Background The majority of syncope emergency department (ED) presentations is due to autonomic syncope, which comprises reflex syncope and orthostatic hypotension. Despite the European Society of Cardiology (ESC) guidelines many patients with autonomic syncope are still admitted. Therefore we studied the indications for, and the factors associated with, clinical admission in the prospective SYNERGY database. Methods We performed a post-hoc-analysis of patients visiting the ED with an adjudicated diagnosis of autonomic syncope from the SYNERGY database. We analyzed admission indications based on the ESC guideline risk (initial diagnosis+risk stratification); RISC-score, and clinical admission indications. We combined these admission indications and compared with observed patient management. Furthermore, we analyzed the factors associated with the decision for admission. Results We analyzed 388 adjudicated autonomic syncope patients, of whom 39.4%(n = 153) were admitted. 2.8%(11/388) had a guideline risk admission indication, 14.0%(53/388) had a RISC-score admission indication; 26.0%(101/388) had clinical admission indications. The combination of clinical indications and guideline risk yielded 26.3%(102/388) admission indications, combination with the RISC-score yielded 33.5% (130/388) for high-risk and 46.9% (182/388) for intermediate-risk admission indications.Factors associated with admission were age; diagnostics/consultations unrelated to syncope; and any ECG abnormalities without guideline ECG-risk features. In contrary, execution of an active-standing test was associated with a lower likelihood of admission. Conclusions Patients with autonomic syncope are frequently admitted to the hospital, over one-third of these admissions is not guideline-indicated. Optimizing the implementation of the guideline-based initial evaluation process may reduce unindicated admissions of autonomic syncope patients.
Spinal afferents relay sensory information and regulate cardioprotective reflexes. These afferent signals go to cell bodies in the dorsal root ganglia (DRG) and ultimately to the central nervous system. However, the morphology and distribution of spinal afferent terminals in the heart have not been well delineated. This is partly due to challenges, including limited surgical access to the upper thoracic DRGs, tissue thickness, and tracer options. In this study, we injected tracer dextran biotin (DB) into the left DRG (C8-T3) of male Sprague-Dawley rats (3-5 months). After 16 days, the animals were sacrificed, and the left and right ventricles were separated from the rest of the heart. Next, these samples were stained with diaminobenzidine and mounted for visualization under brightfield microscopy. DB-labeled axons were identified and digitally traced using the Neurolucida system. Our findings showed that spinal afferent neurons of the left DRG project individual axons that enter the ventricles from the base. These axons are distributed across various regions within both ventricles. While these axons are present in the epicardial and myocardial layers, they were not identified in the endocardial layer. Within the epicardial and myocardial layers, spinal afferents form extensive terminal arborizations and make presumptive contact with cardiac muscle, blood vessels, and adipose tissue. This investigation marks the first anterograde characterization of spinal afferent axon terminal distribution and morphology in flat-mount preparations of whole rat ventricles.
Parental fructose consumption has been associated with early cardiometabolic dysfunction in the offspring, potentially involving autonomic and inflammatory mechanisms related to the cholinergic anti-inflammatory pathway (CAP). Therefore, we investigated whether splenectomy or autonomic splenic denervation could modulate neuroinflammatory and cardiometabolic alterations in offspring of rats exposed to fructose overload. Male and female Wistar rats received 10% fructose in drinking water or a standard diet for a period of 60 days, before being mated. Parental fructose overload was maintained until the end of lactation. At 21 days of age, the offspring were allocated into four groups: control, fructose, fructose splenectomized, and fructose splenic autonomic-denervated. Splenectomy and splenic denervation were performed at 21 days of age. Metabolic, hemodynamic and autonomic parameters, systemic inflammation, and pro-oxidant markers were evaluated at 51 days of life. Offspring from fructose-fed parents exhibited reduced insulin sensitivity, increased systolic, diastolic, and mean arterial pressure, increased vascular sympathetic modulation, elevated arterial pressure variability, and impaired baroreflex sensitivity. In addition, the fructose group showed increased pro-inflammatory cytokines, NADPH oxidase activity, nitrite, and hydrogen peroxide levels, associated with reduced anti-inflammatory cytokines. The splenectomized and splenic denervation fructose groups attenuated insulin resistance, improved hemodynamic parameters, heart rate, and arterial pressure variability, baroreflex sensitivity, reduced inflammatory cytokines, and attenuated pro-oxidant markers. In conclusion, parental fructose consumption induced early cardiometabolic, autonomic, inflammatory, and redox alterations in the offspring. Moreover, interruption of spleen-related signaling pathways attenuated these dysfunctions, suggesting the involvement of CAP-related mechanisms in the developmental programming induced by parental fructose overload.
