Plaque, atherosclerotic

The concentration of t-PA in human blood is 2—5 ng/mL, ie, 2—5 ppb. Plasminogen activation is accelerated in the presence of a clot, but the rate is slow. The dissolution of a clot requites a week or more during normal repair of vascular damage (17). Prevention of irreversible tissue damage during a heart attack requires that a clot, formed by mpture of an atherosclerotic plaque, be dissolved in a matter of hours. This rapid thrombolysis (dissolution of the clot) must be achieved without significant tibrinogenolysis elsewhere in the patient. 

General trends in radiopharmaceutical research emphasize the use of small peptides. These molecules, of which the agents mentioned for thrombosis localization are an example, exhibit rapid and specific binding, and rapid blood clearance, two important parameters for a successflil radiopharmaceutical. Peptides are readily labeled with Tc and lend themselves to formulation as lyophilized kits that can be rapidly and rehably reconstituted. Possible targets for these molecules are quite varied, ranging from atherosclerotic plaque to P-amyloid (for Alzheimer s disease), to a variety of somatic receptors the populations of which are increased or decreased in disease. 

In general, arterial thrombi are platelet-rich ( white clots ) and form at ruptured atherosclerotic plaques, leading to intraluminal occlusion of arteries that can result in end-organ injury (e.g., myocardial infarction, stroke). In contrast, venous thrombi consist mainly of fibrin and red blood cells ( red clots ), and usually form in low-flow veins of the limbs, producing deep vein thrombosis (DVT) the major threat to life results when lower extremity (and, occasionally, upper extremity) venous thrombi embolize via the right heart chambers into the pulmonary arteries, i.e., pulmonary embolism (PE). 

The calcification of atherosclerotic plaques may be induced by osteopontin expression, since osteopontin is a protein with a well-characterized role in bone formation and calcification. Vascular smooth muscle cell migration on osteopontin is dq endent on the integrin av 33 and antagonists of av 33 prevent both smooth muscle cell migration and restenosis in some animal model [8]. 

The atherosclerotic plaque overexpresses another chemoattractant, eotaxin, that may mediate mast cell... 

Libby P, Aikawa M (2002) Stabilization of atherosclerotic plaques new mechanisms and clinical targets. Nat Med 8 1257-1262... 

Atherosclerotic plaques are lesions in the arterial vessels which arise during the process of atherogenesis. Most cases of acute heart attacks are caused by rupture of an atherosclerotic plaque. 

Furthermore, there is some evidence for pleiotrophic effects (e.g., effects on hemostasis, vascular function, anti-inflammatory effects, and stabilizing effects on atherosclerotic plaques) of statins. The clinical relevance of this (and the potential difference between the various statins) is at present uncertain but subject to intense investigation. 

The innermost layer of an artery, which consists of loose connective tissue covered by a monolayer of endothelium that resides on a basement membrane. In human arteries, the intima often contains resident smooth muscle cells even early in life. Atherosclerotic plaques form in the intima. 

An episode of acute regional ischemia in the brain leading to neuronal death. It is usually caused by thrombi or emboli from atherosclerotic plaques. 

An episode of acute cardiac ischemia that leads to death of cardiomyocytes. It is usually caused by a thrombotic atherosclerotic plaque. 

Kamat BR, Galli SJ, Barger AC, Lainey LL, Silverman KJ Neovascularization and coronary atherosclerotic plaque cinematographic localization and quantitative histologic analysis. Hum Pathol 1987 18 1036. 

The intima of the arterial wall contains hyaluronic acid and chondroitin sulfate, dermatan sulfate, and heparan sulfate proteoglycans. Of these proteoglycans, dermatan sulfate binds plasma low-density lipoproteins. In addition, dermatan sulfate appears to be the major GAG synthesized by arterial smooth muscle cells. Because it is these cells that profiferate in atherosclerotic lesions in arteries, dermatan sulfate may play an important role in development of the atherosclerotic plaque. 

Hemostasis is the cessation of bleeding from a cut or severed vessel, whereas thrombosis occurs when the endothelium lining blood vessels is damaged or removed (eg, upon rupmre of an atherosclerotic plaque). These processes encompass blood clotting (coagulation) and involve blood vessels, platelet aggregation, and plasma proteins that cause formation or dissolution of platelet aggregates. 

CEA involves exposure of the carotid bifurcation in the neck to a point along the internal carotid artery (ICA) beyond which the atherosclerotic plaque terminates. 

The relationship between LAA and early recurrence is likely to be largely mediated by arterial embolism from atherosclerotic plaque, although recurrent low-flow stroke may also occur due to severe vessel stenosis or occlusion. In recently symptomatic individuals with moderate-or-severe ICA stenosis, platelet-fibrin embolic signals (ES) are commonly detected in the MCA using transcranial Doppler (TCD) ultrasound and have been reported to independently predict a fivefold increase in 90-day recurrence. " ... 

Carotid artery disease is one of the major causes of ischemic stroke. The predominant mechanisms by which it causes stroke are (a) arterial embolism from atherosclerotic plaques (b) hemodynamic changes, leading to watershed infarcts and (c) distal propagation of thrombus originating from acute carotid occlusion. ... 

It has been pointed out that some of the histopatholog-ical changes in rheumatoid synovitis are similar to those noted adjacent to atherosclerotic plaques. For example, accumulation of mononuclear cells at the extraluminal surface of endothelial cells in the adventitia and the deposition of immune complexes have been reported in both diseases (Rothschild and Masi, 1982). 

Ischemic heart disease (IHD) is also called coronary heart disease (CHD) or coronary artery disease. The term ischemic refers to a decreased supply of oxygenated blood, in this case to the heart muscle. Ischemic heart disease is caused by the narrowing of one or more of the major coronary arteries that supply blood to the heart, most commonly by atherosclerotic plaques. Atherosclerotic plaques may impede coronary blood flow to the extent that cardiac tissue distal to the site of the coronary artery narrowing is deprived of sufficient oxygen in the face of increased oxygen demand. Ischemic heart disease results from... 

Lipid-laden macrophages, smooth muscle cells, and necrotic debris from the death of foam cells accumulate in the subendothelial space, leading to enlargement of the fatty streak. A collagen matrix forms a fibrous cap that covers the lipid core of the lesion to establish a fibrous plaque called an atherosclerotic plaque. Initially, the diameter of the coronary artery lumen is... 

The hallmark feature in the pathophysiology of chronic stable angina is an established atherosclerotic plaque that impedes... 

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