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)

A significantly higher platelet malondialdehyde-like material (MDA--LM) content after physical and N-ethylmaleimide (NEM) stimulation is found in chronic ischemic heart disease (CHD) patients when compared to the control group. In subjects under aspirin treatment "in vivo" (1 gr/day) no difference is found between CHD and control group. It is suggested that the enhanced amount of lipid peroxides in CHD platelets is produced by a cyclooxygenase-dependent mechanism. This enhanced platelet lipid peroxide production in CHD may be another platelet-dependent risk factor for atherosclerosis in these patients.
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PMID:Elevated lipid peroxide levels in platelets of chronic ischemic heart disease patients. 681 50

Mast cells were examined in the left ventricular myocardium of 134 patients who had died of different diseases. Myocardial mast cells were smaller in quantity and size and somewhat degranulated where coronary arteries were stenosed due to atherosclerosis. These changes in mast cells can be used as a criterion of chronic myocardial ischemia. The findings are suggestive of functional insufficiency in myocardial mast cells associated with coronary disease.
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PMID:[Effect of stenosing coronary arteriosclerosis on myocardial mast cells]. 685 57

Coronarography was used to study the state of haemocoagulation in 83 patients with chronic ischaemic heart disease. No essential differences in the figures of the blood coagulation in patients with intact and slightly sclerosed coronary arteries have been found; certain parameters, the blood heparin, dissolved fibrin were changed towards hypercoagulation with the vessels intact. Marker growth of the haemocoagulation potential was seen only with total lesion of the heart arteries reaching over 50 and 75%. The rise of haemocoagulation activity was noted also as the sensitivity of microvessels to adrenaline rose. It has been concluded that in the development of hypercoagulation not only atherosclerosis of the vascular wall, but changes of its reactivity take part.
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PMID:[Structural and functional state of the vascular wall and hemostasis in chronic ischemic heart disease]. 728 91

Total cholesterol and triglycerides as well as their distribution among the different hyperlipoproteinemia types were studied in three patients groups: 47 normotensive patients with myocardial infarction, 35 normotensive patients with cardiosclerosis (chronic ischemic heart disease), 29 hypertensive patients without symptoms or signs of clinical atherosclerosis. Their results were compared to those of 45 normal controls. There was no decrease in HDL cholesterol nor increase in LDL cholesterol in patients with chronic or acute ischemic heart disease. A large percentage of patients from these groups had normolipoproteinemia. The most prominent lipidic changes were observed in hypertensive patients: no patient had a HDL cholesterol level above normal values, thirty three per cent had a HDL cholesterol level below 35 mg/dl. A high percentage of patients with acute myocardial infarction or hypertension exhibited atypical lipoproteinemia anomalies (hyper HDL triglyceridemia, hyper LDL triglyceridemia, hyper VLDL cholesterolemia) when they could have normolipoproteinemia. This suggested lipoproteinic metabolism disturbances in such cases.
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PMID:[Changes in serum lipid levels, lipid composition and lipoprotein fractions in patients with ischemic cardiopathies or arterial hypertension]. 733 37

Renal hemodynamics were studied in patients suffering from atherosclerosis with predominant localization of the process not in the renal artery (in patients with chronic ischemic heart disease) and with normal or periodically increased arterial pressure (to 160/95 mm Hg). The data obtained were compared with the findings in groups of healthy persons and patients with III stage hypertensive disease. A history of myocardial infarction was the criterion of the presence of atherosclerosis. It was established that the changes progress from age involution to those more pronounced in atherosclerosis and are of a quantitative character; they are of a similar trend. An increase of arterial pressure contributes to deterioration in the blood supply to the kidneys, besides marked quantitative changes (mainly due to increased resistance of the renal vessels) new qualitative shifts occur (increase in the filtration fraction) which aggravate renal hemodynamics and thus contribute to the fixation of the nephrogenic factor in the further development of arterial hypertension.
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PMID:[Renal hemodynamics in arteriosclerosis and its changes under increased arterial pressure]. 737 4

In this work, an x-irradiation/high fat/high cholesterol diet-induced atherogenic model was invoked to examine the effects of severe diffuse atherosclerosis on myocardial metabolism in the in vivo porcine heart. This model was studied using spatially localized 31P-nuclear magnetic resonance (NMR) to monitor pH and the levels of inorganic phosphate, phosphomonoesters, creatine phosphate, and adenosine triphosphate as a function of workload transmurally in control swine and in animals suffering from chronic ischemic heart disease. These preliminary studies revealed that the development of severe atherosclerosis and the accompanying chronically diseased state produce changes in high energy phosphates and that increases in rate pressure products result in demonstrable signs of ischemia in the myocardium which span the entire left ventricular wall. Ischemic changes include a global increase in inorganic phosphate and corresponding decreases in creatine phosphate, ATP, and pH. Importantly, changes in intracellular pH are noted with even the slightest increase in workload suggesting that these diseased hearts display elevated glycolytic activity. By challenging these animals with increased cardiac workload, we directly visualize how the chronically compromised heart responds to severe oxygen challenges in a clinically relevant model of this situation.
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PMID:31P-nuclear magnetic resonance studies of chronic myocardial ischemia in the Yucatan micropig. 781 9

The possibility that Fas/APO 1 is involved in the apoptosis of advanced human coronary atherosclerosis was examined in the present study. Coronary arteries with atherosclerosis were obtained from human hearts with chronic ischemic heart disease at cardiac transplantation. Normal vessels were used as controls. Fas/APO 1 was detected by immunohistochemistry with a monoclonal antibody. Apoptotic cells were stained in situ by terminal deoxynucleotidyl transferase mediated-dUTP nick end labeling (TUNEL) and DNA fragmentation into oligonucleosomes was checked by gel electrophoresis. Bcl-2, an antiapoptotic oncoprotein, was detected by immunohistochemistry and Western blot. Apoptotic cells were present in the neointima in all stages of atherosclerosis, and in intraplaque small vessels. In initial lesions, only a few cells were undergoing apoptosis. By contrast, in advanced lesions, many cells were found to undergo apoptosis. Apoptosis was further confirmed by genomic DNA analysis using gel electrophoresis. Apoptotic cells were either smooth muscle cells or macrophages, but also endothelial and blood borne cells. Fas/APO 1 was present in foam cells. Most of the Fas/APO 1 positive cells were stained for the macrophage marker CD68 and for alpha-smooth muscle actin in serial sections. Several anti-Fas/APO 1 positive foam cells were revealed to undergo apoptosis by double staining. Bcl-2 was detected in Fas/APO 1 expressing plaques. A number of CD3-positive T-lymphocytes were found around foam cells expressing Fas/APO 1. This data suggests that Fas/APO 1 regulated apoptosis is involved in the development of advanced human atherosclerotic lesions and that it probably determines the amount of tissue mass in the diseased vessels.
Atherosclerosis 1997 Jun
PMID:The role of Fas/APO 1 and apoptosis in the development of human atherosclerotic lesions. 919 70

The aim of this study was to assess the presence of Chlamydia pneumoniae antibodies in patients with angiographically verified atherosclerotic coronary artery disease. A total of 114 consecutive patients were investigated between April 1995 and June 1996. Patients were divided into two groups: 72 patients with acute myocardial infarction (AMI; 53 men, 19 women, mean age 62.27 +/- 10.1 years), and 42 patients with chronic ischemic heart disease (CAD; 37 men, 5 women, mean age 62.75 +/- 9.2 years). A control group of 50 normal subjects matched for age (mean 62 +/- 9 years), sex, social status and geographical area was used. Identification of Chlamydia pneumoniae was carried out with the microimmunofluorescence method, on two serum samples taken from patients on admission and after 15 days. The IgM, IgG and IgA anti-Chlamydia pneumoniae titers were assessed, values > or = 1:16, > or = 1:32 and > or = 1:8 being respectively considered positive. Acute (IgM > or = 16 or four fold rise of IgG titer) and chronic (IgG > or = 128 e IgA > or = 32 or only elevated IgA titer) infections were analyzed. IgM antibodies were not found in AMI, CAD and control groups. IgG positivity (IgG > or = 32) was found in 38% of the control group, in 58.3% of the AMI group (p < 0.05) and 42.8% of the CAD group (p < 0.01). IgA positivity > or = 8) was found in 22% of the control group, in 31.9% of the AMI group (NS) and in 33.3% of the CAD group (p < or = 0.05). Acute infection was observed in 5.5% of AMI patients and in 12% of CAD patients (NS), whereas no subject of the control group showed these values. Chronic infection was observed in 9.7% of AMI patients and in 16.6% of CAD patients (NS) whereas nobody of the control group showed these values. In conclusion, our results suggest that Chlamydia pneumoniae infection is present only in the AMI and CAD groups. It is possible to suppose that this infection may be linked to atherosclerosis through an endothelial damage or a systemic endogenous procoagulant and inflammatory activity.
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PMID:[Chlamydia pneumoniae infection and cardiac ischemic syndromes]. 992 69

The heart and the vascular system are frequent and characteristic targets of several systemic autoimmune diseases, in particular Systemic Lupus Erythematosus (SLE), Rheumatoid Arthritis (RA) and Systemic Sclerosis (SSc). In this chapter we review the classic cardiac abnormalities and the more recent data about cardiovascular involvement as part of a major disease complication determining a substantial morbidity and mortality. In addition to the classic cardiac abnormalities involving the heart structures, acute and chronic ischemic heart disease and cerebrovascular accidents are threatening clinical manifestations of SLE and RA associated to an early accelerated atherosclerosis. Immune-mediated inflammation is now recognized as an important factor involved in the pathogenesis of atherosclerosis. Ongoing clinical studies are being devised to find specific risk factors associated with systemic autoimmune diseases and/or treatment regimens. Hopefully, prophylactic measures should be available within the next few years.
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PMID:Cardiac involvement in systemic autoimmune diseases. 1240 11

AIM: To elucidate possibilities of multiplane transesophageal ultrasound for assessment of localization and structure of atherosclerotic plaques in the thoracic aorta as well as relationship between changes of elastic-tonic properties, processes of aortic wall remodeling, stage of aortic atheromatosis, and coronary atherosclerosis. MATERIAL: Patients with chronic ischemic heart disease and atherosclerosis of thoracic aorta (n=120), healthy volunteers (n=11, all men, mean age 51-/+8 years). METHODS: Multiplane transesophageal ultrasound with subsequent calculation of parameters of elasticity and stiffness. The classification of C. Pitsavos et al. (1997) was used for grading aortic atheromatosis. RESULTS. Atherosclerotic plaques were found in 109 patients (91%) and 69 patients (58%) had pronounced (stage 3-5) atheromatosis of thoracic aorta. The plaques were most frequently (87%) localized in descending aorta. Calcinated hyperdense plaques, soft plaques with low density, soft plaques with heterogeneous density prevailed in ascending aorta, aortic arch, and descending aorta, respectively. Sensitivity and specificity of thoracic atherosclerosis as predictor of atherosclerotic lesions in coronary vessels were 90 and 65%, respectively. Pronounced diffuse atherosclerosis of thoracic aorta decreased its elastic-tonic properties as evidenced by significant lowering of parameters of elasticity and increase of stiffness index. This process was associated with remodeling of thoracic aorta (progressive passive dilatation, thickening of its wall and lowering of amplitude of systolic excursion). Atheromatosis stage correlated inversely with systolic excursion and parameters of elasticity and directly with stiffness index, intima-media thickness, systolic and diastolic diameters of the aorta. There was also a direct correlation between stage of aortic atheromatosis and age and total score of coronary artery involvement. CONCLUSION: Multiplane transesophageal echocardiography is a highly informative noninvasive method of assessment of morpho-functional changes of thoracic aorta caused by atherosclerosis.
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PMID:[Morpho-Functional Changes of Thoracic Aorta in Atherosclerosis: Multiplane Transesophageal Ultrasound Study] 1246 2


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