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Infarct borderzone

After promising results in experimental models of myocardial ischemia (58,59), multiple clinical trials were initiated. As in 2005, data from six clinical trials applying BM or peripheral blood-derived stem cells in patients with chronic HF and seven trials in patients with AMI were published (Tables 2 and 3). Stamm et al. injected 1.5 X 106 AC 133 + BM stem cells into the infarct borderzone of patients, who underwent concurrent CABG. However, in contrast to myoblast studies, this study examined patients treated shortly after AMI. Atotal of 12 patients were treated, and they showed increased perfusion in treated areas and improved LV dimensions and EF compared with the controls (10,60). Further, unlike patients in myoblast trials, the improvements in this trial occurred without any incidence of electrical abnormalities. Whether this represents a difference in patient population, cell type, or even cell dose, remains unknown. [Pg.429]

Bogousslavsky, Moulin T (1995) Borderzone Infarcts. In Bogousslavsky J, Caplan LR (eds) Stroke syndromes, 1st edn. Cambridge University Press, Cambridge, pp 358-365... [Pg.15]

Mokri B (2001) The Monro-Kellie hypothesis applications in CSF volume depletion. Neurology 56 1746-1748 Naruse S, Horikawa Y, Tanaka C, Hirakawa K, Nishikawa H, Yoshizaki K (1982) Proton nuclear magnetic resonance studies on brain edema. J Neurosurg 56 747-752 Nedergaard M, Vorstrup S, Astrup J (1986) Cell density in the borderzone around old small human brain infarcts. Stroke 17 1129-1137... [Pg.147]

MCA infarcts are mainly caused by cardioembolism, internal carotid artery (ICA) thrombosis, dissection or embolism and rarely (in Caucasians) by intrinsic MCA disease. MCA atherothrombotic territory infarctions related to intrinsic MCA disease often cause concomitant small cortical (territorial or borderzone) and subcortical infarcts (Min et al. 2000). [Pg.210]

MCA stenosis causes subcortical stroke either by occlusion of a single penetrating artery to produce a small lacunar infarct or by artery to artery embolism with impaired clearance of emboli that produces multiple small cerebral infarcts, mainly in borderzone regions (Wong et al. 2002). [Pg.212]

Subcortical white matter infarcts may mimic a superficial MCA infarct causing a partial anterior circulation syndrome or present as a lacunar syndrome (pure motor, ataxic hemiparesis or sensori motor stroke). Superficial perforating artery infarcts (medullary branches) are often accompanied by cortical spotty lesions. Borderzone and white matter medullary branches infarctions are usually caused by hypoperfusion due lo large vessel occlusion or stenosis (Bogousslavsky 1993 Donnan and Yasaka 1998), but white matter medullary branches infarction can also be caused by cardioembolism (Lee et al. 2003). [Pg.212]

Cerebellar infarcts can be grouped in territorial (superior cerebellar artery, anterior inferior cerebellar artery, posterior inferior cerebellar artery and combined), borderzone and lacunar. They are often combined with brain stem infarcts and with superficial posterior cerebral artery or thalamic infarcts. The most common isolated cerebellar infarcts are located in the superior cerebellar artery and posterior inferior cerebellar artery territories (Amarenco 1993 Amarenco et al. 1993,1994). [Pg.218]

Lee PH, Bang OY, Oh SH et al (2003) Subcortical white matter infarcts. Comparison of superficial perforating artery and internal borderzone infarcts using diffusion-weighted magnetic resonance imaging. Stroke 34 2630-2635 Leys D, Mounier-Vehier F, Lavenu I et al (1994) Anterior choroidal artery territory infarcts. Study of presumed mechanisms. Stroke 25 837-842... [Pg.222]

In the past, two different basic mechanisms have been proposed to account for ischemic events in ICA occlusive disease (1) intracranial embolism and (2) a low-perfusion state also referred to as hemodynamic insufficiency. In the post-mortem arteriographic and pathologic study by Rodda and Path (1986), massive infarcts involving two major cerebral artery territories were associated with distal ICA occlusion, middle cerebral artery (MCA) territory infarcts were seen when the ICA was occluded or stenosed, and borderzone infarcts were characterized by ICA disease and limited circle of Willis anastomosis. [Pg.226]

Infarcts occurring as a consequence of cardiac arrest or severe hypotension (see Chap. 16) follow similar topographical patterns with bilateral lesions in the borderzones between the major cerebral arteries - a... [Pg.227]

Fig 15.1. Diffusion-weighted imaging demonstrates different patterns of acute stroke in occlusive internal carotid artery disease 1, territorial stroke 2, subcortical stroke 3, territorial stroke with fragmentation 4, disseminated small lesions 5, borderzone infarction... [Pg.227]

Kang et al. (2002) 35 > 70% or occlusion Territorial lesion (n=21) Borderzone lesion with or without a territorial lesion (n=10) Bilateral hemispheric lesions (n=4) Acute ischemic lesion in ICA occlusive disease is mainly multiple borderzone infarction was mostly associated with territorial infarction... [Pg.228]

Szabo et al. (2001) 102 >50 or occlusion Territorial stroke (n=30) Subcortical stroke ( =13) Territorial infarction with fragmentation (n=ll) Disseminated small lesions (n=15) Borderzone lesions (n=33) The degree of ICA stenosis may favor certain stroke patterns. In patients with high-grade stenosis the highest frequency of lesions occurs in the hemodynamic risk zones... [Pg.228]

Fig. 15.7. The theoretical concepts of stroke in hemodynamic risk zones - dot-like microembolic lesions in the most distal arterial branches resulting from more proximal vessel pathology and impaired emboli washout (left) and the complete infarction of the compromised tissue in the borderzone territory (right). The bottom row gives DWI examples of these lesion patterns... Fig. 15.7. The theoretical concepts of stroke in hemodynamic risk zones - dot-like microembolic lesions in the most distal arterial branches resulting from more proximal vessel pathology and impaired emboli washout (left) and the complete infarction of the compromised tissue in the borderzone territory (right). The bottom row gives DWI examples of these lesion patterns...
Hendrikse and coworkers (2001) investigated whether the presence of borderzone infarcts is related to the collateral ability of the CW in symptomatic and asymptomatic patients with unilateral occlusion of the ICA. They found that in patients with unilateral ICA occlusion, the presence of collateral flow via the posterior communicating artery in the circle of Willis is associated with a low prevalence of borderzone infarcts and that asymptomatic patients with an ICA occlusion do not have an increased collateral function of the CW. Figure 15.10 shows the four patterns of collateral flow via the CW to the hemisphere ipsilateral to the ICA occlusion. [Pg.233]

Bazner H, Hennerici M (2004) Georg Friedrich Handel s strokes. Cerebrovasc Dis 17 326-331 Bogousslavsky J, Regli F (1986a) Borderzone infarctions distal to internal carotid artery occlusion prognostic implications. Ann Neurol 20 346-350... [Pg.236]

Del Sette M, Eliasziw M, Streifler JY et al (2000) Internal borderzone infarction a marker for severe stenosis in patients with symptomatic internal carotid artery disease. Stroke 31 631-636... [Pg.236]


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See also in sourсe #XX -- [ Pg.218 , Pg.219 , Pg.226 , Pg.228 , Pg.229 , Pg.230 , Pg.232 , Pg.245 ]




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