buy Sunitinib One day after implantation diaphragmatic

One day after implantation, diaphragmatic stimulation was observed when the patient was in the seated position, and it could not be resolved by reprogramming the device. We decided to replace the LV lead; however, there were no other vein branches suitable for CRT in the lateral region of the LV (Fig. 2A and B). We tried to insert the lead into an upper branch of the posterolateral vein, but we could not obtain a suitable pacing threshold. We replaced the LV lead more proximally in the same posterolateral vein, and confirmed that buy Sunitinib stimulation was not observed on fluoroscopy during pacing at outputs of up to 10V. A postoperative 12-lead ECG showed a QRS duration of 128ms during biventricular pacing (Fig. 1B). The operation was performed under general anesthesia. A thoracoscopic procedure was carried out with a 3-port technique: 1 camera port (11.5mm) was placed in the eighth intercostal space at the mid-axillary line, and 2 working ports (5mm each) were placed in the fifth intercostal space at the anterior and posterior axillary lines. The left phrenic nerve was carefully detached from pericardial adipose tissue (Fig. 3A), and electrical insulation was accomplished with a 4×5cm2 Gore-Tex patch inserted between the phrenic nerve and the pericardium (Fig. 3B). The operative time was 112min and total blood loss was 3mL. No intraoperative or postoperative complications were observed. Following the procedure, the LV pacing threshold was 1.8V at 0.4ms and the impedance was 674Ω. The R-wave sensing threshold was 30.0mV. Diaphragm stimulation was not observed in any position during pacing at outputs of up to 10V.
Discussion The present case report describes a patient who underwent successful thoracoscopic LV lead insulation to eliminate phrenic nerve stimulation during CRT. An echocardiography conducted at 2 years after implantation showed significant reverse remodeling (LV ejection fraction=48.9%, LV end-diastolic diameter=50mm, LV end-systolic diameter=35mm, and LV end-systolic volume=55.8mL). CRT has been demonstrated to improve systolic function in heart failure patients with conduction system disorders [1,2]. The stimulation site within the LV might play an important role in the outcome of CRT [3,4]. Transvenous LV lead implantation depends on the coronary venous anatomy. Coronary sinus angiography revealed that there were no other branches suitable for CRT (Fig. 2B). Lead insertion in the anterior or mid-cardiac vein may not result in optimal LV synchronization [5–7]. Furthermore, repeated implantation procedures are associated with an increased risk of device infection. Therefore, we decided not to perform LV lead replacement using a coronary vein-based lead system [8]. An epicardial LV lead implanted surgically was an option for the elimination of phrenic nerve simulation [9,10]. The surgical LV lead implantation could be performed using a thoracoscopic approach. Even though the epicardial side of the surgically implanted epicardial lead was insulated, in rare instances, this might cause phrenic nerve stimulation [11]. In most cases, a suitable site away from the phrenic nerve can be found. However, in CRT, the suitable area was limited to the mid-lateral region of the LV, and CRT with an epicardial lead implanted at the mid-lateral region of the LV can potentially result in a recurrence of phrenic nerve twitching [11]. Furthermore, the surgically implanted LV lead has to be connected with a subcutaneous CRT-D generator. In our case, a 12-lead ECG during biventricular pacing showed a narrow QRS width, and except for the phrenic nerve stimulation, the implanted lead position was appropriate for LV synchronization. We considered that the thoracoscopic placement of Gore-Tex insulation on the transvenous lead was a less invasive option than surgical LV lead implantation. Injury to the phrenic nerve and phrenic nerve paralysis are considerable potential complications of phrenic nerve electrical insulation. Furthermore, thoracoscopic phrenic nerve insulation requires general anesthesia, the risks of which should also be considered. We believe that replacement of the LV lead using a transvenous approach is the method of choice for the avoidance of phrenic nerve stimulation. However, when acceptable results cannot be obtained using the transvenous approach, as in our case, thoracoscopic phrenic nerve insulation represents a potential option for the management of uncontrollable phrenic nerve stimulation during CRT [12].
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Introduction
Case report A 52-year-old male with known dextrocardia and CCTGA presented with a 2-month history of recurrent presyncope and effort intolerance. His examination revealed a resting pulse rate of 52beats/min (bpm) and a blood pressure of 130/80mmHg. The apex beat and heart sounds were appreciated on the right side of the sternum, whereas gastric tympany was noted below the left diaphragm. A 12-lead electrocardiogram (ECG) revealed sinus rhythm with an atrial rate of 80bpm, complete atrioventricular block, and a narrow QRS escape with a rate of 50bpm. The normal P wave axis (+60°) indicated normal atrial situs, the progressive decrease in the height of the R waves from V1 to V6 suggested dextrocardia, and the absence of septal q waves in the lateral leads was suggestive of CCTGA (Fig. 1). A posteroanterior chest radiograph confirmed dextrocardia with situs solitus. A transthoracic echocardiogram confirmed the diagnosis of situs solitus, dextrocardia, and CCTGA with adequate systemic ventricular function and no other associated abnormality. The temporary pacemaker lead, which was inserted from the right femoral vein just prior to PPI, was seen to course along a right-sided inferior vena cava, further confirming the atrial situs as solitus. Under local anesthesia using 1% lignocaine hydrochloride, a 3-cm long incision was made one fingerbreadth below the right clavicle across the deltopectoral groove such that two-thirds of the incision was medial and one-third was lateral to the groove, and an attempt was made to isolate the cephalic vein. Since the cephalic vein was not of adequate caliber, venous access was obtained through two separate extrathoracic axillary venous punctures using an 18G needle and two guide wires that were inserted into the venous system. A 7F active fixation lead (model 4076, 58cm, Medtronic Inc., Minneapolis, MN, USA) was inserted through a 7F peel-away introducer (Medtronic Inc., Minneapolis, MN, USA) over one guide wire. The lead was manipulated into the pulmonary artery over a stillette that was given a distal curvature. The lead withdrawn from the pulmonary artery into the venous ventricle acquired a position that appeared to be septal in the anteroposterior (AP) view, but appeared to point laterally in the right anterior oblique view (RAO). Since the true position of the lead was not quite clear, angiographic delineation of the right heart chambers was considered an option. Through the second access that was meant for the atrial lead, a 6F valved introducer with a side port (AVANTI®+, Cordis Corporation, Miami, FL, USA) was inserted, and the distal tip was positioned in the superior vena cava. Through the side port, 10mL of non-ionic intravenous contrast (iohexol) was rapidly injected by hand, and cine films were acquired in the AP, left anterior oblique (LAO), and RAO views. This was performed to define the position of the venous atrium and its appendage, the relationship of the venous atrium to the venous ventricle, and anatomical details of the venous ventricle. The acquired films confirmed the lateral wall position of the previously placed lead and served as roadmaps to facilitate further lead positioning (Fig. 2). After failed attempts at obtaining a stable lead position in the septal region because of the smooth-walled morphologic left ventricle, the lead was screwed to the apex, where sensed R waves of 18mV, a threshold of 0.9V, pulse width of 0.4ms, and lead impedance of 780ohms were obtained. The 6F valved introducer was then exchanged over a guide wire for a 7F peel-away introducer, and an atrial straight active fixation lead (model 4076, 52cm, Medtronic Inc., Minneapolis, MN, USA) was inserted through it. The lead was positioned in the right atrial appendage over a curved stillette, with the previously acquired cine films serving as a roadmap. Satisfactory pacing parameters were obtained, with P waves of 4.4mV, threshold values of 0.5V at a pulse width of 0.5ms, and a lead impedance of 550ohms (Fig. 3). After confirming the stable positions of both leads, the leads were secured to the muscle. A dual chamber pulse generator (Model Relia DDD, Medtronic Inc., Minneapolis, MN, USA) was attached to the leads and placed in a pre-pectoral pocket, and the wound was closed in layers. A post-procedural 12-lead ECG revealed atrial sense and ventricular paced complexes with a right bundle branch block pattern and left axis deviation. The patient׳s post-procedural course was uneventful.