• 2018-07
  • 2019-04
  • 2019-05
  • Nakai et al showed that RTc and Tpeak


    Nakai et al. showed that RTc and Tpeak-end dispersion can be used to evaluate the spatial distribution of myocardial repolarization [15,16]. We measured RTc and Tpeak-end dispersion in the acute and chronic periods in the case reported herein. Both variables were increased during the acute period after CRT, suggesting that repolarization heterogeneity was augmented before being modified by amiodarone. These changes are consistent with previous reports of prolongation of the Tpeak-end interval with LV pacing. On the follow-up SAVP-ECG, RTc and Tpeak-end dispersion had decreased to within safe ranges. There is no standard index for use of antiarrhythmic agents, and it is difficult to make the decision to stop an antiarrhythmic agent once it is started, even if the patient is free of arrhythmia. In the present case, RTc/Tpeak-end dispersion increased in the acute phase after CRT, suggesting a potential substrate for ventricular arrhythmia, but both measures decreased to within normal range with amiodarone administration and with time. We controlled the dose of amiodarone in response to the low risk for ventricular arrhythmia indicated by the SAVP-ECG. Our experience in this case highlights the importance of risk stratification for lethal arrhythmia after CRT.
    Conflict of interest
    Introduction When BV6 Supplier lead fracture occurs, the lead impedance usually BV6 Supplier increases drastically and often becomes immeasurable [1]. Here, we experienced the case of a patient with pacemaker lead fracture caused by a cardiac fibroma in which no great change in lead impedance was observed.
    Case report A high echoic mass was incidentally found on a routine transthoracic echocardiogram (TTE) in June 2011. The mass was 28mm in diameter and seemed to adhere to the tricuspid valve and a ventricular lead (Fig. 1). The patient did not have subjective symptoms, and there was no evidence of infection. The pacing threshold and lead impedance remained unchanged compared to those recorded 6–24 months previously. Therefore, we decided to follow the patient carefully. He underwent TTE several times thereafter, but the size of mass did not change. The lead impedance was measured every 4–6 weeks by a programmer and was maintained at around 500–600Ω between March 2011 and January 2012. The patient complained of dyspnea on exertion, and pacing failure was observed on an electrocardiogram in January 2012. He underwent urgent pacemaker check, and we found that the pacemaker did not sense the R-wave and did not pace at all. Although the lead impedance was only slightly increased (689Ω), a chest X-ray showed that the pacemaker lead was fractured at the tricuspid level (Fig. 2). A TTE showed new severe tricuspid valve regurgitation and a floating mass around the ventricular lead. Acute decompensated heart failure was diagnosed, and we attempted surgical treatment. We extracted the fractured lead, enucleated the tumor, replaced the tricuspid valve under cardiopulmonary bypass, and implanted an epicardial lead. Macroscopic examination revealed that the tumor surrounded the fractured lead and covered the stump (Fig. 3A, B). Pathological examination revealed that the tumor had no granulation, fibrin agglomeration, or inflammatory cell invasion but was composed of fibrous connective tissue with calcification (Fig. 3C). The tumor and the fractured lead were subjected to bacteriological studies, and no microorganisms were detected. Consequently, the tumor was diagnosed as a cardiac fibroma.
    Discussion Cardiac tumors are rare and most of them are myxomas [2]. Cardiac fibroma accounts for only a small percentage of all cardiac tumors [2]. Furthermore, there have been no reports showing that cardiac fibroma may be related to pacemaker lead fracture. The incidence of pacemaker lead fracture is about 2.6–3.6% [3,4]. However, most cases of pacemaker lead fracture occur within the pacemaker pocket or the subclavian vein between the clavicle and the first rib [3,4], and fracture at the tricuspid valve level is rare [5–7]. When lead fracture occurs, the lead impedance becomes greatly elevated and immeasurable by pacemaker telemetry [1]. However, the present case showed only a slight increase in the lead impedance after the fracture of the lead. Had the pacemaker lead system in this case been bipolar, the lead impedance might have increased greatly. We presume that an electric current continued flowing through the stump of the fractured unipolar lead to the generator, which might have caused the limited increase in lead impedance in this case. In addition, a remote monitoring system was not used in this case to measure the lead impedance. It may have been possible to detect a partial fracture before the completion of the lead fracture if this patient used a remote monitoring system [8,9].