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)

In patients with coronary artery disease, angina pectoris provides an unreliable underestimation of disease activity and risk. Unheralded myocardial infarction and sudden death are common clinical presentations. Furthermore, objective testing, in hospital and more recently during the patient's normal daily activities, has demonstrated frequent and asymptomatic episodes of ischemia, as indicated by transient ST-segment depression. Since the underlying pathophysiologic disturbances of myocardial perfusion appear to be similar in painful and painless episodes, it seems appropriate to consider them together as the "total ischemic burden" on the myocardium. Research into this functional expression of coronary disease has indicated that active ischemia is associated with an increased risk of morbid events in all clinical subgroups of patients, including those with stable angina, unstable angina, peripheral vascular disease and following myocardial infarction. If this is confirmed in prospective trials, the assessment of total ischemic burden is likely to become part of the clinical investigation of patients with coronary disease. Clinical trials testing the efficacy of interventions will need to examine the effect on ischemic activity during normal daily life, in addition to symptoms and exercise tolerance. Evidence is still required to demonstrate whether therapy aimed at reducing the total ischemic burden will prolong life. The total ischemic burden provides a marker to follow the dynamic changes of the atherosclerotic lesion. Future research may have to concentrate on treatment aimed at altering the natural history of obstructive coronary atherosclerosis in order to affect the long-term outlook for patients with coronary artery disease.
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PMID:Total ischemic burden in patients with coronary artery disease. 209 78

To investigate the prostaglandin I2 (PGI2) half-life regulated by high density lipoprotein (HDL) in patients with coronary artery disease (CAD), we determined the stability of PGI2 and serum apolipoprotein A-I (Apo A-I) and apolipoprotein A-II (Apo A-II) levels in four age-matched groups of patients: controls (n = 17), angina pectoris (n = 18), unstable angina pectoris (n = 17), myocardial infarction (n = 19) (acute phase, 3.6 +/- 1.7 hours from onset; subacute phase, 75 +/- 15 hours from onset in the same patients). Serum PGI2 half-life and total serum Apo A-I levels were lower in the CAD group than in the control group. PGI2 was least stable in patients with unstable angina and the acute phase of myocardial infarction. In these patients, the molar ratio of Apo A-I to Apo A-II and HDL-associated Apo A-I levels were decreased, and free Apo A-I levels were increased. After in vitro incubation of HDL with increasing amounts of Apo A-II, Apo A-I in HDL was displaced by Apo A-II, with the parallel decrease in stability of PGI2. Free Apo A-I cannot stabilize PGI2. HDL-associated Apo A-I, whose amount is affected by Apo A-II, stabilized PGI2 and correlated well with stability of PGI2 in patients with CAD and control patients. Decreased PGI2 half-life may play an important role in the pathogenesis of atherosclerosis and thrombus formation in the coronary arteries, especially thrombus formation during an acute coronary event.
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PMID:Prostaglandin I2 half-life regulated by high density lipoprotein is decreased in acute myocardial infarction and unstable angina pectoris. 211 45

One hundred and ninety one consecutive patients over 70 years of age (127 men and 64 women, average age 75.6 years) underwent percutaneous transluminal coronary angioplasty (PTCA) between January 1986 and February 1989. One hundred and sixty patients had severe angina (20 Class III and 140 Class IV), 72 patients had previous myocardial infarction, 36 of which were recent (less than 1 month), and 6 patients had previously undergone coronary bypass surgery. The coronary lesions affected one vessel in 67 patients and more than one vessel in 124 patients. The left ventricular ejection fraction was less than 50% in 15 patients. Angioplasty was attempted on 245 lesions (228 stenoses and 17 occlusions): 1 lesion in 141 patients, 2 lesions in 46 patients, 3 lesions in 4 patients, with a primary success rate of 81% in stenotic and 41% in occluded arteries. There were 9 deaths (4.7%) 6 of which occurred in patients with multivessel disease and unstable angina; there were 6 Q-wave infarctions (3.1%), 8 non Q-wave infarctions (4.2%) and 3 emergency coronary bypass operations (1.6%). The first 123 patients of this series were followed up for an average of 18.8 months (7 to 37 months). Follow-up of the 100 patients successfully dilated (4 lost to follow-up) showed that 55 remained improved (53 asymptomatic), 25 had recurrent angina after the initial improvement due to restenosis in 19, progression of coronary athero-sclerosis in 3, restenosis and an evolution of coronary atherosclerosis in 1 and a lesion which had been neglected in 2 cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Coronary angioplasty in patients aged 70 and over. Immediate results and later outcome]. 212 26

The relationship of thrombus to atherosclerosis is complex and far more wide-reaching than the obvious causal association of a thrombotic occlusion in a coronary artery with myocardial infarction. An atherosclerotic plaque may be eccentric (localized primarily along one segment of the arterial wall) or concentric (localized circumferentially) and is a complex structure composed of connective tissue, calcium, inflammatory cells and lipid in proportions differing from plaque to plaque. The consistency of plaques depends on the proportion of their component elements: a heavily fibrotic and calcified plaque is hard, whereas a plaque composed predominantly of cholesterol-ester and lipid-containing macrophages is soft. Plaques with a soft lipid core may be covered by a relatively thin cap of fibrous connective tissue separating the plaque material from the luminal blood flow. A rupture or fissure of this cap allows blood to enter the plaque causing dissection of its structure and deposition of fibrin in the plaque. Fissuring commonly promotes thrombosis also in the lumen of the artery and may be followed by thrombus fragmentation and embolization. Mural thrombi may wax and wane, causing intermittent occlusions and fleeting, minor clinical symptoms. Further episodes of thrombosis increase the mass of the mural thrombus in the already restricted lumen and may herald the onset of ischemic symptoms, abruptly aggravate a stable clinical state and produce the crescendo type of unstable angina, dysrhythmias, myocardial infarction or sudden coronary death. The episodic dynamic progress of atherosclerotic disease and local thrombosis governs the episodic evolution of the clinical course.
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PMID:Coronary atherosclerosis and thrombosis. 219 40

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

In order to evaluate the evolution (progression and regression) of coronary atherosclerosis, 61 patients (8 with stable angina, 9 with unstable angina, 15 with a recent myocardial infarction, 29 with multivessel coronary artery disease and treated with successful one-vessel angioplasty) were enrolled in a prospective study. In the angioplasty group, only untreated vessels were considered for the analysis. All patients underwent coronary angiography before hospital discharge and after one year, in accordance with the study protocol. In 13 patients (21%) a repeat angiography was performed at 6.3 +/- 2.7 months for clinical reasons (myocardial infarction, changing pattern angina, angina recurrence). All patients were asymptomatic or mildly symptomatic on medical therapy between the angiographic studies. Progression (decrease in internal luminal diameter at the site of stenosis greater than or equal to 20%; new onset of lesions, new episodes of total occlusions) was found in 16 out of 216 stenoses (7%) and in 14 out of 61 patients (23%). Regression (increase greater than or equal to 20% in internal luminal diameter; reopening of a previously occluded vessel) was found in 11 out of 227 lesions (5%) and in 7 out 61 patients (11%). At repeat angiography, the increase in severity was found more frequently in stenoses greater than 5 mm in length and with a reduction of greater than or equal to 75% in luminal diameter. Regression was more frequent in the occluded vessel supplying a recently infarcted area. No significant relationship was observed between lesion morphology (concentric, eccentric, with plaque ulceration, thrombi, border irregularities) and progression or regression. Lesions with plaque ulceration (with or without superimposed thrombi) were found only in patients submitted to coronary angiography close to an acute ischemic attack. Morphologic regression (disappearance of ulceration, border irregularities, thrombi) was also observed, without any significant changes occurring in the severity of the underlying stenosis. Progression may occur independently of worsening in the clinical status; on the contrary, regression was only found in patients without new cardiac events. Nevertheless, clinical status does not seem to be closely correlated to progression, regression, or changes in plaque morphology.
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PMID:[A prospective study of the evolution of coronary lesions: clinico-morphologic correlations]. 221 Jan 60

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

Accelerated atherosclerosis occurs in chronic renal failure. The role of percutaneous transluminal coronary angioplasty (PTCA) in chronic renal failure patients requiring dialysis has not been characterized. We studied 17 chronic dialysis patients requiring PTCA over a 6-year period. Their mean age was 60 years, four were diabetic, eight had severe hypertension, and seven had unstable angina. Angiographic success was achieved in 47 of 49 (96%) stenoses attempted, including multivessel PTCA in 12 patients. There was one procedural death, two non-Q wave myocardial infarctions following PTCA, and one additional in-hospital noncardiac death. The 15 survivors were asymptomatic on discharge (mean stay 11 days), but recurrent angina developed within 6 months in 12 patients. Angiography in 11 of these 12 patients demonstrated restenosis of 26 of 32 (81%) dilated sites. Repeat PTCA in six patients was followed by return of angina in four patients with restenosis in 11 of 12 sites. Bypass surgery was ultimately performed in four patients with long-term angina relief. During follow-up (mean 20 months), seven patients died (five from chronic renal failure, two cardiac deaths). Thus although PTCA in chronic dialysis patients is technically feasible and provides relief of angina, aggressive restenosis limits the long-term benefit. Coronary bypass surgery may be the preferred therapy for this unique patient group.
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PMID:Short- and long-term outcome of percutaneous transluminal coronary angioplasty in chronic dialysis patients. 230 93

This is a study of type A behavior pattern in patients with coronary heart diseases (CHD). Type A behavior pattern (coronary-prone behavior pattern) has been recognized as a risk factor for CHD in western countries. Three hundred patients with new onset of CHD (243 cases of acute myocardial infarction and 57 cases of unstable angina pectoris) between 1981 and 1987 were analysed from the standpoint of behavior pattern. Type A behavior pattern assessed by Jenkins Activity Survey (JAS) was found in 64.6% of subjects and in 43.0% of healthy controls (p less than 0.05). Concerning occupational position, the majority of patients in the administrative class showed type A behavior pattern. Type A behavior pattern was not related with other traditional risk factors (hypertension, hypercholesterolemia and smoking) and was related with angiographically documented severity of coronary atherosclerosis. Emotional stress load by mirror drawing test (MDT) evoked more elevation of blood pressure and plasma catecholamine level in type A patients than in type B patients. A follow-up of post CHD patients, whose occupational position belonged to the administrative class and/or whose work load did not decrease after CHD, modification of type A behavior pattern seemed to be difficult. In conclusion, we consider that type A behavior pattern exists also in Japanese CHD patients, and plays an important role in the development of CHD.
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PMID:Type A behavior pattern as a risk factor for coronary heart diseases. 239 27

Thirty patients (26 men, 4 women) aged from 32 to 73 years (mean 54 years) who developed anterior (14 cases) or posterior (16 cases) myocardial infarction received intravenous streptokinase in doses of 1,500,000 units 2 to 10 hours (mean 4 hours) after the onset of infarction. Coronary angiography, performed 18.6 days on average after thrombolysis, showed a distinct predominance of asymmetrical stenosis with irregular walls and a narrow neck (10 cases, 33 p. 100) or of complete occlusion (12 cases, 40 p. 100) in the artery responsible for the infarction. Complete occlusion probably was the ultimate stage of stenosis. In contrast, the various angiographic images observed in arteries unrelated to the infarction were evenly distributed. The radiological morphology of coronary arterial lesions after a recent infarction is suggestive of ruptured atheromatous plaque, sometimes complicated by thrombosis in situ. Identical images are seen in unstable angina. These findings indicate that one single therapeutic approach should be applied to the most severe types of coronary disease due to atherosclerosis.
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PMID:[Angiographic morphology of the coronary arteries after a recent myocardial infarction treated by intravenous thrombolysis]. 249 70


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