Percutaneous Transluminal Angioplasty of the Symptomatic Atherosclerotic Carotid Arteries
Results, Complications, and Follow-up
Background and Purpose Carotid endarterectomy reduces stroke risk in patients with >70% symptomatic stenosis. We present our results of percutaneous transluminal angioplasty (PTA) as an alternative treatment.
Methods Ninety-eight patients with symptomatic >70% stenosis of the internal carotid artery were considered for PTA. Details of the procedure, complications, and 4-year follow-up were registered.
Results Eighty-five PTAs were performed in a 4-year period. Transient cardiovascular effects were frequent: hypotension (54.1%), bradycardia (67.1%), asystole (25.9%), and syncope (16.5%). Transient ischemic attack occurred in 3 of 82 patients (3.7%), and disabling stroke occurred in 4 (4.9%); mortality was 0%. After a mean follow-up period of 18.7 months, 4 patients died, 1 due to fatal stroke. The overall probability of surviving any stroke or death was 86.7%. Restenosis (>70%) was seen in 6 cases (7.4%).
Conclusions PTA may be a reasonable treatment for symptomatic atherosclerotic stenosis, at least in patients at high risk for carotid endarterectomy.
Although CEA reduces stroke risk in patients with symptomatic severe (>70%) stenosis,1 2 perioperative risks of stroke or death of 7.5%1 and 5.8%2 have been reported. PTA could be used as an alternative treatment to reduce risk and improve outcome. In this study we review our current experience with carotid PTA.
Subjects and Methods
Since 1991 a total of 85 PTAs were performed in 82 patients with symptomatic >70% atherosclerotic stenosis of the ICA in the neck (Table 1⇓). Eleven of them were not eligible for CEA (10 because of severe ischemic cardiopathy). All patients were informed of the experimental nature of the PTA and provided informed consent accepting the procedure. Electroencephalography, electrocardiography, ECD, transcranial Doppler, and CT or MRI were performed in all patients. In patients with reversible ischemic neurological deficit or minor stroke, PTA was postponed at least 3 months.
Premedication with dexamethasone, droperidol, and fentanyl citrate was administered in 38 patients (43.5%). In 2 patients with marked sinus bradycardia, a temporary pacemaker was inserted. Patients were monitored with continuous electroencephalography, electrocardiography, and blood pressure readings. Four-vessel digital subtraction angiography was performed by a transfemoral arterial approach. Carotid stenosis was measured according to the NASCET protocol.3 Angiographic exclusion criteria for PTA were as follows: (1) <70% stenosis; (2) severe siphon stenosis; (3) kinking of the ICA; (4) highly calcified lesion; (5) intramural thrombus; and (6) electroencephalographic slowness when one attempted to insert the guidewire or the balloon through the stenosis.
Before the procedure, an intravenous bolus of 5000 U heparin was given. The diameter of the balloon was approximately the same as that of the vessel. The balloon was inflated 1 to 4 times to 8 to 10 atm lasting up to 10 seconds each. Intravenous atropine was given in cases of bradycardia. A neurological examination was performed after each inflation. The residual lumen of the vessel was checked by digital subtraction angiography. Heparin infusion was maintained for 7 days in severe dissection (intimal flap >10 mm). All other patients received 250 mg ticlopidine BID. PTA-associated risk included all strokes or deaths within 30 days.
Long-term prospective follow-up consisted of ECD and clinical assessment by study neurologists 1 month after PTA, every 3 months for the first year, and every 6 months thereafter. Carotid angiography was repeated 1 week later in cases of severe dissection or in the follow-up when restenosis (>70%) was shown by ECD. Restenosis, stroke, myocardial infarction, or death was registered.
Cumulative proportion survival was studied by means of Kaplan-Meier survival curves. Several analyses defined treatment failure as (1) any nonfatal ischemic stroke ipsilateral to the carotid lesion; (2) any stroke ipsilateral to the carotid lesion; (3) all strokes or vascular death; and (4) all strokes or all deaths.
Ninety-eight patients were considered for PTA. Of them, 11 patients (11.2%) were excluded by angiographic exclusion criteria. Insertion of the balloon through the stenotic area was impossible in 5 cases (5.1%) considered as technical failures.
PTA with <50% residual stenosis was successful in 78 arteries (91.8%). In 58 (74.4%) the residual lumen was > 80%. In 5, residual stenosis ranged from 50% to 75%. PTA-induced vessel wall dissection was seen in 22 arteries (25.9%), with a severe intimal flap in 5. In 3 of them, a repeated digital subtraction angiography performed 1 week later showed resolution of the dissection. Asymptomatic transient spasm of the ICA was seen in 7 procedures (8.2%). It was severe in 3, disappearing after intra-arterial nimodipine.
Thirty-day morbidity and mortality are shown in Table 2⇓. Ipsilateral TIA occurred in 3 patients who did not received intravenous heparin during the PTA. Disabling stroke occurred in 4 patients. One had multiple embolic occlusions of distal middle cerebral artery branches. Another had an ICA dissection with occlusion. The third had a stroke 30 minutes after a technically uncomplicated PTA with 0% residual stenosis. An embolus was seen in the middle cerebral artery with a fresh anterograde thrombus. The fourth patient, also with a severe dissection, developed a completed stroke 18 hours after PTA with carotid occlusion. Thus, the overall neurological complication rate was 8.5%, the severe complication rate was 4.9%, and the mortality rate was 0%.
Transient cardiovascular effects and local pain were frequent. Groin hematoma occurred in 3 patients. There was no myocardial infarction in the 30-day perioperative period.
All but one patient were followed-up for a mean period of 18.7 months (Table 3⇓). One died because of an ipsilateral cerebral hemorrhage 7 months after PTA. Three others died for reasons other than stroke. No ipsilateral ischemic stroke occurred, and 3 patients had myocardial infarction. Survival rates calculated by life-table methods were as follows: After 4 years, percentages of patients without (1) ipsilateral disabling ischemic stroke, (2) ipsilateral disabling stroke and/or vascular death, or (3) any ipsilateral disabling stroke and/or death were 95.3%, 91.5%, and 86.7%, respectively.
In 81 arteries of patients without perioperative end points, 6 cases (7.4%) of asymptomatic restenosis (>70%) occurred, 5 of them between the third and sixth months. Of 75 arteries without restenosis, 65.3% had a stable 100% residual lumen.
ECST and NASCET studies have shown rates of 7.5% and 5.8%, respectively, for all perioperative strokes and deaths.1 2 For these reasons, exploration of any new therapy for carotid stenosis with potential for improving those results, such as PTA, might be encouraged.4
In our series of 85 PTAs performed for symptomatic >70% carotid stenosis, combined 30-day mortality (0%) and major morbidity (4.9%) rates were not different from those shown in ECST and NASCET1 2 but better than those found in another recent analysis of CEA for symptomatic stenosis.5 TIA, attributed to cerebral embolism due to dislodgment of atheromatous material or thrombus from the vessel wall, occurred in 2.2% to 13.1% of the patients.6 7 8 9 10
Cardiovascular symptoms are related to excessive stretching of the carotid sinus. The site of stenosis has been considered responsible,4 but we could not find any statistical correlation between symptoms and location. A temporary pacemaker is mandatory in cases with persistent sinus bradycardia of any origin.
Intimal dissection occurred in 25% of our patients. When severe, this condition may be responsible for distal embolism or occlusion.11 12 Stenting may help to avoid these consequences. Treatment with heparin after PTA is mandatory. We tried to relate dissection with several variables such as location, size of the plaque, or presence of ulcer or calcium. Only the absence of calcium was negatively related with the risk of dissection (relative risk estimate, 0.80; 95% confidence interval, 0.61 to 0.94). The stiff tip of the balloon catheter may be responsible for vessel spasm7 12 that, as in our patients, was reversed by local nimodipine infusion.
The rate of recurrent stenosis (>70%) was similar to that published in other PTA series12 13 and in the low range of the rates reported for CEA.8 Restenosis was always asymptomatic and occurred between three and six months after PTA. Myointimal hyperplasia9 was deemed responsible. The mean clinical prospective follow-up was 18.7 months. Life-table analysis disclosed a probability of surviving at 48 months without ipsilateral stroke of 95.3% and without any stroke or death of 86.7%. These figures are very similar to those observed in ECST and NASCET.1 2
Although our results show that PTA may be a valid alternative to CEA in patients with >70% symptomatic atherosclerotic carotid stenosis, the definitive answer regarding the benefit-risk ratio of these two techniques will only be determined by ongoing prospectively randomized trials.10 14 In the meantime, PTA may be considered an alternative to CEA, at least in patients at high risk for CEA, provided that they undergo rigorous and careful evaluation of safety and efficacy as part of an ethically approved study.
Selected Abbreviations and Acronyms
|ECD||=||extracranial continuous-wave Doppler|
|ECST||=||European Carotid Surgery Trial|
|ICA||=||internal carotid artery|
|NASCET||=||North American Symptomatic Carotid Endarterectomy Trial|
|PTA||=||percutaneous transluminal angioplasty|
|TIA||=||transient ischemic attack|
This study was partially supported by a grant from the Spanish National Health Service (FIS 94/0737).
Presented in part at the Fourth European Stroke Conference, Bordeaux, France, June 1-3, 1995.
- Received June 25, 1996.
- Revision received September 16, 1996.
- Accepted September 19, 1996.
- Copyright © 1996 by American Heart Association
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