [9]. Quantification of LV dyssynchrony provides diagnostic and prognostic data, which may be useful in selecting patients for and guiding the delivery of CRT therapy [10-12].

Heart rate is an important determinant of myocardial performance, and several studies have confirmed the existence of chronotropic effects on myocardial contractility (the positive force-frequency relation) in normal human subjects, but not in patients with HF [13-15]. Several studies using human cardiomyopathic muscle or other experimental models of the failing heart have demonstrated an impaired force-frequency relation that was deteriorated further by calcium and acetylstrophanthidin, but improved by increasing intracellular cyclic adenosine monophosphate with an adenylate cyclase activator or a beta-adrenergic agonist, suggesting an abnormality in calcium handling within the myocytes [16-18]. LV dyssynchrony may worsen as heart rate increases in HF patients because of the non-homogenous distribution of ultrastructual changes, potential myocardial ischaemia, or calcium handling abnormalities within the myocytes secondary to cardiac disease, leading to further impairment of the force-frequency relation in the whole heart [18]. However, the relationship between baseline heart rate and LV dyssynchrony remains unknown. Accordingly, the purpose of the present study was to test the hypothesis that LV dyssynchrony is augmented as heart rate increases in patients with HF and normal QRS duration.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 5. Limitations
 References
 
Fifty-two consecutive patients with non-ischaemic heart disease referred for elective cardiac catheterization at Mie University Hospital were enrolled in the study. Patients were stratified into 3 groups: normal QRS duration (<120 ms) without HF (control subjects, n=20), normal QRS duration with HF (n=20), and CLBBB with HF (n=12). The diagnosis of HF was based on the Framingham criteria and clinical evidence of HF with shortness of breath, symptomatic exercise limitation, and peripheral oedema with a disease history of at least 6 months. Patients with an echocardiographic ejection fraction over 50% were excluded. Patients with normal QRS duration without HF, who had atypical chest pain, no significant coronary artery disease by coronary catheterization, and preserved LV systolic and diastolic function by 2-D echo, were enrolled as control subjects. All patients with HF (n=32) were treated as clinically indicated with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor antagonists (n=30), beta-blockers (n=16), diuretics (n=23), digitalis (n=10), and antiarrythmics (n=4) before enrolment in the study (Table 1). All medications except diuretics were withheld for at least 48 h before cardiac catheterization. Patients were excluded from the study if they had atrial fibrillation, symptomatic ventricular tachycardia, LV apical thrombus, aneurismal wall motion, primary valvular heart disease, or had received any inotropic agents within 4 weeks of the study. The study protocol was approved by the institutional ethics committee of Mie University School of Medicine, and written informed consent was obtained from all subjects.


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  		Table 1 Patient characteristics

 
2.1. Cardiac catheterization procedures
After right and left heart catheterization, left ventriculography and coronary arteriography, a 6F single-field conductance catheter (Webster Laboratories, Baldwin Park, CA), with a 2F micromanometer (Millar Instruments, Inc., Houston, TX) placed within its lumen was advanced to the LV apex and connected to a digital stimulator microprocessor (Sigma V, Leycom [dual-field system], Zoetermeer, Netherlands) to measure LV volume. The conductance catheter technique and its principles have been fully described previously [10,19-22]. Real-time pressure-volume diagram generation and analog/digital conversion (333 Hz) were performed using a 16-bit microcomputer system (PC-9801VX, NEC Co., Tokyo, Japan). At the beginning of the study, the conductance catheter signal gain was calibrated using a thermo dilution-derived stroke volume. A calibration offset (parallel conductance) was corrected by matching a conductance catheter signal at end-diastole with an end-diastolic volume measured by biplane ventriculography using an area-length method. Each measurement represents the mean value of at least 30 consecutive sinus beats. A temporary pacing lead was positioned in the right atrium to increase heart rate.

2.2. Study protocol
Three sets of steady-state LV pressure-volume loops were recorded over a 15-second recording period. After baseline data were measured, right atrial pacing was initiated for control subjects and HF patients with normal QRS duration and CLBBB. Heart rate was increased by 40 bpm and data were collected again after 20 min.

2.3. Data analysis
Steady-state haemodynamic measurements were determined from signal-averaged cardiac cycles, combining 5 to 10 sequential beats. Stroke volume was calculated as end-diastolic minus end-systolic volume. The derivatives of LV pressure (+dP/dt) were calculated using the 5-point Lagrangian method as an isovolumetric phase index of the inotropic state. The LV contractile state was assessed by end-systolic elastance (Ees) using a single-beat formula, which is sensitive to changes in contractile state but relatively insensitive to changes in loading conditions [23]. The rate of LV relaxation was analyzed by determining the time constant of the isovolumetric fall of LV pressure, which was calculated by regressing LV pressure vs. the peak rate of fall in LV pressure (–dp/dt) during the isovolumic relaxation phase. The total systemic resistance was calculated as end-systolic pressure divided by cardiac output.

2.4. Mechanical dyssynchrony
Assessment of LV dyssynchrony from segmental LV volume measurement has been previously described for cine-angiography and the conductance catheter [10,11,22]. Time-varying segmental volumes, as measured with the conductance catheter, have been validated by means of cine-angiography [22]. The segmental signals obtained by the conductance catheter reflect instantaneous volume slices perpendicular to the LV long axis as obtained by cine-computerized tomography. Mechanical ventricular dyssynchrony, as measured with the conductance catheter, has been validated by means of tissue Doppler echocardiography [10]. At each time point, a segmental signal was defined as dyssynchronous if its change (i.e., dVseg/dt) was opposite to the simultaneous change in the total LV volume (dVLV/dt). Segmental dyssynchrony was quantified by calculating the percentage of time within the cardiac cycle that a segment was dyssynchronous. Overall LV dyssynchrony (DYS) was calculated as the mean of the segmental dyssynchrony measurements. DYS can be calculated within each specified time interval: we determined DYS during systole (DYSS) and diastole (DYSD), with systole defined as the period between dP/dtmax and dP/dtmin [10].

2.5. Internal flow
Non-uniform contraction and filling is associated with ineffective shifting of blood volume within the LV. This internal flow (IF) is quantified by calculating the sum of the absolute volume changes of all segments and subtracting the absolute total volume change: IF(t)=[{Sigma}|dVseg,i(t)/dt|–|dVLV(t)/dt|)/2. Note that dVLV(t)/dt represents the effective flow into or out of the LV. Thus IF measures the segment-to-segment blood volume shifts that do not result in effective filling or ejection. Division by two takes into account that any non-effective segmental volume change is balanced by an equal but opposite volume change in the remaining segments. IF fraction (IFF) is calculated by integrating IF(t) over the full cardiac cycle and dividing by the integrated absolute effective flow [10]. Off-line analysis was performed using custom-designed software.

2.6. Statistical analysis
All results are presented as the mean value±SD. One-way analysis of variance was used for the comparison between the three groups. Two-way analysis of variance with repeated measures was used to compare heart rate at baseline vs. heart rate increased by 40 bpm. Bonferroni correction was applied to adjust for multiple comparisons. A p value <0.05 was interpreted as statistically significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 5. Limitations
 References
 
3.1. Patient characterization
The mean plasma BNP levels in HF patients with normal QRS duration were less than those with CLBBB (Table 1). QRS duration in HF patients with CLBBB was significantly longer than in the other two groups, while there was no difference in QRS duration between control subjects and HF patients with normal QRS duration (Table 2). There was no significant difference in PR interval among three groups. Ejection fraction in HF patients with normal QRS duration was higher than that with CLBBB, while there was no difference in end-diastolic pressure.


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  		Table 2 Baseline haemodynamic data

 
3.2. Baseline haemodynamics
At baseline, there were no differences in heart rate and LV end-systolic pressure among the three groups. End-diastolic pressure and volume in HF patients with normal QRS duration and CLBBB were greater than those in control subjects. LV ejection fraction in control subjects was significantly higher than in HF patients with normal QRS duration and CLBBB.

3.3. Effect of RA pacing on LV mechanical dyssynchrony
Typical LV segmental and total volume recordings during 3 consecutive heart cycles at baseline heart rate and at heart rate increased by 40 bpm in a control subject are shown in Fig. 1. Time-volume loops from control subjects are very smooth and show little dispersion in the onset of contraction and in the peak LV volume between the segments, which was unchanged as heart rate increased (Fig. 1). IF is largely restricted to the isovolumic contraction and relaxation periods, which is consistent with normal physiology because, with the mitral and aortic valves closed, changes in LV shape result in internal segment-to-segment flow. By contrast, in HF patients with normal QRS duration, loops fluctuate and show a substantial dispersion in the onset of contraction and in the peak LV volume between the segments, which is exacerbated as heart rate increased. Contraction patterns are substantially more dyssynchronous in HF patients compared to control subjects. Furthermore, ineffective IF was present throughout the cardiac cycle in HF patients, which was exacerbated as heart rate increased. Contraction patterns are substantially more dyssynchronous in HF patients with CLBBB, compared to control subjects and HF patients with normal QRS duration, which was exacerbated as heart rate increased.


Figure 01
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  		Fig. 1 Typical example of segmental and total left ventricular (LV) volume signals and calculated internal flow at baseline (left panel) and during pacing (right panel) in a control subject. HR indicates heart rate; LVV, LV volume; LVP, LV pressure; DYS, % dyssynchrony; and IFF, internal flow fraction.

 
QRS duration was unchanged after pacing in all groups (Fig. 2). PR intervals were significantly prolonged during atrial pacing in all patients although there was no significant difference between the three groups (186±22 ms in control, 192±53 ms in normal QRS duration, and 202±56 ms in CLBBB). In control subjects, LV contractility estimated by Ees and positive dP/dt was significantly increased as heart rate was increased by RA pacing. Baseline % systolic dyssynchrony was 25.2±5.1% and baseline IFF was 7.2±2.1%, which were unchanged during pacing (25.5±5.9%, 8.4±2.7%, respectively; Fig. 3). By contrast, in HF patients with normal QRS duration, LV contractility was unaffected by increased heart rate. Baseline % systolic dyssynchrony and IFF were 37.4±4.8% and 14.8±10.9% respectively, which increased significantly to 43.2±4.4% and 24.0±12.2% during tachycardia (both p<0.01, Fig. 3). Furthermore, the values of % systolic dyssynchrony and IFF during pacing in HF patients with normal QRS duration were close to the values observed at baseline in HF patients with CLBBB. In HF patients with CLBBB, baseline % systolic dyssynchrony and IFF were 44.0±3.9% and 21.6±6.4%, which increased significantly to 48.1±4.1% and 23.8±10.9% during pacing.


Figure 02
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  		Fig. 2 QRS duration, left ventricular (LV) end-systolic pressure, end-systolic elastance (Ees) and peak positive dP/dt at baseline (Base) and during pacing (Base+40) in control subjects, patients with heart failure (HF) accompanied by normal QRS duration (Normal QRS), and by complete left bundle branch block (CLBBB). *p<0.01 vs. Base in Control, {dagger}p<0.01 vs. Base+40 in Control, {ddagger}p<0.05 vs. Base in HF with Normal QRS, §p<0.05 vs. Base+40 in HF with Normal QRS, ||p<0.01 vs. Base in HF with CLBBB.

 


Figure 03
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  		Fig. 3 % Systolic dyssynchrony and internal flow fraction at baseline (Base) and during pacing (Base+40) in control subjects, patients with heart failure (HF) accompanied by normal QRS duration (Normal QRS), or complete left bundle branch block (CLBBB).

 
Segmental conductance catheter signals do not provide an anatomical view but represent the total volume of slices perpendicular to the LV long axis. The proposed dyssynchrony indexes therefore reflect inter-segmental differences in contraction and may underestimate phase changes obtained by comparing regional lateral and septal wall motions, e.g., using tissue Doppler imaging. Accordingly, tissue-Doppler measurements were performed to compare conductance catheter-derived indexes of mechanical dyssynchrony and septal-to-lateral delay in the timing of peak systolic myocardial velocity as obtained by tissue-Doppler echocardiography. The septal-to-lateral delay times were significantly correlated with dyssynchrony index using linear regression analysis (y=0.2134x+24.125, r=0.90, p=0.002).


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
5. Limitations
 References
 
The present study demonstrates that in HF patients with normal QRS duration, LV mechanical dyssynchrony and internal flow fraction markedly increase when heart rate is increased by right atrial pacing. These findings highlight the importance of baseline heart rate in the assessment of LV dyssynchrony in patients with HF.

LV mechanical dyssynchrony is an important co-determinant of cardiac dysfunction in HF. In patients with HF and wide QRS complexes signifying electromechanical delay, cardiac resynchronization in the form of biventricular pacing has shown significant beneficial effects [5-8]. LV dyssynchrony is not uncommon in patients with HF with normal QRS duration, although it is more prevalent in patients with wide QRS complexes. In a tissue Doppler echocardiographic study, it was shown that patients with HF and normal QRS duration have dyssynchronous LV contraction compared with individuals with normal ventricular function. The mechanism of the discrepancy between mechanical and electrical dyssynchrony is unclear [24-27]. Firstly, electrocardiography may not be sensitive enough to detect the presence of an electromechanical delay in all the regions of the LV. Secondly, some patients may have mechanical dyssynchrony without significant electrical delay as a result of deposition of extracellular matrix, myocyte loss, and pathological hypertrophy. Finally, ultrastructual changes within the myocytes secondary to cardiac disease, such as decreased amounts of mitochondria, contractile proteins, or functional enzymes for oxidative phosphorylation may adversely affect myocardial contractility.

The effect of heart rate on mechanical dyssynchrony is currently unknown. Consistent with previous studies, we have demonstrated that the force-frequency relation was lost in patients with HF, while it was preserved in control subjects [15-18]. In the present study, we clearly showed that LV mechanical dyssynchrony was augmented as heart rate increased in patients with HF and normal QRS duration. The heart rate dependent dyssynchrony may be in part contributing to the impaired force-frequency relation in the whole heart. In a recent study, Vollmann et al. [28] evaluated the force-frequency relationship in 22 patients with HF during biventricular, LV, and right ventricular pacing. Results showed that increasing heart rates enhanced cardiac contractility during biventricular pacing, whereas this effect was absent during single-site LV or right ventricular stimulation, suggesting that LV dyssynchrony can be an important modulator of the force-frequency relationship in selected HF patients.

The precise mechanism of increased LV mechanical dyssynchrony with increased heart rate is unclear, it may be related to altered sarcoplasmic reticulum Ca handling or delayed mechanical restitution due to inadequate time for recovery of the Ca release channel [18]. Non-homogenous distribution of deposited extracellular matrix, myocyte loss, and pathological hypertrophy or other ultrastructual changes within the myocytes secondary to cardiac disease may be attributable to the increased mechanical dyssynchrony. Previous studies have demonstrated that sodium-nitroprusside, nitroglycerin, cardiomyoplasty and partial left ventriculectomy improve segmental synchrony, probably by reducing myocardial afterload stress and wall stress [21,27,29,30].


   5. Limitations
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
References
 
Optimally, the conductance catheter is placed in a straight position from the aortic valve to the LV apex using angiography. The distance from the pigtail to the first measurement electrode is ~2 cm. Therefore volume changes in the most apical part of the LV are not measured. If this region is highly dyssynchronous, as might be the case in patients with apical infarcts, underestimation of dyssynchrony by this methodology might be expected.

We cannot ignore the differences in patient characteristics at baseline which could affect the degree of LV dyssynchrony. Plasma BNP levels were significantly higher and ejection fraction lower in HF patients with CLBBB than those with a normal QRS duration, suggesting that LV remodelling was more progressive in patients with CLBBB. The degree of LV dyssynchrony before atrial pacing in HF patients with normal QRS duration might be worse as LV remodelling was progressive.

With the exception of diuretics, all medications including beta-blockers were withheld for at least 48 h before cardiac catheterization to minimize the effects of these medications on AV conduction, despite this we cannot rule out the possible effects of these medications on LV dyssynchrony.

Finally, the effect of atrial pacing on A-V conduction could affect LV dyssynchrony. In the present study, A-V conduction estimated by PR interval was prolonged in all patients, which might affect atrio-ventricular synchrony, diastolic filling time, and LV filling pattern, although there were no significant differences in PR interval between the 3 groups.

In conclusion, our data show that LV dyssynchrony was augmented as heart rate was increased by right atrial pacing in patients with HF and normal QRS duration. This finding suggests that we should consider the effect of heart rate during the evaluation of LV dyssynchrony, and that dyssynchrony dependent on heart rate may contribute to the impairment of the force-frequency relation in the clinical setting.


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

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