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)

Rupture of an atherosclerotic plaque associated with partial or complete thrombotic vessel occlusion is fundamental to the development of ischemic coronary syndromes. Plaques that produce only mild-to-moderate angiographic luminal stenosis are frequently those that undergo abrupt disruption, leading to unstable angina or acute myocardial infarction. Plaques with increased lipid content appear more prone to rupture, particularly when the lipid pool is localized eccentrically within the intima. Macrophages appear to play an important role in atherogenesis, perhaps by participating in the uptake and metabolism of lipoproteins, secretion of growth factors, and production of enzymes and toxic metabolites that may facilitate plaque rupture. In addition, the particular composition or configuration of a plaque and the hemodynamic forces to which it is exposed may determine its susceptibility to disruption. Exposure of collagen, lipids, and smooth muscle cells after plaque rupture leads to the activation of platelets and the coagulation cascade system. The resulting thrombus may lead to marked reduction in myocardial perfusion and the development of an unstable coronary syndrome, or it may become organized and incorporated into the diseased vessel, thus contributing to the progression of atherosclerosis. In unstable angina, plaque disruption leads to thrombosis, which is usually labile and results in only a transient reduction in myocardial perfusion. Release of vasoactive substances, arterial spasm, or increases in myocardial oxygen demand may contribute to ischemia. In acute myocardial infarction, plaque disruption results in a more persistent thrombotic vessel occlusion; the extent of necrosis depends on the size of the artery, the duration of occlusion, the presence of collateral flow, and the integrity of the fibrinolytic system. Thrombi that undergo lysis expose a highly thrombogenic surface to the circulating blood, which has the capacity of activating platelets and the coagulation cascade system and may lead to thrombotic reocclusion. Measurements aimed at reversing the process of atherosclerosis via cholesterol reduction and enhanced high density lipoprotein activity are encouraging. Active research is being focused on the development of new antithrombotic tools, such as inhibitors of thrombin, thromboxane, and serotonin receptor antagonists, and monoclonal antibodies aimed at blocking platelet membrane receptors or adhesive proteins. These compounds may prove useful when immediate and potent inhibition of the hemostatic system is desired. Intensive research is still needed in the areas of pathogenesis and therapeutic intervention in atherosclerosis.
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PMID:Atherosclerotic plaque rupture and thrombosis. Evolving concepts. 220 64

Some controversy has always existed regarding the presence and extent of the vasa vasorum--the nutrient vessels in the wall of the human aorta--in the coronary arteries. Now, cinemicrographic studies using silicone polymer injections in cleared human hearts have identified the vasa vasorum of coronary arteries, revealing evidence of neovascularization in the region of atherosclerotic plaques. These studies suggest an important role for the vasa vasorum in the pathogenesis of coronary atherosclerosis and its sequelae, especially intramural hemorrhage and vascular spasm. The wall of the human coronary artery in regions of atherosclerotic injury may be particularly rich in capillary vessels of the vasa vasorum. From this, the evidence suggests that with the morning increase in blood pressure, fragile neovascular structures of the vasa vasorum may be more prone to rupture and may be responsible, in part, for the circadian variation in myocardial infarction.
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PMID:Rupture of coronary vasa vasorum as a trigger of acute myocardial infarction. 223 13

We conducted a study on the clinical and angiographic characteristics of 140 patients with unstable angina. Average age of 57, male/female ratio 4 to 1. The most frequent risk factors: tobacco smoking (73%) and arterial hypertension (42%). They had old infarct (57%), and unstable angina at rest (37%). We did early submaximal stress test to 31% of them; in 38.6% test was stopped due to angina, 25% for fatigue. 91% had ischemic changes, there weren't any severe complications. Regarding significant coronary obstruction: 20% had one vessel, 26% two, 50% three and left trunk 4%. Normal ventriculogram 43%. Eight patients died; the causes were: disease of the trunk (37.5%) and "active" angina (87.5%), 25% during catheterization . All survivors responded to medical treatment. 54 patients were not candidates for surgical treatment, among them 70.3% were released in class I (NYHA). At follow up 90% were in class I-II, 12% had unstable angina recurrence, 3% had acute infarct. In the pathogenesis of unstable angina intervene fixed atherosclerosis, obstructive lesions, repetitive spasms and non-occlusive thrombosis, this physiopathologic behavior is responsible for the stages of ischemic activity. Treatment should be directed to maintain the balance between the distribution and the demand of O2, and also treating spasm and thrombosis.
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PMID:[Unstable angina: clinical and angiographic characteristics of 140 cases]. 224 1

The aim of the present study was to evaluate the vasomotion of the entire coronary tree in variant angina, particularly focusing the attention on the behaviour of the "non spastic" epicardial vessels, using a quantitative coronary technique. Two different groups of patients served as controls. The first group consisted of 10 patients with accessory nodal pathway but without any sign of myocardial ischemia (Group I). The second group included 8 patients with stable exertional angina pectoris and coronary artery disease (Group II). The third group (Group III) consisted of 16 patients presenting with variant angina and spontaneous or hyperventilation-induced (HV: 30 cycles/min for 5 min) ST segment elevation. All patients underwent coronary angiography before and 2 min after HV testing; the evaluation of the coronary diameters was performed on baseline and after HV. In Group III, the HV testing caused a 26 +/- 12% reduction of the "non spastic" coronary vessels, with the mean control diameter of 2.00 +/- 0.61 mm that decreased to 1.48 +/- 0.55 mm. The patients of Group I showed only a mild degree of vasoconstriction (9 +/- 6%) of the epicardial coronary vessels; the Group II patients, also, showed a moderate response to vasoactive stimulus (11 +/- 8%), with the mean control diameter of 2.36 +/- 0.69 mm that decreased to 2.09 +/- 0.65 mm. The greater amount of vasoconstriction showed by patients with variant angina was statistically significant compared to both control groups (p less than 0.001). A further analysis of the coronary vasomotion, in Group III patients, showed that the 6 patients with normal or near normal coronary angiograms exhibited a 34% reduction in the vessel diameter. The remaining 10 patients who presented with a diffuse atherosclerotic involvement of the epicardial vessels (organic stenosis greater than or equal to 50% at the site of spasm) showed a lesser (20%) but yet significant extent of vasoconstriction compared to both control groups (p less than 0.001). In conclusion, our data indicate that: patients with variant angina exhibit a marked and diffuse coronary narrowing of the coronary vessels during vasoconstrictor stimuli; focal spasm occurs more frequently at the level of atherosclerotic coronary segments, whether they are critical or not. An interaction between these 2 phenomena, ie atherosclerosis and abnormal vasoconstriction, is supposed to be a cause of the occurrence of focal coronary spasm in variant angina.
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PMID:[Variant angina which interacts with two phenomena: local hypersensitivity and abnormal response in the coronary tree to vasoconstrictor stimuli]. 226 56

Casts were produced of the arterial networks of 25 human hearts obtained at autopsy from subjects who were not diagnosed as having cardiovascular disease. Many casts showed imprints of atherosclerotic plaques, remnants of calcified masses, and fine vascular meshes near the lumen of the major coronary arteries. Of 25 casts produced, 14 contained one or more of these anomalies, seven contained vascular meshes, and five of these related to imprints and/or calcified masses. Analysis of these findings in the context of atherosclerosis, intramural hemorrhage, and vascular spasm, suggests possible relationships between them. The findings support the hypothesis that neovasculature in the walls of coronary arteries may play a role in the pathogenesis of vascular disease and malfunction.
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PMID:Vasculature in the walls of human coronary arteries. 240 50

Growing collateral arterial blood vessels are super-sensitive to serotonin. Advanced atherosclerosis causes platelet activation, and activated platelets release sufficient serotonin that collateral arterial spasm occurs as a response. The development of ketanserin, the 5-HT2-receptor blocker, has both identified the receptor responsible for the arterial spasm and provided new approaches to treatment.
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PMID:Collateral arterial tree and responses to serotonin. 244 67

The review examines the effects of smoking on blood parameters, concentrating on those seen as responses or reactions to the insult of smoking, and finds evidence that smoking causes chronic leucocytosis, macrocytosis and raised haematocrit, raised plasma fibrinogen concentration, reduction of the serum ratio of high to low density lipoprotein (HDL/LDL ratio), and platelet changes. Each of the changes resolved on "quitting", though for fibrinogen the evidence was indirect. Reports that elevations of the white cell count (WCC), and plasma fibrinogen and reduction of the HDL/LDL ratio each predict myocardial infarction, and that higher haematocrit increases the risk of cerebro-vascular incidents are reviewed, with reports of associations with other forms of arterial disease and COPD, and of their significance for the prognosis of established disease. After noting pathological mechanisms which implicate each of these factors, and platelets, in reactions likely to contribute to the development of atherosclerosis, infarction, arterial spasm, and/or lung damage, the author concludes that the evidence in man, backed up by experimental data, provides very strong support for the view that elevations of WCC, haematocrit, plasma fibrinogen and reduction of the HDL/LDL ratio represent (or are closely associated with) intermediate causal mechanisms through which smoking induces arterial disease and probably lung disease, and that experimental evidence indicates that platelet changes and macrocytosis also contribute. Differences in the extent of these responses to smoking could be valuable in differentiating the relative harmfulness of different types of cigarette (or of other inhaled pollutants) in terms of these diseases, and in predicting the susceptibility of individuals to these smoking-related diseases.
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PMID:Reactive changes in the blood of smokers and the development of arterial diseases and COPD, a review: evidence of associations between changes and subsequent disease with implications for the evaluation of harmful effects of cigarettes, and for susceptibility to the chronic effects of inhaled pollutants. 248 24

We would like to emphasize three points. First, atherosclerosis produces a profound alteration of vascular responses, which may lead to spasm in several vascular beds. Second, we have proposed that leukocytes as well as platelets may play a critical role in the pathophysiology of vasospasm. Third, there is bad news and good news in relation to regression of atherosclerosis. Maximal vasodilator capacity does not improve consistently during regression of atherosclerosis, but endothelium-dependent relaxation improves, hypersensitivity of blood vessels subsides, and we speculate that susceptibility to vasospasm may be abolished.
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PMID:What causes spasm of atherosclerotic arteries? Is regression of plaques beneficial? 248 35

The aim of this study was to evaluate the effects of hyperventilation (HV) and of ic nitroglycerin (NTG) on coronary diameters and hemodynamics in 32 patients with angina pectoris. Of these, 10 patients had stable angina and critical coronary artery disease (CAD, Group I), 12 patients with variant angina (VA) and no or minor coronary atherosclerosis (Group II), and 10 patients with angina and normal coronary arteries (syndrome X (SX), Group III). All patients underwent coronary angiography as well as right heart catheterization; measurements of left anterior descending coronary diameters (mid segment), great cardiac vein blood flow, aortic pressure and coronary resistance were performed on baseline, after HV and following NTG. HV caused coronary spasm in 4 patients with VA and significantly (p less than 0.001) reduced coronary diameters and regional blood flow both in Groups II and III, but not in Group I. NTG resulted in increased coronary diameters in all patients, however variations were greater in VA and SX (44 and 39%, respectively) than in Group I (18%; p less than 0.025). NTG induced an increase of coronary blood flow only in patients with CAD. We conclude that patients with VA and SX present a similar coronary response to vasomotor stimuli, either after HV or following NTG. Response is abnormal if compared to that of patients of group I, and it involves both epicardial and intramural coronary vessels. Thus, we suggest that SX and VA belong to a single pathogenetic entity with a spectrum of clinical manifestations.
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PMID:[Abnormal coronary response to vasomotor stimuli: analogies between variant angina and X syndrome]. 250 49

Renal artery stenosis in 201 patients with hypertension was treated with percutaneous transluminal renal angioplasty (PTRA). A total of 213 procedures were performed as treatment of 262 separate stenosis. The stenosis was caused by atherosclerosis in 134 cases and by fibromuscular dysplasia (FMD) in 52 cases; the cause was indeterminate in 27 cases. Of the 213 procedures, 172 were successful or resulted in improvement, for a technical success rate of 80.8%. The initial clinical results could be evaluated in 210 cases; cure or improvement was achieved in 80%. There were 23 cases in which neither technical nor clinical success was achieved. Data on the remaining 187 cases were the basis of this long-term follow-up study. The cumulative patency rate at 5 years was 80% in the atherosclerosis group, 89% in the FMD group, and 74% in the indeterminate group. The mortality was less than 1%. Because spasm occurred in 33 cases, causing an infarction in ten instances, antispasmodic medication seems warranted. These long-term results indicate that PTRA is the treatment of choice in patients with renovascular hypertension.
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PMID:Percutaneous transluminal renal angioplasty: initial and long-term results. 252 80


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