Purpose Diabetic neuropathy can lead to decreased peripheral sensation and motor neuron dysfunction associated with impaired postural control and risk of falling. However, the relationship between decreased peripheral sensation and impaired vestibular function in diabetes mellitus is poorly investigated. Therefore, the aim of this study was to investigate the relationship between peripheral and autonomic measurements of diabetic neuropathy and measurements of vestibular function. Methods A total of 114 participants with type 1 diabetes (n = 52), type 2 diabetes (n = 51) and controls (n = 11) were included. Vestibular function was evaluated by video head impulse testing. Peripheral neuropathy was assessed by quantitative sensory testing and nerve conduction. Autonomic neuropathy using the COMPASS 31 questionnaire. Data were analyzed according to data type and distribution. Results Measurements of vestibular function did not differ between participants with type 1 diabetes, type 2 diabetes or controls (all p-values above 0.05). Subgrouping of participants according to the involvement of large-, small- or autonomic nerves did not change this outcome. Correlation analyses showed a significant difference between COMPASS 31 and right lateral gain value (ρ = 0.23, p = 0.02,), while no other significant correlations were found. Conclusion Diabetic neuropathy does not appear to impair vestibular function in diabetes, by means of the VOR. Clinical trials NCT05389566, May 25th, 2022.

Prospective studies applying fluoroscopy for assessment of right ventricular (RV) lead position have failed to show clear benefits from RV septal pacing. We investigated the impact of different RV lead positions verified by computed tomography (CT) on the risk of pacing-induced cardiomyopathy (PICM). We retrospectively included 153 patients who underwent routine fluoroscopy-guided pacemaker implantation between March 2012 and May 2020. All patients had normal pre-implant left ventricular ejection fraction (LVEF). Patients attended a follow-up visit including contrast-enhanced cardiac CT and transthoracic echocardiography. Patients were classified as septal or non-septal based on CT analysis. The primary endpoint was PICM (LVEF < 50% with ≥10% decrease after implantation). Based on CT, 48 (31.4%) leads were septal and 105 (68.6%) were non-septal. Over a median follow-up of 3.1 years, 16 patients (33.3%) in the septal group developed PICM compared to 31 (29.5%) in the non-septal group (p = 0.6). Overall, 13.1% deteriorated to LVEF ≤ 40%, 5.9% were upgraded to cardiac resynchronization therapy device, and 14.4% developed new-onset atrial fibrillation, with no significant differences between the groups. This study demonstrated a high risk of PICM despite normal pre-implant left ventricular systolic function with no significant difference between CT-verified RV septal or non-septal lead position.

Background Right ventricular (RV) pacing may induce significant left ventricular (LV) dyssynchrony resulting in pacing-induced cardiomyopathy (PICM). LV activation sequence is affected by RV pacing site and previous studies suggest that RV septal pacing may be superior compared to traditional RV apical pacing. However, results are conflicting and randomized controlled trials have failed to show clear benefits from RV septal pacing. Traditionally, studies have applied fluoroscopy to determine RV lead implantation site. However, locating pacing site using this method is known to be inaccurate and poorly reproducible compared with cardiac computed tomography (CT). The purpose of our study was to evaluate the association between RV pacing site determined by cardiac CT and risk of PICM. Methods We retrospectively included 153 patients with pre-implant LV ejection fraction (LVEF) ≥50% who underwent fluoroscopy-guided dual chamber pacemaker implantation due to high-degree atrioventricular block between March 2012 and May 2020. All patients attended a follow-up visit including cardiac CT and transthoracic echocardiography. RV lead position was evaluated from CT dividing the RV into three segments: apical, septum or free wall (Figure 1). Furthermore, RV lead position estimated by the implanting physician, using fluoroscopy during pacemaker implantation, was retrieved from medical records. The primary endpoint was PICM defined as ≥10% decrease in LVEF from time of pacemaker implantation to follow-up, resulting in LVEF &lt;50%. Results Mean duration of follow-up was 3.7 years (range 2.1–8.7). The implanting physician estimated 131 (85.6%) leads to be located septal, 5 (3.3%) located non-septal and 17 (11.1%) were unknown. Based on CT, 48 (31.4%) leads were located septal and 105 (68.6%) were located non-septal of which 31 were located on the free wall (20.4%). With CT as the golden standard, 47 (35%) leads were estimated correctly during fluoroscopy-guided implantation. No significant differences between patient characteristics in the CT-estimated septal and non-septal groups were observed except for ischemic heart disease (P=0.05) (Table 1). There were 16 (33.3%) patients in the septal group who developed PICM compared to 31 (29.5%) in the non-septal group (P=0.6). Adjusting for ischemic heart disease did not change this result. In the septal group, the change in LVEF from baseline to follow-up was −9.0±10.4% compared to −7.5±9.1% in the non-septal group (P=0.4). Conclusion In total 31% developed PICM despite having a normal pre-implant LVEF with no observed difference between RV septal and non-septal pacing. With CT as the golden standard, RV leads were inaccurately located during fluoroscopy-guided pacemaker implantation with only 35% being located correctly. Misclassification of pacing sites in previous studies may have contributed to the inconsistent results. Funding Acknowledgement Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Svend Andersens FondKarl G Andersens Fond