Diabetes and Stroke: Does an Excess Risk of Hemodynamic Cerebral Ischemia Exist?

Embolic and hemodynamic mechanisms are the main causes underlying ischemic strokes of carotid origin. The hemodynamic cerebral ischemia (HCI) risk depends on the contribution of the contralateral internal carotid artery (ICA) and vertebral arteries via the circle of Willis, the ipsilateral external carotid artery via the ophthalmic artery and the leptomeningeal arteries. During carotid surgery, impaired collateral flow is associated with the need for shunt insertion.

When HCI is present, cerebral perfusion is initially maintained by vasodilation of precapillary arterioles and the increased extraction coefficient of oxygen. Secondarily, vascular reserve exhaustion by degradation of arterial lesions engenders a loss of cerebral autoregulation, ischemic penumbra and cerebral infarction.

Carotid revascularization with an incomplete circle of Willis enhances the postoperative ischemic stroke risk. The loss of cerebral autoregulation, attributable to HCI combined with ipsilateral carotid tight stenosis, heightens the risk of hyperperfusion and cerebral hemorrhage.

Carotid occlusion is the primary cause of HCI. Carotid occlusions and tight stenoses lead to loss of cerebral autoregulation and cerebrovascular reserve, and have been associated with a 4-fold-increased stroke risk.

Diabetes in an independent risk factor for ischemic stroke, whose associated mortality rate is higher and sequelae more serious than for nondiabetics. Diabetes increases the risk of stroke or death after surgical carotid revascularization or endoluminal angioplasty.It is, with contralateral ICA occlusion, 1 of the 7 factors doubling the stroke risk after carotid endarterectomy. Diabetes also enhances the cerebral hemorrhage risk associated with carotid surgery, thrombectomy or thrombolysis revascularization of the cerebral arteries.