History
The patient underwent bypass surgery (left internal mammary artery to left anterior descending artery and saphenous vein graft to distal right coronary artery) 13 years previously. Three months later, routine Holter electrocardiogram (ECG) monitoring revealed asymptomatic episodes of second-degree and third-degree atrioventricular block. The patient refused pacemaker implantation because of lack of symptoms.
In December 2002 the patient developed dyspnea (New York Heart Association [NYHA] class II). Another 24-hour ECG showed not only high-degree atrioventricular block but also sinus bradycardia. A dual-chamber pacemaker was implanted in February 2003. Follow-up was uneventful, and right ventricular pacing was reported to be almost 100%.
In December 2005 angiography was performed for atypical chest pain and a slight increase in dyspnea. No significant stenosis was present, but his left ventricular ejection fraction (LVEF) had decreased to 25%. Therefore an upgrade to a cardiac resynchronization therapy defibrillator (CRT-D) was carried out in February 2006.
In May 2007 the patient was free from dyspnea and echocardiography showed a normal LVEF of 73%.
The patient remained asymptomatic, and no arrhythmias, apart from paroxysmal atrial fibrillation, were recorded in the implantable cardioverter-defibrillator (ICD) memory. In July 2011 the battery was depleted (elective replacement indicator). Another echocardiogram confirmed a preserved LVEF of 60%. The patient was in NYHA class I. During VVI pacing with 30 bpm, no intrinsic ventricular activity is present.
Current Medications
The medications the patient was taking in February 2003 were atorvastatin 10 mg daily and aspirin. In February 2006 he was taking ramipril 7.5 mg daily, metoprolol 50 mg twice daily, torsemide 10 mg daily, atorvastatin 20 mg daily, and aspirin. In July 2011 he was taking ramipril 7.5 mg daily, metoprolol 50 mg twice daily, torsemide 10 mg daily, simvastatin 80 mg daily, and warfarin.
Current Symptoms
The patient had no angina, dyspnea, or peripheral edema.
Physical Examination
Laboratory Data
Electrocardiogram
Findings
The electrocardiogram revealed atrioventricular sequential pacing, paced QRS complex at 168 ms, and positive findings in lead V1 (Figure 30-1).
FIGURE 30-1 12-Lead electrocardiogram with cardiac resynchronization therapy “on.”
Echocardiogram
Findings
The echocardiogram showed the patient’s left ventricular end-diastolic volume to be 110 mL, left ventricular end-systolic volume of 43 mL, an LVEF of 60%, left ventricular mass index of 120 g/m2, and delta P over tidal volume of 15 mm Hg.
Focused Clinical Questions and Discussion Points
Question
Is a downgrade to a CRT pacemaker (CRT-P) an option to consider in this case?
Discussion
No guidelines or randomized trials have addressed this question. Also, no studies evaluated patient preferences in such situations. Cardiologists who hold the opinion “once ICD, always ICD” will perform ICD generator replacement. The reasons downgrading was chosen in this case are as follows:
1. If this patient would present now with a normal LVEF and third-degree atrioventricular block, he would receive a VDD or DDD pacemaker, because no data support “prophylactic” CRT implantation in this situation. In addition, no indication exists for ICD.
2. In a 2011 paper from our group,3 subgroup analysis of patients with a CRT-D and a primary prevention indication showed that only 1 in 46 patients whose LVEF improved to greater than 35% experienced ICD therapy beyond the first year (single episode antitachycardia pacing delivered for ventricular tachycardia) during a mean follow-up of 35 months. Device replacement was performed in 22 patients after a mean of 43 months. In none of the 8 patients who had not previously received ICD therapies were ICD therapies observed during an additional follow-up of mean 27 months.
3. Even though the patient most probably will not need ICD therapy, he still has a risk for inappropriate therapy. This risk is approximately 8% in patients with coronary artery disease with a primary prevention indication and a mean follow-up of 30 months.4 Even if an ICD would be programmed with a cutoff rate of greater than 230 bpm, considerable risk still exists for noise sensing because of lead fracture.
Question
Is downgrading to CRT-P or DDD pacing an option in this patient?
Discussion
Given the fact that the most likely cause for impaired left ventricular function and heart failure in this patient is dyssynchrony induced by right ventricular pacing, downgrading to CRT-P or DDD seems to not be a good idea. In addition, the difference in cost between a DDD device and a CRT-P device is much smaller than between CRT-P and CRT-D.
Discussion
This patient’s condition is obviously much better than before CRT implantation, regarding both LVEF and symptoms. However, the reason for this is unclear (e.g., biventricular stimulation, improved heart failure medication after CRT-D implantation, natural course, teetotalism). Therefore therapy with the angiotensin-converting enzyme inhibitor should be continued. The dosage of the diuretic can be reduced, as long as the patient takes his weight on a regular basis. No evidence shows that beta blockers in patients with normal LVEF improve their prognosis, so the dosage might be reduced or even stopped. On the other hand, if the patient tolerates it, why change a winning strategy?
Question
Should noninvasive stress testing or coronary angiography be done before a treatment decision is made?
Discussion
In nonischemic cardiomyopathy, no stress testing would be indicated. This patient has ischemic heart disease, but is free from angina since the coronary artery bypass graft performed 13 years previously. As long as an ICD is implanted, the patient is potentially protected from deleterious effects of severe ischemia or myocardial infarction, that is, ventricular fibrillation. Apart from treatment of risk factors, no intervention can reduce the risk for infarction, not even percutaneous coronary intervention. However, in patients with stable coronary artery disease, the annual risk2 for myocardial infarction (∼1.5%) or cardiovascular death (∼1%) is very low. To exclude severe ischemia as a potential trigger of ventricular fibrillation, myocardial perfusion scintigraphy or stress echocardiography would be the best option (class IIA, level B).1 In the case of a positive test, coronary angiography should be performed and the stenosis(es) treated. However, this would not change our attitude toward downgrading to CRT-P.
Final Diagnosis
The patient was diagnosed with chronic right ventricular pacing–induced impairment of LVEF.
Plan of Action
The decision was made to upgrade to CRT-D.
Intervention
Downgrade to CRT-P was performed after recovery of LVEF and no arrhythmias during a follow-up of 65 months. Twelve months after downgrading, no ventricular arrhythmias were documented in the CRT-P memory, but he was in atrial fibrillation and cardioversion was suggested.
Outcome
The outcome in this patient was favorable.
Selected References
1. Fox K., Garcia M.A., Ardissino D. et al. Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology; ESC Committee for Practice Guidelines (CPG).Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology. Eur Heart J. 2006;27:1341–1381.
2. Fox K.M. Efficacy of perindopril in reduction of cardiovascular events among patients with stable coronary artery disease: randomised, double-blind, placebo-controlled, multicentre trial (the EUROPA study). Lancet. 2003;362:782–788.
3. Schaer B.A., Osswald S., Di Valentino M. et al. Close connection between improvement in left ventricular function by cardiac resynchronization therapy and the incidence of arrhythmias in cardiac resynchronization therapy-defibrillator patients. Eur J Heart Fail. 2010;12:1325–1332.
4. Schaer B., Sticherling C., Szili-Torok T. et al. Impact of left ventricular ejection fraction for occurrence of ventricular events in defibrillator patients with coronary artery disease. Europace. 2011;13:1562–1567.
