NEW YORK — Although carotid angioplasty and stenting have emerged as treatment alternative to carotid artery stenosis, there are still unavoidable complications associated with the procedures.
Both embolization and hypotension during the carotid angioplasty and stenting (CAS) have been linked to neurologic injury, and the current standard remains carotid endarterectomy (CEA), said Dr. Peter H. Lin at the Veith symposium on vascular medicine sponsored by Montefiore Medical Center.
Stroke after CAS is assumed to be embolic. “Disruption of atherosclerotic plaque is a disadvantage with carotid stenting. There are eight times more embolizations seen with CAS than with CEA,” said Dr. Lin of Baylor College of Medicine, Houston. “Neurologic deficit remains the most feared of all procedure-related complications.”
Dr. Lin and colleagues conducted a study showing the significance of carotid plaque echomorphology in assessing the embolization risk during CAS. Results from a total of 234 CAS procedures performed in 213 patients with a mean stenosis of 85% showed that the incidence of embolization was increased with hypoechoic plaque. The researchers concluded that that neuroprotective devices should be used in such procedures.
At the session, Dr. Klaus D. Mathias agreed that embolic injury to the brain is the main problem associated with carotid stenting procedures. “Clinically silent embolic showers occur frequently during CAS. Any phase of stenting can produce emboli, which is not good for the brain. There is 3–5 times more embolic material released to the brain with unprotected carotid stenting than with surgery,” said Dr. Mathias of the department of radiology at Klinikum Dortmund (Germany).
According to Dr. Mathias, filter protection is the preferred embolic protective device. A 60% reduction in complications from 3.5% to 1.5% has been reported in previous studies of neuroprotective filters. “The German PROCAS registry showed a 30%–60% reduction in neurologic events with protective filters, but we are still missing prospective trials,” said Dr. Mathias.
Another feared periprocedural complication leading to neurologic injury is hypotension. “Hemodynamic changes are common events during CAS and CEA, occurring in up to 30% of patients,” said Marc van Sambeek, Ph.D., head of the section of vascular surgery at University Hospital, Rotterdam (the Netherlands).
Hypotension, if sufficiently severe, may cause watershed infarction. Lesser degrees of hypotension may render an otherwise inconsequential microembolic shower very relevant if washout is impaired washout, and also lead to a reduction in adequate collateral blood flow to an ischemic territory in the brain.
Hemodynamic instability is well recognized in patients after endarterectomy, where postoperative hypertension has been known to be associated with stroke or death, and studies suggest that CEA is also associated with hypotension. CAS is being investigated as a promising alternative, but despite favorable results from initial series, hemodynamic instability may complicate this procedure,” said Dr. Sambeek.
Hemodynamic instability can be caused by the triggering of baroreceptors of the carotid sinus, as well as the release of catecholamines. “Hemodynamic instability is greater during CAS than in CEA,” said Dr. Sambeek. “Complications are clearly related to hypotension and bradycardia during the procedure.”
In a study presented at the meeting, Dr. Sambeek and colleagues evaluated the patterns of adrenaline and noradrenaline release in CAS, compared with CEA. They found that patterns of catecholamine release were significantly different in patients undergoing CAS and CEA with much higher and more variable surges occurring in CEA patients.
“CAS should be performed with cerebral protection using filter devices,” said Dr. Ron Fairman, chief of the division of vascular surgery at the Hospital of the University of Pennsylvania, Philadelphia, when asked to comment on this article.“In our own series, we have experienced occasional hypotension requiring continuous pharmacologic support for 24–36 hours following CAS. Other troubling phenomenon include troponin “leaks” in association with hypotension, as well as symptoms of cerebral reperfusion which seem to occur with greater frequency than following CEA. Physicians should anticipate these events and be prepared to intervene in order to prevent cardiac and cerebral compromise” he concluded.