History
This 68-year-old man had a history of non-ST elevation myocardial infarction in 2008 and percutaneous coronary intervention with incomplete revascularization to triple-vessel disease. He developed atrial fibrillation and congestive heart failure in 2010. An echocardiogram showed a left ventricular ejection fraction (LVEF) of 19%, left ventricular end-diastolic volume of 146 mL, and left ventricular end-systolic volume of 119 mL. The QRS width was 144 msec. He remained in New York Heart Association (NYHA) class III while on optimal medical therapy for heart failure. He received a cardiac resynchronization therapy (CRT) pacemaker with bipolar right ventricular lead in the right ventricular apex and bipolar left ventricular lead positioned at the posterior branch of the great cardiac vein together with atrioventricular nodal ablation in 2010. On follow-up, anodal stimulation was detected on device interrogation and testing and the anodal stimulation threshold was 2.0 V at 0.4 msec, which was only slightly higher than the left ventricular lead pacing threshold, at 1.5V at 0.4 msec. The left ventricular lead output was set at 3.0 V at 0.4 msec, which was above the anodal stimulation threshold. No V-V delay was set for the patient. At follow-up examination at 6 months, improvement in symptoms with NYHA class II was noted. An echocardiogram showed an increase in LVEF to 25% and reduced left ventricular end-systolic volume of 91 mL.
Current Medications
The patient was taking clopidogrel 75 mg daily, simvastatin 20 mg daily, lisinopril 10 mg daily, carvedilol 12.5 mg twice daily, and aspirin 80 mg daily.
Current Symptoms
The patient’s heart failure symptom has improved to NYHA class II. He enjoys light exercise mainly in terms of brisk walking and reports no angina.
Physical Examination
Laboratory Data
Electrocardiogram
Findings
Figure 43-1, A, shows biventricular pacing at maximum output that resulted in anodal stimulation and triple site stimulation (i.e., right ventricular ring, right ventricular tip, and left ventricular tip). Figure 43-1, B, shows biventricular pacing below the anodal stimulation threshold, with subtle change in aVL and aVR, in contrast to triple site stimulation. In Figure 43-1, C, further decrement in left ventricular lead output can be seen, which resulted in loss of left ventricular capture, with the electrocardiogram (ECG) morphology basically the same as in right ventricular pacing alone. As shown in Figure 43-1, D, on testing by left ventricular pacing alone at maximum output, the ECG is very similar to what would be seen with biventricular pacing because of simultaneous right ventricular ring anodal stimulation and left ventricular pacing. Decrement of left ventricular lead output, as seen in Figure 43-1, E, led to loss of anodal stimulation and activation starts from the left ventricular pacing lead with marked change in ECG morphology.
FIGURE 43-1
Focused Clinical Questions and Discussion Points
Question
How is anodal stimulation recognized in a patient with a CRT?
Discussion
Most CRT devices use a bipolar lead for right ventricular pacing and a unipolar or bipolar lead for left ventricular pacing. Configuration of the left ventricular tip or ring as the cathode and the right ventricular lead ring as the anode is sometimes employed to prevent phrenic nerve stimulation or optimize the threshold for the left ventricular lead. In this configuration, potentially the right ventricular ring electrode can capture the myocardial tissue directly and result in the phenomenon of anodal stimulation.1,2,4,5 Anodal sitmulation typically occurs with high left ventricular lead output,1,2,4,5 and it is demonstrated by a change in 12-lead ECG morphology during increment of pacing output above pacing threshold during left ventricular only pacing (with the right ventricle output programmed off). In the presence of anodal stimulation, the ECG morphology is the same as simultaneous left and right ventricular (biventricular) pacing. It is reported that anodal stimulation can be detected in 78.4% of cases.2 Anodal stimulation can also be seen during biventricular pacing when the QRS morphology becomes narrower at high left ventricular lead pacing output. This can be observed in only 41.4% of cases.2 In this case report, very subtle change was observed that best could be appreciated in leads aVL and aVR, with loss of anodal stimulation when left ventricular lead output was decremented to 2.0 V at 0.4 msec when testing in the biventricular pacing configuration (see Figure 43-1). With further decrease in left ventricular lead output to 1.5 V, loss of left ventricular capture and only right ventricular capture were noted. Loss of anodal stimulation was more obvious when tested in the left ventricular pacing alone configuration. The reason why anodal stimulation may not be apparent when testing with biventricular pacing is because of the close proximity of the right ventricular lead ring and tip so that triple site stimulation may not cause significant change in QRS morphology in contrast to biventricular pacing.
One obvious question is whether anodal stimulation resulted in suboptimal CRT. In a small case study, 3 of 46 patients with left ventricular tip to right ventricular ring configuration were noted to have anodal stimulation and all of them were nonresponders to CRT.3 Also, in a study of the hemodynamic effect of anodal stimulation by echocardiogram, no statistical difference was found in the hemodynamic effect of anodal stimulation on biventricular pacing. However, in 2 patients, worsening of hemodynamic status was noted with the presence of anodal stimulation.7 Obviously, these studies are small in sample size and no definitive conclusion can be drawn. Another potential drawback of anodal stimulation is the elimination of the effect of V-V delay because of simultaneous capture of the right ventricular ring (anodal stimulation) and left ventricular tip.6
Final Diagnosis
This patient had clinically detectable anodal stimulation. As a result the device was to allow triple site stimulation, with favorable response in terms of functional class and left ventricular reverse remodeling after CRT.
Plan of Action
The plan for this patient was to enable triple site pacing.
Selected References
1. Bulava A., Ansalone G., Ricci R. et al. Triple-site pacing in patients with biventricular device-incidence of the phenomenon and cardiac resynchronization benefit. J Interv Card Electrophysiol. 2004;10:37–45.
2. Champagne J., Healey J.S., Krahn A.D., ELECTION Investigators et al., et al. The effect of electronic repositioning on left ventricular pacing and phrenic nerve stimulation. Europace. 2011;13:409–415.
3. Dendy K.F., Powell B.D., Cha Y.M. et al. Anodal stimulation: an underrecognized cause of nonresponders to cardiac resynchronization therapy. Indian Pacing Electrophysiol J. 2011;11:64–72.
4. Tamborero D., Mont L., Alanis R. et al. Anodal capture in cardiac resynchronization therapy implications for device programming. Pacing Clin Electrophysiol. 2006;29:940–945.
5. Thibault B., Roy D., Guerra P.G. et al. Anodal right ventricular capture during left ventricular stimulation in CRT-implantable cardioverter defibrillators. Pacing Clin Electrophysiol. 2005;28:613–619.
6. van Gelder B.M., Bracke F.A., Meijer A. The effect of anodal stimulation on V-V timing at varying V-V intervals. Pacing Clin Electrophysiol. 2005;28:771–776.
7. Yoshida K., Seo Y., Yamasaki H. et al. Effect of triangle ventricular pacing on haemodynamics and dyssynchrony in patients with advanced heart failure: a comparison study with conventional bi-ventricular pacing therapy. Eur Heart J. 2007;28:2610–2619.
