Vaso vagal syncope (VVS) recurrence is a relevant clinical problem [1]. Indeed, despite the rapid onset, the short duration of the acute crisis, and the spontaneous complete recovery after the event, VVS may be complicated by physical injury and worse prognosis [1], [2]. However, VVS has a frequency between 15% and 39%, with annual number of episodes about 18.1–39.7 per 1000 patients [3]. To date, VVS has an incidence of 6.2 per 1000 person-years, that grows up after 70 years of age with rate annual 19.5 per thousand individuals after 80 years [3]. However, VVS recurrence rate is about 35%, causing a physical injury until the 29% [3]. The patients with type 2 diabetes mellitus (T2DM) represent a percentage about the 30% of all the VVS subjects [4]. Different mechanisms might explain the link between VVS recurrence and T2DM, such as the abnormalities of autonomic nervous system [5]. The autonomic nervous system regulates the hemodynamic stability by maintaining a stable blood pressure and the heart rate under normal and abnormal physiologic conditions [5]. Consequently, the dysfunction of this complex regulatory system, and of its interaction with sensor systems as baroreceptors, mechanoreceptors, and chemoreceptors might alter the vascular reactivity, leading to the VVS and its recurrence [5]. Moreover, autonomic system alterations might cause both VVS event and VVS recurrence, as the result of an inappropriate response of the autonomic nervous system, with excessive vagal tone, and sympathetic tone withdrawal [2]. As first, T2DM patients have higher rate of autonomic system dysfunction [6]. Secondly, in T2DM patients the cardiac autonomic deregulation might be persistent, severe and known as cardiac autonomic neuropathy (CAN), [6]. To date, in T2DM with CAN there is a parasympathetic heart denervation, with an early augmentation of sympathetic tone, then leading to impaired heart rate variability (HRV), resting tachycardia, exercise intolerance, abnormal blood pressure regulation, and orthostatic hypotension [7]. However, in T2DM patients all these alterations look to be the compensatory response of the cardiac sympathetic tone increase to subclinical peripheral denervation [7]. Actually, the association between T2DM and autonomic dysfunction, such as between T2DM and VVS event and its recurrence is not well established and under investigated. Therefore, the recent studies cannot come to definitive conclusions about the link between T2DM the VVS events and VVS recurrence. Intriguingly, different studies proposed the HRV as a simple, reproducible and well-recognized method for evaluating sympatho vagal activity and autonomic dysfunction [8], [9]. However, in this study we evaluated the entity of autonomic dysfunction by HRV alterations, and its relevance to cause VVS and the VVS recurrence in T2DM vs. non T2DM patients (controls) at 12 months of follow up.