18. Endocardial Left Ventricular Lead

Published on 02/03/2015 by admin

Filed under Cardiovascular

Last modified 22/04/2025

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History

The patient was a 65-year-old retired man seeking treatment for dilated cardiomyopathy with normal coronary arteries for about 10 years. Risk factors are dyslipidemia and obesity (91 kg, 173 cm). Two procedures of ablation for atrial fibrillation and atrial tachycardia were performed 6 and 2 years earlier. One year previously, a new episode of atrial fibrillation was treated with direct current shock and amiodarone. The patient is currently in sinus rhythm and remains in New York Heart Association (NYHA) class III under medical therapy. The patient has no pulmonary disease, and respiratory tests are normal.

Comments

This is a long history of heart failure in a patient being followed adequately and benefiting from currently available therapeutic techniques. The cardiomyopathy is considered idiopathic, and atrial arrhythmias are events that do not fully explain the current heart failure status of the patient.

Medications

The patient was taking bisoprolol 2.5 mg daily, ramipril 5 mg daily, rosuvastatin 20 mg daily, furosemide 40 mg daily, warfarin with international normalized ratio (INR) between 2 and 3, amiodarone 200 mg daily.

Comments

The patient could not tolerate the recommended dosages of beta blockers and angiotensin-converting enzyme (ACE) inhibitors because of symptomatic hypotension. The spironolactone that was given previously had to be stopped for occurrence of hyperkalemia. Thus medical treatment is not optimal, because patient ideally should require 10 mg daily each of bisoprolol and ramipril. The statin is given for the hypercholesterolemia. Amiodarone and warfarin are for rhythm control and prevention of thromboembolism, respectively. The furosemide dosage is sufficient for controlling the heart failure symptoms.

Current Symptoms

The patient is in NYHA class III, with predominant dyspnea on exertion, accompanied with palpitations, fatigue, and mild peripheral edema.

Comments

The patient never experienced symptoms of acute heart failure even during the occurrence of atrial tachyarrhythmias. Increasing the dosage of furosemide did not minimize symptoms.

Physical Examination

Comments

Although the patient had symptoms of heart failure, no objective sign can be observed except from sinus tachycardia and hypotension. This may occur in patients with chronic heart failure.
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FIGURE 18-1 Baseline electrocardiogram.

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FIGURE 18-2 The cardiothoracic ratio is over 50%. Some pulmonary overloading can be observed.

Laboratory Data

Electrocardiogram

Findings

The electrocardiogram (ECG) showed sinus rhythm 82 bpm, P duration 80 ms, P axis 40 degrees, PR interval 320 ms, QRS 120 ms, and QRS axis −30 degrees; QTc 489 ms (Figure 18-1).

Comments

The ECG showed first-degree atrioventricular block, and the QRS was not prolonged. QRS morphology could correspond to left anterior hemiblock, although left axis deviation is not that important. This ECG tracing does not fit a cardiac resynchronization therapy (CRT) indication.

Echocardiogram

Findings

The echocardiogram revealed left ventricular ejection fraction (LVEF) 25%; moderate left ventricular dilation, with end-diastolic volume 87 mL/m² and end systolic volume 65 mL/m²; global hypokinesia; left ventricular filling time less than 40% of the RR duration; left ventricular preejection time 160 ms; normal right ventricular function; dilation of the atria; no valvular abnormality; and increased filling pressures (Figure 18-2).
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FIGURE 18-3 In spontaneous rhythm, dP/dtmax is very low (481 mm Hg/sec) with a low left ventricular systolic pressure found at 88 mm Hg.

Comments

A discrepancy was seen between low LVEF and moderate left ventricular dilation, although the patient’s heart failure history is 10 years. The short left ventricular filling time is related to the prolonged PR interval. The prolonged preejection time may be related to left ventricular dyssynchrony. Increased filling pressure is compatible with the high BNP level.

Catheterization

A coronary angiogram was performed again (the first since 2006) to exclude coronary artery disease. The examination provides an opportunity to assess the coronary sinus network during venous-phase recording. This examination shows a huge distribution of very small and tortuous veins that predict major difficulties in case of a decision for a CRT implantation.
Analysis of the effects of atriobiventricular pacing with an endocardial left ventricular lead placed at different sites within the left ventricle is performed, and three temporary leads are introduced: one at the atrial appendage and one at the right ventricular apex via the right femoral vein and one left ventricular lead introduced via the right femoral artery from the groin. A radial approach was used for the coronary angiogram, to introduce a pressure wire to record left ventricular pressure, and to calculate left ventricular dP/dt. All pacing configurations are applied in the VDD mode, with the AVD set at 100 ms. Three left ventricular lead positions are tested in biventricular pacing: apical, anterolateral, and posterior. Each pacing is applied for 2 minutes before a 10-second recording to measure mean dP/dtmax and dP/dtmin. Between each pacing configuration, the baseline intrinsic rhythm is restored (Figures 18-3, 18-4, 18-5, and 18-6).
In conclusion, both dP/dtmax and dP/dtmin increase during biventricular pacing at all left ventricular sites in contrast to baseline spontaneous rhythm. However, the left ventricular pacing site does influence the result—when the left ventricular lead is placed at the left ventricular apex, the improvement in dP/dtmax is 7% (not significant), whereas it is 45% at the anterolateral left ventricular site, and 67% at the midposterior left ventricular site.

Comments

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FIGURE 18-4 During atriobiventricular pacing with the endocardial left ventricular lead placed at the apex, dP/dtmax rises to 517 mm Hg/sec, without change in the left ventricular systolic pressure, but the difference is not significant.

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FIGURE 18-5 During atriobiventricular pacing with the endocardial left ventricular lead placed at the anterior and lateral site, dP/dtmax rises significantly to 697 mm Hg/sec, with a slight increase in left ventricular systolic pressure.

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FIGURE 18-6 During atriobiventricular pacing with the left ventricular lead placed at the posterior site, left ventricular dP/dtmax rises further to 806 mm Hg and systolic pressure to 102 mm Hg. dP/dtmin is also higher than in the spontaneous condition, demonstrating faster left ventricular relaxation.

Implantation

Implantation of the atriobiventricular system is performed under general anesthesia. The atrial lead is placed at the right atrial appendage, the right ventricular lead (a single-coil implantable cardioversion defibrillator lead) at the apex (rather than at the right ventricular free wall close to the apex, as suggested by the postprocedure chest radiographic examination). The left ventricular lead is placed through a transseptal puncture, from the left subclavian vein, to the location designated by the temporary preoperative hemodynamic test, which provided the maximal dP/dtmax increase, that is, the posterior endocardial site. The lead being used was the Select Secure (Medtronic, Northridge, Calif.). This implantation is currently done in the context of the ALternate Site Cardiac ReSYNChronization (ALSYNC) feasibility trial, assessing the feasibility and safety of the left ventricular endocardial pacing through an atrial transseptal approach.

Postoperative Radiograph

The postoperative radiographic examination includes four views: anteroposterior, lateral, right anterior oblique, and left anterior oblique. It confirms that the location of the left ventricular lead is close to the site of pacing applied during the preoperative hemodynamic study. See Figure 18-7.

Postoperative Electrocardiogram

The recorded ECG under biventricular pacing shows right deviation of the QRS axis. QRS duration (~130 ms) does not really differ from the intrinsic QRS complex (120 ms). Atrioventricular delay is set at its nominal value (120 ms) and VV interval at 0 ms (Figure 18-8).
When left ventricular pacing alone is programmed, the ECG shows the classic QRS pattern of left posterior pacing with large QRS (160 ms) (Figure 18-9).
Electrical performance of the left ventricular lead is excellent—650 Ω impedance and 0.5-V pacing threshold at 0.4-ms pulse width.
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FIGURE 18-7 Postoperative chest radiographic examination showing the location of the three leads: atrial lead at the lateral wall of the right atrium, right ventricular lead at the right ventricular paraapical site, and left ventricular lead at the midposterior wall of the left ventricular endocardium. A, Anteroposterior view. B, Lateral view. C, right anterior oblique view. D, Left anterior oblique view.

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FIGURE 18-8 Postoperative electrogram recorded in DDD mode during atrio–left ventriciular pacing.

Electrical Activation Pattern

A new system (EcVUE, CardioInsight, Cleveland, Ohio) that noninvasively generates maps of the electrical activity of the heart, has been developed. A vest consisting of 252 electrodes is placed on the patient’s thorax. One beat is recorded, and an electrocardiographic map can be obtained that is plotted on a three-dimensional anatomic image of the patient’s heart obtained with computed tomography. This map allows analysis of the electrical activation of the atria and ventricles.
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FIGURE 18-9 Postoperative electrogram recorded in DDD mode during atrial left ventricular pacing.

Left ventricular pacing elicits variable electrical activation patterns affecting electrical synchrony. Electrocardiographic mapping produces noninvasive, biventricular electrical activation maps that can be acquired during different pacing configurations. The red color indicates the zone of primary activation, and the dark blue indicates the zone of latest activation. Isochrones delineate the zones of equal activation time. Narrowing of the zones indicates slower conduction. These activation maps can be used in the context of CRT to evaluate electrical synchrony—visual inspection of activation maps at baseline and during pacing, interventricular, and intraventricular quantitative assessments.
In this patient, the intrinsic QRS complex is measured by the system at 118 ms. Left lateral and posterior wall depolarization is delayed in contrast to right ventricular activation. The difference between mean right ventricular and mean left ventricular activations is −64 ms. The pattern of activation is similar to a left bundle branch block pattern. Note also that the midseptal activation cannot be observed.
During biventricular pacing, the activation pattern looks more homogeneous. The paced QRS duration is 126 ms. The posterior and inferior left ventricular wall remains slightly delayed. The difference between mean right ventricular and mean left ventricular activations is −20 ms (Figures 18-10, 18-11, and 18-12).
In conclusion, this technique helps in understanding the ventricular activation patterns according to the lead locations.

Outcomes

During the 3-month follow-up period, the medical treatment has not been changed, but the anticoagulant dosage was reduced. The patient is in NYHA class I, and fatigability is less frequent. He has no symptom of heart failure, and peripheral edema has disappeared. He lost 10 kg of weight. Blood pressure is 106/70 mm Hg.
Laboratory data showed an increase in creatinine level up to 164 mmol/L, with a potassium level of 5.1 mmol/L and urea 15 mmol/L. BNP is 405 pg/mL.
Echocardiographic data improved. The ejection fraction increased to 44%, left ventricular end-diastolic volume to 64 mL/m², and left ventricular end-systolic volume to 43 mL/m². LV preejection time is 120 ms. Right ventricular function is normal, and no mitral regurgitation was seen. Filling pressures are normal. The ECG pattern is the same as at hospital discharge. The left ventricular threshold is 0.5 V at 0.4 ms, and the left ventricular pacing impedance is 560 Ohm. Device memories are free from atrial or ventricular arrhythmias. The patient demonstrated 100% biventricular pacing.

Comments

The patient is a responder to CRT. His NYHA class improved by two grades, ejection fraction had increased, left ventricular end-systolic volume had decreased more than 15%. BNP was reduced, although not totally restored to normal.
Drug dosages were later increased (for beta blocker and ACE inhibitor) in the future as his BP has increased. Furosemide was withheld as filling pressures are normal while urea, creatinine, and potassium levels were increasing. These latter changes could be explained by dehydration. This phenomenon is not infrequent in responders to CRT. In this patient, the drug dosages, including diuretics, are not changed after implantation of the CRT device until the first follow-up visit. As cardiac function improves rapidly with evidence of left ventricular reverse remodeling, the need for diuretics diminishes rapidly, so they can be stopped earlier. The patient no longer reports dyspnea, although he has symptoms of fatigue.

Focused Clinical Questions and Discussion Points

Question

Was the patient recommended for CRT?
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FIGURE 18-10 A, Left anterior oblique view. The right ventricle activates first, and this activation is homogeneous. The left anterior wall is rapidly activated, whereas the lateral wall is much delayed. B, Posteroanterior view. The atrioventricular valves are on the right, and the left ventricular apex is on the left. This view demonstrates the delay in activation of the lateral and posterior wall. C, A posterior and inferior view of the left ventricle (atrioventricular valves on the right, apex on the left). This view confirms the late activation of the posterior wall. The inferior wall is less delayed and activation goes fast (D).

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Figure 18-11 The same views as in intrinsic rhythm and same time scale. During biventricular pacing, the activation pattern is quite altered. Depolarization clearly starts from the spots of lead locations—apical right ventricular and posterior left ventricular walls. As a result, the right ventricular free wall and anterior, posterior, and some inferior left ventricular walls appear to be electrically synchronized. The posterior and inferior left ventricular wall is slightly delayed, and basal segments are the most delayed, but the concerned region is small.

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FIGURE 18-12 The same views as in intrinsic rhythm and biventricular pacing and same time scale. During left ventricular pacing only, the activation pattern is totally reversed with primodepolarization at the lateral left ventricular wall. Two lines of block appear at the anterior wall facing the septum and at the posterior and lateral wall. As a consequence, right ventricular and inferior left ventricular walls are largely delayed. The difference between mean right ventricular and mean left ventricular activations is +110 ms.

Discussion

This patient has most of the criteria for an indication for a CRT device, except a borderline ECG criteria (i.e., QRS 120 msec and a non–left bundle branch block [LBBB] pattern). According to the latest ESC guideline, however, he is not a candidate for CRT.4
Initially, CRT has been proposed to patients with LBBB with QRS longer than 150 ms, to resynchronize a delayed activated left ventricle to the right ventricle, the gross concept being that systolic dyssynchrony is the primary reason for the further decline of cardiac function. Later, recommendations were extended to patients with shorter QRS complex, but still longer than 120 ms, and earlier clinical stages of heart failure. However, as a matter of fact, patients with non-LBBB ECG morphologies are not good responders to CRT. Today, the ESC recommendations rank patients with LBBB and QRS of 120 ms or greater as class IA candidates, whereas patients with non-LBBB morphology with QRS of 150 ms or greater are ranked class IIA candidates.4

Question

What were the reasons for indicating CRT in this patient?

Discussion

In some countries (including France), if a patient does not fit recommendations but objective arguments are found that indicate the patient may benefit from a given therapy, it will be allowed by the administration. This is the reason why a temporary hemodynamic assessment was performed to determine the possible acute benefit over intrinsic rhythm that could be measured during atriobiventricular pacing from endocardial sites, including the left ventricle (a previous coronary artery angiogram with venous return timing demonstrated the prediction of a difficult access to the veins of the coronary sinus network). In addition, the left ventricular endocardial approach provides much more flexibility for moving a catheter inside the left ventricular cavity, thus allowing determination of the optimal site of pacing. Previous studies showed that optimal pacing sites are individualized.2 The designated site can then be used again during the implantation procedure.
The dP/dtmax value is a hemodynamic reference parameter for assessing left ventricular function and has been used during the last decade for atrioventricular and VV-interval optimizations during acute CRT implantation and has been suggested as an option to guide the choice of pacing sites. In this patient, a huge difference was found between intrinsic rhythm condition and biventricular pacing with the left ventricular endocardial lead placed at the midposterior wall. Currently, the use of preoperative acute hemodynamic assessment to predict a good left ventricular reverse remodeling or clinical response to CRT remains controversial.3,6 From what we have observed in the current case, it is conceivable that more studies are needed for the role of using acute hemodynamic-guided placement of left ventricular leads for patients in whom the use of CRT may have less-than-expected benefits, such as those with a borderline QRS duration (e.g., 120 to 150 ms) or non-LBBB pattern of ECG.

Question

Why was this patient implanted with an endocardial left ventricular lead, a technique that is not currently recommended? Why was a surgical epicardial approach not preferred?

Discussion

The surgical epicardial approach is an accepted option in the case of failure or expected major difficulties of the coronary sinus approach. However, the acute hemodynamic evaluation before implantation was performed with an endocardial left ventricular lead, and it cannot be certain that similar effects of epicardial and endocardial pacing would be found at the same spot. Although the patient had no coronary artery disease or scar zone, local conduction disorders might arise, leading to inhomogeneity in the hemodynamic results between the two pacing modalities. The patient was already on anticoagulation therapy for paroxysmal atrial fibrillation, so acceptance of long-term anticoagulation was not an issue even at a higher dosage (with INR between 2.5 and 3.5).
However, this technique is currently under investigation and may have severe drawbacks.5,10 It requires an atrial transseptal puncture, which can be a tricky exercise when sheaths are coming from the upper part of the body. The lead is crossing the mitral valve, and long-term mitral leaflet movement disturbance might be an issue. Clotting must be cautiously prevented. In case of infection, vegetation embolism might occur, and the removal of the lead will probably be done in the cardiac surgical room. Currently, this technique is still investigational, and the ALSYNC trial will address the issues of safety and efficacy of the endocardial approach for left ventricular lead implantation and whether it is superior to the conventional transvenous approach.

Question

What is the usefulness of cardiac activation maps?

Discussion

The new ESC guidelines that restrict the class IA indications to patients with LBBB morphology were discussed earlier. However, some patients exhibit a non-LBBB morphology at ECG, but invasive endocardial and epicardial maps demonstrate a left ventricular activation delay. This delay seems essential to obtain a favorable response after CRT.1,7-9 This is the situation in the patient in this case, who did not show a prolonged QRS complex but had delayed electrical activation of the left ventricle. After CRT, the effect of left ventricular pacing on the activation pattern is clearly shown—inversion of the activation pattern when left ventricular pacing only is applied and significant electrical resynchronization when both left ventricular and right ventricular leads are paced. These noninvasive maps are obtained in nearly real time and require only one heart beat to be displayed. Consequently, this technique can theoretically be useful not only for the diagnosis of electrical dyssynchrony before implantation but also during implantation because it provides fast and reproducible information of the electrical resynchronization. Thus the choice of the optimal pacing site is foreseeable, with the condition that electrical activation resynchronization and mechanical improvement occur in parallel. Finally, this tool potentially can be used for optimization of atrioventricular and VV intervals during follow-up, especially in nonresponders to CRT to better understand the possible mechanism of lack of efficacy and plan ahead the various options of device programming and implantation revision.
Currently, this technique remains investigational and needs the scientific proof to be demonstrated in the clinical setting.

Selected References

1. Bourassa M.G., Khairy P., Roy D. An early proof-of-concept of cardiac resynchronization therapy. World J Cardiol. 2011;3:374–376.

2. Derval N., Steendijk P., Gula L.J. et al. Optimizing hemodynamics in heart failure patients by systematic screening of left ventricular pacing sites: the lateral left ventricular wall and the coronary sinus are rarely the best sites. J Am Coll Cardiol. 2010;55:566–575.

3. Duckett S.G., Ginks M., Shetty A.K. et al. Invasive acute hemodynamic response to guide left ventricular lead implantation predicts chronic remodeling in patients undergoing cardiac resynchronization therapy. J Am Coll Cardiol. 2011;58:1128–1136.

4. McMurray J.J., Adamopoulos S., Anker S.D. et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail. 2012;14:803–869.

5. Ploux S., Whinnett Z., Bordachar P. Left ventricular endocardial pacing and multisite pacing to improve CRT response. J Cardiovasc Transl Res. 2012;5:213–218.

6. Prinzen F.W., Houthuizen P., Bogaard M.D. et al. Is acute hemodynamic response a predictor of long-term outcome in cardiac resynchronization therapy? J Am Coll Cardiol. 2012;59:1198.

7. Rickard J., Kumbhani D.J., Gorodeski E.Z. et al. Cardiac resynchronization therapy in non-left bundle branch block morphologies. Pacing Clin Electrophysiol. 2010;33:590–595.

8. Strik M., Ploux S., Vernooy K. et al. Cardiac resynchronization therapy: refocus on the electrical substrate. Circ J. 2011;75:1297–1304.

9. Strik M., Regoli F., Auricchio A. et al. Electrical and mechanical ventricular activation during left bundle branch block and resynchronization. J Cardiovasc Transl Res. 2012;5:117–126.

10. Whinnett Z., Bordachar P. The risks and benefits of transseptal endocardial pacing. Curr Opin Cardiol. 2012;27:19–23.

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