Accelerated idioventricular rhythm after left bundle branch pacing lead implantation.

Premature ventricular contractions with right bundle branch block morphology induced during left bundle branch (LBB) pacing (LBBP) lead implantation serve as a marker indicating that the lead is close to or has reached the LBB region. However, no reports to date have described accelerated idioventricular rhythm (AIVR) induced by LBBP lead deployment. We herein describe a patient who underwent LBBP for complete atrioventricular block. The patient's intrinsic escape rhythm was overtaken by AIVR induced immediately after LBBP lead deployment. AIVR is another marker indicating that the lead has reached the LBB region.

Gradual development of left bundle branch current of injury during left bundle branch pacing lead implantation.

A larger left bundle branch (LBB) potential or LBB current of injury (COI) indicates a low LBB capture threshold in LBB pacing. During LBB pacing in an 85-year-old woman, achieving a low LBB capture threshold did not initially present with a larger LBB potential or LBB COI, but rather with a new initial negative deflection in a ventricular electrogram. LBB COI gradually developed over 7 min thereafter, which suggested that the lead tip had reached the left ventricular subendocardium. Therefore, this negative deflection may be the first sign to avoid further lead rotation.

Uncommon output-dependent paced QRS morphology transition during left bundle branch pacing.

We report a patient who underwent left bundle branch pacing (LBBP) because of intermittent complete heart block. During unipolar pacing at a deep septal site, a transition in QRS morphology from nonselective to selective pacing (presence of a discrete component on the intracardiac electrogram) was observed, but this was accompanied by concomitant prolongation of the stimulus-to-left ventricular activation time (Stim-LVAT) from 96 to 116 ms. However, with several additional turns of the lead, a transition from nonselective to selective LBBP with a short and constant Stim-LVAT of 78 ms was achieved. Our case suggests that a paced QRS morphology transition from nonselective to selective pacing does not always indicate LBBP. Assessment of high-output pacing is mandatory to achieve LBBP.

Successful resynchronization by permanent His-bundle pacing in a patient with pacing-induced cardiomyopathy.

Right ventricular (RV) pacing has been reported to result in ventricular dyssynchrony, heart failure, and increased mortality. Pacing associated deterioration of left ventricular (LV) systolic function has been termed pacing-induced cardiomyopathy (PICM). While upgrading to biventricular pacing (BiVP) is an effective therapy for PICM, permanent His-bundle pacing (HBP) can be a physiological alternative to BiVP. We present a patient with PICM who responded dramatically to permanent HBP.

Papillary fibroelastoma in the left ventricle resected under the guidance of a gastrointestinal fiberscope.

We report the case of a left ventricular mass in a 72-year-old man with ischemic heart disease. The tumor was deep in the left ventricle, and we considered that it would be difficult to directly visualize. Therefore, we inserted a gastrointestinal fiberscope into the heart. The tumor that was detected appeared to be a papillary fibroelastoma that arose from the left ventricular anterior papillary muscle. We resected the tumor under the guidance of a gastrointestinal fiberscope and performed coronary artery bypass grafting. The gastrointestinal fiberscope was useful for observing and resecting the deep left ventricular tumor.

Dislodgment of an atrial screw-in pacing lead 10 years after implantation.

Dislodgment of an atrial screw-in pacing lead is quite rare. This report describes a rare case of an atrial screw-in lead dislodgment 10 years after implantation. Although it is an uncommon complication, very late dislodgment can occur postoperatively, and careful follow-up is necessary.

Immunohistochemical and immunoelectron microscopical localization of procollagen III peptide in papillary carcinoma of thyroid.

The immunohistochemical localization of procollagen III peptide, a precursor of type III collagen, was examined in 38 papillary carcinomas and 25 follicular neoplasms using an immu-noperoxidase technique. Although localization of procollagen ill peptide was not demonstrated in normal follicular cells, distinct cytoplasmic immunostaining of neoplastic cells was frequently found in the tissues examined, as were stromal fibroblasts. Such cytoplasmic immunostaining was observed in 92.1 % of 38 papillary carcinomas and in 36.0% of 25 follicular neoplasms. Cytoplasmic immunoreactivity in papillary carcinomas was more intense at the peripheral zone of the tumor and correlated with the degree of invasiveness. The controls, in which the primary antibody was preabsorbed with procollagen ill peptide or replaced with normal rabbit serum, showed only faint background staining in all specimens. Immunoelectron microscopical examination revealed that electron-dense deposits, indicating procollagen III peptide, were located in the perinuclear space, Golgi apparatus, and rough endoplasmic reticulum of papillary carcinoma cells. These results suggest that neoplastic cells, especially papillary carcinoma cells, could play an important role in type III collagen production, possibly in connection with the creation of an environment that is conducive to their progression.