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)

Abdominal aortic coarctation is a rare, non-atherosclerotic disease. It is a functionally significant at an early age when associated with aortic branch stenosis and renovascular hypertension. The pathogenesis of aortic constrictive lesions remains unknown, but may be related to developmental error or aortic growth arrest and various hypotheses have been reported. When the renal arteries are involved by the coarctation, severe hypertension is common at an early age and in untreated patients, life-threatening complications commonly occur. Patients who reach the age of 40 years generally have the coarctation below the renal arteries but even when the renal arteries are not involved by the coarctation, renovascular disease may still occur due to secondary atherosclerosis. Aortic thrombosis secondary to abdominal aortic coarctation with renovascular disease and lower limb ischemia, occurring in a 63-year old woman, is reported.
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PMID:Abdominal aortic coarctation inducing aortic occlusion and renovascular hypertension. 175 97

The interaction of platelets with the vessel wall plays an important pathophysiological role in coronary artery disease. While in healthy blood vessels platelets remain inactivated and do not adhere or aggregate, an augmented interaction occurs in coronary artery disease. Due to their strategic anatomical position between the circulating blood and the media of the vascular wall, endothelial cells play an important regulatory role. Indeed, after endothelial denudation, massive platelet adhesion and aggregation at the vessel wall occurs. Platelet-derived substances lead to vasoconstriction and in the long run also to proliferative changes of the vascular wall. Besides other substances, endothelial cells release vasoactive mediators such as endothelium-derived nitric oxide (NO), prostacyclin and endothelin. In healthy human arteries, aggregating platelets cause endothelium-dependent relaxations in spite of the liberation of serotonin and thromboxane A2 and through the luminally released NO also induce a feedback inhibition of the platelets. In contrast, in arteries without endothelium, a marked vasoconstriction (due to thromboxane A2 and serotonin) is noted. Endothelin may also play a role in platelet-vessel wall interaction, since thrombin and transforming growth factor beta (a platelet-derived product) stimulate the production of this potent vasoconstrictor. Oxidized low-density lipoproteins inhibit the relase of NO and thereby activate the platelet-vessel wall interaction. In atherosclerosis even more pronounced dysfunctions of the endothelium occur, which lead to vasoconstriction, ischemia and thrombus formation in patients with coronary artery disease.
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PMID:[Thrombocyte-vascular wall interaction and coronary heart disease]. 176

Etiology and longterm prognosis were prospectively investigated in 155 consecutive patients (96 men, 50 women) ages 16-45 years who were referred to the Neurosurgical Unit with cerebral transient ischemic attacks or infarction during the period 1978-88. All patients underwent neurological and medical-cardiological evaluation, cerebral computerized tomography scanning, electrocardiogram, and laboratory tests. 2-dimensional echocardiography was performed in 123 cases (79%), cerebral angiography in 147 (95%). Atherosclerosis was the leading etiology, occurring in 48 patients (31%). A cardioembolic disorder was considered the probable cause of ischemia in 8 cases (5.1%). Further possible etiologies were though to be: oral contraceptives (5.8% of the total, but 15.3% within the females), spontaneous arterial dissection (4.5%), migraine (4%), puerperium (2.6%), cervical trauma (2.6%), and other, more uncommon conditions. Despite extensive evaluation, the cause of cerebral ischemia remained unknown in 40% of the cases. All patients received antiplatelet medication and 16 underwent surgery. The longterm outcome at a mean followup of 5.8 years was favorable in that 91% of the subjects resumed their workload on a full or parttime basis.
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PMID:Etiopathogenesis and prognosis of cerebral ischemia in young adults. A survey of 155 treated patients. 177 5

The blood levels of 6-keto-PGE1 alpha and thromboxane B2 were measured in the coronary sinus of 15 males during and just after a spontaneous myocardial ischemic episode. The comparison was made in 30 males with coronary heart disease in the presence of exercise-induced angina in whom coronary sinus blood samples were taken during myocardial ischemia provoked by pacing and 6 males suffering from cardialgias without signs of coronary atherosclerosis. The patients with spontaneous anginal attacks had lower baseline 6-keto-PGE1 alpha (179.0 +/- 47.8 pkg/ml) than those with exercise-induced angina (336.0 +/- 65.7 pkg/ml; p less than 0.1). This difference became greater during ischemia (165.0 +/- 49.0 and 350.0 +/- 69.5 pkg/ml, respectively, p less than 0.05) and just after its elimination (166.0 +/- 48.7 and 413.0 +/- 76.0 pkg/ml, respectively, p less than 0.05). Coronary sinus blood thromboxane B2 levels were not substantially different in the presence or absence of myocardial ischemia. Thus, a decrease in the prostacyclin-forming function of the coronary endothelium plays a definite role in the genesis of spontaneous myocardial ischemic episodes.
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PMID:[Coronary sinus blood thromboxane and prostacyclin in spontaneous myocardial ischemia]. 179 81

Recent studies suggest that granulocytes (PMNs) play a role in the pathogenesis of acute and chronic myocardial ischemia and extension of myocardial injury. A positive correlation was also found between leukocyte count and severity of coronary artery disease. Rabbit derived antiserum dependent-reduction of circulating PMNs in the dog or using monoclonal antibody anti-CD11b/CD18 of PMNs resulted in smaller myocardial infarcts. Granulocytes can release a variety of mediators tissue injury and synergize with these different mediators and other cells resulting in amplification of neutrophil stimulation and rising to additional products with enhanced endothelial injury. This paper reviews "in vivo" studies that have been instrumental in demonstrating this role of granulocytes as a mediator of myocardial ischemia. Experience in humans shows the modification of PMNs function in angina and during myocardial ischemia, and data from our group demonstrated that their aggregability is increased in the coronary sinus of patients with angiographically documented coronary disease. Upon re-perfusion PMNs accumulate and produce an inflammatory response resulting in endothelial injury. Free radicals formed during ischemia or re-perfusion produce deleterious effects on cell membranes, endothelial cell and myocardium. On the other hand the PMNs activation occurring during coronary angioplasty (PTCA) by the release of proteolytic enzymes and the generation of oxygen-free radicals, may aggravate the endothelial damage induced by PTCA and further stimulate platelets having potential implications in subsequent development of restenosis. An other aspect of PMNs function is related to leukotriene C4 release; the vasoconstrictor effect of this leukotriene on coronary arteries is synergistic with that induced by platelet-released thromboxane A2, as well as the decrease in coronary flow produced by the combination of both substances is greater than the sum of changes caused by the two eicosanoids separately administered. The potential role of leukocytes, oxygen radicals, leukotrienes and granulocyte enzymes in pathophysiology of myocardial injury due to a regional ischemia and reperfusion is an area of intense investigation. Experimental and clinical studies to elucidate these events should not only provide insights into acute and chronic pathologic tissue damage, but may also lead to the identification of important new targets of pharmacologic intervention.
Atherosclerosis 1991 Nov
PMID:Role of granulocytes in endothelial injury in coronary heart disease in humans. 181 45

Chronic ischemia of the lower extremities with atherosclerosis background is being manifested by intermittent claudication. For treating the intermittent claudication many drugs are used, which may give rise to therapeutical side effects. In 50 patients with diagnosed arteriosclerosis affecting the lower extremities in II stage according to Fontain, a vegetable preparation PADMA-28 was applied for 16 weeks. A marked, statistically significant elongation of the claudication distance was achieved. That was measured, under standardized condition, on an ergometer-treadmill. Moreover, there was also a decrease in the index of blood platelets aggregation, a drop in the level of cholesterol, triglycerides, total lipids, beta lipoproteins, and an increase in ++alpha lipoproteins. Also 50 patients were receiving placebo for 16 weeks, but no positive results were observed in comparison with preparation PADMA-28. The studies were carried out by the method of double blind test, the latter was accomplished by randomized method. Observation, the performed biochemical examinations did not reveal any undesirable effect. Drug tolerance was excellent. The positive influence of the drug may result from summed action of components contained in the preparation namely: bioflavonoides, salicylates, valepotriates, tannins, phenol acids, ethereal oils and esters of acids. PADMA-28 may be a useful adjuvant to therapeutic methods with regard to chronic ischemia of the lower extremities in II stage, according to Fontain.
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PMID:[Treatment of chronic ischemia of the lower extremities with complex herbal preparation]. 181 52

Acute arterial occlusion in an extremity must be treated as a medical-surgical emergency since not only the affected limb is endangered, but the life of the patient as well. The cause of the acute occlusion is an embolism or in situ thrombosis. The most common source of embolism is the heart from which about 30% of the cardiac emboli obliterate the bifurcation of the femoral artery and about 4/5 of all emboli involve the extremities. Arterio-arterial emboli arise from aneurysms or from nonocclusive, ulcerated atheromatous plaques. Acute in situ thrombosis occurs mostly at the site of stenotic arteriosclerotic lesions. Aneurysms and dilated forms of atherosclerosis can be both the cause of in situ thrombosis as well as the source of an embolism. Differentiation between thrombosis and embolism can be extremely difficult but for acute treatment, however, it is of little relevance. There is a peak of both events in the seventh and eighth decades. On complete occlusion without adequate collaterals, the presentation is characterized by "the six Ps": pain, pallor, pulselessness, paresthesia, paralysis and prostration. With acute occlusion of central points such as the aortic bifurcation or the femoral artery bifurcation, there is complete ischemia with onset of rhabdomyolysis after four to six hours which can lead to severe local and generalized symptoms due to the dangerous metabolites released. In contrast, occlusion of isolated lower leg arteries usually only lead to transient symptoms. If arterial occlusion is suspected, prior to transportation to the hospital, 5000 I.E. heparin should be given intravenously. Acute thrombotic occlusion of large arteries is the surgical domain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Therapy of acute peripheral arterial occlusion]. 183 82

Atherosclerotic changes of carotid and lower extremity arteries were studied in the selected industrial population represented by 58 men with arterial hypertension. Affection of peripheral arterial system was detected by means of non-invasive ultrasound methods. Stenoses of carotid arteries were recorded in 19% of cases (11 of 58), stenoses of lower extremity arteries in 7% (4 of 58). Hypertonic individuals did not show neurological symptomatology, including one patients with total occlusion of the arteria carotis interna. One man underwent the attack of cerebrovascular ischemia. Stenoses of lower extremity arteries were also in the subclinical stage and without intermittent claudications. A high number of risk factors of atherosclerosis was found in the series: obesity in 90%, smoking 57%, hypercholesterolemia in 47%. Peripheral arterial changes were associated with combined risk factors (two and more). This indicates their involvement in the origin and development of atherosclerotic lesions.
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PMID:Carotid and lower extremity arterial disease in hypertensions. 183 75

We investigated incidence, severity, and distribution of coronary atherosclerosis, acute thrombosis, and plaque fissuring in ischemic heart disease (both unstable-acute syndromes and chronic ischemia) and in nonischemic controls. We also studied the structural, immunohistochemical, and biochemical profile of plaques, with and without thrombus, including morphometry, immunophenotyping of inflammatory infiltrates, cytokine presence, and ultrastructural features. Critical coronary stenosis was almost the rule in both acute and chronic ischemic series (greater than 90%) whereas it reached 50% in control subjects. Thrombosis was principally characteristic of unstable-acute ischemic syndromes (unstable angina, 32%; acute myocardial infarction, 52%; cardiac sudden death, 26%) but was also found in chronic ischemia (stable angina, 12%; ischemic cardiomyopathy, 14%) and in control subjects (4%). Plaque fissuring without thrombus occurred in low percentages in lipid-rich, severe eccentric plaques in most series. Major differences were found between pultaceous-rich versus fibrous plaques rather than between plaques with or without thrombus. Pultaceous-rich plaques were frequent in sites of critical stenosis, thrombosis, and ulceration. Inflammatory infiltrates, i.e., T cells, macrophages, and a few beta cells, mostly occurred in lipid-rich, plaques unrelated to thrombus. In adventitia, infiltrates were a common finding unrelated to any syndrome. Necrotizing cytokines such as alpha-TNF were immunohistochemically detected in macrophages, smooth muscle, and intimal cells and detected by immunoblotting in 67% of pultaceous-rich plaques, either with or without thrombus. Immune response mediators such as IL-2 were also expressed in analogous plaques but in a minor percentage (50%-40%). Media were extensively damaged in severely diseased vessels with and without thrombus. Ultrastructural study showed that the fibrous cap was either highly cellular or densely fibrillar. Intimal injury with collagen exposure was often associated with platelet adhesion, whereas foamy cell exposure was not. In conclusion, investigated parameters were essentially similar in plaques, both with and without thrombus, whereas major differences were found between pultaceous-rich and fibrous plaques. Since platelets adhere to exposed collagen and not to foam cells, the type of exposed substrates could play a major role in thrombosis.
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PMID:Coronary atherosclerotic plaques with and without thrombus in ischemic heart syndromes: a morphologic, immunohistochemical, and biochemical study. 189 66

The age and advanced stage of atherosclerosis in this patient population require careful preoperative evaluation and attention to detail in the perioperative period in an effort to avoid complications in other organ systems resulting from diffuse occlusive disease. The keys to accurate diagnosis and successful management of patients with acute or chronic mesenteric ischemia include a detailed history, focusing on the quality and temporal relation of the symptoms; an accurate vascular assessment on physical examination, with attention directed to ruling out nonvascular causes of the symptoms; a high index of suspicion of vascular origin for otherwise unexplainable abdominal pain in the patient population at risk; an aggressive diagnostic approach with a low threshold for obtaining mesenteric angiography; CT of the abdomen to rule out occult pancreatic carcinoma; expeditious correction of metabolic and electrolyte abnormalities and optimization of cardiac function; and early surgical intervention, with directed revascularization in an effort to minimize loss of bowel from infarction.
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PMID:Mesenteric artery occlusive disease. 191 32


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