Yoichiro Nakagawa

Pulmonary vein isolation (PVI) is an established treatment for atrial fibrillation (AF). While it is known to affect the autonomic nervous system, the relationship between left atrial (LA) remodeling and PVI-mediated neuromodulation remains unclear. We aimed to assess the neuromodulatory effects of PVI using skin sympathetic nerve activity (SKNA). SKNA was recorded one day before and 2–3 days after PVI in 28 paroxysmal AF (PAF) and 33 persistent AF (PerAF) groups. Baseline low frequency to high frequency (LF/HF) ratio was higher in the PAF group (1.23 [interquartile range {IQR}: 0.79–1.76] vs. 0.74 [IQR: 0.49–1.38], p = 0.017). After PVI, the PAF group demonstrated significant reductions in burst amplitude (1.46 [IQR: 1.04–2.84] vs. 1.09 [IQR: 0.78–2.17] μV, p = 0.015) and LF/HF ratio (0.91 [IQR: 0.73–1.52] vs. 0.71 [IQR: 0.48–1.21], p = 0.012), whereas the PerAF group exhibited no such changes. A weak positive correlation was observed between the percentage change in LF/HF ratio and LA volume index in the PAF group (r = 0.572, p = 0.002). PVI significantly decreased SKNA in PAF patients but not in PerAF. LA remodeling may hinder the effectiveness of PVI-mediated neuromodulation.

Danon disease (DD) is a rare lysosomal storage disorder resulting from pathogenic variants of the lysosome-associated membrane protein type 2 (LAMP-2) gene. The disease is characterized by severe cardiomyopathy, which rapidly progresses to end-stage heart failure. This case, with DD caused by a missense variant, exhibited slow progressive cardiomyopathy and survived for an extended period despite being a male. A pathological analysis revealed that only a minority of the samples exhibited autophagic vacuoles with unique sarcolemmal features (AVSFs), which are typical of DD. Importantly, LAMP-2 expression was absent and the myocardial tissue contained a substantial amount of p62-positive aggregates.

While autonomic dysregulation and repolarization abnormalities are observed in subarachnoid hemorrhage (SAH), their relationship remains unclear. We aimed to measure skin sympathetic nerve activity (SKNA), a novel method to estimate stellate ganglion nerve activity, and investigate its association with electrocardiogram (ECG) alterations after SAH. We recorded a total of 179 SKNA data from SAH patients at three distinct phases and compared them with 20 data from controls. Compared with control data, in the acute phase data (days 1–3 of SAH), T peak‐to‐end (Tp‐e) interval was significantly prolonged (81 [interquartile range {IQR}: 71–93] vs. 58 [IQR: 54–64] ms, p < 0.001), non‐burst amplitude of SKNA was significantly increased (2.4 [IQR: 1.3–4.1] vs. 0.7 [IQR: 0.5–1.7] μV, p < 0.001), and the ratio of low frequency to high frequency (HF) was significantly decreased (0.8 [IQR: 0.5–1.1] vs. 1.1 [IQR: 0.7–1.3], p = 0.028). Linear mixed model revealed a relationship between Tp‐e interval and SKNA. Although these abnormalities gradually normalized, delayed cerebral ischemia episodes were associated with increased HF oscillation. Transient sympathetic dysregulation contributes to repolarization impairment after SAH. SKNA may have the potential to monitor adverse outcomes.

We report the case of a man in his 60s who had dilated cardiomyopathy with severe functional mitral regurgitation. Four years after a cardiac resynchronization therapy (CRT) device with an implantable cardioverter defibrillator was implanted, this device was replaced with an adaptive CRT device because of battery consumption. Seven months after replacement of this device, the left ventricular pacing to right ventricular activation and the atrioventricular delay from automatic adjustments contributed to less functional mitral regurgitation. The findings from our case suggest that optimal CRT, by measuring intracardiac conduction parameters, is effective for functional mitral regurgitation.