| 1. |
- Baumgartner, R W, et al.
(författare)
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Microembolic signal counts increase during hyperbaric exposure in patients with prosthetic heart valves
- 2001
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Ingår i: Journal of Thoracic and Cardiovascular Surgery. - : Elsevier BV. - 1097-685X .- 0022-5223. ; 122:6, s. 1142-1146
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Patients with prosthetic heart valves have an increased risk of thromboembolic events, and transcranial Doppler sonography reveals microembolic signals. Whereas microembolic signals were initially assumed to be of particulate matter, recent studies suggest that they are partially gaseous in origin. If this is true, alteration of environmental pressure should change microembolic signal counts. We undertook this study to evaluate the influence of hyperbaric exposure on microembolic signal counts in persons with prosthetic heart valves. METHODS AND RESULTS: Microembolic signal counts were monitored by transcranial Doppler sonography of both middle cerebral arteries under normobaria (normobaria 1), 2 subsequent periods of hyperbaria (2.5 and 1.75 bar), and a second period of normobaria (normobaria 2) in 15 patients with prosthetic heart valves. Each monitoring period lasted 30 minutes. Compression and decompression rates were 0.1 bar/min. Microembolic signal counts increased from 20 (12-78) at normobaria 1 to 79 (30-165) at 2.5 bar (P <.01 vs normobaria 1 and 2), decreased to 44 (18-128) at 1.75 bar (P <.01 vs normobaria 1 and 2.5 bar; P <.001 vs normobaria 2), and returned to 20 (8-96) at normobaria 2 (values are medians and 95% confidence intervals). CONCLUSIONS: Our results strongly suggest that gaseous bubbles are underlying material for part of the microembolic signals detected in patients with prosthetic heart valves.
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| 2. |
- Benninger, D H, et al.
(författare)
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Mechanism of ischemic infarct in spontaneous carotid dissection
- 2004
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Ingår i: Stroke: a journal of cerebral circulation. - 1524-4628. ; 35:2, s. 482-482
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: It is unclear whether stroke in patients with spontaneous dissection of the cervical internal carotid artery (ICAD) is due to thromboembolism or impaired hemodynamics. This study investigated the mechanism of stroke in ICAD by examining brain imaging and cerebrovascular findings of such patients. METHODS: We retrospectively evaluated the prospectively collected brain CT, MR, and ultrasound findings of 141 consecutive patients with 143 ICADs causing ischemic stroke. Eleven patients were not included because they had an inappropriate temporal bone window (n=6) or were treated with thrombolysis (n=5). Thus, the data of 130 patients (76 men, 54 women) with 131 ICADs were analyzed. RESULTS: All patients had territorial infarcts; 6 patients (5%) also had border-zone infarct patterns. Territorial infarcts affected the middle cerebral artery (MCA) in 130 of 131 cases (99%) and the anterior cerebral artery (ACA) in 1 case (1%). Additional vascular territories were affected in 8 patients with MCA infarcts (ACA, n=5 [4%]; posterior cerebral artery, n=3 [2%]). The pattern (hemodynamic versus thromboembolic) and extent of infarction were not influenced by vascular findings (MCA stenosis or occlusion, ACA occlusion, degree of obstruction in the dissected ICA, pattern of cross-flow in 115 patients with >80% ICA stenosis or occlusion). CONCLUSIONS: This study suggests that thromboembolism, not hemodynamic infarction, is the essential stroke mechanism in ICAD.
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| 3. |
- Kremer, Christine, et al.
(författare)
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Prognosis of asymptomatic stenosis of the middle cerebral artery
- 2004
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Ingår i: Journal of Neurology, Neurosurgery and Psychiatry. - : BMJ. - 1468-330X .- 0022-3050. ; 75:9, s. 1300-1303
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The risk of ischaemic events in asymptomatic intracranial atherosclerosis is unknown. OBJECTIVE: To follow up patients with asymptomatic atherosclerotic middle cerebral artery stenosis (MCAS) to evaluate the long term stroke risk in its territory. METHODS: Consecutive white patients with asymptomatic atherosclerotic MCAS were enrolled. Patients with MCAS of possible or proven non-atherosclerotic origin were excluded. MCAS was assessed by transcranial colour duplex sonography according to published angiography validated criteria. Medical treatment was given at the discretion of the treating physician. RESULTS: 50 patients were included and followed for (mean (SD)) 815 (351) days; three were lost to follow up. MCAS was < 50% in 38 and > or = 50% in 12. No patient suffered an ischaemic event in the MCAS territory; one had a transient ischaemic attack in the contralateral hemisphere. Three patients died, one from a subdural haematoma in the contralateral hemisphere, and two from non-stroke-related causes. Medical treatment at baseline included antithrombotic drugs in 42 cases (antiplatelet agent, n = 39; warfarin, n = 3), and statins in 22; at the end of follow up 45 of the 47 survivors were on antithrombotic drugs (antiplatelet agent, n = 37; warfarin, n = 8), and 30 were on statins. CONCLUSIONS: Asymptomatic MCAS of atherosclerotic origin appears to have a benign long term prognosis with a low risk of ipsilateral stroke in medically treated white patients.
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