Unusual presentation of asymptomatic subacute lead-related ventricular perforation beyond the pericardium without pericardial effusion: a case report.

The clinical manifestations of subacute pacemaker lead-related cardiac perforations are highly variable. Patients with subacute perforations can present with a variety of symptoms, whereas those with acute perforations usually present with cardiac tamponade that necessitates emergent pericardiocentesis. A 32-year-old woman underwent pacemaker implantation for sick sinus syndrome. An active-fixation atrial lead was fixed to the right atrial appendage, and a ventricular lead was fixed to the right ventricle (RV) apex, with acceptable parameters. Two weeks postoperative, the patient visited the clinic for routine examination of the pacemaker parameters. Chest X-ray showed migration of the RV lead beyond the cardiac silhouette. Echocardiography revealed no evidence of pericardial effusion or tamponade. Computed tomography revealed that the RV lead was positioned beyond the RV and pericardium and into the anterior chest wall. Procedural lead revision was performed with cardiothoracic surgery backup. The lead was retracted after loosening the active-fixation screw and inserting the stylet. The lead was placed in the RV septum with active fixation. The procedure was completed without complications, and the patient was discharged after 3 days. Subacute lead perforations can present with various symptoms, and some patients may be asymptomatic without pericardial effusion. Altered lead parameters frequently provide the first indication for the diagnosis of cardiac perforation. Transvenous lead revision with surgical backup is an alternative to surgical extraction.

ECG features and proarrhythmic potentials of therapeutic hypothermia.

OBJECTIVE: Hypothermia can induce ECG J waves. Recent studies suggest that J waves may be associated with ventricular fibrillation (VF) in patients with structurally normal hearts. However, little is known about the ECG features, clinical significance or arrhythmogenic potentials of therapeutic hypothermia (TH)-induced J waves. METHODS: We analysed ECGs from 240 patients who underwent TH at six major university hospitals in Korea between August 2010 and December 2013. The prevalence, amplitudes and distributions of the J waves and the development of malignant arrhythmia were analysed. RESULTS: The average patient body temperature was 33.5±1.0°C during TH. J waves were observed in 98 patients (40.8%). They were newly developed in 91 cases, and pre-existing J waves were augmented in seven patients. J waves during TH were primarily observed in leads II, III, aVF and V4-6. The average amplitude of the J waves was 0.239±0.152 mV. There were four VF events during TH. These events occurred in three patients who were finally diagnosed with Brugada syndrome, idiopathic VF or early repolarisation syndrome, respectively, and in one patient with non-cardiac aetiology (asphyxia). CONCLUSIONS: J waves were recorded in about 40% of the patients who received TH. They were most frequently observed in the inferior limb leads or lateral precordial leads. Life-threatening VF occurred only rarely (1.7%) during TH and were mainly observed in patients with primary arrhythmic disorder. Although a causal relationship between TH-induced J waves and VF remains unknown, administering TH to this potentially susceptible, high-risk population may require careful attention.