Blood Pressure Instability after Percutaneous Carotid Angioplasty and Stenting

Mun Jye Poi and Peter H. Lin

Endovascular treatment of carotid stenosis by way of balloon angioplasty and carotid artery stenting (CAS) may be accompanied by bradycardia or hypotension. The incidence of CAS-induced bradycardia varies widely in the literature, ranging from 5% to 76%. Similarly, the incidence of hypotension resulting from endovascular carotid interventions showed a wide range from 14% to 28%, based on available reports. The wide disparity in the reported incidence of CAS-induced hemodynamic instability may be due in part to the lack of uniformity with regard to the definitions of hemodynamically significant bradycardia or hypotension. Considering all available reports, most researchers agree that hypotension is defined as a decrease of baseline systolic blood pressure by 30 mm Hg after carotid intervention. Persistent hypotension is defined as blood pressure reduction lasting more than 1 hour following carotid interventions. The significance of these conditions have been associated with adverse clinical outcomes following catheter-based carotid interventions.

Pathophysiology of Hemodynamic Instability Associated with Carotid Interventions

The causative factor contributing to CAS-related hemodynamic instability is the physical stimulation of the carotid sinus baroreceptors brought on by dilation of an angioplasty balloon catheter or deployment of an intravascular stent. Baroreceptors are located within cardiovascular structures that respond to blood pressure alteration and provide instant feedback information to the brain in response to changes in arterial blood pressure.

The baroreceptor nerve endings are located primarily in the adventitia of arteries, predominantly in the region of the carotid sinus and aortic arch. Baroreceptors can also be found in other arterial regions including the brachiocephalic artery and pulmonary artery. The baroreceptor sensory nerves in the carotid sinus are part of the glossopharyngeal nerve, and the other baroreceptor sensory nerves are part of the vagus nerve. The carotid sinus and aortic arch baroreceptors are tonically active at normal levels of arterial pressure, and they increase or decrease their rate of firing in response to the mean level as well as the pulsatile component of arterial pressure. The frequency of baroreceptor firing is directly proportional to the mean arterial pressure and the rate of change in pressure.

This afferent input controls a variety of reflex responses encompassing autonomic and endocrine adjustments, each toward maintaining cardiovascular homeostasis. Impulses are propagated through the glossopharyngeal and vagus nerves to the nucleus tractus solitarius of the medulla, with resultant activation of parasympathetic nuclei and inhibition of sympathetic nuclei. From the nucleus, second-order neurons pass to the caudal portion of the ventrolateral medulla. From there, third-order inhibitory neurons pass to the rostral ventrolateral medulla, the location where the cell bodies of the neurons control blood pressure. The axons of these neurons descend into the spinal cord and innervate the cell bodies of the blood pressure–regulating preganglionic sympathetic neurons in the intermediolateral gray column of the spinal cord. The axons of the preganglionic neurons leave the spinal cord and synapse on the postganglionic neurons in the ganglionic chain and collateral ganglia and the catecholamine-secreting cells in the adrenal medulla. The axons of the postganglionic noradrenergic neurons innervate the blood vessels and the heart. Impulses from the carotid sinus also initiate excitatory impulses from the nucleus tractus solitarius to the nucleus ambiguus and dorsal vagal nucleus. The increase in vagal activity results in a decrease in heart rate.

Baroreceptor sensitivity is a physiologic measure of the ability of the cardiovascular autonomic system to buffer acute fluctuation in blood pressure. It is defined as changes in the heart rate in response to changes in systolic blood pressure. This value generally decreases with age and can differ widely among individuals, ranging from 2 and 30 ms/mm Hg. Low baroreceptor sensitivity has been reported in experimental atheromatous animal models as well as in patients with unilateral or bilateral carotid stenosis. Rigid atheroma in the carotid sinus and proximal internal carotid artery are believed to be associated with decreased baroreceptor sensitivity. Therefore, with the removal of the thickened atheroma by carotid endarterectomy, improvement in baroreceptor sensitivity through greater stimulation of the stretched baroreceptors may be expected. However, reports on clinical outcomes following carotid endarterectomy reveal conflicting alterations in blood pressure with baroreceptor stimulation. In this regard, it has been postulated that chronic hypertension can lead to desensitization of baroreceptors, which can diminish response to baroreceptor stimulation following carotid endarterectomy.

Hemodynamic Instability Triggered by Carotid Artery Interventions

Hemodynamic instability is often seen during CAS procedures, primarily at the time of inflation of an angioplasty balloon catheter. Modification of the elasticity or compliance of the arterial wall during balloon angioplasty and stent placement can alter the sensitivity of carotid baroreceptors. Balloon dilatation causes stretching of a vessel wall, resulting in superficial splitting of the intima and atherosclerotic plaque. Retraction of the intima and distention of the media results in a permanent increase in vessel diameter.

It has been demonstrated in a canine model that balloon angioplasty of nondiseased carotid arteries increases the sensitivity of carotid sinus baroreceptors. This has been attributed to increased sensitivity to changes in the mechanical properties of the carotid sinus, such as greater compliance and increased diameter for a given arterial blood pressure. Enlargement of the canine carotid sinus diameter by balloon angioplasty or vein patch grafting has also produced decreases in blood pressure in normal and hypertensive dogs that persisted for days in the presence of normally active arterial baroreceptors at other sites. Adaptation of carotid sinus receptors to changes in mechanical properties in that setting appears slow and incomplete.

Long-term and short-term changes in autonomic activity after CAS have also been observed. Some researchers have postulated that the presence of a carotid stent could cause persistent stimulation of the carotid sinus, causing continuous vagal stimulation during the periprocedural period. Others have reported that CAS could change an expansile artery to a relatively rigid tube, causing dysfunction of the adventitial baroreceptors and decrease of baroreceptor sensitivity. In one study, baroreceptor sensitivity is found to be decreased for 1 month after CAS and resumed to near-baseline level at 6 months after intervention. However, this observation may be a result of the compensatory ability of the aortic and contralateral carotid baroreceptors that contribute partially to the recovery of baroreceptor sensitivity after CAS on one side.

Only gold members can continue reading. Log In or Register to continue

Share this:

• X
• Facebook

Related

Related posts:

1. Embolic Protection Devices to Prevent Stroke during Percutaneous Angioplasty and Stenting
2. Management of Acute Limb Ischemia Complicating Aortic Reconstruction
3. Treatment of Dyslipidemia and Hypertriglyceridemia
4. Intraoperative Assessment of the Technical Adequacy of Carotid Endarterectomy

Stay updated, free articles. Join our Telegram channel

Join

Full access? Get Clinical Tree