Improvement in Cerebral Hemodynamics After Carotid Angioplasty
Background and Purpose Carotid percutaneous transluminal angioplasty (PTA) may offer an alternative treatment to carotid endarterectomy. However, in contrast to carotid endarterectomy, which has been shown to normalize impaired cerebral hemodynamics, the effects of carotid PTA are unknown. Therefore, we prospectively studied the effect of carotid PTA on both perioperative and postoperative cerebral hemodynamics.
Methods Eleven patients undergoing carotid PTA for symptomatic carotid artery stenosis were prospectively studied. Transcranial Doppler recordings from the ipsilateral middle cerebral artery (MCA) were performed during the procedure. In addition, MCA blood flow velocity and CO2 reactivity were determined before PTA and at 2 days, 1 month, and 6 months after the procedure. The results were compared with those in 11 similar patients undergoing carotid endarterectomy in whom measurements were performed before and 1 month after the operation.
Results During carotid PTA, in 2 of 11 patients during passage of the balloon catheter through the stenosis, MCA blood flow velocity fell transiently. In 6 of 11 patients there was a reduction in flow velocity (>50%) during balloon deflation, but this lasted only a few seconds. After the procedure there was a significant improvement in ipsilateral hypercapnic reactivity: preoperative value, 59.8±42.2% (mean±SD); 2 days, 77.9±31.4%; 1 month, 88.7±45.0%; 6 months, 89.8±33.9%; and (ANOVA P=.003) preoperative value versus 1 month, P<.02; versus 6 months, P<.02. In all cases in which reactivity was significantly impaired preoperatively, it returned to the normal range. Pulsatility index also increased significantly: preoperative value, 0.827±0.251 (mean±SD); 2 days, 0.992±0.262 (P=.002). Contralateral MCA hypercapnic reactivity also improved after carotid PTA. There was a similar improvement in ipsilateral hypercapnic reactivity after carotid endarterectomy.
Conclusions Carotid PTA results in a normalization of impaired hemodynamics, as assessed by CO2 reactivity. The degree of improvement is similar to that seen after carotid endarterectomy.
Stenosis of the ICA is associated with an increased risk of stroke, and in symptomatic patients with 70% or greater diameter stenosis, carotid endarterectomy has been shown to result in a significant stroke reduction.1 2 However, carotid endarterectomy carries a small risk of stoke in addition to the general risks of anesthesia, including myocardial ischemia, in patients with coexistent ischemic heart disease. Carotid PTA has a number of potential advantages, including shorter hospitalization, lack of general anesthetic and surgical incision, and the possibility of dilating surgically inaccessible lesions such as high ICA stenoses.3 It may be suitable for patients unfit for carotid endarterectomy.
Treating ICA stenosis may prevent stroke both by reducing embolization and by improving perfusion pressure. ICA stenosis results in impaired ipsilateral hemodynamics if it reduces blood flow significantly in the presence of inadequate collateral supply. In such cases, resting cerebral blood flow is usually normal, but the impairment in hemodynamics can be demonstrated by an increased oxygen extraction fraction or reduced vasodilatory reserve.4 In the presence of a hemodynamically critical stenosis, the distal circulation is already nearly maximally vasodilated and can vasodilate only a little further in response to a vasodilatory stimulus such as CO2 or acetazolamide.5 Carotid endarterectomy has previously been shown to normalize impaired cerebral hemodynamics, as assessed by oxygen extraction fraction or perfusion pressure, in individuals in whom it was reduced preoperatively.6 7 The effects of carotid PTA on cerebral hemodynamics are unknown. To investigate alterations in both perioperative and postoperative cerebral hemodynamics, we performed a prospective study in patients undergoing carotid PTA and compared them with a group of similar patients undergoing carotid endarterectomy. We used TCD to measure cerebral blood flow velocity and combined it with the administration of CO2 to estimate cerebral CO2 reactivity, a measure of perfusion reserve.5
Subjects and Methods
Patients studied were patients randomized into an international multicenter trial (Carotid and Vertebral Artery Transluminal Angioplasty Study [CAVATAS]) evaluating carotid and vertebral PTA. Patients with carotid stenosis suitable for surgery are randomized between carotid endarterectomy and carotid PTA, and patients unsuitable for surgery are randomized between carotid PTA and best medical therapy.3 In the trial, randomization occurs within centers, ensuring comparability of patients in both arms within an individual center. Patients undergoing both carotid PTA and carotid endarterectomy were studied. Details regarding the patients are provided in “Results.”
Carotid PTA was performed by the femoral artery route. A 6F sheath was placed in the femoral artery, through which a 5F Mani cerebral catheter was passed into the common carotid artery, and angiography was performed to confirm the degree of stenosis. An exchange wire was passed across the stenosis, and a balloon catheter was passed over this. An Optiplast Vasacath was used, with a diameter of the inflated balloon of 5, 6, or 7 mm and a balloon length of 2 cm. Inflations were performed for 5 to 10 seconds, except for one 30-second inflation in one patient; the number of inflations was 1 in 1 subject, 2 in 3 subjects, 3 in 5 subjects, 4 in 1 subject, and 5 in 1 subject. Immediately after PTA, selective arterial angiography of the angioplastied artery was performed.
In patients undergoing carotid PTA, CO2 reactivity measurements were performed before PTA, during the procedure, and at 2 days, 1 month, and 6 months after PTA. In carotid endarterectomy cases, CO2 reactivity was measured preoperatively and at 1 month and 6 months. Duplex carotid ultrasound was performed at each measurement point. In the one patient with a distal ICA stenosis that was too distal to be identified on B-mode ultrasound, patency was determined by TCD by the submandibular route and degree of stenosis evaluated once during follow-up by MR angiography.
The same transcranial pulsed Doppler ultrasound machine with a 2-MHz probe (TC2000 S, Eden Medizinische Elektronik GmbH) was used for all cerebral hemodynamic studies. The MCA was insonated by the transtemporal route at a depth of 46 to 54 mm, with a sample volume of 10 mm. The probe was fixed in position with the use of a head strap. During reactivity measurements, mean VMCA was recorded continuously onto an IBM-compatible microcomputer for off-line analysis. Subjects wore a face mask; both inspiratory and expiratory ports were fitted with one-way valves. End-tidal CO2 was monitored continuously (Normacap 200, Datex). Baseline VMCA during normocapnia was measured, followed by VMCA during inspiration of 8% CO2 and then during hyperventilation. For these measurements subjects rested until VMCA and end-tidal CO2 were stable, and then mean VMCA over 30 seconds was recorded. Subjects then breathed 8% CO2 in air; this was continued until end-tidal CO2 and VMCA were stable, when mean VMCA over 30 seconds was recorded. The period of hypercapnia lasted 3 to 6 minutes. Then, after 2 minutes of breathing room air, the subject was instructed to vigorously hyperventilate. This was continued until end-tidal CO2 and VMCA were stable, when mean VMCA over 30 seconds was recorded. The period of hyperventilation lasted 2 to 3 minutes.
The vasodilatory response to hypercapnia was calculated from the following formula:
Eight percent CO2 results in a maximal vasodilatory response as assessed by TCD,5 and therefore the increase in flow velocity was not divided by the rise in end-tidal CO2. An exhausted reactivity was defined as a reactivity below 30%, calculated from the mean reactivity minus 3 SDs in our studies in individuals without any carotid stenosis.
The vasoconstrictor response to hypocapnia (hyperventilation) was calculated from the following formula:
Changes in hemodynamics, both reactivity and peak systolic velocities, before and after PTA were evaluated with the use of a one-way ANOVA followed by Scheffé’s multiple comparisons test for examination of differences between individual groups.
Details of Subjects
Sixteen subjects underwent attempted PTA. In 2 patients adequate Doppler signals could not be obtained from the MCA. In 3 patients the guide wire could not be passed through the carotid stenosis. In 11 subjects technically successful carotid PTA was performed, and the data from these 11 patients are presented. Mean±SD age was 61.1±7.5 years; 8 subjects were male and 3 female. The mean degree of ICA stenosis determined angiographically1 was 76.1±13.0%; the degree of stenosis was 50% to 59% in 1, 60% to 69% in 2, 70% to 79% in 1, 80% to 89% in 4, and 90% to 99% in 3. Stenosis was in the proximal ICA in 9, the distal ICA in 1, and the common carotid artery in 1. No patients had significant MCA stenosis or additional ICA stenoses distal to the lesion undergoing PTA. The mean±SD degree of contralateral ICA stenosis was 28.6±24.0%. Patients had presented with amaurosis fugax or retinal infarct (6), nondisabling stroke (1), TIA (3), and amaurosis fugax and TIA (1).
Eleven patients undergoing carotid endarterectomy for symptomatic proximal ICA stenosis were studied. Mean±SD age was 61.2±4.8 years; 10 patients were male and 1 female. The mean±SD degree of ICA stenosis determined angiographically was 79.3±16.1%; degree of stenosis was 50% to 59% in 1, 60% to 69% in 3, 70% to 79% in 1, 80% to 89% in 1, and 90% to 99% in 5. Patients had presented with amaurosis fugax or retinal infarct (4), nondisabling stroke (5), and TIA (2).
Monitoring During PTA
In 2 subjects ipsilateral VMCA fell during passage of the balloon catheter through the carotid stenosis to 55% and 39% of the value immediately before passage of the catheter. Ipsilateral VMCA fell transiently (to <50%) during balloon inflation in 6 of 11 subjects. Individual values of mean VMCA during balloon inflation, expressed as the percentage of preinflation values and averaged over inflations within the same individual patients, were 35%, 39%, 90%, 20%, 12.5%, 100%, 69%, 12%, 100%, 35%, and 100%. In all cases VMCA returned to normal within seconds of balloon deflation. In 2 patients there was a transient increase in pulsatility index after balloon deflation lasting approximately 2 minutes.
Only 1 patient experienced neurological symptoms during the procedure; he developed dysphasia and right-sided weakness and numbness immediately after the balloon deflation. VMCA was not significantly reduced at the time of balloon inflation (69% of preinflation flow velocity), and it was assumed that the event was embolic. Embolic signals were detected after balloon deflation in the ipsilateral MCA in this patient; however, embolic signals have been shown to be demonstrated in 90% of subjects after balloon deflation, usually in the absence of symptoms.6 The deficit rapidly resolved over the next hour, and no new lesions were seen on a repeated CT brain scan.
Hemodynamics Before and After PTA
During the postoperative follow-up period, no patient suffered TIA or stroke. Changes in ipsilateral hemodynamics are summarized in Table 1⇓. On the ipsilateral side, VMCA was unaltered after PTA. In contrast, hypercapnic reactivity increased significantly by a mean of 30.3% at 2 days and 48.3% at 1 month; in contrast, the response to hyperventilation remained unaltered. In all 4 patients in whom hypercapnic reactivity was decreased below the normal range (<30%) before PTA, it returned to normal by 2 days after PTA. Pulsatility index increased significantly. The hemodynamic improvements were more marked at 1 month than at 2 days after PTA and were maintained at 6 months. This paralleled the improvement in degree of stenosis, as reflected by a significant fall in the mean±SD ICA peak systolic velocity in the 9 patients with proximal ICA stenosis: preoperative value, 2.6±1.0 m/s; 2 days, 1.13±0.39 m/s; 1 month, 0.99±0.34 m/s; 6 months, 1.28±0.76 m/s; preoperative value versus 2 days, P<.003; versus 1 month, P<.0008; versus 6 months, P<.006. After carotid PTA, all arteries remained patent as determined by carotid duplex at 2 days, 1 month, and 6 months after PTA; in the one case in which the stenosis was in the distal ICA, TCD of the distal ICA by the submandibular approach demonstrated normal flow velocities and no spectral broadening at all time points, and MR angiography after 6 months showed no stenosis. In many subjects there was a further fall in ICA peak systolic velocity from 2 days to 1 month after PTA (Table 2⇓), but in 2 patients there was an increase between 1 and 6 months consistent with a degree of restenosis (patients 2 and 8 in Table 2⇓). In subject 2, despite the evidence of restenosis there was no corresponding reduction in CO2 reactivity, but in subject 8 the increase in ICA peak systolic velocity was accompanied by a fall in CO2 reactivity from 115% to 63%.
A significant increase in both hypercapnic reactivity and full vasodilatory reserve was seen on the contralateral side after PTA (Table 3⇓), although differences between individual time points were not significant.
Hemodynamics Before and After Carotid Endarterectomy
CO2 reactivity, measured 1 month postoperatively, increased significantly by a mean of 44.2% (Table 4⇓). In the two cases in which it was outside the normal range preoperatively (<30%), it returned to the normal range postoperatively. Reactivity to hyperventilation did not change. Pulsatility index increased significantly. All operated carotid arteries remained patent as determined by carotid duplex at 1 month after surgery. There was no evidence of restenosis at 1 month. During the postoperative follow-up period, no patient suffered a TIA or stroke.
These results demonstrate that carotid PTA results in a significant improvement in cerebral hemodynamics, as determined by measurement of CO2 vasodilatory perfusion reserve. In all patients in whom hypercapnic reactivity was reduced below the normal range before PTA, it returned to the normal range after the procedure. The changes seen were similar to those seen in patients with carotid endarterectomy, in whom there was also a significant improvement in CO2 reactivity and a return to the normal range in those patients in whom it was reduced preoperatively. This is consistent with previous studies showing normalization of impaired cerebral hemodynamics after carotid endarterectomy.7 8 Although the improvement was evident in the PTA patients by day 2, there was a further improvement in reactivity over the next month. This paralleled a further reduction in ICA peak systolic velocity, which is directly related to degree of stenosis, between day 2 and 1 month after PTA. This delayed fall in peak systolic velocity is consistent with delayed remodeling after PTA; we have noted this on serial carotid duplex studies and in a few patients in whom angiography has been repeated at 1 year, and we are currently prospectively evaluating this in a separate study. No patients in the present study underwent repeated intra-arterial angiography during the 6-month follow-up period. During the follow-up period, 2 subjects developed evidence of restenosis on duplex ultrasound. In one case CO2 reactivity fell, but in the other case it remained normal despite having been reduced preoperatively; in this case it is likely that collateral supply was established during the restenosis period.
In this study we also demonstrated an improvement in contralateral hemodynamics in patients undergoing carotid PTA. This has been reported previously for carotid endarterectomy8 and is thought to represent an improved collateral supply through the ipsilateral ICA and the circle of Willis to the contralateral hemisphere.
The significance of impaired vasodilatory reserve in patients with ICA stenosis has not been evaluated in large prospective studies, but in a prospective follow-up study in patients with carotid artery occlusion a severely reduced reactivity has been shown to be associated with a markedly increased stroke rate.9
Recording during PTA revealed reductions in VMCA in approximately half the patients during balloon inflation. However, these were short-lived, and flow velocity rapidly returned to normal after balloon deflation; they are likely to be shorter than the reduction in VMCA seen in some patients during carotid endarterectomy even in the presence of shunt insertion. In 2 patients with tight stenosis and poor collateral flow, VMCA fell during passage of the balloon catheter, but this was asymptomatic; the use of TCD allowed detection of this flow reduction and measures to be taken to restore flow rapidly.
In summary, carotid PTA results in a return of impaired cerebral hemodynamics to the normal range in a manner similar to that of carotid endarterectomy. It may result in transient falls in VMCA, but these are usually asymptomatic; TCD monitoring allows detection of reduced VMCA in the minority of patients in whom it drops during passage of the balloon catheter, and this may allow prevention of prolonged ischemia. Although these results are encouraging, the true role of carotid PTA in the management of ICA stenosis remains to be determined by large randomized trials that compare it with carotid endarterectomy.
Selected Abbreviations and Acronyms
|ICA||=||internal carotid artery|
|MCA||=||middle cerebral artery|
|PTA||=||percutaneous transluminal angioplasty|
|TCD||=||transcranial Doppler ultrasonography|
|TIA||=||transient ischemic attack|
|VMCA||=||MCA blood flow velocity|
This study was supported by the British Heart Foundation.
- Received September 27, 1995.
- Revision received December 28, 1995.
- Accepted January 3, 1996.
- Copyright © 1996 by American Heart Association
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