Dynamic contrast-enhanced MR angiography and MR imaging of the carotid artery: high-resolution sequences in different acquisition planes.
(9/264)
BACKGROUND AND PURPOSE: First-pass contrast-enhanced MR angiography has become the technique of choice for studying the carotid bifurcation, but this method has some limitations. We evaluated the clinical utility of performing 3D contrast-enhanced MR angiography in the axial plane immediately after performing angiography in the coronal plane. METHODS: Cervical carotid arteries of 80 consecutive patients were studied on a 1.5-T MR imager with phased-array coils. Coronal 3D MR angiography was performed after administering a bolus injection of contrast material (20 mL) with automatic triggering. This was immediately followed by an axial acquisition. We measured carotid diameters on the contrast-enhanced MR angiograms as well as on intra-arterial digital subtraction angiograms according to established criteria. We also evaluated original source MR angiograms. RESULTS: Angiograms obtained in the axial plane correlated better with the intra-arterial digital subtraction angiograms than did the coronal angiograms. When first-pass contrast-enhanced MR angiography was incomplete because of a failure of triggering, the second-phase acquisition provided sufficient image quality. Original source images suffered from ring artifacts, low axial resolution, and a low level of soft-tissue visualization. Axial-based source images showed flow-independent contrast filling to the patent lumen with sufficient visualization of plaque morphology, thickened arterial wall, and surrounding disease processes, such as tumors. CONCLUSION: With the addition of a 1-minute second-phase 3D acquisition in a different plane immediately after first-pass contrast-enhanced MR angiography, one can obtain a more accurate depiction of the carotid bifurcation, insurance against failure of triggering, and diagnostic source images. (+info)
Transcranial Doppler-directed Dextran-40 therapy is a cost-effective method of preventing carotid thrombosis after carotid endarterectomy.
(10/264)
OBJECTIVES: perioperative stroke reduces the clinical effectiveness of carotid endarterectomy (CEA). Postoperative thrombotic stroke may be reduced in incidence by the use of transcranial Doppler-directed Dextran-40 therapy. This programme requires the purchase of additional equipment and employment of more staff. This study examined whether this additional financial outlay was cost-effective in terms of saving expenditure by preventing postoperative thrombotic stroke. MATERIALS AND METHODS: data was collected prospectively on a series of 600 consecutive CEAs. The costs of the monitoring programme were analysed over 1- and 5-year periods. Formulae were derived allowing other units to calculate whether this technique will be cost-effective for them. RESULTS: after the introduction of TCD monitoring the postoperative thrombotic stroke rate fell from 2.7% to 0% (8 strokes prevented). Our local unit cost for the treatment of stroke was 25,702 pounds. After allowing for the additional costs of the monitoring programme, we calculate that postoperative TCD has saved 171,393 pounds. CONCLUSIONS: postoperative TCD monitoring is a clinically effective and also cost-effective method of reducing the stroke rate associated with CEA. For units performing more than 50 CEAs per year who experience occasional postoperative carotid thrombosis, its introduction should be considered. (+info)
Clinical and pathophysiological features of amaurosis fugax in Japanese stroke patients.
(11/264)
OBJECTIVE: It has been emphasized that amaurosis fugax (AmF) is caused by thromboembolism due to atheromatous lesions of the extracranial carotid artery (EC-CA) in Caucasian populations. However, there have been few studies of AmF in Japan. We analyzed the clinical and pathophysiologic features of AmF in 43 Japanese AmF patients. SUBJECTS AND METHODS: Forty-three patients presented with AmF from a group of 2,056 Japanese patients with acute ischemic stroke. We investigated angiographic and transcranial Doppler findings, precipitating factors, medical treatment and prognosis, to elucidate the pathogenetic mechanism of AmF. RESULTS: Angiographic findings revealed an intracranial lesion in 22 patients (51%), extracranial lesion in 16 (37%), and no abnormality in 5 (12%). Blood flow in the ophthalmic artery (OA) examined by the transcranial Doppler ultrasonography (TCD) showed normal antegrade flow in 24 patients and reversed flow in 7. Precipitating factors for AmF were seen in 7 out of 43 patients. Regarding the pathogenesis of AmF, the micro-thromboembolism originated from the internal carotid artery (ICA) in 25 patients, the thromboembolism was via the external carotid artery (ECA) in 7, the hemodynamic retinal vascular insufficiency in 6 patients showed various atheromatous changes in the intracranial carotid artery (IC-CA) or EC-CA, and the cause was unknown in 5. CONCLUSION: In this series of patients, AmF was mainly caused by thromboembolism from IC-CA atheromatous lesions. Micro-thromboemboli from the ECA or hemodynamic retinal vascular insufficiency, although less frequent, should also be considered as possible etiologies for AmF. (+info)
Delayed bilateral internal carotid artery thrombosis following accidental strangulation.
(12/264)
A 24-yr-old male presented after a fishing accident in which he was pulled underwater by a rope attached to a crayfish pot. He was winched out of the water with the rope still around his neck, sustaining serious neck injuries that ultimately led to his death. After initial resuscitation, he remained fully conscious for approximately 8 h, after which there was a rapid and sudden deterioration in his level of consciousness. The presentation, investigation, management and subsequent postmortem findings are presented and discussed. (+info)
Fulminant cerebral infarction in a patient with nephrotic syndrome.
(13/264)
Fulminant cerebral infarction secondary to arterial thrombosis in adults with nephrotic syndrome is rare. We report a 42 year old male with fulminant right anterior cerebral and middle cerebral artery infarction. Minimal change disease of the kidney was documented by renal biopsy. The possible pathogenesis is discussed and pertinent literature reviewed. (+info)
Vascular release of plasminogen activator inhibitor-1 impairs fibrinolysis during acute arterial thrombosis in mice.
(14/264)
The role of plasminogen activator inhibitor-1 (PAI-1) in the plasma, blood platelets, and vessel wall during acute arterial thrombus formation was investigated in gene-deficient mice. Photochemically induced thrombosis in the carotid artery was analyzed via transillumination. In comparison to thrombosis in C57BL/6J wild-type (wt) mice (113 +/- 19 x 10(6) arbitrary light units [AU] n = 15, mean +/- SEM), thrombosis in PAI-1(-/-) mice (40 +/- 10 x 10(6) AU, n = 13) was inhibited (P <.01), indicating that PAI-1 controls fibrinolysis during thrombus formation. Systemic administration of murine PAI-1 into PAI-1(-/-) mice led to a full recovery of thrombotic response. Occurrence of fibrinolytic activity was confirmed in alpha(2)-antiplasmin (alpha(2)-AP)-deficient mice. The sizes of thrombi developing in wt mice, in alpha(2)-AP(+/-) and alpha(2)-AP(-/-) mice were 102 +/- 35, 65 +/- 8.1, and 13 +/- 6.1 x 10(6) AU, respectively (n = 6 each) (P <.05), compatible with functional plasmin inhibition by alpha(2)-AP. In contrast, thrombi in wt mice, t-PA(-/-) and u-PA(-/-) mice were comparable, substantiating efficient inhibition of fibrinolysis by the combined PAI-1/alpha(2)-AP action. Platelet depletion and reconstitution confirmed a normal thrombotic response in wt mice, reconstituted with PAI-1(-/-) platelets, but weak thrombosis in PAI-1(-/-) mice reconstituted with wt platelets. Accordingly, murine (wt) PAI-1 levels in platelet lysates and releasates were 0.43 +/- 0.09 ng/10(9) platelets and plasma concentrations equaled 0.73 +/- 0.13 ng/mL. After photochemical injury, plasma PAI-1 rose to 2.9 +/- 0.7 ng/mL (n = 9, P <.01). The plasma rise was prevented by ligating the carotid artery. Hence, during acute thrombosis, fibrinolysis is efficiently prevented by plasma alpha(2)-AP, but also by vascular PAI-1, locally released into the circulation after endothelial injury. (+info)
Pulse dispersion due to atrial fibrillation causes arterial thrombosis in a rabbit experimental model.
(15/264)
Thrombosis associated with atrial fibrillation (AF) is usually caused by a left atrial (LA) thrombus, but it is not always detected. The present study was based on the hypothesis that abnormalities in peripheral artery are responsible for the ischemic stroke associated with AF. Peripheral arterial coagulability was investigated in a rabbit experimental model in which AF was induced by high-frequency stimulation of the right atrium, creating stenosis of the carotid artery together with endothelial damage. The rabbits were classified into 4 groups: (i) sinus rhythm only (group 1), (ii) sinus rhythm after 6 h of pacing (group 2), (iii) short AF (continuous pacing for 5 min; group 3) and (iv) long AF (continuous pacing for 6 h: group 4). The carotid blood flow developed a typical pattern, called cyclic flow reductions (CFRs), the frequency of which (CFRF) was 18.59+/-2.85 in AF (group 3+4) compared with 14.46+/-2.1 in sinus rhythm (group 1+2) (p<0.0005). Among the groups with AF, correlation analysis showed an association between CFRF and pulse dispersion (p<0.02, r=0.58). This study suggests that the distinctive hemodynamic effects with AF, in particular pulse dispersion, substantively influence thrombus formation on injured vascular endothelium. (+info)
Nonpeptide factor Xa inhibitors II. Antithrombotic evaluation in a rabbit model of electrically induced carotid artery thrombosis.
(16/264)
SK549 (mol. wt. 546 Da) is a synthetic, selective inhibitor of human coagulation factor Xa (fXa) (K(i) = 0.52 nM). This study compared the antithrombotic effects of SK549 and a series of benzamidine isoxazoline fXa inhibitors with aspirin, DuP 714 (a direct thrombin inhibitor), recombinant tick anticoagulant peptide, or heparin in a rabbit model of electrically induced carotid arterial thrombosis. Compounds were infused i.v. continuously from 60 min before electrical stimulation to the end of the experiment. Values of ED(50) (dose that increases the carotid blood flow to 50% of the control) were 0.12 micromol/kg/h for SK549, 0.56 micromol/kg/h for aspirin, 0.14 micromol/kg/h for DuP 714, 0.06 micromol/kg/h for recombinant tick anticoagulant peptide, and >100 U/kg/h for heparin. The EC(50) (plasma concentration that increased blood flow to 50% of the control) for SK549 was 97 nM. Unlike aspirin and heparin, SK549 was efficacious and, at 1.5 micromol/kg/h i.v. (n = 9), maintained carotid blood flow at 87 +/- 6% of control level for greater than 90 min. Unlike heparin, SK549 inhibited ex vivo fXa activity but not ex vivo thrombin activity. There was a highly significant correlation between K(i) (fXa) and ED(50) of a series of fXa inhibitors (r = 0. 85, P <.001). Therefore, these results suggest that SK549 is a novel, potent, and effective antithrombotic agent in a rabbit model of arterial thrombosis. It is likely that SK549 exerts its antithrombotic effect through selective inhibition of fXa. Furthermore, SK549 may be clinically useful for the prevention of arterial thrombosis. (+info)