Severe Internal Carotid Stenosis Research Articles

Functional MRI evaluation of cognitive effects of carotid stenosis revascularization.

IntroductionSevere internal carotid stenosis, if left untreated, can pose serious risks for ischemic stroke and cognitive impairments. The effects of revascularization on any aspects of cognition, however, are not well understood, as conflicting results are reported, which have mainly been centered on paper‐based cognitive analyses. Here, we summarized and evaluated the publications to date of functional MRI (fMRI) studies that examined the mechanisms of functional brain activation and connectivity as a way to reflect cognitive effects of revascularization on patients with carotid stenosis.MethodsA PubMed and Google Scholar (covering the relevant literature until November 1, 2021) search yielded eight original studies of the research line, including seven resting‐state and one task‐based fMRI reports.ResultsFindings demonstrated treatment‐related alterations in fMRI signal intensity and symmetry level, regional fMRI activation pattern, and functional brain network connectivity. The functional brain changes were associated largely with improvement in cognitive function assessed using standard cognitive test scores.ConclusionsThese findings support the contribution of fMRI to the understanding of brain functional activation and connectivity changes revealing cognitive effects of revascularization in the management of severe carotid stenosis. The review also highlighted the importance of reproducibility through enhancing experimental designs and cognitive task applications with future research for potential clinical translation.

Management of severe internal carotid stenosis with unruptured intracranial aneurysm

To investigate the safety and feasibility of endovascular treatment for severe internal carotid artery stenosis (≥70%) with unruptured intracranial aneurysms. We retrospectively reviewed 213 cases with severe stenosis or occlusion of internal carotid artery, and those patients had been treated at Peking University Third Hospital, between January 2012 and July 2015. In the study, 14 (6.6%) cases were coexistence with unruptured intracranial aneurysms. The medical records, imaging data, treatment and prognosis were analyzed. There were 15 aneurysms (11 after the stenosis, 1 before the stenosis, and 3 in the other drainage basin) in those 14 patients with severe stenosis or occlusion of internal carotid artery. One of the 14 patients underwent carotid endarterectomy, and the 11 patients were successfully implanted with an internal carotid stent (residual stenosis 0-30%, mean 6.4%). Two patients with internal carotid artery stenosis remained untreated. One of them had complete occlusion of the initial segment of the internal carotid artery and was not possible to be treated, and the other patient refused to treat with internal carotid stenosis. The sizes of aneurysms were 1.0-7.0 mm, with an average of (2.8±1.5) mm. Three cases were treated with stenosis and aneurysms treated at the same time, and stent assisted coil embolization was performed in all the aneurysms, including 1 case that treated aneurysm before the stenosis. One patient refused surgical treatment of unruptured aneurysm, and no treatment was given to 10 patients who had small unruptured aneurysms (<5.0 mm). No perioperative complications were observed during the perioperative period. Three cases were lost with the follow-up, and the other 11 patients were followed up for 15-55 months, with a median of 37 months, and had good prognosis. Our results suggest that patient coexistance with severe internal carotid stenosis and unruptured intracranial aneurysms should be treated individually according to the location and size of aneurysms. Moreover, the presence of a small intracranial aneurysm (<5.0 mm) does not seem to increase the risk of endovascular stenosis in patients with severe internal carotid stenosis.

Reversible cerebral hyperperfusion syndrome after stenting of the carotid artery—Two case reports

Hyperperfusion syndrome can complicate carotid revascularization, be it endarterectomy or carotid artery stenting (CAS). Although extensive effort has been devoted to reducing the incidence of ischemic stroke complicating CAS, little is known about the incidence, etiology, and prevention strategies for hyperperfusion following CAS. We report two cases (female patients 72 and 81 years) presenting severe internal carotid stenosis (> 90%), who underwent presurgical and therapeutic intervention with CAS. Both patients developed hyperperfusion symptoms at 2 hours and at 30 minutes, respectively, following stenting, in both cases unilateral hyperperfusion was CCT confirmed. Case 1 was presenting with acute edema of the right hemisphere, case 2 with distended focal edema (left fronto-temporoparietally). Hyperperfusion syndrome and neurological symptoms retroceded in both cases (conservative therapy) and both patients returned to full activity (case 2 within 48 hours).

Safety and Security of Carotid Artery Stenting for Severe Stenosis with Contralateral Occlusion

Background: Despite advances in the surgical treatment of patients with severe internal carotid stenosis (ICA), there are selective groups of patients who, due to several reasons, are not good candidates for surgery. Patients with contralateral occlusion are one of these subgroups. Thereby, other therapeutic alternatives, such as angioplasty may be of value. So far, there has been little published data about carotid angioplasty (CA) or stenting (CAS) in those patients. The objective of this study was to evaluate the efficacy and safety of angioplasty and stenting in patients with severe internal carotid stenosis and contralateral occlusion. Methods: Between 1991 and June 2004, 519 consecutive patients who underwent CA or CAS for severe stenosis of the ICA were registered in our prospective CA Data Bank. Of them, we identified 96 with contralateral occlusion (18.5%), who formed the basis of the present analysis. Results: Mean age was 64 ± 9 (range 40–80), 85 (88.5%) were men, and 61 (63.5%) were symptomatic. Thirty-two patients (33.3%) did not meet the criteria to be included in the NASCET. CA was done in 25 patients (26%) and CAS in 71 (74%). Distal protection was used in 38 patients (39.6%). Asymptomatic stenosis was treated in cases of progression (>85%), exhausted vasoreactivity, positive microemboli detection in transcranial Doppler, and/or asymptomatic lesions in CT/MRI. Transient hemodynamic effects were frequent: hypotension (54.5%), bradycardia (61.5%), asystole (33.3%), and syncope (33.3%). TIA occurred in 1 patient (1%), minor stroke in 1 (1%), and disabling stroke in 2 patients (2.1%). Mortality was 0%. Morbidity was 0% in cases done with distal protection. Conclusion: In our experience, CA/CAS performed in patients with severe carotid stenosis and contralateral occlusion compared favorably with the results obtained with carotid endarterectomy (CEA), to the extent that if randomized series comparing CEA and CA/CAS are done, CA/CAS might be considered as the treatment of choice in this subgroup of patients.

Reduced Frequency of Embolic Signals in Severe Carotid Stenosis with Poststenotic Flow Velocity Reduction

Background: We aimed to investigate the effect of poststenotic low blood flow in patients with recently symptomatic severe carotid stenosis on arterio-arterial embolism. Methods: Analyses based on a series of 206 consecutive patients (155 men and 51 women, mean age 65.3 years) with a nondisabling ischemic event in the anterior circulation ≤30 days (median 4.5) before presentation and diagnosis of ipsilateral carotid artery stenosis/occlusion (≧30% local diameter reduction). All patients underwent Doppler/duplex sonography, which included measurement of poststenotic flow velocity as an indicator for poststenotic blood flow as well as a 1-hour transcranial Doppler monitoring for the detection of embolic signals. Results: Thirty-seven of two hundred and six patients had very severe stenosis which was associated with reduced poststenotic flow velocity (<20 cm/s systolic) in 17 patients. Probability of embolic signals increased with increasing degree of stenosis and was maximal in patients with stenoses ≧90% local diameter reduction if poststenotic flow velocity was not reduced. Reduced poststenotic flow velocity in patients with very severe stenosis was associated with a significantly lower frequency of embolic signals compared to patients with the same degree of stenosis but no velocity reduction (adjusted odds ratio 0.15, 95% confidence interval 0.025–0.897, p = 0.038, adjustment for antiplatelet medication and time since ischemia). Conclusions: Low poststenotic flow velocity behind very severe internal carotid stenosis reduces the otherwise high frequency of embolic signals in recently symptomatic patients corroborating the hypothesis that reduced blood flow across carotid stenosis causes reduced embolism.

Intracranial hemorrhage and hyperperfusion syndrome following carotid artery stenting: Risk factors, prevention, and treatment

ObjectivesThe study defined the incidence of cerebral hyperperfusion syndrome and intracranial hemorrhage (ICH) and the risk factors for their development following carotid artery stenting (CAS). BackgroundHyperperfusion syndrome and ICH can complicate carotid revascularization, be it endarterectomy or CAS. Although extensive effort has been devoted to reducing the incidence of ischemic stroke complicating CAS, little is known about the incidence, etiology, and prevention strategies for hyperperfusion and ICH following CAS. MethodsWe retrospectively reviewed the prospective database of 450 consecutive patients who were treated with CAS in our department to identify patients who developed hyperperfusion syndrome and/or ICH. ResultsThe mean age of the patients was 72.7 ± 10.9 years, and the mean diameter narrowing was 84 ± 12.8%. Five (1.1% [95% confidence interval 0.4% to 2.6%]) patients developed hyperperfusion. Three (0.67%) of the five developed ICH. Two of these patients died (0.44%). Symptoms developed within a median of 10 h (range, 6 h to 4 days) following stenting. All five patients had correction of a severe internal carotid stenosis (mean 95.6 ± 3.7%) with a concurrent contralateral stenosis >80% or contralateral occlusion and peri-procedural hypertension. These same risk factors are involved in cerebral hyperperfusion following carotid endarterectomy. The use of platelet glycoprotein IIb/IIIa receptor blockers did not appear to increase the risk ICH. ConclusionsThe hyperperfusion syndrome occurs infrequently following CAS, and ICH occurs in 0.67% of patients. Patients with severe bilateral carotid stenoses may be predisposed to ICH, particularly if there is concurrent arterial hypertension. Patients with these factors may require more intensive hemodynamic monitoring after CAS, including prolongation of hospitalization in some cases.

２．閉塞性頚動脈病変に対する総合診療―脳血管内科医の役割

Recently, the number of patients with severe carotid stenosis is increasing in Japan. During these 2 years (2001-2002), 205 patients with severe internal carotid stenosis were admitted to our hospital, of whom 94 patiens (45.9%) underwent carotid endarterectomy (CEA). According to our criteria of carotid ultrasound sonogram (US), we recommend the precise examination and CEA for the patients with>90% stenosis on the US axial view, over 200cm/sec in peak sysytolic velosity at the most stenotic lesion, and>1.3 in endodiastolic flow velosity ratio of common carotid artery (intact/lesion side). Transoral carotid ultrasonograpy are essential for the assessment of distal internal carotid artery, and trascranial color coded doppler ultrasonography are also useful for the management of the CEA patients to protect against hyperperfusion. Stroke internists should play the coordinator for the comprehensive assessment of the patients with systemic vascular disease with the various medical specialists, to establish the treatment strategy and management of patients with carotid artery disease.

Preventing ischemic stroke in patients with prior stroke and transient ischemic attack : a statement for healthcare professionals from the Stroke Council of the American Heart Association.

Stroke, the third leading cause of death in the United States, is a leading cause of adult neurological disability and accounts for the greatest number of hospitalizations for neurological disease. Although treatment of acute stroke has the potential of reducing death and disability, it is likely that prevention will more effectively reduce the ravages of stroke. The patient who is recovering from a mild stroke or who has had a recent transient ischemic attack (TIA) is at high risk of stroke recurrence, physical and intellectual disability, long-term institutionalization, and death. There is substantial evidence from observational epidemiological studies and clinical trials that recurrent ischemic stroke can be prevented (Table 1⇓). Control of risk factors is important for prevention of a first stroke and is practical after ischemic stroke and TIA have occurred. Identification of the specific ischemic stroke mechanism, eg, TIA or minor stroke ipsilateral to a moderate or severe internal carotid stenosis, guides decision making with regard to recurrent stroke prevention therapy (Table 2⇓). A patient with symptomatic cerebrovascular disease is likely to have other cardiovascular diseases or is predisposed to develop them. Preventive measures should complement reduction in risk of atherothrombotic events in the coronary arteries and other arterial territories. Certain nonmodifiable characteristics identify persons at high risk of stroke and stroke recurrence. These include advancing age, male sex, and black and Hispanic race-ethnic backgrounds. Some risk factors, however, such as elevated blood pressure, cigarette smoking, obesity, impaired glucose tolerance, and physical inactivity, are modifiable. Other conditions, ie, prior cardiovascular diseases such as coronary heart disease with angina or prior myocardial infarction, valvular heart disease, congestive heart failure, atrial fibrillation, increased left ventricular mass, and certain other echocardiographic abnormalities, identify persons at increased risk who may be treated with antithrombotic therapy. More recently, other modifiable risk …

796-1 Non Surgical Revascularization in Carotid Arteries: Role of Percutaneous Transluminal Angioplasty

The role of Percutaneous Transluminal Angioplasty (PTA) in the revascularization of carotid arteries is not well established. The aim of this study was to asses the efficacy of PTA in revascularizing patients with carotid arterial stenosis. Thirteen consecutive patients (mean age 68 ± 7.7 years) underwent 13 PTA procedures in the carotid arteries during September 1992 to March 1994. The indication for revascularization was recurrent ischemic attacks with severe (&gt;50%) carotid stenosis in the 13 cases. Time between symptoms onset to PTA was more than one month in all cases. The lesions were located in the internal carotid arteries (first extracraneal segment) in nine patients and in the common carotid arteries in four. This group included one patient treated by severe internal carotid stenosis with complete occlussion in the contralateral internal carotid vessel. PTA was performed using conventional technique. The balloon/artery ratio was 0.8–0.9/1 in all cases (Mean balloon size 5.3 ± 0.5 mm). PTA was successfully performed in all patients with the diameter stenosis reduced from, 77.5 ± 5% to 19.7 ± 4%. Four patients had bradycardia and hypotension during balloon inflation. Two patients had transient neurologic deficit immediately after the procedure, resolved within 24 hours. No patient had a residual neurologic deficit upon discharge (mean 48 hours). At late clinical follow up (mean time 10 ± 7 months) one patient had restenosis with a new successful PTA. This early experience showed that PTA can be performed successfully and safely in selected cases of patients with symptomatic severe stenosis in carotid arteries. However, larger groups of patients and longer follow-up should need to compare this technique with surgical-endarterectomy.

Usefulness of an intravenous contrast medium in the characterization of high-grade internal carotid stenosis with color Doppler-assisted duplex imaging.

The remaining limitations of ultrasonographic imaging in accurately quantifying internal carotid stenosis or diagnosing internal carotid occlusion may be overcome by enhancing the echogenicity of flowing arterial blood with contrast agents. This study assessed the usefulness of the intravenous (transpulmonary) contrast medium SH U 508 A in improving the characterization and quantification of severe internal carotid stenosis. We examined 32 patients (30 had vessels with a stenosis of greater than 70% luminal narrowing and 2 had vessel occlusions) using a 7.5-MHz linear-array transducer for color Doppler-assisted duplex imaging before and after injection of the contrast medium. The SH U 508 A-induced increase in carotid blood echogenicity began 11 +/- 2 (mean +/- SD) seconds after the start of the bolus injection, peaked at 21 +/- 2 dB, and showed a half-life of 75 seconds. Quantitative vascular measurements (cross-sectional luminal area reduction and plaque length, respectively) obtained before and after contrast application were highly correlated (r > .90). Visualization of the entire length of the intrastenotic residual flow lumen, however, was significantly improved by contrast enhancement (52% versus 83%, P = .01). This pilot study on patients with extracranial carotid artery disease suggested that ultrasonic contrast media may be most useful in improving the ultrasonography-based diagnosis of internal carotid occlusion.

Non-invasive evaluation of patients with extracranial to intracranial bypass.

In selected patients with cerebrovascular insufficiency, an extracranial-intracranial bypass is indicated to increase cerebral blood flow. To assess the effect of this operation upon routine non-invasive testing, 15 patients had oculoplethysmography, carotid phonoangiography and Doppler testing. None of those with a preoperative abnormality were changed after surgery, despite angiographically proven anastomotic patency. Whereas non-invasive tests may correctly identify severe internal carotid stenosis, use of these modalities in their routine form does not predict extracranial-intracranial bypass patency.