Vertebral artery stenosis: long-term follow-up.

Abstract

SUMMARY Ninety-six patients with 2550% unilateral vertebral artery (VA) stenosis were followed up for an average of 4.6 years. In 89 patients (93%) at least one VA origin was involved, while the intracranial VA was affected in 3 patients (3%). Seventy-four patients (77%) had 2=50% stenosis of at least one internal carotid artery, of whom 52 underwent carotid endarterectomy. None of the patients had definite vertebrobasilar transient ischemic attacks (VB TIA). Nineteen patients (19.8%) experienced nonlocalizing symptoms possibly compatible with VB TIA, none of whom had a stroke. Twenty-three patients (24%) had strokes. The only two patients (2%) who sustained a brainstem infarction had fatal strokes and both were known to have basilar artery stenosis in addition to their VA stenosis. The observed stroke rate was 8.5 times the expected infarction rate for a normal population. Forty patients died during follow up. The observed 5-year survival rate was 60% compared to 87% in a matched normal population. Eight deaths (20% of all deaths) were caused by stroke and 21 deaths (52.5% of all deaths) were cardiac related.VA stenosis is most frequently located at the VA origin (93%), and is associated with a low incidence of brainstem infarction. Stroke Vol 15, No 2, 1984 THE PRESENT STUDY describes the stroke and survival rates in a group of patients with angiographically proven vertebral artery (VA) stenosis. Little information is available regarding the natural history of patients with VA occlusive disease. Previous studies suggest that stenosis of the distal VA is more dangerous than stenosis at the VA origin, and that hemodynamic factors may be more important than emboli in producing vertebrobasilar (VB) ischemia.1 " 3 However, lack of precise information about the prognosis in these patients makes recommendations for treatment difficult. The problem is further complicated since the clinical symptoms of VB ischemia are often difficult to define, and non-localizing events such as isolated vertigo may be erroneously labeled as "VB ischemia". MethodsThe records of patients who underwent aortic arch and/or selective vertebral artery angiography at the Cleveland Clinic between 1974 and 1978 were reviewed. The angiographic films of all patients with reported stenosis of at least 1 VA were examined. Ninety-eight patients with ^5 0 % unilateral or bilateral VA stenosis were selected for follow up. Patients with unilateral or bilateral VA occlusion only and patients who underwent VA operative procedures were excluded. Fifty-two patients who underwent carotid endarterectomy (CE) were included in follow up since the benefit of CE in VB ischemia is doubtful.4 These cases were analyzed separately. Follow up was accomplished using a standardized questionnaire and telephone interviews. End points were death or stroke. Vertebrobasilar transient ischemic attacks (VB TIA) were noted but were not sufficient reason for stopping follow up. The recommendations of the ad hoc NINCDS Committee were followed in defining VB From the

Recanalization of Symptomatic Vertebral Ostial Occlusion in Patients with Acute or Subacute Stroke

“…[23][24][25] As VA-origin plaques are hard, smooth, and concentric and are less prone to ulceration or intramural hemorrhage, they are therefore known to have less risk for embolism than carotid bifurcation plaques. 26 However, acute thrombus formation at the stump or due to plaque rupture can cause sudden occlusion of the V1 segment as well as a large thrombus burden. 27,28 The endovascular treatment of VA atheromatous disease remains controversial, as its natural history is poorly understood and no randomized trials have assessed the effectiveness and long-term outcome of this therapy.…”

Vol. 8, No. 2 (Full Issue)

“…Unfortunately, as evidenced by its common usage, the bias of 1 r is often ignored. The expected value of a lag-1 autocorrelation coefficient for a series consisting of N data points was analytically derived by Marriott and Pope (1954) to be:…”

“…This finding was subsequently supported by similarly positive results in observational studies (Marzewski, et al,. 1982;Moufarrij, Little, Furlan, Williams & Marzewski, 1984;Chimowitz, et al, 1995;Thijs & Albers, 2000;Qureshi, et al, 2003) In 1998, the National Institute of Neurological Diseases and Stroke (NINDS) funded the Warfarin vs Aspirin for Symptomatic Intracranial Disease (WASID) study, the first double-blinded, placebo-controlled randomized clinical trial (RCT) to test the superiority of warfarin (International Normalized Ratio [INR] 2 -3) over high-dose aspirin (650 mg twice daily) in this patient population. The protocol called for enrollment of 806 patients with angiographically proven symptomatic intracranial disease to determine a combined endpoint of stroke (ischemic and hemorrhagic) and vascular death.…”

“…Existing literature on warfarin treatment for intracranial stenosis was reviewed (Millikan, et al, 1954;Marzewski, et al, 1982;Moufarrij, et al, 1984;Chimowitz, et al, 1995;Thijs, et al, 2000;Qureshi, et al, 2003). Of the six publications, two studies (Marzewski, et al, 1982;Moufarrij, et al, 1984) insufficiently detailed; focus is placed on the remaining four publications in addition to the article describing the WASID trial results (Chimowitz, et al 2005).…”

Endovascular Angioplasty for Extracranial Vertebral Artery Occlusion Without Visualization of the Stump of the Artery Ostium

“…1,22) After the initial occurrence of untreated vertebrobasilar stroke or transient ischemic attack, the risk of stroke within the following 5 years is 25-35%. 13) Percutaneous endovascular treatment of extracranial VA disease is not as technically challenging as surgical procedures, and as such, endovascular angioplasty is a valuable alternative. 2,7,9,16,20,21) Common endovascular angioplasty is performed after a wire device is navigated across the lesion.…”