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In two decades the invention of transvenous left ventricular (LV) pacing integrated to a conventional pacemaker (cardiac resynchronization pacemaker, CRT-P) or an implantable cardioverter-defibrillator (CRT-D) has offered an effective therapy for patients with mild to severe heart failure (HF). Cardiac resynchronization therapy (CRT) typically involves simultaneous or sequential stimulation of both the ventricles to improve electrical and mechanical dyssynchrony, enhance pump performance, reduce functional mitral regurgitation, halt or reverse adverse ventricular remodeling, and reduce HF symptoms, HF readmission, and mortality. This chapter will focus on appropriate and optimal CRT programming and programming troubleshooting.
Right atrial (RA) pacing is associated with worsening of ventricular dyssynchrony and myocardial performance. RA pacing is associated with left atrial conduction delay, subsequently reducing the LV filling pressures. Often there is additional compensation of atrioventricular (AV) delays (prolongation) with right atrial pacing leads and a loss of LV synchronization due to the predominant contribution of right ventricular pacing wave front to global activation. However, heart failure patients are frequently on medications that can blunt their sinus node function, and RA pacing is often necessary to improve chronotropic compentency and to restore AV synchrony.
CRT requires pacing stimulation in one or both ventricles to improve myocardial pump performance. Programming shorter AV delays results in trunction of LV filling, thereby worsening AV valve regurgitation and worsening of pump function. Although there are no ideal universal AV delays, programming extremly short AV delays (<80 msec) or long AV delays (>200 msec) can result in loss of benefit from CRT. Particular attention must be paid to rate-adaptive AV delays to avoid LV filling truncation or inadequate contribution of LV pacing to global activation. Acute hemodynamic studies suggest improvement in LV performance occurs with V-V interval optimization when there is fusion from LV pacing and native RV conduction. However, long-term benefit of optimization has not been proven.
Most LV pacing leads are passive leads. Macro lead dislogement or chronic change in pacing thresholds above the programmed output can lead to loss of CRT. Assessing LV capture on electrocardiogram (ECG) is critical to ensure adequate response. Evoked response-based autothresholds can automatically increase outputs to ensure adequate CRT. Multielectrode stimulation with extended vectors provide several options to deal with elevated pacing thresholds after device implant.
Intrinsic conduction above the maximum tracking rate leads to loss of CRT and hemodynamic detioration. The upper tracking rate should be programmed to 75% to 85% of predicted maximal heart rate. Interactions with mode switch rates, sensor-related rates, and therapy zones for arrhythmias should be taken into consideration when programming the maximum tracking rates. Often mode switch rate is also increased to a higher rate to maintain ventricular pacing.
Functional undersensing of atrial activity leads to loss of tracking and ineffective CRT. Postventricular atrial refractory period (PVARP) should be shortened and algorithms that promote PVARP extension after a premature ventricular contraction (PVC) should be turned off in patients without any retrograde conduction. For patients with intact retrograde conduction, PVARP should be programmed slightly longer than the ventriculoatrial (VA) interval measured during ventricular threshold testing. PVARP shortening should be programmed taking into consideration the VA interval at faster and slower rates. Algorithms that promote PVARP extension (pacemaker-mediated tachycardia [PMT] termination) should be turned off.
Frequent atrial and ventricular arrhythmias are the cause of nonresponse to CRT. Tracking reduced percentage of biventricular (BiV) pacing associated arrhythmias, such as atrial fibrillation, may explain the reasons for nonrespone to CRT. Rhythm control with antiarrhythmic drugs, ablation procedures, and AV junctional ablation in patients with rapid ventricular response are frequently needed to deliver effective CRT. Triggered pacing and algorithms to smooth ventricular response should be turned on to facilitate CRT delivery.
Algorithms that recognize loss of ventricular sensing and promote CRT by shortening the AV interval (negative AV hysteresis) or PVARP (atrial tracking) should be turned on. In additon, careful recording and evaluation of faster sensed events will help the operator determine causes of inadequate CRT.
Extended vectors for LV pacing can lead to anodal capture. Increased charge density at an electode away from the LV results in anodal capture. Anodal capture is a frequently unrecognized cause of effectice CRT. Electrocardiography should be performed to confirm biventricular capture when extended vectors are used for CRT delivery.
Phrenic nerve stimulation occurs in about 15% of tbe patients with CRT and can limit BiV pacing. Electronic changing of pacing vectors, use of multielectrode LV leads with extended pacing vectors, and programming LV output to 1.5 times the pacing threshold, when adequate LV margin without phrenic capture is an issue, are several ways of effectively deliving CRT, at the same time minimizing phrenic nerve stimulation.
Several methods of optimization for CRT currently exist. Although prospective echo-based parameters are not predictive of CRT response, individual responses may vary. Device-specific algorithms to optimize AV-VV interals exist and in prospective randomized trials the benefit is modest. However, some nonresponders may respond favorably to these optimzation techniques.
Several manufacturers have specific features to improve clinical outcomes with CRT. The general theme to promote BiV pacing is similar to the concepts that are already outlined. Understanding device-specific features is crucial in programming and troubleshooting CRT devices.
The following features are available in Medtronic (Minneapolis, MN) CRT devices to promote the benefits of CRT.
Although CRT was approved 10 years ago, nonresponder rates up to 30% remain a major issue in clinical practice. The most common reason for CRT nonresponse is suboptimal AV delays. Various clinical trials looked at improvement in echo parameters (ejection fraction [EF], LV volumes), clinical parameters (6-minute walk test, NYHA functional status, quality of life, and peak VO 2 consumption), and heart failure outcomes (mortality, time to transplant, and heart failure hospitalizations as end points to assess CRT response). More recently, clinical composite scores (CCS) are frequently used to assess CRT response.
Several acute hemodynamic studies suggested that synchronized LV pacing resulting in QRS fusion leads to great improvements in left ventricular performance. Clinical trials suggested that LV-only pacing was not inferior to BiV pacing; some nonresponders to BiV pacing did favorably well with LV-only pacing.
An adaptive CRT algorithm was developed to automate AV and interventricular (VV) delays to promote synchronized LV pacing and prevent deleterious right ventricular pacing in appropriate patients. The algorithm is operational in the following three modes ( Fig. 39-1 ):
Adaptive BiV and LV. This is the preferred mode in patients with intrinsic 1 : 1 conduction and a PR interval less than 200 msec. AV delays and VV delays are determined by the algorithm, and dynamic adjustments are made.
Adaptive BiV. This is the preferred mode in patients with underlying AV block. AV and VV delays are optimized by the algorithm. Synchronized LV pacing is not applicable due to AV block.
Nonadaptive CRT. This is the preferred mode in patients with permanent atrial fibrillation (AF). AV and VV interval optimization is not performed.
Synchronized LV pacing is operational when the patient has a regular rhythm with rates less than 100 beats per minute (bpm) with a short AV intrinsic conduction. The details of the algorithm are shown below ( Fig. 39-2 ). The AV interval is extended once every minute to look for the intrinsic AV interval ( Fig. 39-3 ). The following intervals/events are determined:
AV Conduction Interval. The timing between the atrial electrogram and right ventricular (RV) electrogram.
End of P Wave. The timing from the atrial electrogram to end of P wave on a far-field channel (Can-SVC coil/Can to A ring electrode).
RV Timing with Reference to QRS Duration. The timing of the RV electrogram to the end of the QRS duration on a far-field (Can to RV coil) channel. This interval is longer in patients with right ventricular delay and shorter with normal intrinsic right ventricular conduction.
When the conditions for synchronized LV pacing are met, LV pacing is delivered to preempt native conduction by 40 msec ( Fig. 39-4 ). The algorithm converts to BiV pacing when conditions are no longer met.
The AV delay is determined after considering the end of P wave (20 msec after P wave) and to preempt the intrinsic RV conduction by 50 msec. VV interval is determined by a combination of AV interval and the RV-QRS duration interval. The algorithm considers RV sense to end of the QRS as a surrogate of QRS width. Shorter intervals mean better RV conduction and are associated with preemptive LV pacing, as shown in Figure 39-5 .
Use of this algorithm has shown that dynamic ambulatory adjustments of AV and VV delays are safe and the adaptive LV pacing is not inferior to traditional echo-optimized BiV pacing. Substudies analysis suggested that patients who had synchronized LV pacing >50% had better clinical composite scores, fewer HF hospitalizations, and lower AF prevalence and mortality when compared with patients who had synchronized LV pacing <50%.
Attain Performa is a quadripolar LV pacing lead with steroid elution on all four electrodes. Use of narrow spacing between electrodes two and three can reduce the incidence of phrenic nerve stimulation. The lead comes with an IS4 header, which is coated with a yellow color to differentiate from a DF4 connector pin. Using Vector Express, the threshold can be determined for all the 16 possible vectors. Impedance, along with the pacing threshold, is taken into consideration for selecting a better vector ( Fig. 39-6 ).
Triggered LV or BiV pacing is a programmable option. The ventricular sense response (VSR) rate can be programmed to a higher value than the maximum track rate. When dual-chamber pacing mode is enabled, VSR response initiated triggered pacing when PVC was sensed in the AV interval. Safety pacing overrides the VSR response in the safety pacing window, while VSR is active during the remainder of the AV interval. In nontracking modes, triggered ventricular pacing is available as long as it does not violate the maximum VSR rate ( Fig. 39-7 ).
Increase in ventricular pacing rate during an episode of atrial tachyarrhythmia, in response to the patient's intrinsic rate can promote CRT delivery. Beat-to-beat rate adjustments are made according to the algorithm. The response level and rates can be programmed based on ventricular rates during an atrial arrhythmia episode on a histogram. Figure 39-8 shows the operating algorithm of conducted AF response and its effect on ventricular pacing rate.
This algorithm is operational when the atrial rates are below the maximum tracking and mode switch rates. PVCs can lead to atrial events falling in refractory periods and loss of atrial tracing and CRT delivery. When events are sensed in the PVARP period with conduction to the ventricle, PVARP is shortened by 50 msec to promote CRT delivery ( Fig. 39-9 ). The AV interval is extended so the upper tracking rate is not violated.
Prolonged episodes of ventricular sensing with loss of CRT delivery can result in exacerbation of heart failure symptoms. The number of sensed beats to log an episode and the number of paced beats to terminate an episode are programmable parameters. Understanding these episodes can result in programming changes to promote CRT. VSR and VSP (safety pacing) are considered as sensed events even though triggered pacing is often delivered. Figure 39-10 shows a ventricular sensed episode logged by the device showing loss of CRT at rates above the upper tracking rates. Increasing upper tracking rate will effectively improve CRT delivery.
The following features are available through St. Jude Medical (SJM; St. Paul, MN)) devices to promote effective CRT delivery:
The algorithm has two particular components AV delay and VV delay optimization as follows:
AV Delays. Sensed and paced AV delays are determined after eight consecutive sensed and paced intervals. P wave duration measurement on electrograms provides an indirect measure of timing for total atrial activation. The total atrial activation in turn provides an estimate of mitral valve closure. An offset interval of 30 to 60 msec is added to the electrogram duration (30 ms if duration is >100 ms, 60 msec if duration is <100 msec) to account for electro-mechanical delay. This constitutes the optimal sensed AV delay. Optimal paced AV delay is calculated by sensed AV delay with addition of pacing related latency (often 50 msec).
VV Delays. There are three steps involved in calculation of optimal VV delays. During sensed beats, the peak of the R wave correlates with the onset of isovolumic contraction. The delta interval is calculated by measuring the time difference between intrinsic deflections on LV and RV leads (Δ = R LV − R RV ) ( Fig. 39-11A ).
Figure 39-11B shows that the delta interval is the temporal difference of intrinsic deflections sensed on RV and LV leads. Paced interventricular delay is assessed during pacing from both chambers and assessing the delay to the alternate chamber. The difference between the two values is termed as ε. (ε = pIVCD LR − pIVCD RL ) ( Figs. 39-11C and D ). The optimal VV interval is calculated by averaging the sensed and paced interventricular delays as VV = 0.5 (Δ + ε). If the optimal VV delay greater than 0 msec, LV is paced first, and if the optimal VV delay less than 0 msec, RV is paced first to ensure synchronization of wavefronts in the septum.
Quartet multipolar pacing lead offers increasing number of options for choosing a suitable LV pacing vector. All four electrodes can act as a cathode and two as an anode, providing up to 10 possible unipolar and bipolar pacing configurations. Steroid elution is available only on the lead tip electrode ( Fig. 39-12 ). VectSelect Quartet provides the interface for testing pacing thresholds and the propensity for phrenic nerve capture across all vectors. Once the appropriate vector is selected, outputs can be programmed manually or by autocapture algorithm ( Fig. 39-13 ).
This tool/algorithm helps in prioritizing pacing vectors to understand the site of latest activation near the four electrodes on the quartet lead. During sensed or ventricular beats, interventricular conduction delay is calculated as described in the QuickOpt algorithm ( Fig. 39-14 ). The default vector during multivector capture testing is the vector that involves the longest VV delay.
Trigger pacing to promote CRT during sensed ventricular events can programmed up to 150 bpm. The maximum programmable triggered pacing rate should be 30 msec longer than the ventricular tachycardia (VT) detection interval.
This particular feature shortens AV delay to promote forced ventricular pacing ( Fig. 39-15 ). There is a built-in lockout feature between use of the negative AV/PV hysteresis algorithm and others to minimize ventricular pacing (Ventricular Intrinsic Preference). The shortest AV delay is programmable in the algorithm (−10 msec to −120 msec, delta −10 msec). The algorithm is activated when an R wave is sensed in AV interval. Then the AV interval is shortened by programmed delta value (−10 msec) for 32 cycles. If another R wave is sensed during the AV interval, the device will shorten by another delta value for 256 cycles.
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