History
The patient is a 71-year-old man who has been followed for 20 years. He is a former smoker, having smoked from the age of 20, with 50 years of smoking at one pack per day. He formerly had hypertension. His mother had a myocardial infarction at the age of 60 years; no other family members had known premature vascular disease. He initially sought treatment at the age of 52 years with an anterior myocardial infarction. Thrombolysis was performed at that time, and he was placed on aspirin 325 mg daily.
The patient returned to medical attention 9 years ago with worsening angina (Canadian Cardiovascular Society [CCS] III). An exercise methoxyisobutylisonitrile (MIBI) test demonstrated ST depression in the anterior leads starting 6 minutes into exercise. He was able to exercise for 9 minutes. The maximal ST depression was 0.2 mV in amplitude and persisted 3 minutes into recovery. The nuclear images showed a large reversible defect occupying most of the anterior wall and anterior septum. A subsequent angiogram showed 90% stenosis in the proximal left anterior descending (LAD) artery, 40% stenosis of the left mainstem artery, 50% stenosis of the proximal and mid–right coronary artery, and 60% stenosis of the circumflex artery. Angioplasty was performed, and a bare metal stent was placed in the proximal LAD. He was then started on an angiotensin-converting enzyme (ACE) inhibitor, a statin, and a thienopyridine in addition to his aspirin and was enrolled in a cardiac rehabilitation program.
His echocardiogram at that time showed an ejection fraction of 50%, normal right ventricular function, mild-to-moderate mitral regurgitation, mild tricuspid regurgitation (no other valvulopathy), and right ventricular systolic pressure of 25 mm Hg.
One year ago the patient returned to medical attention with an acute inferior myocardial infarction. He had been on holiday camping and sought treatment 30 hours after the onset of pain. He underwent an angiogram, which revealed an occlusion of the proximal right coronary artery. Collaterals from the circumflex artery filled the distal right coronary artery. The stenosis of the circumflex artery was 75%. The stenosis of the left mainstem artery was 60%. The LAD artery now had a 70% stenosis in its midportion. The left ventricular angiogram showed an ejection fraction of 45% with severe mitral regurgitation.
A subsequent echocardiogram confirmed an ejection fraction of 45% and demonstrated severe mitral regurgitation. Akinesis of the inferior wall and hypokinesis of the anterior wall were noted. The mitral valve appeared morphologically normal. The mitral regurgitation jet was directed posteriorly, thought to be due to a tethered posterior leaflet resulting from the inferior wall motion abnormality.
Coronary artery bypass surgery and mitral valve repair or replacement was recommended. This was undertaken before discharge. He received the following grafts: left internal thoracic artery to mid-LAD with a skip graft to the second diagonal artery; saphenous vein graft from the aorta to a large first obtuse marginal artery with a skip graft to the second obtuse marginal artery; and saphenous vein graft from the aorta to the distal right coronary artery. On examining the mitral valve, the surgeon thought the best result would be obtained with a mechanical mitral valve replacement, which was implanted simultaneously.
The patient’s immediate postprocedure echocardiogram showed no mitral regurgitation and an ejection fraction of 20%. Despite this, his hospital stay was complicated by pulmonary and peripheral edema. He was discharged to home 10 days after surgery on aspirin, an ACE inhibitor, a statin, a diuretic, and a low-dose beta blocker.
He has been attending the heart function and heart failure clinic weekly; his medications have been slowly increased to his target doses. He has had no hospital admissions for heart failure.
He is referred to a cardiac electrophysiologist 3 months after surgery for an opinion regarding device therapy.
Comments
In summary, this patient is a 71-year-old retired electrician with ischemic heart disease and persistently reduced ejection fraction despite revascularization and maximal medical therapy.
Current Medications
The patient’s medications are ramipril 10 mg, aspirin 81 mg, and coumadin (dose titrated to achieve an international normalized ratio of 2.5-3.5) every morning and bisoprolol 10 mg, spironolactone 25 mg, and atorvastatin 80 mg every evening.
Comments
The patient appears to be on optimal medical therapy.
Current Symptoms
The patient currently denies orthopnea and paroxysmal nocturnal dyspnea. He is able to walk one block on a flat surface and has to stop because of shortness of breath.
Comments
He has New York Heart Association class III heart failure symptoms despite being revascularized and on optimal medical therapy.
Physical Examination
Comments
The patient appears mildly volume overloaded.
Laboratory Data
Comments
The patient’s renal insufficiency is long-standing. He has had three previous episodes of acute renal insufficiency resulting from prerenal azotemia. His creatinine has been at this level over the last 12 months.
Electrocardiogram
Findings
The 12-lead electrocardiogram (ECG) shows sinus bradycardia at a rate of 60 bpm, right bundle branch block (RBBB), and left and anterior hemiblock (Figure 3-1).
Comments
The important finding on ECG is that the RBBB is very wide, with a QRS duration of 220 msec.
Echocardiogram
Findings
The echocardiogram performed the week before the patient was referred for device therapy demonstrated an ejection fraction of 20%. The left ventricular end-diastolic and end-systolic dimensions are 66 and 52 mm, respectively. Mitral valve hemodynamics are normal, and paradoxical septal motion was noted. Left atrial diameter was 62 mm.
Comments
The parasternal long axis image shown in Figure 3-2 demonstrates the very dilated left ventricle with poor ejection fraction.
FIGURE 3-1
FIGURE 3-2
Focused Clinical Questions and Discussion Points
Question
What is the benefit of a biventricular implantable cardioverter defibrillator (Bi-V ICD) over an implantable cardioverter-defibrillator (ICD)?
Discussion
Dyssynchrony is defined as the lack of synchronization between chambers or between the walls within the same chamber. This can refer to atrioventricular dyssynchrony, which is lack of synchronization between the atria and ventricles; V-V dyssynchrony (also known as interventricular dyssynchrony), which is lack of synchronization between the left and right ventricles; or intraventricular dyssynchrony, which is dyssychrony between the walls within one of the ventricles.
BBB creates V-V dyssynchrony by delaying the activation of the ipsilateral ventricle. This is one reason why investigators attempted to improve the symptoms of patients with heart failure and BBB by adding a left ventricular lead and resynchronizing the chambers.
Both randomized and nonrandomized trials have shown the efficacy of biventricular ICDs and pacing in patients with wide QRS duration and reduced ejection fraction. These trials included patients with left bundle branch block (LBBB) and RBBB. However, to date only four randomized trials have examined the efficacy of biventricular pacing on death or hospitalization for heart failure in subgroups stratified by QRS morphology.
The Comparison of Medical Therapy, Pacing and Defibrillation in Heart Failure (COMPANION) trial; the Cardiac Resynchronization in Heart Failure (CARE-HF) trial; the Multicenter Automatic Defibrillator Implantation with Cardiac Resynchronization Therapy (MADIT-CRT) study; and the Resynchronization–Defibrillation for Ambulatory Heart Failure Trial (RAFT) showed the benefit of biventricular pacing or ICD over medical therapy or a biventricular ICD over standard ICD therapy.1,3,5,6 In each of these trials, patients with LBBB and RBBB were included and as a group had a significant reduction in the primary end points (usually mortality and hospitalization for heart failure or a cardiovascular event) (Table 3-1). In each of these trials, there was no benefit of bi-ventricular pacing in the RBBB subgroup or the combined RBBB and intraventricular conduction delay subgroup.
It would appear that although patients with LBBB and RBBB have interventricular dyssynchrony, additional factors such as left ventricular intraventricular dyssynchrony must be present that confer a benefit from biventricular pacing. Are these factors and RBBB mutually exclusive or are there patients with RBBB who have these factors and thus will benefit from biventricular pacing?
In the RAFT trial the efficacy of biventricular pacing was further analyzed by QRS duration in the group of patients with RBBB. In the group of patients with a QRS duration of less than 160 msec, there was no benefit to biventricular ICD over ICD. However, in the patients with RBBB and a QRS duration of 160 msec or greater, benefit was seen of the cardiac resynchronization therapy device (CRT-D) over ICD in reducing mortality and heart failure hospitalizations.1
On further review of the patient’s chart, it was noted that he previously had an LBBB (Figure 3-3). Presumably, the previous LBBB was actually very slow left bundle conduction and not complete LBBB. The left bundle actually conducted, but so slowly that it appeared to be ‘blocked’. This was only apparent when there was right bundle branch block present. This demonstrates that patients with RBBB may have underlying left bundle disease.
Question
Would there be an expected improvement in mortality or morbidity with a Bi-V ICD if the QRS showed nonspecific interventricular conduction delay?
Discussion
Three of the trials described previously analyzed the efficacy of biventricular pacing in patients with nonspecific intraventricular conduction delay (IVCD). In the CARE-HF trial, only 10 patients randomized had IVCD. There appeared to be no difference in the event rates between the group randomized to biventricular pacing (2/4) and the group randomized to medical therapy (2/6).4 In the 308 patients with IVCD in the MADIT-CRT trial no benefit was seen to biventricular pacing with respect to the end point of heart failure event or death.7 In the RAFT trial, death and heart failure hospitalization event rates were similar in the 207 patients with IVCD who were randomized between biventricular ICDs and ICDs alone.6
FIGURE 3-3
TABLE 3-1
Trials That Analyzed the Efficacy of Biventricular Pacing Depending on QRS Morphology
| Trial | No. | Control | Intervention | End Point | RRR Overall (%) | RRR in Non-LBBB |
| COMPANION | 1520 | Medical therapy | Biventricular pacemaker/ICD | Death from or hospitalization from heart failure | Biventricular pacemaker 34% Biventricular ICD 40% |
No difference |
| CARE-HF | 813 | Medical therapy | Biventricular pacemaker | Death or hospitalization for a major cardiovascular event | 37% | No difference |
| RAFT | 1798 | ICD | Biventricular ICD | Death or heart failure hospitalization | 25% | No difference∗ |
| MADIT-CRT | 1820 | ICD | Biventricular ICD | Death or heart failure event | 44% | No difference |
CARE-HF, Cardiac Resynchronization in Heart Failure trial; COMPANION, Comparison of Medical Therapy, Pacing and Defibrillation in Heart Failure trial; ICD, implantable cardioversion defibrillator; LBBB, left bundle branch block; MADIT-CRT, Multicenter Automatic Defibrillator Implantation with Cardiac Resynchronization Therapy study; RAFT, Resynchronization–Defibrillation for Ambulatory Heart Failure Trial; RRR, Relative Risk Reduction.
∗ See text: Overall no difference was found in the RBBB group, but when analyzed by QRS width, patients with RBBB and a QRS >160 msec derived benefit from biventricular ICD therapy.
Question
What are the additional risks in implantation of a CRT-D over an ICD?
Discussion
Both the MADIT-CRT and RAFT trials randomized patients between CRT-Ds and ICDs alone.5,6 Both trials enrolled patients during a time when currently available coronary sinus access tools and subselection sheaths were used and where left ventricular lead deployment techniques were well known. The risk for hemothorax and pneumothorax was higher in CRT-D than ICD implantation (RAFT, 1.2% vs. 0.9%; MADIT-CRT, 1.7% vs. 0.8%). The risk for pocket hematoma requiring intervention occurred more commonly in the CRT-D group than the ICD group (RAFT, 1.6% vs. 1.2%; MADIT-CRT, 3.3% vs. 2.5%). Device pocket infection occurred more commonly in the CRT-D group than the ICD group (RAFT, 2.4% vs. 1.8%; MADIT-CRT, 1.1% vs. 0.7%). An increased rate of lead dislodgement occurred, requiring intervention in the CRT-D group in contrast to the ICD group (RAFT, 6.9% vs. 2.2%; MADIT-CRT, 4% need for left ventricular lead repositioning). In addition, patients in the CRT-D group had a 0.7% to 1.2% risk for coronary sinus dissection.
Final Diagnosis
The patient is a 71-year-old man with ischemic heart disease and mitral regurgitation. After mitral valve replacement, coronary artery bypass graft surgery, and optimal medical therapy, he had persistently low ejection fraction and NYHA III symptoms. His ECG shows a RBBB with a QRS duration of 220 msec.
Plan of Action
After a discussion with the patient regarding the risks and benefits of implantation of a CRT-D versus ICD, the patient wished to proceed with a CRT-D.
Intervention
CRT-D was undertaken; the coronary sinus venogram identified a suitable posterolateral coronary sinus branch within which a left ventricular lead was inserted (Figure 3-4). At the time of the procedure a high-voltage ICD lead was inserted first, followed by a right atrial pace and sense lead. After this, a coronary sinus venogram was performed (Figures 3-5 and 3-6). The only suitable vein for a coronary sinus lead was a lateral branch of the coronary sinus. An angioplasty wire was required to advance the wire to its final position (Figure 3-7).
FIGURE 3-4
FIGURE 3-5
The device was programmed DDDR to 50 to 120 bpm. The sensed atrioventricular delay was programmed to 180 msec, and the programmed atrioventricular delay was programmmed to 150 msec. The V-V delay was programmed so the left ventricular stimulus was delivered 20 msec before the right ventricular stimulus.
The patient’s follow-up ECG shows sinus rhythm with biventricular pacing. The QRS is much more narrow than before the procedure.
His chest radiograph shows cardiomegaly (Figures 3-8 and 3-9). The position of both the right ventricular and right atrial leads are satisfactory. The left ventricular lead is in the lateral left ventricle (Figure 3-10).
FIGURE 3-7
Selected References
1. Birnie D.H., Ha A., Higginson L. et al. Importance of QRS duration and morphology in determining response to cardiac resynchronization therapy: results from the Resynchronization-Defibrillation for Ambulatory Heart Failure Trial (RAFT). Heart Rhythm,. 2012;9(Suppl 5):S295–S296.
2. Bristow M.R., Saxon L.A., Boehmer J. et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med. 2004;350:2140–2150.
3. Cleland J.G., Daubert J.C., Erdmann E. et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med. 2005;352:1539–1549.
4. Gervais R., Leclercq C., Shankar A. et al. Surface electrocardiogram to predict outcome in candidates for cardiac resynchronization therapy: a sub-analysis of the CARE-HF trial. Eur J Heart Fail. 2009;11:699–705.
5. Moss A.J., Hall W.J., Cannom D.S. et al. Cardiac-resynchronization therapy for the prevention of heart-failure events. N Engl J Med. 2009;361:1329–1338.
6. Tang A.S., Wells G.A., Talajic M. et al. Cardiac-resynchronization therapy for mild-to-moderate heart failure. N Engl J Med. 2010;363:2385–2395.
7. Zareba W., Klein H., Cygankiewicz I. et al. Effectiveness of cardiac resynchronization Therapy by QRS Morphology in the Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy (MADIT-CRT). Circulation. 2011;123:1061–1072.
