Cardiac resynchronization therapy: haemodynamic background and perspectives
1 Department of Cardiology, Heart Center Brandenburg in Bernau/Berlin, Ladeburger Str. 17, 16321 Bernau b. Berlin, Germany
2 Department of Cardiology, Heart Center Leipzig, Germany
* Corresponding author. Tel: +49 3338 69 46 10; fax: +49 3338 69 46 44. E-mail address: c.butter{at}immanuel.de
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Abstract |
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Cardiac resynchronization therapy (CRT) has become an accepted routine therapy for a subgroup of heart failure patients. Haemodynamic evaluations have yielded data that are essential to our current understanding of the mechanisms of CRT and nearly every step of CRT innovation has been introduced following studies employing relatively complex, invasive haemodynamic measurement techniques, such as conductance catheters for constructing pressure–volume loops and sensor tipped pressure wires in the left ventricle. These studies have been valuable in demonstrating the importance of selecting optimal pacing site and to understand the interactions between right and left ventricles, including the optimal timing for stimulation. The invasive measurements were the only investigations which showed that CRT decreased oxygen consumption and improved work efficacy without additional oxygen demand as seen with catecholamines. The acute haemodynamic effects also appear to be chronically maintained. Even if the invasive haemodynamic evaluations are time-consuming and not always applicable in routine clinical practice, their use should be considered in patients with new or borderline CRT indications to avoid deleterious effects by suboptimal lead placement or programming.
Key Words: Cardiac resynchronization therapy • Haemodynamics • Heart failure
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Introduction |
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TopAbstractIntroductionAsynchrony, haemodynamics, and...Optimized pacing site and...Simultaneous or sequential...Concerns with cardiac...Final considerationsAcknowledgementReferences |
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Cardiac resynchronization therapy (CRT) has become an accepted therapy for a subgroup of heart failure patients with systolic left ventricular (LV) dysfunction. Current understanding of the underlying mechanisms of action and most technological advances have been based on acute invasive haemodynamic measurements. Nearly every step of CRT innovation has been introduced following studies employing relatively complex, invasive haemodynamic measurement techniques, by means of conductance catheters for recording pressure–volume loops or sensor-tipped pressure wires in the left ventricle. Compared with the widespread application of CRT therapy, these studies have involved only a small number of patients. Within the past decade, beginning from the understanding of mechanical asynchrony and of the optimal LV pacing site up to the development of programming features for atrioventricular (AV) and interventricular intervals optimization, less than 600 patients have participated in trials. Because of their invasive nature, trials typically included few patients, but are nonetheless considered to be landmark because they provide very specific and valuable information. However, the general applicability of the findings from small numbers of highly selected patients to a broad population of patients now receiving CRT has not been addressed.
Accordingly, this paper will focus on the role of haemodynamic studies in the development of CRT and the potential critical issues raised by these data.
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Asynchrony, haemodynamics, and patient selection |
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TopAbstractIntroductionAsynchrony, haemodynamics, and...Optimized pacing site and...Simultaneous or sequential...Concerns with cardiac...Final considerationsAcknowledgementReferences |
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Intraventricular conduction delay (IVCD), particularly left bundle branch block (LBBB), is relatively common in dilated cardiomyopathies, being observed in 20–40% of patients. The presence of LBBB is associated with a poor prognosis. IVCDs result in loss of coordinated ventricular activation, which, in turn, results in uncoordinated myocardial contraction and depressed systolic pump function. Mechanical inefficiency occurs for several reasons. First, the early activated portion contracts at low chamber pressure, whereas the opposing non-contracting wall remains distensible, wasting work as the shortening of one region is largely converted into pre-stretch of another. Secondly, the late-activated region elicits contraction at higher wall stress because the early-activated part is already showing systolic stiffening. Lastly, the late activated segment can stretch the early activated region as the latter begins to relax, again wasting energy. The resulting internal transfer of work from one part of the heart to another reduces chamber efficiency.1
More than 20 years ago Burkhoff et al.2 performed pacing studies in isolated canine hearts investigating the influence of pacing site on LV systolic performance. They observed a significant influence of pacing site on the magnitude, but not on the time course of isovolumic ventricular pressure waves. Interestingly, it was already demonstrated that pacing from different sites of the ventricle resulted in different chamber contractile strengths. There was a linear inverse relationship between changes in QRS duration and changes in contractile strength. This information became relevant during the initial investigations into CRT and in the patient selection process 10 years later, when clinicians sought to reverse electrical and mechanical dyssynchrony in heart failure patients by pacing.
In an animal model with artificial LBBB, Leclercq et al.3 demonstrated that LV pacing increased electrical dispersion over that observed with LBBB or biventricular (BiV) pacing, despite improving mechanical function and coordination. Their results support clinical data showing no correlation between change in QRS duration and mechanical response to LV or BiV pacing. The underlying mechanisms of this dissociation between electrical and mechanical properties are not completely understood. Interestingly, mechanical dyssynchrony rather than electrical dispersion seems to be the most relevant aspect when mechanical LV efficiency is concerned.
This interpretation was not supported by other animal studies with artificial LBBB which found a significant difference in electrical asynchrony between short and intermediate AV delays.4,5 Whether these animal data can be easily transferred to patients with substantial structural heart disease with scarred areas, areas with hypertrophy, and intraventricular conduction disturbances is also not fully understood.
Nevertheless, the general approach to identifying pacing candidates has been QRS prolongation on the surface ECG. Recent studies have reported a weak but significant positive correlation between basal QRS width and systolic response to pacing.6 This conclusion has been obtained by comparing the outcomes of patients with narrow and wide QRS complexes. Nelson et al.7 demonstrated that QRS duration also correlates inversely with basal contractile function, as reflected by the maximal rate of pressure rise (dP/dtmax) suggesting that this may provide another predictor of response to CRT. QRS duration and dP/dtmax are indirect markers of the presumed primary abnormality, mechanical dyssynchrony, so direct measures of dyssynchrony might better predict benefit from CRT.
Invasive measurement of global LV contractility is not currently part of routine patient selection. The majority of patients with a wide QRS have mechanical dyssynchrony. Most centres focus on measures of intraventricular asynchrony by echocardiography in narrow QRS patients. Whether LV contractility (dP/dt) determined by Doppler assessment of mitral regurgitating flow adds important clinical information is presently unknown.
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Optimized pacing site and extent of haemodynamic response |
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TopAbstractIntroductionAsynchrony, haemodynamics, and...Optimized pacing site and...Simultaneous or sequential...Concerns with cardiac...Final considerationsAcknowledgementReferences |
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Right ventricular vs. left ventricular pacing
Conventional right ventricular (RV) pacing was reported as beneficial in a small study of congestive heart failure patients; this observation was not confirmed in the following years. In contrast, other reports raised significant concerns about RV pacing. Attempts to optimize the RV pacing site showed no convincing improvement of LV function in patients with both narrow and wide QRS-complexes. These conflicting results should be interpreted in the light of underlying AV dyssynchrony and of AV-delay programming. As a general rule, improvement in LV function occurred when the AV-delay was optimized, independently of RV pacing site.
Initial invasive investigations mainly involved pulmonary capillary wedge and systemic arterial pressure changes during pacing. Later, tip pressure and conductance catheters were used to measure left and RV pressures, offering the opportunity to create pressure–volume loops. Recent investigations used a 0.0014 in. tip pressure wire, which was placed and stabilized by a guiding catheter in the left ventricle. The changes in pulse pressure (PP) (a surrogate of stroke volume) and the change in LV +dP/dtmax (index of global LV contractility) have been used for comparison of different pacing sites and modes.
Using a fixed AVD of 100 ms, Blanc et al.8 observed no significant impact on PCW or arterial pressure with RV apical or with outflow tract pacing.
Similar observations were made by Varma et al.9 They took the same fixed AVD for both ventricles and different pacing sites within the RV. Due to the study design it is not surprising that pacing at RVApex and RVOutflowTract did not significantly increase global LV contractility and was not significantly better than LV or BiV pacing.
Also Kass et al.10 could not demonstrate a significant improvement in LV +dP/dtmax with RV apical or septal pacing in patients without typical pacemaker indication despite programing the AVD at 3–4 different values. By carefully optimizing the RV site and AVD, the deleterious effects on LV function may be at best reduced. Unfavourable effects of RV stimulation were also observed in patients with near normal LV function.11 Applying RV stimulation at two sites is also not better than single-site pacing in patients with advanced AV block or post-AV junctional ablation requiring permanent RV stimulation.12 When combined with LV pacing, the RV stimulation site seems to be of minor importance. The high septum provides no overall advantage as an alternative pacing site in BiV stimulation compared with apical stimulation. Thus, a change in the typical CRT implantation technique cannot be recommended at the moment.13
In summary, no LV function benefit in congestive heart failure can be expected by RV stimulation at any site.
In contrast, several studies have shown using invasive measurements that LV or BiV stimulation can improve haemodynamic parameters in patients with CHF and ventricular conduction delay.1,8–10,14,15 The extent of PP and LV +dP/dtmax increase is comparable in both modes and depends on AVD optimization especially for the LV only mode. Furthermore, the extent of baseline mechanical asynchrony, which is not adequately reflected by QRS widening, predicts the effect of CRT. Achieving the maximum improvement in LV function with LV only stimulation requires both intrinsic conduction via the AV node and dedicated programming of the AVD,10,14,16 which is crucial and limits its application to selected patients.
Table 1 summarizes the effects of LV and BiV stimulation on LV +dP/dtmax and PP in studies regardless of their different study designs.
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Overall an increase in LV +dP/dtmax of more than 20% on average can be achieved with simultaneous BiV pacing. A comparable effect can be obtained by pacing the free wall of the left ventricle alone. PP can be increased by
12–13% with both pacing modes. Whether to prefer BiV stimulation over LV stimulation for daily activity is under discussion. An early study17 demonstrated that BiV pacing is better for modulation of heart rate and systolic function as it results in increased contractility and decreased LV end-diastolic pressure. This effect seems independent of AV dyssynchrony, being observed also in atrial fibrillation.
Anterior vs. free-wall pacing of the left ventricle
Owing to the fact that the latest myocardial activation in CHF patients with left bundle branch block occurs in the postero-lateral region (also called LV free wall) it has been suggested that stimulation in that region might achieve the greatest benefit. Nevertheless, first attempts at CRT either by epicardial lead placement via mini thoracotomy or by transvenous access ended up in non-optimal positions. Epicardial LV leads placed by thoracotomy were most commonly found at the apex,14 but also sometimes on midlateral segments. Up to 30% of chronic implanted transvenous LV leads in MUSTIC and MIRACLE trials were placed anteriorly due to suboptimal early coronary sinus leads and delivery tools.
Invasive investigations15,18 clearly demonstrated that the pacing site within the left ventricle is essential for optimal haemodynamic improvement.
Within individual patients, significant differences in the improvement in PP and LV +dP/dtmax were observed depending on the epicardial vein used for stimulation. When the LV lead was positioned in the anterior vein (which occurred in nearly one-third of the patients) short AVDs caused deterioration in LV performance. In other areas, an increase was achieved, but always less compared with LV free-wall stimulation. Overall, free-wall stimulation produces an improvement in global LV contractility and stroke volume, which is twice that of anterior wall stimulation, and is independent of univentricular or BiV application.
Thus, nowadays LV lead placement should always be achieved via the coronary sinus system targeting tributaries on the free wall. Anterior placement should remain the exception, in the rare cases where targeting a free-wall pacing site is not feasible.
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Simultaneous or sequential pacing |
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TopAbstractIntroductionAsynchrony, haemodynamics, and...Optimized pacing site and...Simultaneous or sequential...Concerns with cardiac...Final considerationsAcknowledgementReferences |
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When initially introduced, CRT resynchronization was technically feasible just by splitting the RV channel using a Y-adaptor. These pioneering attempts at CRT did not allow delivery of a different magnitude of current to each ventricle, did not allow use of separate delays in activation, and caused sensing problems. During the following years it became obvious that simultaneous stimulation would not achieve total resynchronization in all patients. Several observations support this conclusion.
First, depending on the underlying heart disease, the dimensions of the left and right atria and their individual timing of contraction are unpredictable. It is important for optimal effectiveness that the timing between left atrial contraction and the diastolic LV filling be optimized, especially in severe heart failure patients. Secondly, in normal hearts, the activation of the two ventricles does not occur simultaneously, i.e. epicardial RV depolarization starts a few milliseconds earlier than LV depolarization. Thirdly, in CRT, the left ventricle is paced from the epicardial surface, which could account for a delay in the transmission of the stimulus that needs to reach the subendocardial conduction system before spreading to the remaining ventricle. Fourthly, in advanced cardiomyopathy, the RV to LV interactions can be different from those in normal hearts. As a consequence, the best mechanical efficiency may be achieved with different patterns of ventricular activation. Fifthly, the baseline ventricular conduction defect differs considerably from case to case; in patients with a QRS duration >150 ms, the conduction delay is possibly due not only to isolated bundle branch block, but also to a generalized anisotropic disturbance of the conduction system and/or myocardial scars. Sixthly, the ventricular catheters (particularly LV leads) are placed in quite different anatomical positions depending on the operator's choice and the constraints of the coronary sinus anatomy leading to ventricular activation patterns during pacing that differ from patient to patient. Lastly, different lead polarities with the opportunity for anodic or cathodic pacing might play a role in activation patterns (Figure 1).19
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These considerations motivated manufacturers to develop devices that allow different settings for RV and LV pacing. Programmability of different AV-delays and V–V delays yielded a very large number of potential programming options, which did not ease the implant procedure or follow-ups. As a result of the non-uniformity of nomenclature between companies, which is confusing for a majority of cardiologists performing device follow-up, the acceptance of these multiple time-consuming programming options has been rather low. Since their introduction, only a few studies have investigated the invasive haemodynamic responses to sequential AV and V–V delay programming compared with a simultaneous stimulation mode. Hay et al.,12 Lee et al.,16 Perego et al.,19 van Gelder et al.,20,21 and Kurzidim et al.22 found that LV +dP/dtmax increased by 0.5–8% with sequential ventricular pacing compared with simultaneous stimulation (Table 2). Interestingly, a wide range of effects between simultaneous and sequential pacing was observed. In one study, only 11% of the patients had significant benefit from early LV activation,20 while in another study 75% of patients improved more by early LV activation than by simultaneous pacing19 (Figure 2).
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In our own study performed in Bernau and Berlin, we first optimized the AV delay according to PP and LV +dP/dtmax and then alternatively stimulated the LV first and the RV first in 20 ms steps. In contrast to the aforementioned studies, we used a fluid-filled system for PP and LV +dP/dtmax measurements. This method allows detection of the relative changes observed in the different pacing modes compared with baseline intrinsic conduction, accepting the physical errors associated with this simple but readily applicable system. In less than 50% of patients (23/49), we found sequential pacing to be superior to simultaneous pacing (Figure 2A), the majority of these improving more by LV stimulation first. When we compared the invasively detectable effects using either PP or LV +dP/dtmax, PP seemed to be the more stable and reproducible parameter (Figure 2B). Thus, we recommend using this invasive parameter for optimizing AV and RV–LV timing.
In conclusion, optimization of the AV delay and RV–LV pacing timing is a laborious process. Comparison of non-invasive parameters using EGM or finger plethysmography have shown good correlation with invasive measurements.23,24 Owing to the individual variations in conduction, electro-mechanical coupling, underlying heart disease and lead placement, no general formula for LV timing can be recommended, but in the majority of patients, LV activation first yields better acute haemodynamic effects. Even though van Gelder20 stated that sequential pacing has never been worse than intrinsic conduction, it cannot be concluded that it is always better than simultaneous stimulation.
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Concerns with cardiac resynchronization therapy: deterioration of right ventricular function? |
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TopAbstractIntroductionAsynchrony, haemodynamics, and...Optimized pacing site and...Simultaneous or sequential...Concerns with cardiac...Final considerationsAcknowledgementReferences |
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Not much attention has been paid to the change in RV function in the past. The majority of all previous investigations focused on LV function as the sole target to improve patient outcome. However, according to the improved survival of CRT patients, we are confronted more and more with patients suffering from progressive and untreatable right heart failure. Within the overall heart failure cohort, nearly two-thirds suffer from coronary heart disease, in which RV dysfunction is seen less frequently than in patients with idiopathic or postmyocarditic dilated cardiomyopathies. Evaluating RV dysfunction prior to CRT as well during follow-up is difficult. The geometry of the right ventricle does not allow exact measurement of the ejection fraction by echocardiography or angiography. Invasive parameters like RV +dP/dtmax and RV –dP/dtmin strongly depend on pre- and afterload, which are of limited value for long term observations. Nevertheless, in some studies, data concerning RV function have been reported.
Auricchio et al.14 observed almost no change in RV +dP/dtmax with RV and LV pacing in an open chest setting with epicardial leads. A slight increase in the same parameter was seen with simultaneous BiV pacing, but the average changes in RV systolic parameters were also relatively small and inconsistent.
Despite the observation that in a few patients RV +dP/dtmax decreased when LV +dP/dtmax was optimized using different AVDs for both ventricles Perego et al.19 found no deterioration in RV pressure on average. Moreover, changes in LV dP/dtmax and RV dP/dtmax were not correlated in individual patients. Thus they concluded that LV-based optimization of AV and VV delays are not associated with worsening of RV dP/dtmax.
A recent study by Lee et al.16 supported concerns about RV function with BiV stimulation. They used conductance catheters in both ventricles and varied the degree of early stimulation of the LV. As in other studies, they also found that LV pacing produces systemic haemodynamic improvements similar to BiV pacing. The effect strongly depends on the critical timing between intrinsic RV conduction and LV pacing. They concluded that their study is the first to demonstrate that BiV pacing can adversely affect RV haemodynamics while LV pacing maintains or improves existing RV function.
In conclusion, the effects of CRT on RV function seem not to be negligible especially in patients already having evidence of pre-existing RV failure. Avoidance of RV stimulation might be beneficial in the long-term in these patients.25 Dedicated programming of different AVDs for RV and LV should be performed with the intention of creating fusion of intrinsic RV conduction and LV pacing. Whether this time consuming procedure is also relevant in patients with maintained RV function is unknown at the moment.
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Final considerations |
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TopAbstractIntroductionAsynchrony, haemodynamics, and...Optimized pacing site and...Simultaneous or sequential...Concerns with cardiac...Final considerationsAcknowledgementReferences |
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Haemodynamic evaluation has yielded information that is essential to our current understanding of the mechanisms of CRT. The data have been valuable in demonstrating the importance of selecting optimal pacing site and to understand the interactions between RV and LV, including the optimal timings for BiV stimulation.
Thanks to invasive measurements, it was demonstrated that CRT decreases oxygen consumption and improves work efficacy without additional oxygen demand as opposed to the effect of catecholamines. The acute haemodynamic effects also appear to be maintained chronically.26 Even if the invasive haemodynamic evaluations are time-consuming and not always applicable in routine clinical practice, their use should be considered in patients with new or borderline CRT indications to avoid deleterious effects by suboptimal lead placement, and to optimize device programming.
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Acknowledgement |
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TopAbstractIntroductionAsynchrony, haemodynamics, and...Optimized pacing site and...Simultaneous or sequential...Concerns with cardiac...Final considerationsAcknowledgementReferences |
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The authors would like to thank Dan Burkhoff for his critical review of the manuscript.
Conflict of interest: none declared.
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References |
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TopAbstractIntroductionAsynchrony, haemodynamics, and...Optimized pacing site and...Simultaneous or sequential...Concerns with cardiac...Final considerationsAcknowledgementReferences |
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