Hemodynamic instability after pulmonary veins isolation in a patient with dual chamber pacemaker: The phantom injury of the ventricular lead

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Abstract

Introduction:

The standard treatment of sinus node dysfunction (SND) is the pacemaker implantation, and the ideal methodology for the management of atrial fibrillation (AF) is rhythm control, but this is sometimes very hard to accomplish. For such actions, complete isolation of all pulmonary veins (PVI) is currently widely accepted as the best endpoint.

Case Presentation:

In this case, we report a female patient, 81 years old, with controlled hypertension, without coronary artery disease, bearer of bilateral knee replacement, and dual chamber pacemaker implanted 1.5 years ago owing to sinus node disease, presenting the following symptoms: presyncope episodes associated with sustained irregular palpitation tachycardia. The evaluation of the pacemaker-recorded episodes of atrial fibrillation, the echocardiogram-presented normal systolic function and measurements, as well as the resting myocardial scintigraphy and with drug use did not demonstrate ischemia and/or fibrosis. The patient was in use of valsartan 320 mg daily, amlodipine 10 mg daily, sotalol hydrochloride 120 mg 2 times daily, and dabigatran 110 mg 2 times daily. At the end of the PVI, the patient presented hemodynamic instability, with a decrease in heart rate to 30 bpm and invasive arterial blood pressure to 60/30 mmHg. The pericardial puncture was quickly carried out with the possibility of cardiac tamponade as the first hypothesis, but no pericardial effusion was found. Next, we detected acute capture loss from the ventricular pacemaker lead, unvarying with high voltage and pulse width, even with stable impedance, sense and keeping the same position visualized by fluoroscopy. And there was soon afterwards induction of sustained ventricular tachycardia degenerating to spontaneous ventricular fibrillation. Electrical cardioversion-defibrillation was performed with 200J, and the sinus rhythm was reestablished, but there was a dead short, and the pacemaker generator was burned and disabled.

Conclusions:

So, we can speculate that application of atrial radiofrequency for PVI diffused through the tissues, affecting in some way the tip of the ventricular electrode, causing a microlesion in this structure and making it impossible to capture the right ventricle by the pacemaker. As we cannot see it, we can call it of phantom injury of the ventricular lead.

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