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    • br Discussion Implantation of a

    2019-05-28


    Discussion Implantation of a defibrillation patch under thoracotomy has been used for implantation in the beginning and is still in use in cases where venous access is inadequate, and studies have reported postoperative BMS354825 Supplier failure in 3 of 35 ICD patients treated with a defibrillation patch [1]. In such cases, heart failure was considered to be related with the epicardial patch, resulting in removal of the patch. It is important to be attentive towards diastolic dysfunction before surgery [2]. In our case, heart failure due to diastolic dysfunction was observed before surgery and an epicardial patch was considered to be harmful for this patient. Subcutaneous ICD, which is widely used in western countries, may be an alternative in cases where sinus bradycardia is absent, but in our patient atrial pacing would have been required with such an approach. In this case, lead insertion from the BMS354825 Supplier left subclavian vein via the L-SVC was feasible. Persistent left superior vena cava (PLSVC) is a congenital venous malformation occurring in 0.3–0.5% of the general population [3], but its presence in the absence of the R-SVC is a very rare congenital anomaly [4]. ICD placement is a complicated procedure in PLSVC cases, but is nevertheless still feasible [5]. A report indicated that lymphedema occurs in approximately 50% of cases with a history of mastectomy [6], which in turn leads to a decrease in the patients׳ quality of life. Lead implantation from the left subclavian vein via the L-SVC would have been precarious owing to the increased risk of lymphedema; therefore, lead implantation from the right subclavian vein via the L-SVC was the alternative option. However, the right brachiocephalic vein was compressed on entry into the L-SVC leading to an increased risk of lead dislodgement and was therefore considered to be unfeasible. A transthoracic transatrial approach was quite a distinct choice for lead placement, and earlier reports of 35 patients who were treated in this way as the transvenous approach was difficult showed that 8 patients were without any particular complications for up to 14 years [7,8]. We chose this approach in our case, and the postoperative course was uneventful.
    Conclusion
    Conflict of interest
    Case report An 80-year-old woman with a history of acute myelocytic leukemia in remission was hospitalized to undergo cardiac resynchronization therapy (CRT) for refractory congestive heart failure due to doxorubicin-induced cardiomyopathy. Twelve-lead electrocardiography during sinus rhythm revealed a complete left bundle branch block (CLBBB) and a 156-ms QRS (Fig. 1A). The cardiothoracic ratio on chest radiography was 58%. Transthoracic echocardiography revealed diffuse left ventricular (LV) hypokinesis, an ejection fraction of 34%, a 55-mm end-diastolic diameter, and overt dyssynchrony. An inextensible false tendon, 3mm in its widest diameter, was visible with a hyperechoic shadow between the mid-septal and mid-lateral walls (Fig. 1C). Two-dimensional speckle tracking-derived displacement curves showed that the lateral LV wall contracted during systole and relaxed during diastole, whereas the septum expanded during systole and contracted during diastole (Fig. 2A). Neither myocardial perfusion scintigraphy nor magnetic imaging revealed the presence of prominent myocardial injury or septal fibrosis. Septal-to-posterior wall motion delay, an index of intraventricular dyssynchrony, was increased to 403ms (upper normal limit, 129ms). CRT-D was implanted with leads placed at the right ventricular apex and in the posterolateral tributary of the coronary sinus. After achieving the best V–V delay of 0mms based on the echographic measurements, the QRS width was shortened to 124ms (Fig. 1B). The result of a speckle tracking analysis in apical 4-chamber view during CRT showed a nearly unchanged and normal LV lateral wall motion, as well as an unchanged, dyssynchronous, mid-septal motion at the point of attachment of the false tendon, while a decrease to 100ms in the septal-to-posterior wall motion delay was limited to the basal septum (Fig. 2B). Similarly, the result of a speckle tracking analysis in short-axial view during CRT showed normal LV anterior, lateral, posterior, and inferior wall motions, as well as dyssynchronous, anteroseptal, and septal motions at the point of attachment of the false tendon, which was characterized by dyssynchronous motion during mid and late systolic phases after a small synchronous motion during an early systolic phase (Fig. 3B). The shape and length of the false tendon remained fixed during the entire cardiac cycle, regardless of the presence or absence of CRT. However, a dyssynchronous apical motion was not normalized during the CRT.