A sudden rise in pacing threshold of left ventricular lead associated with myocardial ischemia

We report for the first time a sudden rise in the pacing threshold of the left ventricular lead due to myocardial ischemia after cardiac resynchronization therapy with defibrillator implantation, and its recovery to the baseline after the revascularization.


| INTRODUC TI ON
Myocardial ischemia may become a cause of increases in pacing lead threshold after implantation of a cardiovascular implantable electronic device. Acute changes in the right ventricular (RV) and atrial lead pacing threshold following myocardial infarction have been demonstrated. Here, we report for the first time a sudden rise in the pacing threshold of the left ventricular (LV) lead because of myocardial ischemia after cardiac resynchronization therapy with defibrillator (CRT-D) implantation, and its recovery to the baseline after revascularization.

| C A S E REP ORT
A 73-year-old man suffered symptomatic heart failure with the left ventricular (LV) ejection fraction of 28% and intraventricular conduction disturbance (QRS duration 170 ms, Figure 1A) because of broad anterior wall myocardial infarction diagnosed 24 years previously. He had a past history of diabetes. Elective implantation of CRT-D (Quadra Assura MP™, Abbott) was performed. In the present case, clopidogrel was used after a prior myocardial infarction. The use of clopidogrel (75 mg/d) was discontinued 2 days before CRT-D implantation and was resumed 4 days after CRT-D implantation. The LV pacing lead was positioned in the posterolateral vein because of preserved coronary artery blood flow in the targeted area observed on coronary angiography 7 days before CRT-D implantation ( Figure 1B). At baseline, LV capture was found at the multiple pacing vectors (Table 1) Figure 3D).

| D ISCUSS I ON
A quadripolar LV pacing lead enables to overcome a high pacing threshold after device implantation by means of a range of programmed configurations. However, acute changes in the pacing lead threshold can occur following device implantation because of lead displacement and myocardial tissue inflammation just after lead positioning. Also, an acute rise in the pacing threshold following myocardial infarction has been reported after RV or right atrial lead positioning. In our case, lead displacement was excluded using fluoroscopy. In addition, changes in pacing lead threshold attributed to myocardial tissue inflammation might have been less likely because LV pacing lead was positioned in the venous system, and the influence of lead positioning on myocardial tissue could be small.
Therefore, myocardial ischemia was considered as the main cause of a sudden rise in the LV lead pacing threshold. Furthermore, the relationship between myocardial ischemia and a change in the pacing lead threshold might be supported by LV pacing failure at the multiple pacing vectors despite LV capture was achieved across a range of area at baseline. However, detection of myocardial ischemia was difficult, because the patient was asymptomatic for cardiac ischemia because of diabetes, and ST-segment could not be evaluated during pacing rhythm. Although unipolar electrocardiograms recorded from the electrodes has been reported to be useful for demonstrating myocardial ischemia, the unipolar electrocardiograms of the LV lead were not recorded during the acute phase. In the present case, we initially detected the LV pacing failure from electrocardiographic findings, and then coronary angiography revealed a complete occlusion of the OM branch, perfusing the area around the implanted LV lead electrodes. After revascularization of the occluded coronary artery, the LV pacing lead threshold was improved.
In conclusion, myocardial ischemia was associated with a sudden rise in the pacing threshold after CRT-D implantation. In case of a sudden rise in the pacing lead threshold, the presence of myocardial ischemia should be considered as one of the differential diagnosis.