Type 2 Diabetes Intensifies Nocturnal and Early Morning Circadian Autonomic Dysregulation After Ischaemic Stroke

Cardiac autonomic neuropathy (CAN) is a frequent but under-recognised complication of diabetes that may exacerbate cardiovascular risk after stroke. This study aimed to characterise circadian patterns of heart rate (HR) and HR variability (HRV) in patients with acute ischaemic stroke, comparing those with and without type 2 diabetes.

We conducted a retrospective case-control study of 157 patients with acute ischaemic stroke who underwent 7-day continuous electrocardiographic (ECG) monitoring (80 with type 2 diabetes, 77 without diabetes). Patients with paroxysmal atrial fibrillation, insufficient ECG data (<7 days), or obstructive sleep apnoea were excluded. HR and HRV indices (standard deviation of NN intervals [SDNNs], root mean square of successive differences [RMSSDs], pNN50, high-frequency [HF], low-frequency [LF] and LF/HF ratio) were derived from 5-min segments. Circadian variation was analysed using generalised additive mixed models (GAMMs) adjusted for demographic, clinical and treatment factors.

Compared with patients without diabetes, those with type 2 diabetes exhibited persistently higher HR and lower HRV across both time- and frequency-domain measures. Differences were most pronounced at night and in the early morning, indicating blunted autonomic fluctuations despite a preserved HR rhythm. Among patients with diabetes, poorer glycaemic control (glycated haemoglobin [HbA1c] > 7% [53 mmol/mol]) was associated with higher HR and lower HRV, particularly during nocturnal hours, supporting a dose-response relationship.

Type 2 diabetes is associated with attenuated circadian autonomic regulation after ischaemic stroke, characterised by elevated HR and reduced HRV, most evident during sleep and early morning periods. Continuous ECG monitoring may facilitate early detection of nocturnal autonomic dysfunction, and interventions that enhance parasympathetic tone-such as improved glycaemic control and potentially cholinergic modulation-warrant further investigation to mitigate post-stroke cardiovascular risk.