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)

This report examines the correlation of serum apoprotein D with other lipoprotein lipids and apoproteins in a healthy, male population and compares the levels of high density lipoprotein apoprotein D of this control population with 2 samples composed of male, acute myocardial infarction patients and their healthy, male, first-degree relatives. Highly significant correlations were observed with very low density lipoprotein lipids (negative), high density lipoprotein lipids (positive) and serum triglycerides (negative). Serum and low density lipoprotein apoprotein B was not correlated with serum apoprotein D, whereas apoprotein A-I from serum and high density lipoproteins was strongly correlated with apoprotein D. A significant reduction in high density lipoprotein apoprotein D was observed in male, myocardial infarction patients. Their male, first-degree relatives also had lower apoprotein D levels, but the difference was not significant.
Atherosclerosis 1986 Apr
PMID:Apoprotein D in a healthy, male population and in male myocardial infarction patients and their male, first-degree relatives. 308 85

Recent clinical, angiographic, and pathologic evidence has prompted reexamination of the natural history of coronary atherosclerosis. Abrupt anatomic complications of atherosclerotic plaques or thrombosis on a plaque may precipitate the "malignant" syndromes of sudden death, acute myocardial infarction, or unstable angina before the plaque itself is large enough to limit coronary flow. This concept of a bimodal pattern of presentation has important clinical and therapeutic implications.
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PMID:Bimodal presentation of the clinical syndromes of coronary atherosclerosis: a review. 315 31

In 4,649 autopsies performed, in 1972-1985, 824 cases of acute myocardial infarction were found. Of these, 104 (12.6%) had cardiac rupture. Ten cases had rupture of the interventricular septum. The clinical and pathological records were reviewed, and the rupture group was compared with a control group of 100 patients who died from acute myocardial infarction without rupture. Of the patients with rupture, 85% died during the first week after the onset of myocardial infarction; three patients with rupture died suddenly without previous clinical evidence of myocardial infarction. Rupture occurred only in hearts with transmural infarcts, and predominantly in the anteroseptal wall. Patients with rupture had significantly higher blood pressure, fewer previous infarcts, higher frequency of coronary thrombi, less myocardial scar tissue and lower heart weight compared to the control group. There were no significant differences regarding age and sex distribution, physical effort at the symptom debut or death, medication, previous and present diseases other than infarcts, complications or the degree of atherosclerosis in the coronary arteries or aorta.
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PMID:Cardiac ruptures in northern Norway. A retrospective study of 104 cases. 318 80

Angiographically irregular coronary stenoses usually represent plaque rupture with or without superimposed thrombi. Long-segment coronary stenoses with diffuse irregularities (type IIB morphology) have been shown to be more prevalent than focal irregular lesions (type IIA morphology) in survivors of cardiac arrest without acute myocardial infarction. To further understand the pathogenetic importance of type IIB morphology, the clinical and angiographic characteristics in 59 such patients were analyzed. Type IIB lesions accounted for 63% of all type II lesions. Type IIB patients were older than type IIA patients (p less than 0.05). There was a tendency for type IIB morphology to be associated with more extensive disease than other types of lesion morphology (p less than 0.10). Type IIB morphology probably reflects more advanced atherosclerosis. Platelet microemboli may precipitate spasm and/or acute ischemic ventricular tachyarrhythmias. It is possible that long-segment coronary ulcerations are associated with a higher risk for local coronary thromboembolism, and hence with sudden death, than focal lesions.
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PMID:Long-segment coronary ulcerations in survivors of sudden cardiac death. 319 27

Clinical, angiographic, and pathologic data support the contention that atherosclerosis, platelet aggregation, and coronary vasomotility work in unison to cause coronary thrombosis, which in turn leads to myocardial infarction. A patient is described in whom, 2 months after an acute myocardial infarction, inducible coronary artery spasm and a nonocclusive thrombus were angiographically demonstrated at the site of a minimal atherosclerotic narrowing in the infarction-related vessel. This report, to the best of our knowledge, is the first time that these three pathophysiologic mechanisms have been shown, in vivo, to be occurring concomitantly in an infarct-related vessel. Documentation of the unified occurrence of these phenomena support the current concept of the pathophysiology of myocardial infarction.
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PMID:Angiographic demonstration of atherosclerotic stenosis, arterial spasm, and thrombus formation in an infarct-related coronary artery. 319 7

The lipid and lipoprotein profile was examined in male patients with acute myocardial infarction (AMI) at the time of infarction (group A) and in male patients who had survived AMI 2-3 years before the study (group B), and compared to that of healthy controls. The myocardial infarction (MI) patients exhibited similar total cholesterol and LDL-cholesterol levels as the controls. However, the LDL mass concentration was higher in patients than in controls (P less than 0.01 for group A, P less than 0.001 for group B). In composition, patients' LDL in both groups was rich in protein and triglycerides but poor in cholesterol. The compositional changes in patient LDL were evident at all levels of LDL-cholesterol. The mean total HDL and HDL2 mass concentrations were lower in patients than in controls (P less than 0.001 for both groups), but there was no difference in HDL3 levels. Upon admission to hospital the patients with AMI at the time of examination (group A) had higher serum total triglyceride concentration than controls, but on the fasting morning samples serum triglyceride and VLDL lipid levels did not differ between patients and controls. Patients who had survived AMI 2-3 years prior to study (group B) exhibited higher serum total triglyceride and VLDL levels than the control subjects. On stepwise discriminant analysis, HDL2 protein concentration was the single best variable for distinguishing between patients and controls. The most powerful discriminatory parameter was the HDL/LDL protein ratio or the HDL2/LDL protein ratio.
Atherosclerosis 1988 Nov
PMID:Serum lipoproteins in patients with myocardial infarction. 321 82

Eight patients with severe peripheral vascular atherosclerosis scheduled for abdominal aortic surgery were investigated to detect coexisting coronary artery disease. None of the patients had a history of angina pectoris or previous myocardial infarction. Preoperative computerised thallium-201 dipyridamole myocardial scintigraphy was abnormal in all patients, showing either myocardial scar tissue and/or ischaemia with redistribution and/or low washout. In all but one patient, the serum level of creatin kinase was elevated during the first postoperative days. In two patients, the serum concentrations of aspartate aminotransferase and lactate dehydrogenase were elevated. None of the patients showed clinical or electrocardiographical signs of acute myocardial infarction. Thallium-201 dipyridamole myocardial imaging is a new noninvasive method for detection of ischaemic heart disease in patients with severe peripheral atherosclerosis who are unable to perform a bicycle exercise test. The new programme for determination of regional washout appeared to be very precise and may be especially applicable in the case of low washout values.
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PMID:Thallium-201 myocardial scintigraphy during dipyridamole-induced coronary hyperaemia. First experiences with a new regional washout programme. 321 87

Different patho-anatomical and functional factors are considered to be involved in patients with unstable angina pectoris. Among these are a pre-existing plaque based on coronary atherosclerosis, the development of fissures or dissections of the plaque (often combined with thrombus formation at the site of the plaque) coronary vascular tone, and theoretically primary aggregation of platelets at a site of apparently normal vascular endothelium. Several comprehensive studies on patients who died from acute myocardial infarction or unstable angina, have convincingly shown that complications of an atherosclerotic plaque like fissures, dissections and thrombus formation may be present in 60 to 90% of cases. In addition, two groups of investigators, who have applied coronary angioscopy for direct visualization of offending coronary arteries, have confirmed these results, since in about 60-80% of patients with unstable angina complicated atheromata, i.e. rupture, ulceration, thrombus formation, could be documented, whereas in all patients with stable angina an uncomplicated atheroma was seen angioscopically. On the basis of these results a hypothetical sequence of events in patients with stable angina, unstable angina and acute myocardial infarction has been proposed. Stable angina pectoris may be seen in patients with uncomplicated atheroma in one of the major coronary artery branches. When dissections, ulcerations and thrombus formation occur as a complication of a formerly smooth plaque, patients show the clinical syndrome of unstable angina. If an occlusive thrombus develops, the patient will run into a fresh myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiology of unstable angina pectoris--correlations with coronary angioscopic imaging. 324 55

The mechanisms of inflammation responsible for the myocardial tissue damage seen after an acute myocardial infarction (AMI) have not been clearly identified. Recent lines of evidence, demonstrating depressed sera levels of individual complement components in patients after myocardial infarction, have suggested involvement of the complement (C) system in micro- and macrovascular injury subsequent to AMI. The present study assessed the role of complement as a mediator of myocardial inflammation by quantifying products of complement activation including, the terminal complement complex (TCC) the cytolytic component of the complement system, C1rC1s-C1 inhibitor complex and C3bBbP complex, formed following activation of the classical and alternative pathway, respectively, and anaphylatoxins C3a and C5a in 41 patients following AMI. Plasma TCC and C1rC1s-C1 inhibitor complex concentrations increased up to 32-fold (P less than 0.001) and 8-fold (P less than 0.001), respectively, while the C3bBbP complex, C3a des-Arg and C5a des-Arg each increased over 2-fold (P less than 0.001) 16 h after AMI, and were only minimally detectable during non-inflammatory myocardial conditions. Furthermore, TCC concentrations increased over 150% (P less than 0.001) one day after patients reinfarcted, subsequent to hospitalization for a primary AMI. These results demonstrate activation of complement after AMI and suggest that inflammatory mediators of the complement system may contribute to myocardial tissue damage during the infarction process.
Atherosclerosis 1988 Mar
PMID:Detection of the terminal complement complex in patient plasma following acute myocardial infarction. 325 20

Hypertension is associated with an increased risk of coronary events. Treatment of hypertension in controlled trials has not reduced the incidence of coronary events, although the risk of stroke is reduced. In untreated hypertension, about one-half the deaths were due to hypertensive heart failure, whereas myocardial infarction caused 10%-12% of deaths. In treated hypertension, coronary events cause about 40% of deaths. Although in autopsy serious coronary atherosclerosis is commonly found in hypertension, in severe hypertension, dilated coronary vessels free of atheroma were a common finding. No correlation was noted between the height of blood pressure and degree of coronary atherosclerosis. The relationship between coronary disease and hypertension is consistent with an association between them rather than hypertension being a causal factor. The factors that cause acute myocardial infarction may differ from those which predispose to coronary atherosclerosis.
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PMID:Does hypertension predispose to coronary disease? Conflicting epidemiological and experimental evidence. 329 99


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