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Introduction Perforation of a cardiac chamber has been reported as a relatively rare complication of pacemaker implantation; in particular, attachment of the active-fixation atrial lead to the atrial wall carries the risk of perforation that can result in cardiac tamponade [1–10].
Case report A 72-year-old woman who complained of dyspnea on exertion was referred to our hospital on January 21, 2010. Electrocardiography (ECG) on admission showed complete atrioventricular block with a junctional escape rhythm of 35bpm. Although chest radiographs revealed pulmonary congestion and an increased cardiothoracic ratio of 55%, echocardiography showed no evidence of structural buy diazoxide disease or other abnormalities. Laboratory data were within normal limits, with the exception of an elevated amino-terminal fragment of the B-type natriuretic peptide prohormone concentration of 653pg/mL. Permanent pacemaker implantation via the left subclavian vein was performed subsequently with bipolar active-fixation leads (Medtronic CapSureFix Novus, model 5076, Minneapolis, MN, USA) positioned in the right atrial appendage and at the right ventricular basal septum without any difficulty. The atrial pacing threshold was 0.7V at 0.5ms, the pacing impedance was 615Ω, and the P-wave amplitude was 3.1mV. The ventricular pacing threshold was 0.5V at 0.5ms, the pacing impedance was 888Ω, and the R-wave amplitude was 6.2mV. A generator (Sensia DR model SEDR01; Medtronic) was then connected, and ECG showed normal dual-chamber pacing. Movement of the cardiac silhouette on cinefluoroscopy in a 30° left anterior oblique view was normal at the end of the procedure. Chest radiographs obtained in the operation room showed the right atrial lead positioned in the right atrial appendage (Fig. 1). An ECG recorded 40min after the implantation demonstrated that the pacemaker was normally functioning with atrial sensing followed by ventricular pacing (Fig. 1). Approximately 3.5h after the procedure, the patient complained of nausea, and the systolic blood pressure decreased to less than 60mmHg. Echocardiography revealed a large pericardial effusion with evidence of cardiac tamponade and right atrial and ventricular notching. Emergent pericardiocentesis was performed, yielding 850mL of blood, and a pericardial drainage catheter was left in place. However, the patient׳s hemodynamic status did not stabilize. Repeat echocardiogram showed a large, nonhomogeneous, echodense mass, consistent with thrombus, in the epicardial space. Cardiac tamponade due to a large thrombus was suspected. She was taken to the operating room to undergo thoracotomy to remove the thrombus and determine its etiology. On arrival to the operating room, sudden cardiac arrest occurred. Cardiopulmonary resuscitation was performed immediately and simultaneous thoracotomy was undertaken. A surgeon performed open chest heart massage and the heart began to beat. After evacuation of 1400mL of hemopericardium along with several thrombi, bright red blood was seen gushing out from the right coronary artery (Fig. 2). When the surgeon pressed the right coronary artery to control the bleeding, a semi-circle of the atrial lead helix was found to be penetrating the right atrial appendage apex, which was located near the bleeding site (Fig. 3). The screw tip of the atrial lead was protruding 1.8mm out through the wall of the right atrium. There was no active bleeding from the helix penetration site, and a thorough inspection of the pericardium and heart revealed no other bleeding sites. The right coronary artery perforation was repaired using autologous pericardium-reinforced 7-0 prolene mattress sutures. The tip of the screw on the atrial wall was covered by autologous pericardium to prevent further cardiac injury. The distance between the right coronary artery perforation site and the tip of the lead helix was estimated to be less than 10mm.