History
The patient is a 54-year-old man with a history of a nonischemic dilated cardiomyopathy. He was initially referred for consideration of a third procedure for atrial fibrillation. He had undergone pulmonary vein isolation procedures 1 year and 3 months previously. In addition to pulmonary vein isolation, linear ablation of both the left and right atria had been performed, as well as targeting of complex fractionated atrial electrograms. Despite this, the patient experienced early recurrences of atrial fibrillation and atypical atrial flutter soon after each ablation. In addition, amiodarone, digoxin, and beta blockade were used as adjunctive therapy, yet rate control remained poor. Heart rates during waking hours averaged approximately 110 bpm. Left ventricular systolic function was globally reduced, and the ejection fraction was estimated to be approximately 20%. His symptom was New York Heart Association (NYHA) class II to III dyspnea, yet he had no history of hospital admissions for heart failure, no palpitations, and no presyncopal symptoms.
The patient had failed an antiarrhythmic strategy using a combination of medication and ablation. Furthermore, he was failing a rate control strategy using three different atrioventricular nodal blocking agents. He remained tachycardic and symptomatic, and therefore the following therapeutic options were discussed with him and his family: (1) a third catheter ablation for atrial fibrillation, (2) permanent pacemaker implantation with adjunctive atrioventricular nodal ablation, and (3) open surgical cut-and-sew maze procedure. The patient elected to proceed with atrioventricular nodal ablation and permanent pacemaker implantation.
Current Medications
The patient was taking digoxin 250 mcg daily, furosemide 20 mg daily, losartan 50 mg daily, amiodarone 300 mg daily, metoprolol 100 mg twice daily, spironolactone 25 mg daily, and warfarin to maintain international normalized ratio between 2 and 3.
Current Symptoms
The patient’s predominant symptom was dyspnea on exertion. His exercise tolerance was limited to flat surfaces. In addition, he was frequently becoming dyspneic with simple activities of daily living while working on his farm. He had not had any syncopal episodes and was not aware of any palpitations.
Physical Examination
Laboratory Data
Electrocardiogram
Findings
Figure 25-1 shows the electrocardiogram (ECG) obtained before device implantation. The rhythm is atrial fibrillation with a fairly rapid ventricular response. The QRS duration is less than 100 ms, and no evidence of acute ischemia is present.
Figure 25-2 shows the ECG obtained after atrioventricular node ablation and device implantation. The rhythm is atrial fibrillation, with evidence of biventricular pacing. Frequent premature ventricular contractions occurred, with varying degrees of fusion.
Chest Radiograph
Findings
The chest radiograph showed the heart size to be normal. Mild pulmonary venous hypertension was noted (Figure 25-3).
Echocardiogram
Findings
The electrogram revealed mild-to-moderate left ventricular enlargement with severe decrease in systolic function. The left ventricular ejection fraction was estimated to be 20%. Severe generalized left ventricular hypokinesis was evident. Mild right ventricular enlargement with a mild decrease in systolic function was noted. The estimated right ventricular systolic pressure was 44 mm Hg. No significant valvular heart disease was seen. No pericardial effusion was present. The left atrial volume index was 52 mL/m2. Moderate right atrial enlargement was noted.
FIGURE 25-1
FIGURE 25-2
Physiologic Tracings
Findings
Before Device Implantation
The patient was given a 24-hour Holter monitor 1. The patient’s minimum heart rate was 62 bpm, maximum heart rate was 177 bpm, and average heart rate was 103 bpm. The basic rhythm was atrial fibrillation, with the rate varying between 62 and 177 bpm. Very frequent premature ventricular contractions or aberrant beats occurred singly at times and bigeminy in pairs and in runs of ventricular tachycardia or aberrancy 3 to 13 beats in duration. The maximum ventricular tachycardia or aberrant conduction rate was 193 bpm. Also seen were frequent episodes of an accelerated idioventricular rhythm 3 to 4 beats in duration. No symptoms were recorded in the patient’s diary.
After Atrioventricular Node Ablation and Device Implantation
The patient was given a 24-hour Holter monitor 2. The basic mechanism was a ventricular pacemaker with fusion beats. The underlying rhythm was atrial fibrillation, with a ventricular rate of 58 to 94 bpm and an average heart rate of 64 bpm. Very frequent premature ventricular or aberrantly conducted beats (31.2% of total ventricular beats) occurred singly and in bigeminy and in 3- to 4-beat runs of accelerated idioventricular rhythm (AIVR) and in 3- to 11-beat runs of ventricular tachycardia (vs. aberrant beats in a series). The minimum AIVR rate was 75 bpm. The maximum ventricular tachycardia rate was 182 bpm.
Computed Tomography
Findings
Computed tomography (CT) of the heart shows no intracardiac thrombus. Two left and three right pulmonary veins with no pulmonary vein stenosis were noted. All coronary arteries in the right dominant coronary system were patent. Biatrial enlargement and moderately severe left ventricular dilation were observed.
Focused Clinical Questions and Discussion Points
Question
Should a biventricular device or standard dual-chamber implantable cardioverter-defibrillator (ICD) pacemaker be implanted?
Discussion
It is well recognized that the left bundle branch block pattern that ensues with obligate right ventricular pacing after atrioventricular nodal ablation provides electrical dyssynchrony for the contracting myocardium. In light of the patient’s symptomatic status and depressed left ventricular function, consideration of cardiac resynchronization therapy CRT is warranted. However, assuming that the basis for his ventricular dysfunction is indeed a tachycardia-mediated cardiomyopathy,3,6 it is possible that with effective rate control alone (after atrioventricular node ablation) his ejection fraction may improve. In contrast, obligate right ventricular pacing in the context of depressed left ventricular function does hold the potential for further systolic decline and worsening symptoms of heart failure. The physician caring for him elected to recommend biventricular pacing in favor of right ventricular apical pacing.
FIGURE 25-3
Question
Should all patients undergoing CRT with atrial fibrillation and rapid ventricular rates undergo simultaneous atrioventricular node ablation?
Discussion
Atrioventricular node ablation provides the most reliable method for rate control in patients with atrioventricular fibrillation. Randomized controlled trials are still needed to confirm the impact of this procedure on symptom status and survival in patients with atrial fibrillation, heart failure, and biventricular pacing. Several studies, though, have suggested improvements in these fundamental outcomes, and a recent meta-analysis alludes to substantial reductions in all-cause mortality and cardiovascular mortality in those patients who underwent atrioventricular node ablation. In addition, improvements were also seen in the NYHA functional class in the atrioventricular node–ablated groups in contrast to that with medical therapy.2
Question
Does evidence suggest that a high premature ventricular contraction burden is a potential cause of CRT nonresponse?
Discussion
It is clear from large studies and registries that a higher percentage of biventricular pacing is associated with improved symptoms and a reduction in mortality.4 Of interest, it appears that there is potential benefit in improving biventricular percentage pacing above 95%. The Latitude registry has demonstrated that patients with biventricular pacing percentage above 99.6% experienced a 24% reduction in mortality in contrast to the other groups, including patients receiving biventricular pacing more than 95% of the time.4 Conceptually then, it is not necessary for the patient to sustain 20% or 30% ectopy for the salutary effects of biventricular pacing to be diluted.
Although atrial fibrillation with native conduction appears to be the most frequent offender in reducing biventricular percentage pacing, frequent ventricular ectopy is also recognized.5 Frequent ventricular ectopy also has been identified as a cause of reversible left ventricular dysfunction remedial to ablation.1,6 Moreover, ablation of the premature ventricular contraction focus has been shown to be associated with improvement in left ventricular function and functional class in CRT nonresponders.5,7 The largest benefit was seen in patients with a preablation premature ventricular contraction burden greater than 22% of their total beats.
Final Diagnosis
The final diagnosis is nonischemic cardiomyopathy with persistent atrial fibrillation to which tachycardia or ectopy has likely contributed.
Plan of Action
The plan for this patient was atrioventricular node ablation and implantation of a biventricular pacemaker, along with subsequent catheter-based premature ventricular contraction ablation.
Intervention
The patient underwent implantation of a biventricular ICD. This was performed without complications using a standard device and delivery system. The coronary sinus lead was placed in a lateral branch of the venous system, and no phrenic stimulation was noted.
At the patient’s 3-month follow-up visit, it was noted that he was receiving biventricular pacing only 67% of the time. His device interrogation and 24-hour Holter monitoring showed evidence of frequent ventricular ectopy of two different morphologies. The amiodarone had been discontinued, and his symptomatic status was still NYHA class II to class III. A 24-hour Holter monitor showed that approximately one third of his beats were premature ventricular contractions. A discussion around additional antiarrhythmic therapy (i.e., flecainide or mexiletine) versus ablation was undertaken, and the patient ultimately elected to go ahead with an ablation procedure. Two predominant premature ventricular contractions were mapped and ablated. The first was ablated from an epicardial aspect on the left ventricular summit a safe distance from the left circumflex artery. The second originated from the aortomitral continuity and was ablated from an endocardial approach. The patient was seen 3 months after the procedure. Device interrogation showed biventricular pacing to be occuring 98% of the time.
Findings
The patient’s transthoracic echocardiogram at 1 year after atrioventricular node ablation and 9 months after premature ventricular contraction ablation showed a marked improvement in ventricular function with the ejection fraction improving to 45%. In addition, his symptom status was improved to NYHA class II and he continues to actively work on his farm.
Selected References
1. 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;4:863–867.
2. Ganesan A.N., Brooks A.G., Roberts-Thomson K.C. et al. Role of AV nodal ablation in cardiac resynchronization: in patients with coexistent atrial fibrillation and heart failure a systematic review. J Am Coll Cardiol. 2012;59:719–726.
3. Grogan M., Smith H.C., Gersh B.J. et al. Left ventricular dysfunction due to atrial fibrillation in patients initially believed to have idiopathic dilated cardiomyopathy. Am J Cardiol. 1992;69:1570–1573.
4. Hayes D.L., Boehmer J.P., Day J.D. et al. Cardiac resynchronization therapy and the relationship of percent biventricular pacing to symptoms and survival. Heart Rhythm. 2011;8:1469–1475.
5. Lakkireddy D., Di Biase L., Ryschon K. et al. Radiofrequency ablation of premature ventricular ectopy improves the efficacy of cardiac resynchronization therapy in nonresponders. J Am Coll Cardiol. 2012;60:1531–1539.
6. Stulak J.M., Dearani J.A., Daly R.C. et al. Left ventricular dysfunction in atrial fibrillation: restoration of sinus rhythm by the Cox-maze procedure significantly improves systolic function and functional status. Ann Thorac Surg. 2006;82:494–500 discussion 500-491.
7. Yarlagadda R.K., Iwai S., Stein K.M. et al. Reversal of cardiomyopathy in patients with repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract. Circulation. 2005;112:1092–1097.
