27. Prevention of Effective Cardiac Resynchronization Therapy by Frequent Premature Ventricular Contractions in a Patient with Nonischemic Cardiomyopathy

Published on 26/02/2015 by admin

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Last modified 22/04/2025

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History

In 2002 the patient was diagnosed with Global Initiative for Chronic Obstructive Lung Disease stage II chronic obstructive pulmonary disease and in 2004 with first-degree atrioventricular block. In June 2011 he was admitted for decompensated heart failure. Echocardiography revealed a mildly dilated left ventricle, left ventricular ejection fraction (LVEF) of 20%, and grade III mitral regurgitation. Coronary angiography showed no significant coronary artery disease. Frequent premature ventricular contractions were observed during admission. Medical therapy for heart failure was initiated, and the patient was scheduled for reevaluation.
In October 2011 frequent premature ventricular contractions were reported on a 24-hour Holter monitor (28% of all QRS complexes, with one dominant morphology accounting for 99% of all premature ventricular contractions). Drug therapy with metoprolol 75 mg twice daily was not effective, sotalol was not tolerated, and metoprolol was continued.
In December 2011 the patient was readmitted for intermittent total atrioventricular block reported on a 24-hour Holter monitor. He was in New York Heart Association (NYHA) class III. On an echocardiogram, LVEF was 30%, with grade I to II mitral regurgitation. Despite discontinuation of metoprolol therapy, the total atrioventricular block became permanent. A temporary pacemaker was inserted, followed by cardiac resynchronization therapy defibrillator (CRT-D) implantation.

Current Medications

The patient was taking calcium carbasalate (Ascal) 100 mg daily, spironolactone 12.5 mg daily, simvastatin 40 mg daily, perindopril 4 mg daily, furosemide 40 mg daily, and metoprolol 50 mg twice daily.

Current Symptoms

The patient had marked limitation of physical activity (NYHA class III), with no chest pain or collapse.

Physical Examination

Laboratory Data

Electrocardiogram

Findings

An electrocardiogram revealed biventricular pacing with frequent premature ventricular contractions and QRS during biventricular pacing at 160 ms (Figure 27-1). Premature ventricular contractions occurred with slightly varying morphology, all right bundle branch block (RBBB) type of morphology (defined as dominant R in precordial lead V1), left superior axis, transition V4-5.

Echocardiogram

Findings

An echocardiogram showed a dilated left ventricle, no hypertrophy, and an LVEF of 41%, with akinesia of the basal inferolateral wall, no left ventricular thrombus, and grade I to II mitral regurgitation, with eccentric jet along the lateral wall of the left atrium. The mechanism is likely restriction of the posterior mitral leaflet.

Physiologic Tracings

Findings

The 24-hour Holter monitor showed sinus rhythm with biventricular pacing, and frequent premature ventricular contractions (33% of all QRS complexes) were seen, 96% of which were monomorphic.

Focused Clinical Questions and Discussion Points

Question

When the patient developed total atrioventricular block in December 2011, did he need biventricular pacing or would right ventricular pacing have been sufficient?

Discussion

In December 2011 the patient had marked limitation of physical activity (NYHA class III), impaired left ventricular function (LVEF 30%), grade I to II mitral valve regurgitation, and an indication for permanent ventricular pacing because of total atrioventricular block. Several studies have demonstrated the deleterious effects of chronic right ventricular pacing, which include intraventricular and interventricular mechanical dyssynchrony, ventricular dilation, and decreased LVEF. Also, right ventricular pacing may further aggravate mitral valve regurgitation,1 which was already grade I to II at that stage, despite drug therapy. The deleterious effects on left ventricular function may be particularly important in patients who already have left ventricular dysfunction. The Homburg Biventricular Pacing Evaluation (HOBIPACE) trial was the first study to compare biventricular pacing to right ventricular pacing in patients with reduced left ventricular function and a standard indication for permanent ventricular pacing.5 Using a cross-over design, 30 patients received 3 months of right ventricular pacing and 3 months of biventricular pacing. In contrast to right ventricular pacing, biventricular pacing resulted in smaller left ventricular end-diastolic and end-systolic volumes, a higher LVEF, lower N-terminal prohormone of brain natriuretic peptide concentrations, higher maximum exercise capacity, and better quality of life. According to the current guidelines for cardiac pacing and CRT,6 CRT may be considered in patients with reduced LVEF who require chronic pacing and in whom frequent ventricular pacing is expected. However, the evidence for this approach is limited, as indicated by the class C recommendation.
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FIGURE 27-1 

Question

Are the premature ventricular contractions likely to affect left ventricular function?

Discussion

The causal relationship between cardiomyopathy and frequent premature ventricular contractions is difficult to define because frequent premature ventricular contractions can induce cardiomyopathy, but nonischemic dilated cardiomyopathy also has been associated with frequent premature ventricular contraction occurrences. Of importance, left ventricular dysfunction induced by premature ventricular contractions may be reversible in patients without an underlying cardiomyopathy. In a study by Bogun and colleagues,2 for example, 22 patients with frequent idiopathic premature ventricular contractions and LVEF of 50% or less underwent catheter ablation for premature ventricular contractions, after which left ventricular function normalized within 6 months in 82% of patients.2 However, in patients in whom the underlying cardiomyopathy is causative for the premature ventricular contractions, no data are available on the effect of catheter ablation on left ventricular function. Of note, it may be difficult to differentiate between patients with a premature ventricular contraction–induced cardiomyopathy and those with premature ventricular contractions after impaired left ventricular function. The correct diagnosis may become apparent only if the left ventricular function and dimensions return to normal after successful treatment of the premature ventricular contractions by drug therapy or catheter ablation.
Indeed, in the present case, it is unclear whether the frequent premature ventricular contractions have caused cardiomyopathy or cardiomyopathy causes the ventricular extrasystoles. The lack of frequent premature ventricular contractions during the first admission for decompensated heart failure does, however, suggest that an underlying cardiomyopathy may be the cause of the frequent premature ventricular contractions. Also, in patients with underlying cardiomyopathy, premature ventricular contractions may further depress left ventricular dysfunction. In the present case, left ventricular function improved after implantation of the CRT-D. However, the patient remained in NYHA class III, which may be due to the frequent premature ventricular contractions and ineffective biventricular pacing.

Question

Based on the 12-lead ECG, what is the most likely site(s) of origin of the premature ventricular contraction(s)? What are the implications?

Discussion

The 12-lead ECG morphology shows an RBBB-like morphology with a superior axis, suggesting an origin in the inferior left ventricle. The precordial transition in V4 with an RS pattern in V4 suggests that the origin may be located in the mid-inferior wall, consistent with a site of origin close to the papillary muscle. Indeed, an RBBB-like morphology with superior axis and precordial transition in lead V4-6 has been reported to be typical for papillary muscle arrhythmias.3 This finding has important implications for catheter ablation. Papillary muscle arrhythmias frequently originate from deep within the muscle, which is reflected by large areas of simultaneous activation during electroanatomic mapping. Local activation times typically precede the onset of QRS by only 20 to 30 msec.7 Origins deep in the muscle may be difficult to abolish by radiofrequency energy applications, because even irrigated tip ablation creates lesions of limited depths if the catheter is stable and in good contact. In addition, a stable position with sufficient contact force can be particularly difficult at the papillary muscle, requiring a transseptal or combined retrograde aortic and transseptal approach. Intracardiac echocardiography may be helpful in such cases.

Question

Is catheter ablation of the premature ventricular contractions indicated?

Discussion

In the European Heart Rhythm Association and Heart Rhythm Society Expert Consensus on Catheter Ablation of Ventricular Arrhythmias, catheter ablation of frequent premature ventricular contractions is recommended if presumed to cause ventricular dysfunction. As outlined earlier, premature ventricular contractions may cause ventricular dysfunction in two ways in the present case: directly, by causing (aggravating) cardiomyopathy, and indirectly, by preventing effective biventricular pacing. The potential benefits of abolishing the frequent premature ventricular contractions are likely to outweigh the potential risks in catheter ablation. Vascular complications include groin hematomas and pseudoaneurysms (∼1.4%).4 The risk for transient ischemic attacks and stroke are considered to be low (<1%) in the introduction of irrigated catheters. Tamponade occurs in approximately 0.7% of cases.

Final Diagnosis

Persistent symptoms of heart failure occurred in this patient with CRT-D for total atrioventricular block, likely as a result of frequent premature ventricular contractions that also prevented effective biventricular pacing.

Plan of Action

The plan for this patient was catheter ablation of premature ventricular contractions.

Intervention

The CRT device was set to DDD mode with right ventricular pacing only, which resulted in stable ventricular bigeminy. The premature ventricular contraction had an RBBB morphology with left superior axis and transition in V5. The discrepancy between the precordial transition at the outpatient clinic and the laboratory may be caused by small differences in precordial lead placement. The left ventricle was accessed using a retrograde approach via the aorta. The earliest activation was mapped to a wide area around the posteromedial papillary muscle, with the earliest electrogram occurring at 37 msec before QRS onset (Figure 27-2). Repeated radiofrequency energy applications at the same site temporarily abolished the premature ventricular contraction for only approximately 20 seconds; however, the premature ventricular contraction morphology changed to RBBB, superior axis, and transition in V3 (with R < S in lead V6) morphology (Figure 27-3). The earliest activation was mapped to the same area but just remote from the first site, suggesting a shift in the endocardial exit. After a few additional radiofrequency applications, the premature ventricular contractions were abolished and did not recur during a waiting period of 45 minutes. The left ventricular map during right ventricular pacing demonstrated normal bipolar (>1.50 mV) and unipolar (>8.27 mV) voltages and no abnormal electrograms (Figure 27-4). Although these findings make a compact scar in the left ventricle less likely, the presence of a subepicardial scar or diffuse fibrosis cannot be excluded. The left ventricular lead was located over the latest activated endocardial area during right ventricular pacing (Figure 27-5). During programmed electrical stimulation, ventricular fibrillation was induced with a basic cycle length (BCL) of 400 and three extras (230, 200, and 200 msec). Successful cardioversion was performed. The device was programmed to biventricular pacing, which was now effective and not limited by premature ventricular contractions. Ventricular pacing resulted in an almost tripled effective heart rate in contrast to that before ablation (Figure 27-6). Biventricular pacing produced higher blood pressures than only right ventricular pacing.
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FIGURE 27-2 Electroanatomic activation map of the left ventricle color-coded for local activation time during premature ventricular contractions. The sites with earliest activation are located around the base of the papillary muscle (B, red area). The local activation times around the papillary muscle were similar (A, C, and D). Note the subtle differences in the 12-lead electrocardiogram morphology of the premature ventricular contraction, suggestive for slight alterations of the origin itself or the preferential conduction from the origin. The location of the ablation catheter at the successful ablation site on fluoroscopy is displayed in E. At this site, the local activation time was 37 msec before the onset of the QRS-complex (F). After 8 seconds, the premature ventricular contractions disappeared (G).

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FIGURE 27-3 After a radiofrequency application based on activation mapping of the initial premature ventricular contraction (PCV) morphology, a change in the 12-lead ECG morphology of the premature ventricular contractions was observed, with a dominant S wave in V6 suggesting a shift of the PVC exit site.

image

FIGURE 27-4 A to C, Electroanatomic map of the left ventricle during right ventricular pacing, color-coded for bipolar voltage (bipolar voltage >1.50 mV is considered normal and displayed in purple). The bipolar voltages and the electrogram morphologies were normal (D).

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FIGURE 27-5 Electroanatomic map of the left ventricle during right ventricular pacing, now color-coded for local activation time. The sites that were opposite to the left ventricular pacing lead were identified based on fluoroscopy (B, circles) and subsequently tagged on the map (A, white tags with circles in right upper panel). The left ventricular pacing lead is located in close proximity to the latest activated site.

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FIGURE 27-6 The frequent premature ventricular contractions (PVCs) before ablation did not result in significant cardiac output (A). After ablation of the PVC, right ventricular and biventricular pacing resulted in an almost tripled effective heart rate (B and C). Of note, the blood pressure was higher during biventricular pacing in contrast to only right ventricular pacing.

Outcome

Three months after ablation the patient had no limitation of physical activity (improvement from NYHA class III before ablation to class I after ablation). A 24-hour Holter monitor revealed that the premature ventricular contractions were reduced from 33% of all QRS complexes before ablation to less than 0.01% after ablation. Echocardiography demonstrated that the left ventricular dimensions had significantly decreased (the left ventricular end-diastolic volume from 151 to 148 mL and the left ventricular end-systolic volume from 89 to 73 mL) and the LVEF increased (from 41% before to 51% after ablation). The mitral regurgitation was still grade I to II. Therefore marked improvement in exercise capacity and significant reverse remodeling of the left ventricle had occurred, which may be the result of abolishment of the premature ventricular contractions and effective biventricular pacing.

Selected References

1. Barold S.S., Ovsyshcher I.E. Pacemaker-induced mitral regurgitation. Pacing Clin Electrophysiol. 2005;28:357–360.

2. Bogun F., Crawford T., Reich S. et al. Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: comparison with a control group without intervention. Heart Rhythm. 2007;4:837–863.

3. Bogun F., Desjardins B., Crawford T. et al. Post-infarction ventricular arrhythmias originating in papillary muscles. J Am Coll Cardiol. 2008;51:1794–1802.

4. Bohnen M., Stevenson W.G., Tedrow U.B. et al. Incidence and predictors of major complications from contemporary catheter ablation to treat cardiac arrhythmias. Heart Rhythm. 2011;8:1661–1666.

5. Kindermann M., Hennen B., Jung J. et al. Biventricular versus conventional right ventricular stimulation for patients with standard pacing indication and left ventricular dysfunction: the Homburg Biventricular Pacing Evaluation (HOBIPACE). J Am Coll Cardiol. 2006;47:1927–1937.

6. Vardas P.E., Auricchio A., Blanc J.-J. et al. Guidelines for cardiac pacing and cardiac resynchronization therapy: the Task Force for Cardiac Pacing and Cardiac Resynchronization Therapy of the European Society of Cardiology. Developed in collaboration with the European Heart Rhythm Association. Eur Heart J. 2007;28:2256–2295.

7. Yamada T., Doppalapudi H., McElderry H.T. et al. Electrocardiographic and electrophysiological characteristics in idiopathic ventricular arrhythmias originating from the papillary muscles in the left ventricle: relevance for catheter ablation. Circ Arrhythm Electrophysiol. 2010;3:324–331.

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