Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have developed and tested a rotational, mechanical approach to arterial plaque removal (PTRA or Percutaneous Transluminal Rotational Atherectomy). An elliptical burr is rotated by a helical driveshaft at 150,000 rpm. The tip of the burr is embedded with small diamond chips, 30 micron in diameter. Plaque is thus abraded and particles of 2-5 micron in diameter are released downstream. Preliminary studies in a rabbit model of iliac atherosclerosis showed a reduction in percent diameter stenosis from more than 80% to less than 40%. Perforations are the current principal complication, occurring in 2 of the 13 rabbit arteries. A second rotational catheter system has been developed for removal of fresh thrombus (PRT-Percutaneous Rotational Thrombectomy). Low speed rotation (5000 rpm) of a non-cutting catheter promotes the selective winding of fibrin with subsequent lysis of thrombus. This was effective in 20 out of 21 total thrombotic occlusions in a canine model of fresh clot, with a single perforation early in the experiment.
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PMID:Rotational approaches to atherectomy and thrombectomy. 343 60

To investigate the association between carotid plaque hematoma and symptoms of cerebral ischemia a retrospective review of 200 consecutive carotid endarterectomies at the Neurological Institute of New York was carried out. Data analyzed included cerebral ischemic symptoms, angiographic findings, preoperative use of antithrombotic agents, and microscopic pathology of endarterectomy specimens. No association was found between ischemic symptoms ipsilateral to the endarterectomy and presence, size, or age of plaque hematomas. Plaque hematomas were less common among patients who took antithrombotic agents preoperatively than among those who did not. The presence of plaque hematoma was associated with angiographic carotid cross-sectional area stenosis of greater than 75%. Patients with stenosis of less than 75% were more likely than those with stenosis of greater than 75% to have ischemic symptoms ipsilateral to the endarterectomy, suggesting that criteria for surgical treatment of carotid atherosclerosis differ for those who are symptomatic vs. those who are asymptomatic. These results demonstrate the limitation of using a surgical series to extend causal inferences about the relation between plaque hematoma and cerebral ischemic symptoms to the general population of people with carotid atherosclerosis.
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PMID:Lack of association between carotid plaque hematoma and ischemic cerebral symptoms. 362 46

The effectiveness of partial ileal bypass (PIB) as a counter-measure against atherosclerosis was evaluated in WHHL rabbits. The effects of PIB and sham operation, each performed in five animals, on serum lipids, lipoproteins and plaque formation were investigated. PIB resulted in an immediate and sustained decrease of 52% (range 29-67%) in serum cholesterol, while sham operation had no effect. The main reduction was in LDL cholesterol; VLDL-cholesterol was lowered to a lesser extent. PIB also appeared to change the electrophoretic behaviour of total serum, very low density and low density lipoproteins. Plaque formation, measured 30 weeks after operation in various aortic segments and arteries, was significantly reduced after PIB. It is concluded that an induced lowering of serum cholesterol can prevent atherosclerosis in WHHL rabbits. Also, these animals must be considered as a model for the receptor-defective cellular phenotype of homozygous familial hypercholesterolemia, not for the receptor-negative type, which is the only truly genetically homozygous form.
Atherosclerosis 1983 Sep
PMID:Partial ileal bypass inhibits atherosclerosis in WHHL rabbits. 663 6

Fibrinogen may play an active role in the development and progression of atherosclerotic plaques. We assessed the association between fibrinogen levels and atherosclerotic plaques over three different arterial sites in an asymptomatic never-treated male population with increased cardiovascular risk. We included 652 men aged 40 to 60 years old with at least one of the following cardiovascular risk factors: cholesterol > 6.2 mmol/L and/or systolic blood pressure > or = 160 mm Hg and/or diastolic blood pressure > or = 95 mm Hg, and/or because they smoked. Carotid and femoral arteries and the abdominal aorta were assessed by using ultrasonographic methods for the presence of plaque, and subjects were categorized according to the presence (or absence) and extent (one versus two or three sites) of plaque. Plasma fibrinogen was measured according to the thrombin-time method of Clauss. While the presence of atherosclerosis was significantly related to age, current smoking, systolic pressure, LDL cholesterol, and fibrinogen levels, the extent of atherosclerosis was related to age and triglyceride and fibrinogen levels. Multiple regression analysis indicated independent associations between fibrinogen and the presence and extent of atherosclerosis. Plaque prevalence was significantly more pronounced with increasing tertile of fibrinogen levels. The odds ratio of the upper to lower fibrinogen tertiles for the presence of plaque was 1.6 (95% confidence interval, 1.4 to 1.8) and 1.4 (95% confidence interval, 1.2 to 1.7) for its extent. Adjustment for other risk factors slightly reduced the association between fibrinogen and atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fibrinogen and silent atherosclerosis in subjects with cardiovascular risk factors. 767 Sep 37

Sclerotic involvement of abdominal aorta and lower limb arteries is related to 2 types of fundamental lesions: atherosclerosis and arteriosclerosis. Atherosclerosis is a focal intimal thickening (plaque) of large- and medium-sized arteries, which combines atheroma (lipid deposition) and fibrosis. Plaque rupture is the crucial event in the progression of atherosclerosis, directly causing most acute thrombotic events, and contributing in great part to plaque expansion. Arteriosclerosis is a diffuse fibrosis of the arterial wall with thickening of the intima, and thinning of the media. Two forms of arteriosclerosis probably exist with distinct mechanisms and consequences. Obliterating arteriosclerosis mainly involves leg arteries (causing poor distal run-off) and appears to be essentially enhanced by ageing, diabetes and chronic renal insufficiency. Dilating arteriosclerosis involves large arteries where it provokes aneurysm formation; it is related to ageing, but seems also to be dependent upon an inborn dystrophy of arterial connective tissue. These 3 components of sclerotic arterial diseases of the lower limbs are often combined in the same individual.
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PMID:[Description and mechanisms of sclerotic arterial diseases of the lower limbs]. 772 5

The clinical events resulting from atherosclerosis are directly related to the oxidation of lipids in LDLs that become trapped in the extracellular matrix of the subendothelial space. These oxidized lipids activate an NF kappa B-like transcription factor and induce the expression of genes containing NF kappa B binding sites. The protein products of these genes initiate an inflammatory response that initially leads to the development of the fatty streak. The progression of the lesion is associated with the activation of genes that induce arterial calcification, which changes the mechanical characteristics of the artery wall and predisposes to plaque rupture at sites of monocytic infiltration. Plaque rupture exposes the flowing blood to tissue factor in the lesion, and this induces thrombosis, which is the proximate cause of the clinical event. There appear to be potent genetically determined systems for preventing lipid oxidation, inactivating biologically important oxidized lipids, and/or modulating the inflammatory response to oxidized lipids that may explain the differing susceptibility of individuals and populations to the development of atherosclerosis. Enzymes associated with HDL may play an important role in protecting against lipid oxidation in the artery wall and may account in part for the inverse relation between HDL and risk for atherosclerotic clinical events.
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PMID:Atherosclerosis: basic mechanisms. Oxidation, inflammation, and genetics. 772 36

The major cause of human arterial thrombosis is atherosclerosis. Thrombosis over atherosclerotic plaques is either due to superficial or to deep injury. In superficial injury there is endothelial denudation with thrombi adherent to the surface of the plaque. In deep injury more major plaque disruption exposes the lipid core to the lumen. Blood enters the core and thrombus forms within the plaque expanding its volume rapidly. Later thrombosis may, or may not, extend into the lumen leading to occlusion. Plaque disruptions heal by smooth muscle proliferation. Either form of thrombosis may occur in minor forms which invoke plaque growth alone or in major forms which precipitate clinical symptoms. In large arteries, such as the carotid, plaque disruption leads to chronic ulceration with exposed thrombus acting as a nidus for distal embolisation. Plaques with a high lipid and macrophage content in which smooth muscle cell numbers are low are at the greatest risk of disruption.
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PMID:Pathology of arterial thrombosis. 780 31

The potential of angiotensin-converting enzyme (ACE) inhibitors to protect the heart is a topic that has emerged recently as matter of scientific discussion. Experimental and clinical studies have shown the beneficial effects of ACE inhibitors on the metabolism, function, and structure of healthy and damaged hearts and these studies support the concept of both primary and secondary "cardioprotection" with these drugs. More recently, the prevention of atherosclerotic lesions has been demonstrated in animal models, extending the concept to a more general definition of "cardiovascular" protection with ACE inhibitors involving both the heart and the vessels. The potential role of ACE inhibitors on the primary prevention of atherosclerotic disease in humans is currently evaluated in PHYLLIS (Plaque HYpertension Lipid Lowering Italian Study), a multicenter clinical trial in which fosinopril sodium, a new ACE inhibitor, is administered to hypertensive patients with at least one uncomplicated carotid artery lesion. The primary aim of the study is to evaluate the effect of the drug on the long-term (3 years) progression of carotid artery atherosclerosis, noninvasively detected by B-mode ultrasound imaging. In addition to studies on primary prevention, some large clinical trials have been conducted to establish the role of ACE inhibitors on secondary prevention, in particular in patients with acute myocardial infarction (MI). The beneficial effect of these drugs is well established when administered in the subacute phase of acute MI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The use of zofenopril and fosinopril in acute myocardial infarction and carotid artery disease. 781 43

The treatment of coronary atherosclerosis requires an understanding of the pathophysiology of plaque rupture. The rupture of lipid-laden, macrophage-rich plaques initiates unstable angina, acute myocardial infarction and sudden cardiac death. Plaque rupture occurs when the circumferential tension on a plaque exceeds its tensile strength, an event that cannot be predicted by coronary angiography. The incidence of plaque rupture appears to be reduced in patients receiving cholesterol-lowering therapy, beta-adrenergic blocking agents and, possibly, angiotensin-converting enzyme inhibitors and antioxidants. Not all ruptured coronary plaques produce an acute coronary syndrome. The consequences of plaque rupture depend on the extent of thrombus formation over the fissured plaque. This is determined by flow characteristics within the vessel as well as the activity of the thrombotic and fibrinolytic systems. Recent advances in cardiovascular molecular biology, coronary diagnostic techniques and cardiac therapeutics have opened windows of opportunity to study and modify the factors leading to plaque rupture. The local modification of gene expression to alter plaque composition and to elucidate and subsequently inhibit the prothrombotic and fibrinolytic defects that promote coronary thrombosis may, in future, prevent plaque rupture and its consequences. The application of such a concerted interdisciplinary approach promises a paradigm shift in the management of coronary artery disease toward the prevention of plaque rupture and its sequelae.
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PMID:Toward the quiescent coronary plaque. 810 65

Autopsy cases from Annual Report of Autopsy Cases published by the Japan Society of Pathology showed an increase of myocardial infarction from 13.2% in the years 1958-65 to 26.6% in the years 1983-85. However, cerebral infarction and hemorrhage showed no definite increase during the period. Frequency of diabetes mellitus was extremely increased among the cases of myocardial infarction who were admitted to our hospital. Arteriographic characteristics of coronary atherosclerosis in diabetics consist of multiple tight stenoses in one major artery and two or three arterial obstructions. Carotid arterial blood flow and plaque formation and calcification of the arteries were examined by doppler imaging technology and B-mode (5 MHz) real time ultrasound using ultrasonographic equipment in diabetic patients. Both blood flow volume and blood flow velocity in the elderly patients with diabetes mellitus (over 65 years old) were significantly reduced compared with those in the younger patients with diabetes mellitus (7.4 +/- 0.4 vs. 8.5 +/- 0.2 in blood flow volumes. p < 0.01; 12.4 +/- 0.8 in blood flow velocities. p < 0.01). Plaque formation and calcification of carotid arteries were significantly more frequent in the elderly patients with diabetes mellitus than in the younger patients with diabetes mellitus (p < 0.05). Asymptomatic cerebral infarction was studied in 37 diabetic patients by brain magnetic resonance imaging (MRI) in the absence of prior stroke. T2 weighted MRI imaging showed 27 patients among 37 patients (73%) to suffer from lacunar infarction. Hyperintensities were seen in the brain stem (28.6%), white matter (62.9%), basal ganglia (60.0%), and paraventricular areas (PVH) (20.0%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diabetic macroangiopathy in the elderly]. 831 44


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