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

Previous studies have shown that calcium-antagonists may reduce the development of experimental atherosclerosis, and that nifedipine may slow progression of coronary atherosclerosis in man. The mechanisms responsible for this effect are still unclear. It has been recently proposed that oxygen-free radicals can induce peroxidation of human low-density lipoproteins (LDL), and that peroxidized LDL may be an atherogenic stimulus. Chemical modified LDL are internalized by macrophages via specific cell surface receptor that was termed the scavenger receptor, and could induce foam cells transformation in vivo. Previous studies on other systems have shown that calcium-antagonists may effectively inhibit oxygen radical-induced lipid peroxidation. These drugs, though differing widely in their chemical structure, are lipophilic to various degrees and presumably would concentrate in the lipid domain of the phospholipid-rich membranes. Therefore, the aim of the present study was to investigate whether calcium-channel blockers may reduce human LDL peroxidation. Purified human LDL were exposed to oxygen radicals generated by xanthine-xanthine oxidase (18 hours) after a pre-incubation (30 min) in presence of different concentrations of nifedipine, diltiazem and verapamil. Peroxidation was measured from malonyldialdehyde production. The results show that calcium-antagonists prevent LDL peroxidation. Thus, calcium-antagonists may reduce peroxidation of human LDL in vitro, at clinically relevant concentrations. These data suggest that reduced formation of atherogenic peroxidized LDL may be an additional mechanism for the anti-atherosclerotic effects of calcium-antagonists in vivo.
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PMID:[Calcium channel blockers inhibit human low-density lipoprotein peroxidation induced by oxygen free radicals in vitro]. 129 53

Reconstructive operations in the aorto-iliac and femoro-popliteal segments were performed on 281 patients with obliterating atherosclerosis. An attentive examination of the patients in the nearest postoperative period and within the first 5 years has shown different efficiency of the operation in different patients. Favorable changes took place in regional hemodynamics, while disturbances retained in microcirculation and function of the extremity. Another cause of insufficient efficiency of the interventions was an initial stable suppression of tissue respiration and oxygen utilization in the extremity tissues. The dynamics was positive during a year followed after that by new symptoms of progressing disease.
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PMID:[The physiological aspects of the efficacy of reconstructive operations in arteriosclerosis obliterans of the lower extremities]. 130 37

An examination of 192 patients with obliterating atherosclerosis of lower extremities was made who had different reconstructive operation. Intraoperative measurements of oxygen strain in the foot skin and rheography of the shin have shown that temporary compression of large arteries when making vascular anastomoses cause ischemia of extremities, whose degree and duration is dependent on the technique of the technique of the intervention. Advantages of the method of transprosthetic aortotomy such as less duration and lower degree of ischemia were shown. The possibility was revealed to prognose nearest results of treatment for changing regional hemodynamics and oxygenation of tissues at the moment of termination of the operation.
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PMID:[Intraoperative changes in the peripheral circulation with different methods for reconstructing the arteries of the extremities]. 130 61

Forty-five hospitalized elderly patients with coronary heart disease who died suddenly within 6 hours after the onset of symptoms were analyzed clinically and pathologically and summarized as following. (1) All the cases showed abnormal ST segments or T waves on ECG. (2) Various degrees of cardiac dysfunction were found clinically in all the patients. (3) Pathological examination of 31 cases revealed serious coronary atherosclerosis. New myocardial necrosis and/or multiple myocardial scars existed in about two-thirds of the patients. Based on these findings and characteristics, it is speculated that sudden coronary death in the elderly patients is caused by imbalance between oxygen supply and demand in the myocardium or deterioration of the cardiac function, which may result in fatal ventricular arrhythmia. Therefore, the prevention of sudden coronary death in the elderly patients should be focusing on reduction of myocardial ischemia, improvement of myocardial metabolism and protection of cardiac function.
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PMID:[Clinical and pathological analysis of sudden coronary death in hospitalized elderly patients]. 130 72

Several pieces of evidence suggest that vascular endothelium may be a site of latent herpetic viral infection, and that activation of such infection might cause or aggravate atherosclerosis. The present studies which utilized HSV-1 infection of cultured endothelial monolayers, provide insights into two phenomena seemingly relevant in considerations of atherosclerosis. Thus, mechanisms are reported by which infected endothelium may be damaged by marginated inflammatory cells, and be transformed from an anticoagulant to a procoagulant tissue. First, granulocytes are attracted to, and avidly bind, endothelium infected for very brief periods. This interaction is associated with denudation of intact cells as well as actual cytolysis through release of PMN proteases and toxic oxygen species. Second, several potentially additive abnormalities of HSV-infected endothelium would seem to foster coagulation. These include: a) its loss of surface heparans and thrombomodulin; b) its inability to synthesize prostacyclin with associated incapacity to deter platelet adhesion; c) its disordered membrane lipid conformation which is likely associated with excessive surface thrombin generation; and d) its unique ability to generate and release tissue factor. We speculate that mechanical abrasion may reactivate latent herpes (HSV or CMV) infection in endothelial cells particularly those exposed to high shear forces--for instance, at vessel bifurcations. This may underlie the endothelial damage, clotting and atheroma formation commonly found at these sites.
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PMID:Herpes virus infection of endothelium: new insights into atherosclerosis. 132 3

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.
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PMID:The effects of acute and chronic cocaine use on the heart. 134 9

Lipid peroxidation is considered at present as one of the basic mechanisms involved in reversible and irreversible cell and tissue damage. The current knowledge about the role of peroxidative breakdown of polyunsaturated fatty acids in the pathogenesis of various diseases has been reviewed. Lipid peroxidation leads to degradation of the lipid membrane, interaction of degradation products with intra- and extracellular targets and to the production of new reactive oxygen species during the course of the chain reaction thus leading to damage of cells and tissues. According to our current view lipid peroxidation is implicated in the pathogenesis of cancer, inflammatory processes, atherosclerosis, toxic injury by xenobiotics and ischemic-reperfusion damage.
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PMID:Lipid peroxidation--a common pathogenetic mechanism? 139 19

From January 1985 through January 1990, 244 patients (168 males, 76 females, mean age: 69 +/- 14 years) received epidural spinal cord stimulation for the treatment of advanced, nonreconstructable, peripheral vascular disease of the lower limbs due to atherosclerosis in 180 patients, atherosclerosis and/or diabetes in 49, and thromboangiitis obliterans in 15 patients: previous surgery included 101 bypass-grafts in 70 patients, 51% of which below the knee, and 117 sympathectomies in 113 patients as the last resource in face of distal peripheral vascular disease of the lower limbs. Mean ankle-to brachial systolic pressure ratio was .31 +/- .34 on symptomatic limbs; due to pain and advanced disease, walking capacity was assessed in only 151 patients, either on treadmill in 25, or in a metered corridor in 126; angiogram of the lower limbs was performed in every patient unless one not older than three months was readily available; pain at rest was assessed after an analogical scale; partial transcutaneous oxygen tension was measured on the dorsum of the fore-foot of 77 symptomatic limbs (mean: 13.35 +/- 14 mmHg). According to clinical and functional evaluation, 18 patients had exertional ischemia (group I), 87 had permanent ischemia with pain at rest and no tissue loss (group II), and 139 had chronic tissue loss (group III), including 93 ischemic ulcers (mean surface: 3.7 cm2, mean duration: 3.5 months) in 88 patients, 27 limited gangrene, and 24 previous limited non-healing distal amputation. After temporary spinal cord stimulation at T12-L1 level (mean duration: 9 +/- 4 days) with a percutaneous quadripolar electrode lead had allowed for selection of responders, 212 patients received an implantable neurostimulator.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Electric stimulation of the spinal cord in arterial diseases of the legs. A multicenter study of 244 patients]. 143 7

Spontaneous acute occlusion of the coronary artery produces regional myocardial ischemia and infarction. This coronary occlusion could be due to rapid progression of atherosclerosis or vasospasm. The factors that can precipitate an acute attack of myocardial infarction or coronary spasm are not known. It is proposed that a stress-induced rise of unesterified arachidonic acid could trigger a leukocyte respiratory burst with the release of free radicals such as superoxide anion (O2-), hydrogen peroxide, hydroxyl radical, and singlet oxygen. These free radicals have the ability to inhibit prostacyclin (PGI2) formation and enhance the breakdown of endothelium-derived vascular relaxing factor (EDRF) which are potent vasodilators and platelet anti-aggregators. This may lead to rapid progression of atherosclerosis or coronary vasospasm leading to acute myocardial infarction. If this is true, free radical quenchers and inhibitors of leukocyte oxidative burst may be useful in the prevention of progression of atherosclerosis and coronary vasospasm.
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PMID:Can free radicals induce coronary vasospasm and acute myocardial infarction? 143

The theory of the pathogenetic role of lipoperoxides in atherosclerosis and thrombosis is very topical at present. It unifies the theory on the role of free oxygen radicals with the theory of damage of the vascular wall and with the theory of impaired lipid metabolism. It makes possible also a new interpretation of known risk factors. It is also based on the most recent results of molecular biology (role of monocytes-macrophages).
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PMID:[Lipoperoxides and atherosclerosis]. 147 65


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