History
Since 1980 this patient was treated periodically with venosections as a result of hemochromatosis. He had received medical therapy for hypertension since 1985 and was diagnosed with hypertensive nephropathy in 1994. He had a non-Q anterior myocardial infarction in 1996, with following postinfarction angina pectoris.
The patient was hospitalized in 2004 for unstable angina pectoris. A coronary angiogram demonstrated triple vessel disease, and he successfully underwent coronary artery bypass surgery.
In 2011 he was admitted to hospital because of a paroxysm of atrial fibrillation, which converted spontaneously to sinus rhythm during the stay.
During late winter 2012 the patient experienced increasing exercise intolerance and fatigue. He had no chest pain. He developed pitting edema of the lower extremities, which soon extended above his knees, and he had noticed intermittent palpitation. He had episodes of orthopnea, causing him to sleep sitting in a chair at night.
He was admitted to hospital on April 13, 2012 with signs of congestive heart failure. An electrocardiogram (ECG) showed atrial fibrillation with rapid ventricular response, left bundle branch block (LBBB), and QRS width of approximately 160 ms. An echocardiogram the next day demonstrated a dilated left ventricle with an end-diastolic diameter of 66 mm and obvious dyssynchronous contractility. The left ventricular ejection fraction (LVEF) was reduced, at 20%, because of apical akinesia and inferior and lateral hypokinesia. No significant valvular disease was present. Chest radiography on admission showed cardiac enlargement and signs of pulmonary congestion.
The patient was initially treated with an intravenous diuretic, a beta blocker, an angiotensin receptor blocker, and a mineralocorticoid receptor antagonist, but the uptitration of these drugs was limited by hypotension, renal failure, and a tendency to hyperkalemia. The patient had to be periodically treated with dobutamine and dopamine, and he also received an infusion of levosimendan. Atrial fibrillation and periodic atrial flutter with insufficient rate control was initially treated with amiodarone, and direct current cardioversion was planned. Preparing for cardioversion, transesophageal echocardiography was performed, revealing a thrombus in the left atrial appendage. This finding caused cardioversion to be postponed and amiodarone to be discontinued because rhythm conversion was considered unfavorable in this situation. Instead, digoxin was added. On this treatment the patient showed some improvement clinically and the LVEF increased to approximately 30%, but he was still symptomatic even at minimal physical exertion.
The patient was monitored on telemetry, which revealed short runs of nonsustained ventricular tachycardia. On April 25, 2012, with the patient still hospitalized and on telemetry, a run of ventricular tachycardia degenerated into ventricular fibrillation. He was immediately resuscitated and defibrillated into atrial fibrillation and suffered no neurologic sequelae. Amiodarone was commenced. He had no signs of acute coronary syndrome.
Current Medications
The patient was taking bumetanide 4 mg daily, candesartan 16 mg daily, carvedilol 12.5 mg twice daily, hydrochlorothiazide 25 mg daily, spironolactone 12.5 mg daily, atorvastatin 40 mg daily, warfarin 5 mg daily, amiodarone 200 mg twice daily, and digoxin 0.125 mg daily.
Comments
The patient was intolerant to angiotensin-converting enzyme inhibitors because of cough.
Current Symptoms
The patient was experiencing dyspnea and was in New York Heart Association (NYHA) class III. He also had peripheral edema and ventricular tachyarrhythmia.
Comments
The patient had symptomatic heart failure despite optimal pharmacologic therapy.
Physical Examination
Laboratory Data
Comments
The patient’s estimated glomerular filtration rate was 26 mL/min.
Electrocardiogram
Findings
The ECG obtained on admission on April 13, 2012 showed atrial fibrillation with a ventricular rate of 80 to 130 bpm, LBBB, and a QRS width of approximately 160 ms (Figures 29-1 and 29-2). The ECG obtained after cardiac resynchronization therapy defibrillator (CRT-D) implantation on May 10, 2012 demonstrated a high degree of biventricular pacing, despite atrial dysrhythmia. The QRS width was approximately 120 ms (Figures 29-3 and 29-4).
Chest Radiograph
Findings
A chest radiograph was obtained on admission. Sternal circlages were noted on the frontal and lateral views. The cardiothoracic ratio was 0.57, which indicated cardiac enlargement. Mild enlargement of the perihilar vessels and Kerley B lines were seen, suggestive of pulmonary congestion (Figures 29-5 and 29-6).
FIGURE 29-1
FIGURE 29-2
FIGURE 29-3
FIGURE 29-5
FIGURE 29-6
Echocardiogram
Findings
On the parasternal long-axis echocardiographic view, recorded May 3, 2012, the left ventricle was dilated, with an end-diastolic diameter of 65 mm. The interventricular septum and posterior wall diameters measured 11 mm, and the left atrial anteroposterior diameter was 41 mm (Figure 29-7).
Findings
On the apical view, recorded May 3, 2012, left ventricular contraction was dyssynchronous, with apical hypokinesia. The LVEF was estimated to be 30% (apical two-chamber view not shown). Signs of aortic sclerosis were present, but no stenosis was seen (Figure 29-8).
Focused Clinical Questions and Discussion Points
Question
Does the presence of atrial fibrillation influence the indication for CRT in patients with heart failure?
Discussion
The evidence for the beneficial effects of CRT in patients in heart failure with sinus rhythm is solid. In the current European Society of Cardiology (ESC) guidelines,9 CRT holds a class IA recommendation in patients remaining symptomatic despite optimal pharmacologic therapy, with an LVEF of 30% to 35% or less and a QRS duration of 130 to 150 ms or greater. Most randomized controlled trials evaluating the effects of CRT in heart failure excluded patients in permanent atrial fibrillation, and data regarding CRT in patients with heart failure and atrial fibrillation are mostly observational. The major challenge for CRT in atrial fibrillation is to obtain a sufficient degree of biventricular pacing, because the positive effect of CRT on outcomes depends on this.
ESC guidelines9 state that CRT may be considered in patients with permanent atrial fibrillation, NYHA class III, a QRS width of 120 ms or greater, and an LVEF 35% or less. In addition, according to the guidelines, it is mandatory that the patient is pacemaker dependent as a result of an intrinsic slow ventricular rate, the ventricular rate is well controlled (≤60 bpm at rest and ≤90 bpm on exercise) (class IIB, level C), or pacemaker dependency is induced through atrioventricular node ablation (class IIA, level B). The use of CRT in patients with heart failure and atrial fibrillation is well established in clinical practice; the ESC Cardiac Resynchronization Therapy Survey in 140 European centers demonstrated that 23% of all devices were implanted in patients with atrial fibrillation.1
Question
Should atrioventricular node ablation be performed routinely following CRT implantation in patients with permanent atrial fibrillation?
Discussion
To ensure maximal efficacy of CRT, it is crucial to obtain a high degree of biventricular pacing. Measures must be taken so the percentage of biventricular pacing is increased to the highest possible level, because a further reduction in mortality has been observed if biventricular pacing is achieved in excess of 98% of all ventricular beats.5 Even moderately increased ventricular rates during atrial fibrillation pose a substantial challenge for the delivery of efficient CRT, because rapid and irregular intrinsic conduction will compete with pacing.
A subgroup analysis of patients with permanent atrial fibrillation in the Resynchronization/Defibrillation for Ambulatory Heart Failure Trial (RAFT)6 failed to demonstrate any significant beneficial effect of CRT-D compared to defibrillators without CRT in patients with apparently good rate control. It is important to note that only 34.3% of CRT-treated patients achieved biventricular pacing greater than 95%. Atrioventricular node ablation in patients with atrial fibrillation and CRT theoretically leads to 100% biventricular pacing. Observational data have shown that CRT and atrioventricular node ablation in patients with atrial fibrillation improves left ventricular function and functional capacity to a degree similar to that in patients with CRT with sinus rhythm4 and significantly reduces cardiovascular and all-cause mortality in contrast to pharmacologic rate control in patients with atrial fibrillation treated with CRT.2,3 These observations need to be confirmed in randomized controlled trials. Although a rare event, pacemaker failure is possible after atrioventricular node ablation. Accordingly, it is important to continuously evaluate rate control and efficacy of CRT in patients with atrial fibrillation and consider atrioventricular node ablation if the degree of biventricular pacing is insufficient.
Question
When assessing a patient with CRT and atrial fibrillation, does the device counter accurately quantify the degree of biventricular pacing?
Discussion
Kamath and colleagues8 examined patients with CRT and permanent atrial fibrillation with a 12-lead Holter monitor and demonstrated that CRT device counters overestimate the degree of biventricular pacing delivered. Although device counters reported greater than 90% biventricular pacing, in some patients substantial proportions of these beats were fusion or pseudofusion beats. Only effectively paced patients with a low degree of incomplete capture responded to CRT. This emphasizes the importance of using Holter evaluation when assessing amount of capture, because device interrogation alone may not reveal the presence of ineffective biventricular pacing.
Question
Does evidence show that chronic right ventricular pacing and atrioventricular node ablation for atrial fibrillation can be prevented by CRT?
Discussion
Atrioventricular node ablation and pacemaker implantation is a treatment option for the subgroup of patients with therapy-resistant atrial fibrillation, allowing efficient control of ventricular rate. On the other hand, the subsequent delayed and dyssynchronous left ventricular contraction during chronic right ventricular pacing may lead to left ventricular dysfunction and adverse remodeling. CRT represents a more appealing, physiologic method of pacing that does not result in adverse left ventricular remodeling. A recent meta-analysis of five randomized controlled trials involving a total of 686 patients examined whether CRT is superior to right ventricular pacing in this setting.10 CRT resulted in a significant reduction in heart failure hospitalizations, but did not significantly influence mortality, compared to right ventricular pacing. Further studies are necessary to address the effect on clinical outcomes of CRT versus right ventricular pacing in patients with preserved left ventricular function.7,10
Final Diagnosis
The patient was in NYHA class III, with heart failure resulting from ischemic cardiomyopathy, an LVEF of 20%, atrial fibrillation, and LBBB, with a QRS duration of 160 ms. Ventricular fibrillation was resuscitated.
Plan of Action
CRT-D implantation was planned for this patient. In addition, when he had undergone adequate anticoagulation, at least 3 weeks after the discovery of left atrial thrombus, a transesophageal echocardiogram was to be performed. If thrombus could be ruled out, he would undergo direct current cardioversion attempting to restore sinus rhythm, with subsequent pharmacologic rhythm control. Later, follow-up would focus on trying to maximize the degree of biventricular pacing achieved. If failure to restore sinus rhythm or recurrence of therapy-resistant atrial arrhythmia causing insufficient CRT delivery should occur, atrioventricular node ablation would be considered.
Intervention
The patient underwent CRT-D implantation on May 4, 2012. Sinus rhythm was restored with amiodarone. When the patient was examined at the outpatient clinic on June 11, 2012, the CRT device counter reported biventricular pacing in 94% of all beats and some brief episodes of atrial fibrillation. To optimize CRT delivery, atrioventricular pace and sense delay were reduced from 200 to 180 ms and 150 to 130 ms, respectively.
At a subsequent outpatient visit on September 11, 2012, acceptable values were found, with 97% biventricular pacing, 0% atrial fibrillation burden, some ventricular ectopic beats, and no runs of ventricular tachycardia.
Outcome
In September 2012 the patient was in NYHA class II, had no peripheral edema, and had experienced substantial improvement in clinical status. Echocardiography at this time demonstrated an LVEF of 40% and left-ventricular end-diastolic diameter of 59 mm, which also was an improvement over findings in examinations before the CRT implantation.
Selected References
1. Dickstein K., Bogale N., Priori S. et al. The european cardiac resynchronization therapy survey. Eur Heart J. 2009;30:2450-–2460.
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. J Am Coll Cardiol. 2012;59:719–726.
3. Gasparini M., Auricchio A., Metra M. et al. Long-term survival in patients undergoing cardiac resynchronization therapy: the importance of performing atrio-ventricular junction ablation in patients with permanent atrial fibrillation. Eur Heart J. 2008;29:1644–1652.
4. Gasparini M., Auricchio A., Regoli F. et al. Four-year efficacy of cardiac resynchronization therapy on exercise tolerance and disease progression. J Am Coll Cardiol. 2006;48:734–743.
5. Hayes D.L., Boehmer J.P., Day J.D. et al. Cardiac resynchronization therapy and relationship of percent biventricular pacing to symptoms and survival. Heart Rhythm. 2011;8:1469–1475.
6. Healey J.S., Hohnloser S.H., Exner D.V. et al. Cardiac resynchronization therapy in patients with permanent atrial fibrillation: results from the Resynchronization for Ambulatory Heart Failure Trial (RAFT). Circ Heart Fail. 2012;5:566–570.
7. Jensen-Urstad M. Should all patients undergoing atrioventricular junction ablation receive cardiac resynchronization therapy? Europace. 2012;14:1383–1384.
8. Kamath G.S., Cotiga D., Koneru J.N. et al. The utility of 12-lead Holter monitoring in patients with permanent atrial fibrillation for the identification of nonresponders after cadiac resynchronization therapy. J Am Coll Cardiol. 2009;53:1050–1055.
9. McMurray J.J.V., Adamopoulos S., Anker S.D. et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012. Eur Heart J. 2012;33:1787–1847.
10. Stavrakis S., Garabelli P., Reynold D.W. Cardiac resynchronization therapy after atrioventricular junction ablation for symptomatic atrial fibrillation: a meta-analysis. Europace. 2012;14:1490–1497.
