One of the most overlooked of all serious complications of diabetes is cardiovascular autonomic neuropathy (CAN),1–3 which encompasses damage to the autonomic nerve fibers that innervate the heart and blood vessels, resulting in abnormalities in heart rate control and vascular dynamics.4

The present report discusses the clinical manifestations (eg, resting tachycardia, orthostasis, exercise intolerance, intraoperative cardiovascular liability, silent myocardial infarction [MI], and increased risk of mortality) in the presence of CAN. It also demonstrates that autonomic dysfunction can affect daily activities of individuals with diabetes and may invoke potentially life-threatening outcomes. Advances in technology, built on decades of research and clinical testing, now make it possible to objectively identify early stages of CAN with the use of careful measurement of autonomic function and to provide therapeutic choices that are based on symptom control and that might abrogate the underlying disorder.

Little information exists as to frequency of CAN in representative diabetic populations. This is further complicated by the differences in the methodology used and the lack of standardization. Fifteen studies using different end points report prevalence rates of 1% to 90%.1 The heterogenous methodology makes it difficult to compare epidemiology across different studies. CAN may be present at diagnosis, and prevalence increases with age, duration of diabetes, and poor glycemic control. CAN also cosegregates with distal symmetric polyneuropathy, microangiopathy, and macroangiopathy. Age, diabetes, obesity, and smoking are risk factors for reduced heart rate variability (HRV)5 in type 2 diabetes. Thus, there may be selectivity and sex-related differences among the various cardiovascular risk factors as to their influence on autonomic dysfunction.6 HbA1c, hypertension, distal symmetrical polyneuropathy, retinopathy, and exposure to hyperglycemia were shown to be risk factors for developing CAN in type 1 diabetes.7

### Resting Tachycardia

Whereas abnormalities in HRV are early findings of CAN, resting tachycardia …

Diabetic Cardiovascular Autonomic Neuropathy

This review examines how the sympathetic nervous system plays a major role in the regulation of cardiovascular function over multiple time scales. This is achieved through differential regulation of sympathetic outflow to a variety of organs. This differential control is a product of the topographical organization of the central nervous system and a myriad of afferent inputs. Together this organization produces sympathetic responses tailored to match stimuli. The long-term control of sympathetic nerve activity (SNA) is an area of considerable interest and involves a variety of mediators acting in a quite distinct fashion. These mediators include arterial baroreflexes, angiotensin II, blood volume and osmolarity, and a host of humoral factors. A key feature of many cardiovascular diseases is increased SNA. However, rather than there being a generalized increase in SNA, it is organ specific, in particular to the heart and kidneys. These increases in regional SNA are associated with increased mortality. Understanding the regulation of organ-specific SNA is likely to offer new targets for drug therapy. There is a need for the research community to develop better animal models and technologies that reflect the disease progression seen in humans. A particular focus is required on models in which SNA is chronically elevated.

https://www.physiology.org/doi/pdf/10.1152/physrev.00007.2009

Sympathetic Nervous System Overactivity and Its Role in the Development of Cardiovascular Disease

2017 ACC/AHA/HRS guideline for the evaluation and management of patients with syncope: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society

Introduction
POTS is defined as the development of orthostatic symptoms associated with a heart rate (HR) increment ≥30, usually to ≥120 bpm without orthostatic hypotension. Symptoms of orthostatic intolerance are those due to brain hypoperfusion and those due to sympathetic overaction.

http://www.beyondconformity.org.nz/_literature_91240/SANEVAX_Low_2008_POTS_not_in_the_head

Postural tachycardia syndrome (POTS).

2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines, and the Heart Rhythm Society

Background—Water drinking increases blood pressure profoundly in patients with autonomic failure and substantially in older control subjects. The mechanism that mediates this response is not known....

The pressor response to water drinking in humans : a sympathetic reflex?

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The pressor response to water drinking in humans : a sympathetic reflex?