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Stenosis critical

McPherson CM, Woo D, Cohen PL, Panciob AM, Kissela BM, CarrozzeUa JA, Tomsick TA, ZuccareUo M. Early carotid endarterectomy for critical carotid artery stenosis after thrombolysis therapy in acute ischemic stroke in the middle cerebral artery. Stroke 2001 32 2075-2080. [Pg.133]

In Apo E-deficient animals fed a normal chow diet, fatty streaks are first observed in the proximal aorta at 10 to 12 weeks (15). The xanthoma that forms in the intima contains foam cells and is often called the early atherosclerotic lesion and is critically dependent on monocytes. Smooth muscle cells (SMCs) arrive in the intima at approximately 15 weeks and form a fibrous cap around 20 weeks (16). By 36 weeks, lumen narrowing occurs in the external branches of the carotid artery (incidence -75%), but the lumen size is maintained in the aorta. Lumen narrowing, or stenosis, does not correlate with plaque size but... [Pg.206]

Critical stenosis occurs when the obstructing lesion encroaches on the luminal diameter and exceeds 70%. Lesions creating obstruction of 50% to 70% may reduce blood flow, but these obstructions are not consistent, and vasospasm and thrombosis superimposed on a noncritical lesion may lead to clinical events such as MI. If the lesion enlarges from 80% to 90%, resistance in that vessel is tripled. Coronary reserve is diminished at about 85% obstruction due to vasoconstriction. [Pg.144]

Gould KL, Lipscomb K, Hamilton GW. Physiologic basis for assessing critical coronary stenosis. Instantaneous flow response and regional distribution during coronary hyperemia as measures of coronary flow reserve. Am J Cardiol 1974 33 87-94... [Pg.32]

Ref. (61)]. The interim results confirmed the feasibility and safety of using E2F-I decoy. Analysis of the secondary endpoints using quantitative coronary angiography and three-dimensional intravascular ultrasound demonstrated increased patency and adaptive vessel remodeling characterized by reduction in neointimal size and volume in the treated group one year after treatment, leading to 40% reduction in critical stenosis. These results will now need to be confirmed in adequately sampled and powered phase III studies in patients with coronary and peripheral vessel disease in order to further... [Pg.367]

Damage of the vessel wall is produced by placing a hemostatic clamp on the coronary artery a fixed amount of stenosis is produced by an externally applied obstructive plastic cylinder upon the damaged part of the vessel. In dogs, the stenosis is critical, i.e. the reactive hyperemic response to a 10-second occlusion is abolished (protocol 1) in pigs, the stenosis is sub-critical, i.e. there is a partial reactive hyperemia left (Just et al. 1991a protocol 2). [Pg.278]

In this preparation, coronary thrombosis is induced by delivery of low amperage electrical current to the intimal surface of the artery according to the method described by Romson et al. (1980a). In contrast to the stenosis protocols, an occluding thrombosis is formed gradually without embolism after some hours (protocol 5). As a consequence of this time course, the thrombi formed are of the mixed type and contain more fibrin than the platelet thrombi with critical stenosis. [Pg.278]

Rothwell PM, Pendlebury ST, Wardlaw J et al. (2000a). Critical appraisal of the design and reporting of studies of the imaging and measurement of carotid stenosis. Stroke 31 1444-1450... [Pg.171]

Saini RK, Fulmor IE, Antonaccio MJ. Effect of tiapamil and nifedepine during critical coronary stenosis and in the presence of adrenergic beta-receptor blockade in anesthetized dogs. J Cardiovasc Pharmacol 1982 4(5) 770-6. [Pg.609]

Although myocardial depression has been described in healthy volunteers after the use of 40 or 50% nitrous oxide in oxygen, it is usually mild. It is likely that nitrous oxide can worsen myocardial ischemia in patients with critical coronary stenosis, although this may not be of clinical significance (3,4). [Pg.2550]

As predicted by our understanding of the basic physiology, the fall in filtration after ACEI in a patient with renal artery stenosis is dependent upon the prevaihng sodium status of the patient [27,32-34]. The critical role of sodium balance in this fall in GFR during ACEI has been nicely documented in a case report by Hiicik [34], who showed that GFR decreased more markedly in a patient with a transplant renal artery stenosis when captopril was given in a sodium depleted as compared to a sodium replete situation (Table 1). Moreover, Andreucd et al. reported that intravenous infusion of saline could reverse the fall in creatinine... [Pg.485]

De Zwan C, Bar H, Wellens HJ. Characteristic ECG pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of an impend-ing infarction. Am Heart J 1982 103 730. [Pg.313]

The prototypic percutaneous aortic valve was implanted in a 57-year-old male with calcified critical aortic stenosis who failed previous balloon valvuloplasty and was in cardiogenic shock as well as leg ischemia at the time of procedure. Following the procedure, the aortic pressure rose from a 70 mmHg systolic to 120 mm Hg with the aortic valve gradient decreased from 30 to 6 mm Hg. The calculated valve... [Pg.132]

The higher the degree of carotid stenosis in neuro-logically asymptomatic individuals the higher the risk of stroke and TIA (28,31). Most experts agree that a critical threshold of >80% stenosis is associated with a rise of ipsilateral ischemic neurological events and should trigger an evaluation for carotid revascularization. Nonetheless, it should be clear that lesion severity is only one of many variables that have an impact on future stroke risk. [Pg.169]

The standard antiplatelet regimen for patients undergoing carotid artery stenting include aspirin 325 mg a day and clopidogrel 75 mg a day for at least one week prior to the procedure. Currently, there is no role for elective use of glycoprotein Ilb-IIIa receptor antagonists. All patients should be adequately hydrated to reduce the incidence and severity of intraprocedural hypotension. Traditionally, all antihypertensive medications are withheld on the day of the procedure. This is done to avoid excessive hypotension after CAS, particularly in patients with known severe coronary artery disease or critical aortic stenosis. [Pg.172]

Fig. 8.5 Successful compensatory vasodilation. The patient is a 57-year-old man who presented with 5 days of intermittent dizziness and dysarthria, and was found to have critical stenosis of the proximal left internal carotid artery on CT angiography. There is no evidence of infarction in the DWI image. CBV is elevated throughout the entire visualized left cerebral hemisphere, reflecting autoregulatory vasodilation that is successful in maintaining blood flow, as evidenced by the fact that there is... Fig. 8.5 Successful compensatory vasodilation. The patient is a 57-year-old man who presented with 5 days of intermittent dizziness and dysarthria, and was found to have critical stenosis of the proximal left internal carotid artery on CT angiography. There is no evidence of infarction in the DWI image. CBV is elevated throughout the entire visualized left cerebral hemisphere, reflecting autoregulatory vasodilation that is successful in maintaining blood flow, as evidenced by the fact that there is...
The overall picture is that no clinically important adverse interaction occurs between digoxin and ACE inhibitors in patients with normal renal function, and that serum digoxin monitoring is only needed in those who have a high risk of reversible ACE inhibitor induced renal failure (e.g. patients with congestive heart failure during chronic diuretic treatment, with bilateral renal artery stenosis or unilateral renal artery stenosis in a solitary kidney) however, note these latter two conditions are contraindications to the use of ACE inhibitors. The critical factor does not seem to be the particular ACE inhibitor used but the existence of abnormal renal function or conditions that increase the risk of renal impairment. This needs confirmation. [Pg.904]

Buda, A.J., Gallagher, K.P., Wright, L.A. and Krause, L.C. (1986). Effect of critical stenosis on myocardial blood flow, ventricular function and infarct size following coronary reperfusion. Circulation (Suppl. II), 74, 11-18... [Pg.156]


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See also in sourсe #XX -- [ Pg.28 , Pg.30 , Pg.31 , Pg.32 , Pg.33 , Pg.34 ]




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