Archives

  • 2026-05
  • 2026-04
  • 2026-03
  • 2026-02
  • 2026-01
  • 2025-12
  • 2025-11
  • 2025-10
  • 2025-09
  • 2025-03
  • 2025-02
  • 2025-01
  • 2024-12
  • 2024-11
  • 2024-10
  • 2024-09
  • 2024-08
  • 2024-07
  • 2024-06
  • 2024-05
  • 2024-04
  • 2024-03
  • 2024-02
  • 2024-01
  • 2023-12
  • 2023-11
  • 2023-10
  • 2023-09
  • 2023-08
  • 2023-07
  • 2023-06
  • 2023-05
  • 2023-04
  • 2023-03
  • 2023-02
  • 2023-01
  • 2022-12
  • 2022-11
  • 2022-10
  • 2022-09
  • 2022-08
  • 2022-07
  • 2022-06
  • 2022-05
  • 2022-04
  • 2022-03
  • 2022-02
  • 2022-01
  • 2021-12
  • 2021-11
  • 2021-10
  • 2021-09
  • 2021-08
  • 2021-07
  • 2021-06
  • 2021-05
  • 2021-04
  • 2021-03
  • 2021-02
  • 2021-01
  • 2020-12
  • 2020-11
  • 2020-10
  • 2020-09
  • 2020-08
  • 2020-07
  • 2020-06
  • 2020-05
  • 2020-04
  • 2020-03
  • 2020-02
  • 2020-01
  • 2019-12
  • 2019-11
  • 2019-10
  • 2019-09
  • 2019-08
  • 2019-07
  • 2019-06
  • 2019-05
  • 2019-04
  • 2018-07

    • The mechanism underlying the proarrhythmic effect of CRT is

    2019-04-29

    The mechanism underlying the proarrhythmic effect of CRT is not well understood. One explanation is that transmural dispersion of repolarization increases with LV pacing. Bai et al. studied the effects of LV epicardial pacing and biventricular pacing in a canine model of dilated cardiomyopathy [11] and showed that both LV epicardial pacing and biventricular pacing prolonged the ventricular repolarization time and increased transmural dispersion of repolarization. Prolonged transmural dispersion occurred parallel to augmentation in the Tpeak-end interval. According to Scott et al., CRT with transseptal endocardial LV pacing (in comparison with epicardial LV pacing) reduced QTc and Tpeak-end dispersion, and these authors concluded that transseptal LV pacing may be less arrhythmogenic [12]. Barbhaiya et al. looked at the relationship between ventricular arrhythmia, the QT interval, and Tpeak-end dispersion and found that increases in Tpeak-end dispersion and Tpeak-end/QT ratio were associated with an increased incidence of ventricular arrhythmia in patients with a CRT-D [13]. Another group also reported an association between Tpeak-end dispersion and major arrhythmic events [14]. 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 buy ARCA 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.
    Conclusion
    Conflict of interest
    Introduction When pacemaker lead fracture occurs, the lead impedance usually 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.