Multisite stimulation for correction of cardiac asynchrony
- InParys Clinical Research Associates
- Saint-Cloud, Clinique Georges Bizet
- Institut Jacques Cartier, Paris, France
Cardiac electrical stimulation as primary or adjunctive treatment of congestive heart failure is entering its second decade of existence. Initial trials of conventional DDD pacing1-5 were followed by bifocal right ventricular stimulation.6 The concept of multisite stimulation for haemodynamic support was introduced in 1994.7 8 Various studies have already reported the benefits of this method,9 10 or are in progress.11
The transition from conventional DDD pacing to multisite stimulation was not fortuitous. Successive “advances” in the design of cardiac pacing systems have aimed at correcting anomalies in the sequence of cardiac chamber activation, as well as in the synchronisation of the various phases of myocardial contraction and relaxation. The phenomenon of asynchrony is a consequence of progressive, global or focal degradation of the myocardium. One can easily visualise interstitial fibrosis gradually replacing areas of normal myocardium, and causing heterogeneous propagation of cardiac electrical activity. Such heterogeneity combines, to various degrees, three consecutive atrioventricular, interventricular, and intraventricular asynchrony levels. Among various analytical and modelling methods, Doppler echocardiography is preferred for its ease of application in day to day practice.12
The oldest concept, that of desynchronised atrioventricular sequential activation, applies only to sinus rhythm. It is the product of a mismatch between end of atrial systole and onset of ventricular systole, sometimes facilitated by a disorder of atrioventricular conduction or QRS prolongation. It may be simply described as an abbreviated ventricular filling time with respect to the complete cardiac cycle, and, on occasion, by early passive ventricular filling flow superimposed on atrial systole dependent flow. Dual chamber pacing, by linking ventricular to atrial activation, normalises flow patterns of ventricular filling, provided atrial contraction is mechanically effective (fig 1). This principle guides the optimisation of the atrioventricular delay under Doppler echocardiographic guidance in dual chamber pacing. The end point consists of shortening the atrioventricular delay to a minimum without interrupting the end of the A wave by premature mitral valve closure (fig 2).
The concept of interventricular asynchrony
Atrioventricular resynchronisation alone has not been predictably effective in improving haemodynamics except in some patients with prolonged PR interval.2 Candidates for the implantation of a cardiac stimulator often present with intraventricular conduction disorders expressed as a widened QRS, an anomaly which may also be caused by the pacemaker itself. In the hope of minimising atrioventricular asynchrony, a delay is unfortunately imposed between right and left ventricular activation by stimulating the ventricle from the peripheral Purkinje network instead of preserving the normal sequence via the His bundle. This activation/contraction delay causes a delay in subsequent chamber relaxation, disturbing its filling (fig 3). As a result, the right-to-left electromechanical delay caused by typical pacing from the right ventricular apex may disrupt the synchrony of right and left ventricular systole. This spontaneous or iatrogenic asynchrony can be easily quantified by measuring the delay between the onset of ventricular electrical activation and the onsets of aortic and pulmonic ejection, respectively. The difference between these two intervals represents the interventricular mechanical delay (fig 4), and a shortening in both the pre-ejection delays and the interventricular delay appears to predict a benefit from multisite stimulation (fig5).12
The concept of intraventricular systolo-diastolic asynchrony
Finally, heterogeneity of intraventricular myocardial contraction may be so pronounced as to result, within the same ventricle, in the coincidence of territories in systolic phase, while others are already relaxing.13 A marker of such heterogeneity is the QRS width and, sometimes, its polyphasic morphology. Intraventricular asynchrony is unlikely in presence of spontaneous QRS complexes < 120 ms, and paced QRS complexes < 180 ms in duration, and may be greatly accentuated by stimulation confined to the right heart chambers. It is often present in ischaemic cardiomyopathy, where the propagation of ventricular activation wavefronts may be disrupted by the encounter of scarred or ischemic tissue. This abnormal process is characterised by the presence of myocardial segments contracting as ventricular filling has already begun. This, on time-movement echocardiographic examination (fig 6), appears as segmental wall thickening occurring after the onset of the next early diastolic filling phase. Simultaneous stimulation of left and right cardiac chambers is, currently, not capable of predictably correcting this abnormality. However, its successful elimination often decreases the severity of mitral regurgitation, an important contribution to clinical improvement in some patients.
Multisite stimulation for congestive heart failure is a recent therapeutic method, which will, hopefully, be validated in the year 2000. It should be reserved for patients whose abnormal ventricular function may be corrected or improved by palliating conduction disorders, in the hope of changing the sequence of mechanical events, enhancing contractile efficiency, and, in some cases, lessening the severity of ventriculo-atrial regurgitation9 by changing systolic left ventricular geometry. Other mechanisms have been proposed, which remain speculative. Although the cardiac mechanics related to multisite stimulation are only partially understood, echocardiography has emerged as a non-invasive and easily reproducible test of choice in the selection of candidates for this new treatment. The absence of preimplant visible asynchrony probably predicts little improvement by multisite stimulation, but this point needs confirmation. Conversely determination of the nature of the asynchrony should facilitate the choice of an optimal synchroniser configuration. Modification of the electromechanical intervals in the postoperative course should also provide useful information for assessing the success or the failure of cardiac resynchronisation.