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Cardiovascular autonomic neuropathy (CAN) is an under-recognised yet highly prevalent microvascular complication of diabetes. CAN affects approximately 20% of people with diabetes, with recent studies highlighting the presence of CAN in prediabetes (impaired glucose tolerance and/or impaired fasting glucose), indicating early involvement of the autonomic nervous system. Understanding of the pathophysiology of CAN continues to evolve, with emerging evidence supporting a potential link between lipid metabolites, mitochondrial dysfunction and genetics. Recent advancements, such as streamlining CAN detection through wearable devices and monitoring of heart rate variability, present simplified and cost-effective approaches for early CAN detection. Further research on the optimal use of the extensive data provided by such devices is required. Despite the lack of specific pharmacological interventions targeting the underlying pathophysiology of autonomic neuropathy, several studies have suggested a favourable impact of newer glucose-lowering agents, such as sodium–glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists, where there is a wealth of clinical trial data on the prevention of cardiovascular events. This review delves into recent developments in the area of CAN, with emphasis on practical guidance to recognise and manage this underdiagnosed condition, which significantly increases the risk of cardiovascular events and mortality in diabetes. Graphical Abstract
Cardiovascular autonomic neuropathy (CAN) is an under-recognised yet highly prevalent microvascular complication of diabetes. CAN affects approximately 20% of people with diabetes, with recent studies highlighting the presence of CAN in prediabetes (impaired glucose tolerance and/or impaired fasting glucose), indicating early involvement of the autonomic nervous system. Understanding of the pathophysiology of CAN continues to evolve, with emerging evidence supporting a potential link between lipid metabolites, mitochondrial dysfunction and genetics. Recent advancements, such as streamlining CAN detection through wearable devices and monitoring of heart rate variability, present simplified and cost-effective approaches for early CAN detection. Further research on the optimal use of the extensive data provided by such devices is required. Despite the lack of specific pharmacological interventions targeting the underlying pathophysiology of autonomic neuropathy, several studies have suggested a favourable impact of newer glucose-lowering agents, such as sodium–glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists, where there is a wealth of clinical trial data on the prevention of cardiovascular events. This review delves into recent developments in the area of CAN, with emphasis on practical guidance to recognise and manage this underdiagnosed condition, which significantly increases the risk of cardiovascular events and mortality in diabetes. Graphical Abstract
ContextPost‐bariatric hypoglycemia (PBH) is a complication of bariatric surgery including Roux‐en‐Y gastric bypass (RYGB). It remains unclear why only some individuals develop PBH.ObjectiveTo identify clinical characteristics distinguishing post‐RYGB individuals with PBH, versus without symptomatic hypoglycemia (RYGB non‐hypo).Design and SettingCross‐sectional observational study in academic referral centre. Adults 18–70, without current diabetes, were recruited into three groups: (1) PBH (n = 39); (2) RYGB non‐hypo (n = 25); and (3) individuals without history of upper gastrointestinal surgery (n = 17). Outcome measures included between‐group differences in medical history and medication use, and survey‐based scores for hypoglycemia, dumping syndrome, and autonomic symptoms.ResultsPBH participants were 92% female, age 53.4 ± 11.9 y, BMI 31.2 ± 5.6 kg/m2, versus RYGB non‐hypo (100% female, age 53.2 ± 10.5 y, BMI 32.2 ± 8.0 kg/m2) and controls (65% female, age 44.5 ± 14.6 y, BMI 30.8 ± 6.3 kg/m2). 87% of PBH reported level 3 hypoglycemia, with emergency visits in 28% and vehicle accidents in 8%. Reduced hypoglycemia awareness was reported by 82%; 13%–17% were classified as unaware (modified Clarke/Gold scores). Preoperative hypoglycemia symptoms and family history were reported by 26% and 18% of PBH. PBH had significantly higher survey scores for hypoglycemia, dumping syndrome, and autonomic symptoms, and higher self‐reported neuropathy, autonomic neuropathy, orthostatic hypotension, reflux esophagitis, intestinal dysmotility, and IBS (all p < 0.05 vs. RYGB non‐hypo). Gabapentin and PPI use was more frequent in PBH.ConclusionHigh rates of IBS, dumping symptoms, and orthostatic hypotension suggest disordered autonomic regulation as a potential contributor to PBH. Self‐reported preoperative symptoms and family history of hypoglycemia suggest possible preoperative differences in glucose metabolism in PBH.
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