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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this review, we have highlighted pivotal cellular and molecular events in the initiation and progression of atherosclerosis. Key components of lesion initiation are an enhanced focal intimal influx and accumulation of lipoproteins, including LDL in hemodynamically determined lesion-prone areas, focal monocyte-macrophage recruitment, intimal generation of ROS, and oxidative modification of lipoproteins (including LDL [Ox-LDL]). Modified lipoproteins are taken up by the non-downregulating macrophage scavenger receptor, with foam cell formation and the development of the so-called fatty streak. One transitional event in lesion progression is foam cell necrosis, likely attributable to the cytotoxicity of both intimal free radicals and Ox-LDL, with development of an extracellular metabolically inert lipid core. Another is the migration to and proliferation within the intima of medial SMCs, leading to the synthesis of plaque collagens, elastin, and proteoglycans. Mural thrombosis plays a significant role in the late-stage progression of lesions. Regression of lesions is considered a function of the dynamic balance among components of initiation, progression, plaque stabilization, and removal of plaque constituents--the so-called regression quartet. Here, we critically examine how components of diabetes mellitus might impact not only lesion development, but also lesion regression. It is concluded that some components of diabetes mellitus augment key mechanisms in lesion initiation and progression and will likely retard the processes of plaque regression. Specifically, we focus on the various influences of diabetes mellitus on lipoprotein influx and accumulation, free radical generation and Ox-LDL, monocyte-macrophage recruitment, thrombosis and impaired fibrinolysis, and the reverse cholesterol transport system. The importance of nonenzymatic protein glycosylation in modifying a number of these processes is emphasized.
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PMID:Pathogenesis of the atherosclerotic lesion. Implications for diabetes mellitus. 139 13

The records of all patients with aneurysm of the subclavian-axillary artery who were seen between January, 1960, and January, 1980, were reviewed. There were 31 patients (21 male and 10 female) with a mean age of 47 years. The aneurysm (mean size, 3.0 cm) was located on the right in 20 patients and on the left in 10; one patient had bilateral aneurysms. Mural thrombus was present in 25 patients. Eight patients were asymptomatic and 23 presented with upper extremity pain. Thromboembolism occurred in five patients, one presenting with impending loss of tissue. Two patients had the aneurysm rupture and one of them died. A pulsating mass was palpable in 20 patients, including the eight who were asymptomatic. Vocal cord paralysis occurred in two patients. The cause of the aneurysm was atherosclerosis in 12 patients, trauma in 10, poststenotic dilation secondary in thoracic outlet obstruction in 6, mycotic aneurysm in 2, and Ehlers-Danlos syndrome in one patient. Seven patients had nine aneurysms in other areas. Surgical treatment consisted of thoracic outlet decompression in 4 patients, graft interposition in 11, tangential aneurysmorrhaphy in 8, ligation in 4, and exploratory surgery only in one. One forearm amputation was subsequently performed. Three patients did not undergo surgery. Average length of follow-up was 9.2 years. Except for the patient who underwent amputation, all treated patients had adequate circulation in the extremities. No aneurysm recurred and no complication of the repair developed. We conclude that aneurysms of the subclavian-axillary artery, although rare, are both life- and limb-threatening. Resection and arterial reconstruction are recommended.
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PMID:Subclavian-axillary artery aneurysms. 728 Oct 14

Atherothrombosis defines the occurrence of thrombosis on atherosclerotic lesions. Atherosclerosis is the most prevalent disease of our time and its thrombotic complications are responsible for an exceedingly high number of deaths and disabilities. Over the past few years, experimental investigation and clinical and pathologic observations have led to a better understanding of how a thrombus forms and also of its incidence in acute ischemic syndromes. A thrombus is usually found secondary to atherosclerotic plaque disruption. Mural thrombosis, also at the site of plaque rupture, is an important mechanism in the progression of atherosclerosis even when symptoms are absent. Because atherosclerosis is a silent and asymptomatic disease until complications arise with thrombosis producing clinical symptoms, it is necessary to have models that reproduce the human disease in its early stages. Unfortunately, not all the experimental models of vascular disease have human resemblance and validity. Knowledge of the disease process and of what an experimental animal model can offer is a milestone for a successful investigation. Experimental models of vascular disease have enhanced our understanding of the pathophysiological processes leading to vascular obstruction in both spontaneous and accelerated atherosclerosis and thrombosis. Animal models have provided insight into the role of platelets, lipids, renin-angiotensin system (RAS), cytokines and growth factors in the evolution and progression of atherosclerosis and have suggested potential therapeutic interventions. Significant advances in our understanding of the vascular biology and pathology of atherosclerosis and thrombosis, and of the interactions of blood cells, lipids and proteins with the vascular wall, have allowed us to formulate new experimental hypotheses and to test therapeutic strategies, either pharmacological or surgical.
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PMID:Atherosclerosis and thrombosis: lessons from animal models. 1148 25