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Background/Introduction: Cardiac implantable electronic devices and their integrated thoracic impedance sensors have been used to detect sleep apnea for over a decade now. Despite their usage in daily clinical practice, there are only limited data on their diagnostic accuracy. Methods: AIRLESS and UPGRADE were prospective investigator-driven trials meant to validate the AP scan ® (Boston Scientific, Marlborough, MA, USA) in heart failure cohorts. Patients, who either fulfilled the criteria for implantation of an implantable cardioverter-defibrillator (ICD), cardiac resynchronization therapy (CRT), or upgrading to CRT according to most recent guidelines at the time of study conduction, were eligible for enrolment. Sleep apnea and its severity, measured by apnea-hypopnea index (AHI), were assessed by polysomnography. For direct comparison, the apnea sensor-derived AP scan ® was used from the identical night. Results: Overall, 80 patients were analyzed. Median AHI was 21.6 events/h (7.1-34.7), while median AP scan ® was 33.0 events/h (26.0-43.0). In the overall cohort, the sensor-derived AP scan ® correlated significantly with the AHI (r = 0.61, p < 0.001) with a mean difference (MD) of -12.6 (95% confidence interval (CI) -38.2 to 13.0). Furthermore, the AP scan ® was found to correlate well with the AHI in patients with obstructive sleep apnea r = 0.73, p = 0.011, MD -5.2, 95% CI -22.7 to 12.3), but not central sleep apnea (r = 0.28, p = 0.348, MD -10.4, 95% CI -35.4 to 14.6). Conclusions: In an exclusive heart failure cohort, the AP scan ® correlated well with the PSG-derived AHI. A similar correlation was found in most subgroups except for patients suffering from central sleep apnea.

The impact of chronic cadmium exposure and slow accumulation on the occurrence and development of diabetes is controversial for human populations. Islets of Langerhans play a prominent role in the etiology of the disease, including by their ability to secrete insulin. Conversion of glucose increase into insulin secretion involves mitochondria. A rat model of pancreatic β-cells was exposed to largely sub-lethal levels of cadmium cations applied for the longest possible time. Cadmium entered cells at concentrations far below those inducing cell death and accumulated by factors reaching several hundred folds the basal level. The mitochondria reorganized in response to the challenge by favoring fission as measured by increased circularity at cadmium levels already ten-fold below the median lethal dose. However, the energy charge and respiratory flux devoted to adenosine triphosphate synthesis were only affected at the onset of cellular death. The present data indicate that mitochondria participate in the adaptation of β-cells to even a moderate cadmium burden without losing functionality, but their impairment in the long run may contribute to cellular dysfunction, when viability and β-cells mass are affected as observed in diabetes., Competing Interests: The authors declare no conflict of interest. The founding sponsors had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, and in the decision to publish the results.