An 86-year-old woman with a history of hypertension, congestive heart failure (CHF), and prior ICD implantation presented to the emergency department with severe, stabbing chest pain radiating to the back. The pain had started 2 hours earlier while she was sitting and was exacerbated by inspiration. She denied shortness of breath or cough. Her blood pressure was 198/64 mm Hg, heart rate 60 beats per minute, and oxygen saturation 99% on a 2-L nasal canula.
An electrocardiogram showed a left bundle branch block. A CXR report stated that there were no acute pulmonary findings and that an ICD device with intracardiac leads was present, without mention of lead position (Figure 1, Figure 2). The CT report noted a trace right pneumothorax, pneumomediastinum, small subsegmental pulmonary embolism in the right lower lobe, small right pleural effusion, and pulmonary nodule at the left lung base. A diagnosis of pulmonary embolus was made. Treatment with enoxaparin and warfarin was started. Serial cardiac enzyme results were negative. The patient's chest pain improved, and she no longer had pruritic symptoms. She remained hemodynamically stable on anticoagulants and was discharged 2 days later on enoxaparin and warfarin.
She was readmitted 2 days later with shortness of breath, palpitations, and constant, severe, substernal chest pain radiating to the abdomen. She had new onset atrial fibrillation (AF) with a heart rate of 200 beats per minute, so an electrophysiology consultation was obtained.
Chest CT images showed an ICD lead perforating the apex of the RV, with the tip residing in the left lower lung. On inspection of the chest CT images by the consulting electrophysiologist, a second perforated RV ICD lead was seen extending anteriorly and inferiorly out of the RV. A retrospective evaluation of the CT scan and CXR taken on the first admission demonstrated that both RV ICD lead perforations had been present at that time. Interrogation of the ICD showed that all ventricular tachycardia and ventricular fibrillation detection and therapies were programmed off and the RV pacing outputs had been programmed to minimum. Outside records were requested.
Both RV ICD leads had been implanted 3 months prior at another hospital as an upgrade to a biventricular ICD from a dual-chamber pacemaker previously implanted for sick sinus syndrome. The ICD had been implanted because of an ejection fraction of 35%, symptoms of CHF, and left bundle branch block with intrinsic QRS of 163 ms. Both RV ICD leads were active-fixation St. Jude Medical Durata 7122 leads (St. Paul, MN). The first RV ICD lead was positioned in the RV apex. The day after the ICD implantation, the patient complained of chest pain and the RV threshold was significantly higher. Two days later, a second RV ICD lead was placed in the RV septum. The first RV ICD lead was left in place with the screw retracted. Four weeks later, the patient received 6 inappropriate ICD shocks for noise. At that point, the RV output setting was reduced to minimum and ventricular tachycardia and ventricular fibrillation therapies were turned off. A CXR report did not mention lead position. No other data were available from the records obtained.
After the perforations were diagnosed, the patient refused removal of the leads and requested a "do not resuscitate" order. The patient was evaluated by a psychologist and deemed competent. She was aware of the risk of anticoagulation with the presence of perforated leads, but she wished to continue anticoagulation therapy to prevent a stroke. Initially, the ventricular rate in AF was not controlled, and she developed recurrent CHF symptoms. She was started on amiodarone therapy, the AF terminated, and she maintained sinus rhythm. After 10 days, she was discharged on warfarin and enoxaparin.
The patient was readmitted 2 days later with weakness. The international normalized ratio was 3.9. Despite the perforations and full anticoagulation, she remained stable. After repeated conversations, she agreed to undergo removal of the perforated ICD leads and ICD device. Anticoagulation was discontinued, and the preoperative international normalized ratio was 1.4.
The surgeon performed a left thoracotomy. Both leads extruded from the RV 4-5 cm beyond the pericardium (Figure 3). The pericardium was excised around both leads, and the exit points were secured with 4-0 pledgeted Prolene sutures (Ethicon, Somerville, NJ). The surgeon noted that the leads moved freely with each heartbeat but there was no evidence of blood leakage. Both leads were cut at the site of exit from the myocardium and removed by applying traction at the lead end located in the pocket. The remaining 2 pacemaker leads, 1 in the right atrium and 1 in the RV, were found to be functioning normally and were connected to a new dual-chamber pacemaker. The left ventricular lead, a St. Jude Medical Quartet 1458Q, was capped and left in place. It was not compatible with any biventricular pacemaker. An epicardial left ventricular lead was not placed, because of pericardial adhesions. The patient tolerated the procedure well and was discharged on postoperative day 4.
Two months later, a CXR showed complete resolution of the pleural effusion, pneumothorax, and pneumomediastinum. The patient continued on guideline-directed medical therapy, and her ejection fraction improved to 65%. Her case was reclassified 6 months later as New York Heart Association class 1.