Assessment of platelet inhibition by point-of-care testing in neuroendovascular procedures.

Antiplatelet agents are an important component of the preventive strategies currently used in clinical practice to minimize the risk of thromboembolic events during and after endovascular procedures. Because of the variability in the response to antiplatelet agents, measuring the degree of platelet inhibition may help identify and properly treat poor responders. POC testing is defined as diagnostic testing at or near the site of patient care. Knowledge of the specifics of these devices among practicing neurointerventionalists is relatively limited. In this article, the different POC devices available are presented, and their clinical utility in relation to endovascular procedures is discussed.

Point-of-care testing for anticoagulation monitoring in neuroendovascular procedures.

POC testing is defined as diagnostic testing at or near the site of patient care. Rapid measurement of the intensity of anticoagulation and, more recently, platelet inhibition allows dose titration of adjuvant medications such a heparin and antiplatelet agents during neuroendovascular procedures. However, knowledge among practicing physicians regarding the pathophysiologic basis of these measurements and variations in knowledge about the differences among devices is often limited. This review discusses the role of anticoagulation in endovascular procedures and the currently available POC tests for anticoagulation monitoring.

Occurrence and predictors of futile recanalization following endovascular treatment among patients with acute ischemic stroke: a multicenter study.

BACKGROUND AND PURPOSE: Although recanalization is the goal of thrombolysis, it is well recognized that it fails to improve outcome of acute stroke in a subset of patients. Our aim was to assess the rate of and factors associated with "futile recanalization," defined by absence of clinical benefit from recanalization, following endovascular treatment of acute ischemic stroke. MATERIALS AND METHODS: Data from 6 studies of acute ischemic stroke treated with mechanical and/or pharmacologic endovascular treatment were analyzed. "Futile recanalization" was defined by the occurrence of unfavorable outcome (mRS score of > or = 3 at 1-3 months) despite complete angiographic recanalization (Qureshi grade 0 or TIMI grade 3). RESULTS: Complete recanalization was observed in 96 of 270 patients treated with IA thrombolysis. Futile recanalization was observed in 47 (49%). In univariate analysis, patients with futile recanalization were older (73 +/- 11 versus 58 +/- 15 years, P < .0001) and had higher median initial NIHSS scores (19 versus 14, P < .0001), more frequent BA occlusion (17% versus 4%, P = .049), less frequent MCA occlusion (53% versus 76%, P = .032), and a nonsignificantly higher rate of symptomatic hemorrhagic complications (2% versus 9%, P = .2). In logistic regression analysis, futile recanalization was positively associated with age > 70 years (OR, 4.4; 95% CI, 1.9-10.5; P = .0008) and initial NIHSS score 10-19 (OR, 3.8; 95% CI, 1.7-8.4; P = .001), and initial NIHSS score > or = 20 (OR, 64.4; 95% CI, 28.8-144; P < .0001). CONCLUSIONS: Futile recanalization is a relatively common occurrence following endovascular treatment, particularly among elderly patients and those with severe neurologic deficits.

Intra-arterial recanalization techniques for patients 80 years or older with acute ischemic stroke: pooled analysis from 4 prospective studies.

BACKGROUND AND PURPOSE: Previous studies have demonstrated limited benefit with endovascular procedures such as stent placement in octogenarians. We evaluated the safety and effectiveness of intra-arterial recanalization techniques to treat ischemic stroke in patients 80 years or older presenting within 6 hours of symptom onset. MATERIALS AND METHODS: We pooled the data from 4 prospective studies by evaluating intra-arterial recanalization techniques for treatment of ischemic stroke. Clinical and radiologic evaluations were performed before treatment and at 24 hours, 7 to 10 days, and 1 to 3 months after treatment. We performed multivariate analyses to evaluate the effect of ages 80 years and older on angiographic recanalization, favorable outcome (modified Rankin scale of 0-2), and mortality rate at 1 to 3 months. RESULTS: A total of 101 patients were treated in the 4 protocols. Of these, 24 were 80 years or older. There was no significant difference between the 2 age groups in sex, initial stroke severity, time to treatment, site of vascular occlusion, and rate of symptomatic and asymptomatic intracranial hemorrhage (ICH). In logistic regression analysis, age 80 years or older was associated with a lower likelihood of a favorable outcome (odds ratio [OR], 0.40; 95% confidence interval [CI], 0.13-1.2; P = .11) and recanalization (OR, 0.36; 95% CI, 0.12-1.1; P = .07) and with higher mortality rate (OR, 3.17; 95% CI, 1.05-9.55; P = .04) after adjusting for study protocol. After adjusting for recanalization in addition to study protocol, the older age group still had a lower likelihood of favorable outcomes (OR, 0.34; 95% CI, 0.1-1.1; P = .07) and higher mortality rates (OR, 3.62; 95% CI, 1.15-11.36; P = .027). CONCLUSIONS: Our study demonstrates that patients 80 years and older are at higher risk for poor outcome at 1 to 3 months following intra-arterial recanalization techniques. This relationship is independent of recanalization rate and symptomatic ICH supporting the role of other mechanisms.

Endovascular interventions following intravenous thrombolysis may improve survival and recovery in patients with acute ischemic stroke: a case-control study.

BACKGROUND AND PURPOSE: Since the introduction of recombinant tissue plasminogen activator (rtPA) into clinical practice in the mid 1990s, no adjunctive treatment has further improved clinical outcomes in patients with ischemic stroke. The safety, feasibility, and efficacy of combining intravenous (IV) rtPA with endovascular interventions has been described; however, no direct comparative study has yet established whether endovascular interventions after IV rtPA are superior to IV rtPA alone. A retrospective case-control study was designed to address this issue. MATERIALS AND METHODS: Between 2003 and 2006, 33 consecutive patients with acute ischemic stroke and National Institutes of Health Stroke Scale (NIHSS) scores >/=10 were treated with IV rtPA in combination with endovascular interventions (IV plus intervention) at a tertiary care facility. Outcomes were compared with a control cohort of 30 consecutive patients treated with IV rtPA (IV only) at a comparable facility where endovascular interventions were not available. RESULTS: Baseline parameters were similar between the 2 groups. We found that the IV-plus-intervention group experienced significantly lower mortality at 90 days (12.1% versus 40.0%, P = .019) with a significantly greater improvement in NIHSS scores by the time of discharge or follow-up (P = .025). In the IV-plus-intervention group, patients with admission NIHSS scores between 10 and 15 and patients /=10, there was a suggestion of incremental clinical benefit among patients receiving endovascular interventions following standard administration of IV rtPA.

Maternal cerebral hemodynamics in pregnancy-related hypertension. A prospective transcranial Doppler study.

AIM: To compare maternal cerebral hemodynamics, as assessed by transcranial Doppler studies, with the clinical and radiological findings in different types of pregnancy-related hypertension and to determine their pathophysiology. METHODS: A prospective study of 66 consecutive pregnant women with hypertensive disorders (eclampsia, n = 3; pre-eclampsia, n = 41; isolated hemolysis, elevated liver enzymes, and low platelet count (HELLP)-syndrome, n = 12; pre-eclampsia superimposed on chronic hypertension, n = 5; chronic hypertension, n = 5) and 21 women with uncomplicated pregnancies. Mean blood flow velocities (Vmean) were assessed serially by means of transcranial Doppler in all basal arteries and correlated with changes in mean arterial blood pressure (MABP) and the clinical course. RESULTS: Patients with the pre-eclampsia/eclampsia syndrome showed significantly elevated Vmean values as compared to controls. In the course of the illness Vmean over the whole length of all insonated basal arteries rose simultaneously. The three eclamptic patients showed the highest Vmean values (156, 182, 192 cm/s, respectively), of the middle cerebral artery (MCA) while MABP was 135, 135, and 150 mmHg, respectively. In pre-eclamptic patients the maximal Vmean MCA ranged from 80 (67, 93) to 145 (114, 151) cm/s [median (25th, 75th percentile)] depending on the severity of clinical presentation. In patients with isolated HELLP-syndrome changes in Vmean were either mild (5/12 cases) or absent (7/12 cases). CONCLUSIONS: Considerable differences in cerebral hemodynamics were observed in the various types of pregnancy-related hypertensive disorders examined in this study. Our findings in patients with pre-eclampsia/eclampsia syndrome suggest a breakdown of autoregulation with hyperperfusion and vasogenic edema being the most probable pathophysiological mechanism.

Posterior cerebral artery territory infarcts in the New England Medical Center Posterior Circulation Registry.

BACKGROUND: Infarcts in the territory of the posterior cerebral arteries (PCAs) are common. Although associated clinical symptoms and signs are known, the mechanisms of stroke and the anatomical distribution of PCA territory lesions caused by the various stroke mechanisms are less well defined. Published reports have selected only special subgroups of patients. PATIENTS AND METHODS: We studied stroke mechanisms, infarct distribution, and clinical findings among 79 patients in the New England Medical Center Posterior Circulation Registry in whom brain imaging scans showed infarcts that involved 1 or more cortical territories of the PCA. RESULTS: Forty-eight patients (61%) had infarcts limited to the PCA territory (pure PCA), while 31 (39%) also had infarcts in other territories (PCA+). Infarcts were in the cortical territory of the PCA in 47 patients (59%) and were cortical and deep in 32 (41%). Infarcts that were cortical and deep were more common in PCA+ lesions. Stroke mechanisms were embolism of cardiac origin (32 [41%]), proximal arterial disease (25[32%]), cryptogenic embolism (8[10%]), intrinsic PCA disease (7[9%]), vasoconstriction (4[5%]), and coagulopathy (3[4%]). Patients with cardiogenic embolism and intrinsic PCA disease often had pure PCA territory infarcts, while patients with proximal arterial disease more often had PCA+ infarcts. Visual abnormalities were present in 66 patients (84%). Motor weakness, cognitive and behavioral abnormalities, and ataxia were found in 20 patients (25%); only 12 (15%) had sensory signs. CONCLUSIONS: The great majority of pure PCA and PCA+ territory infarcts are caused by cardiac or intra-arterial embolism. Intrinsic PCA disease, vasoconstriction, and coagulopathy are less common causes of infarction.

Anatomy of sensory findings in patients with posterior cerebral artery territory infarction.

BACKGROUND: Posterior cerebral arteries (PCAs) supply the ventrolateral thalamic sensory nuclei and white matter sensory tracts to the somatosensory parietal cortex. Patients with PCA territory strokes often have visual, memory, cognitive, and sensory signs. Clinicoanatomic correlation of visual, cognitive, and memory functions are well defined but, to our knowledge, no systematic study has analyzed the anatomy of sensory abnormalities. OBJECTIVE: To assess the frequency and anatomic correlation of sensory symptoms and signs in patients with PCA territory infarction. PATIENTS AND METHODS: Sixty patients with hemispheral and hemispheral and deep PCA territory infarcts apparent on computed tomographic and magnetic resonance imaging scans were studied for the presence of sensory findings and location of infarcts. RESULTS: Sensory symptoms or signs were present in 15 (25%) of 60 patients. Among patients with sensory findings, 11 of 15 had infarcts in the ventrolateral thalamus in the territory of the thalamogeniculate or lateral posterior choroidal arteries. The other 4 patients had no ventrolateral thalamic or white matter infarction but had severe proximal vascular occlusive lesions that could have caused temporary thalamic ischemia. One of these 4 patients had a medial thalamic infarct and transient hemisensory symptoms. Twelve patients had thalamic infarcts and no recorded sensory findings. Seven patients with thalamic infarcts (6 medial and 1 ventrolateral) had no sensory findings, and sensory findings could not be accurately assessed in 4 patients with ventrolateral and 1 patient with medial thalamic infarcts. CONCLUSIONS: All patients with PCA territory infarcts and sensory findings either had thalamic infarcts in thalamogeniculate or lateral posterior choroidal artery territory or had thalamic ischemia. Sensory findings in PCA territory infarction indicate ventrolateral thalamic ischemia.