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)

Coronary artery disease has emerged as an important cause of death in young patients with SLE. We report three cases of acute myocardial infarction in young lupus patients who underwent emergent coronary angiography. One patient had a large coronary aneurysm and died five months later from myocarditis. The other two patients underwent coronary angioplasty. The difficulty in distinguishing coronary arteritis from premature atherosclerosis and its relevance to methods of treatment is discussed.
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PMID:Evaluation and treatment of acute myocardial infarction complicating systemic lupus erythematosus. 173 66

Literature data suggest that identification of the conditions preventing lecithin:cholesterol acyltransferase (LCAT) to produce normal cholesterol esterification might be of utmost importance in the follow-up of atherosclerosis. Interrelationship between LCAT activity, and total cholesterol (TC), unesterified cholesterol (UC), esterified cholesterol (EC), low and high density lipoprotein cholesterol (LDL-C, HDL-C), triglycerides (TG), phospholipids (PL), free fatty acids (FFA), l-lactate (LAC), and electrolytes, i.e. zinc (Zn), calcium (Ca) and magnesium (Mg), was investigated in 60 patients with acute myocardial infarction (AMI), 30 patients with coronary heart disease (CHD) and 30 healthy control subjects. Results of the study revealed LCAT activity to be significantly decreased in atherosclerotic patients, with a significantly increased ratio of unesterified-esterified cholesterol (UC/EC), as compared to the control group of normal subjects. A decreased LCAT activity was accompanied by elevated values of phospholipids and LDL-C, a moderate increase in triglycerides, and a decreased quotient of HDL3/HDL2 cholesterol. Accordingly, a decreased activity of LCAT could with great certainty be considered a high-risk biochemical factor for atherosclerosis.
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PMID:Lecithin:cholesterol acyltransferase activity in patients with acute myocardial infarction and coronary heart disease. 175 Aug 5

In the Western world the percentage of subjects over the age of 60 years is rapidly increasing. Therefore, elderly individuals represent a progressively increasing proportion of patients with ischemic heart disease (IHD), which is the most prevalent disease in this age range. In the elderly both the clinical presentation and the outcome of IHD have some peculiar features which may have important therapeutic implications. The prevalence of both coronary atherosclerosis and uncomplicated angina pectoris increases up to the sixth decade when it reaches a plateau. Conversely, the prevalence of myocardial infarction increases progressively at increasing ages without reaching any plateau at all. These findings indicate that the higher prevalence of myocardial infarction in the elderly is not caused by a worsening of the atherosclerotic background, but rather by a greater prevalence and/or severity of the functional factors such as local smooth muscle hyperreactivity, local thrombotic stimuli and alterations of the systemic thrombosis-thrombolysis equilibrium which are more directly responsible for the irreversible occlusion of a coronary artery branch. Therefore, the prevention of IHD in the elderly should focus mainly on the ischemic stimuli leading to coronary thrombosis rather than on the atherosclerotic background. Another important feature of IHD in the elderly is the high short and medium-term mortality of acute myocardial infarction. This excess of mortality is caused mainly by a much higher incidence of cardiac rupture, which does not appear to be related to the severity of coronary atherosclerosis nor to the infarct size.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Morphofunctional changes in the left ventricle of the elderly person and the vulnerability to myocardial necrosis]. 184 1

To study past histories of patients who died suddenly, we selected cases from all the summary death certificates in which death occurred within 24 hours from the onset of symptoms spanning 1984 to 1986 in Niigata prefecture with a population of 2.5 million. We then re-examined all information on the death certificates to determine the underlying causes. Sudden deaths due to cardiovascular diseases other than acute myocardial infarction and cerebrovascular accident (OCD) accounted for the largest proportion (51.4%). The proportion of death of unknown etiology increased with the decrease in age in both sexes aged 15 to 54 years, accounting for 67.8% in males and 51.1% in females. The number of cases with histories of diseases related to atherosclerosis (e.g. hypertension, old cerebrovascular accident, etc) increased with age in both sexes, accounting for 38.5% in males and 36.4% in females, both aged 75 years old and over. Except diseases related to atherosclerosis, the past histories accounted for 2.5% or greater were as follows: alcoholism (4.1%), psychiatric disorder (PSY, 2.9%) and valvular heart diseases (VD, 2.6%) in 15-54-year-old males; ischemic heart diseases (IHD, 9.4%), arrhythmia without organic heart diseases (ARR, 2.5%) and VD (2.5%) in 55-74-year-old male; IHD (11.4%), bronchial asthma (3.7%), common cold within one month (CC, 3.6%), cor pulmonale or its related diseases (3.0%) and ARR (2.6%) in male of 75 years old and over; PSY (8.7%), IHD (5.8%), VD (5.1%), pregnancy, delivery or related diseases (4.4%), chronic renal failure (3.6%) and CC (2.9%) in 15-54-year-old females; IHD (10.2%), VD (3.2%) and ARR (2.6%) in 55-74-year-old females; and IHD (11.8%) in females of 75 years old and over. When diseases related to atherosclerosis were included, half of the sudden death cases due to OCD had past histories of underlying cause. As descriptions of past histories are often incomplete, there were probably more cases with past histories. The results of this study indicate that investigation of past histories may aid in elucidating and preventing sudden death.
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PMID:[Past histories of sudden death without specific underlying disease]. 184 23

Acute myocardial infarction is a potentially fatal complication of SLE. Reported mechanisms include atherosclerosis, arteritis and coronary arterial spasm. The following case report presents a fourth possible cause; intracoronary thrombus with angiographically normal coronary arteries in a patient with active lupus and AMI.
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PMID:Myocardial infarction due to intracoronary thrombi without significant coronary artery disease in systemic lupus erythematosus. 186 45

A total of 34 severely obese men with a history of heavy snoring and excessive daytime sleepiness indicative of obstructive sleep apnoea syndrome (OSAS) were studied prospectively. Their mean age was 46 years, and mean body mass index was 41.6 kg m-2. During a 4-year follow-up, 15% (5/34) of these subjects died (three cases of acute myocardial infarction and two cases of pulmonary oedema), all of them suddenly and unexpectedly, outside hospital. On autopsy the degree of atherosclerosis was found to be moderate in all cases. In 68% (15/22) of the men a pathological apnoea index (mean value 46 +/- 20) confirmed the OSAS diagnosis. Exercise tests and neurological examinations did not reveal any other causes of daytime sleepiness. Mean blood pressure at rest and during exercise was normal, and mean serum lipid and blood glucose levels were normal. Spirometry revealed intrapulmonary restrictive changes that could not be attributed to the heavy thoracic wall. Compliance was reduced to about 50% of reference values, and the mean pCO2 level (5.8 kPa) was close to the upper reference limit. Blood tests suggested that high alcohol consumption may be an important factor contributing to OSAS. These results demonstrate that morbidly obese men with a history of OSAS have a high risk of sudden cardiovascular death, despite the absence of other conventional risk factors.
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PMID:The sleep apnoea syndrome in obesity: risk of sudden death. 186 65

The aim of this study was to find out the contributing factors for cardiac rupture in the course of acute myocardial infarction (AMI). Past medical histories and autopsy data of 80 patients were analyzed. The first group consisted of 30 patients who died due to heart rupture in the course of AMI and the control group of 50 patients who died from the other, more common complications of AMI. There was no difference between the groups according to age and sex of the patients. All patients who died from the rupture of the heart had a history of heavy chest pain, while it was lacking in 30% of the patients of the control group (p less than 0.01). All the first group patients showed electrocardiograms diagnostic for AMI, while it was lacking in 14% of the second group patients (p less than 0.05). Almost a half of the second group patients (47%) were in the class I of the Killip's classification, while only 20% of the control group did not developed left ventricular failure. Pathological study showed that the rupture of the heart most commonly occurred in the course of an anterior myocardial infarction. There was no difference according to the size of infarctions between observed groups, but the thickness of the left ventricular wall was significantly less (p less than 0.05) in the control group, and the heart weights were higher (p less than 0.05) in the control group. There was advanced atherosclerosis of the coronary arteries and about two thirds of the first group patients showed acute coronary thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Factors contributing to the onset of heart rupture in acute infarct]. 189 Sep 17

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 incidence of minimal residual atherosclerotic coronary obstruction after successful intravenous thrombolytic therapy was evaluated in 799 patients with acute myocardial infarction. Minimal residual coronary obstruction (less than or equal to 50%) was observed on selective coronary angiography performed 90 min after initiation of thrombolytic therapy in 43 patients (5.5%). In 42 other patients (5.4%), a greater than 50% but less than 100% residual stenosis noted at 90 min demonstrated further resolution of obstruction to less than 50% at an angiographic follow-up study 7 to 10 days later. Patients with minimal residual coronary obstruction were significantly younger (52 +/- 10.7 versus 56.7 +/- 10 years; p = 0.002) and had less multivessel coronary disease (p less than 0.001), better initial left ventricular ejection fraction (54 +/- 12% versus 50.2 +/- 11.4%; p = 0.006) and a lower in-hospital mortality rate (1% versus 7%; p = 0.04) than did patients who had a significant (greater than 50%) residual coronary obstruction after intravenous thrombolysis. Long-term follow-up study of patients with a minimal coronary lesion (average 1.5 +/- 0.6 years) and those with significant residual stenosis (average 1.6 +/- 0.7 years) demonstrated that the incidence of death (2.4% in patients with minimal stenosis versus 3.5% in those with significant stenosis) and recurrent myocardial infarction (5% each) were similar in both groups. New strategies are needed to prevent coronary rethrombosis in patients with minimal atherosclerosis after thrombolytic therapy for acute myocardial infarction.
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PMID:Myocardial infarction with minimal coronary atherosclerosis in the era of thrombolytic reperfusion. The Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) Study Group. 189 33

The natural history of coronary artery disease is punctuated by clinical manifestations of unstable angina, acute myocardial infarction, and ischemic sudden death. These acute coronary syndromes share common pathophysiologic mechanisms that include fissuring of a plaque followed by varying degrees of dynamic coronary obstruction, which is due to vasoconstriction and coronary thrombosis. The response to plaque fissure is likely to be modulated by local and/or systemic procoagulant and anticoagulant-fibrinolytic activities. The key role of coronary thrombosis in acute coronary syndromes has substantial implications for prevention and treatment of complications of coronary atherosclerosis.
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PMID:Pathophysiology of acute coronary syndromes. 195 Oct 98


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