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 unique case is described of a 64-year-old white woman who had silent thromboembolic occlusion of the right pulmonary artery. Over the ensuing months, severe pulmonary hypertension developed, as manifested by marked dilatation and atherosclerosis of the right and left pulmonary arteries and severe right ventricular hypertrophy. Nevertheless, she remained fully ambulatory and felt generally well throughout this time. Eventually, however, the pulmonary arteries became so dilated that they compressed the recurrent laryngeal nerve as it looped under the aortic arch, and it was the resulting hoarseness that first caused the patient to seek medical attention. A work-up disclosed normal peripheral lung fields on x-ray study and a large dense right hilar mass. Accordingly, the patient was subjected to an exploratory thoracotomy on the reasonable but mistaken diagnosis of bronchogenic carcinoma. After the following operation, her condition deteriorated. She developed bronchopneumonia which, when superimposed on her already precariously reduced cardiopulmonary function, precipitated respiratory insufficiency. An independent stroke was the immediate cause of death.
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PMID:Silent, chronic, massive pulmonary thromboembolism masquerading as bronchogenic carcinoma. 96 90

Homozygous familial hypercholesterolaemia is characterized by cutaneous xanthoma development from infancy, precocious and accelerated atherosclerosis with clinical signs of ischemic heart disease and frequent involvement of left heart valves resulting in stenosis and/or incompetence. Two cases are described of this condition, both associated with aortic stenosis. In one case mitral incompetence and thromboembolic pulmonary hypertension were also found. The mitral valve is involved in the atherosclerotic process at the level of the cusps. These become thickened and stiff. Aortic stenosis is mainly due to atheromas infiltrating the Valsalva sinuses and the ascending aorta. Pulmonary hypertension, never reported before in this disease, is probably due to concomitant atheromatosis involving the pulmonary artery with secondary fatty embolism.
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PMID:[Involvement of the heart valves and great vessels in homozygote familial hypercholesterolemia]. 129 17

Endothelial cells produce the 21-amino acid peptide endothelin, which is formed from its precursor, big endothelin, via the activity of converting enzyme. The basal production of the peptide is stimulated by epinephrine, angiotensin II, arginine vasopressin, transforming growth factor beta, thrombin, interleukin-1, and hypoxia. In vascular smooth muscle, endothelin binds to a specific receptor (ETA-subtype), which activates phospholipase C, leads to the formation of inositol trisphosphate, diacylglycerol (which activates protein kinase C), and increased intracellular Ca2+. In certain blood vessels, the endothelin receptor on vascular smooth muscle is linked to a voltage-operated Ca2+ channel via a G-protein. This explains why Ca2+ antagonists inhibit endothelin-induced contractions in certain, but not all, blood vessels. In the human forearm circulation, Ca2+ antagonists do prevent endothelin-induced contractions and unmask endothelin-induced vasodilation mediated by endothelial prostacyclin production (via the ETB-receptor). The pulmonary circulation plays an important role in the metabolism of endothelin, as the lungs take up large quantities of the peptide during passage. Endothelin has profound vasoconstrictor effects in the pulmonary circulation (and also in bronchial tissue), and its production is augmented in pulmonary hypertension. In systemic hypertension, the circulating endothelin levels appear to be normal. In atherosclerosis and other forms of vascular disease, circulating endothelin levels are increased. Thus, endothelin is a potent mediator in the systemic and pulmonary circulation and, in particular, in diseases of the vasculature.
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PMID:Endothelin: systemic arterial and pulmonary effects of a new peptide with potent biologic properties. 133 60

Growing experience in terms of immunosuppression, recipient and donor selection as well as organ preservation has established thoracic organ transplantation as a therapeutic option for many children with end-stage cardiopulmonary diseases. While dilated cardiomyopathy and isolated myocardial failure represent the main indications for cardiac transplantation, replacement of the lungs or heart and lungs is necessitated in cystic fibrosis, primary and secondary pulmonary hypertension as well as some types of complex congenital heart defects involving the pulmonary arteries. We have performed a total of 20 heart, 4 heart-lung, 2 single lung and 1 double lung transplantation in the paediatric group up to 17 years of age. While with respect to the limited experience worldwide, early mortality after lung and heart-lung transplantation is still high (50%), long-term results in isolated cardiac transplantation using triple drug immunosuppression are excellent (79% survival after 6 years) without major impairment of renal function, arterial blood pressure, growth development and physical rehabilitation as well as social reintegration. Freedom from graft atherosclerosis of the allografted heart is documented over a 5 year follow up, while no data are available on the incidence of obliterative bronchiolitis after lung transplantation in the paediatric group. Despite only limited evidence of long-term dysfunction, diagnosis and prevention of chronic rejection should be given utmost attention to allow for a normal life span in this younger age group.
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PMID:Thoracic organ transplantation in the paediatric age group. The Hannover experience. 134 7

Fatal haemopericardium in a 27 year old pregnant woman was caused by rupture of a dissecting aneurysm of the pulmonary artery. She had an uncorrected patent ductus arteriosus and severe pulmonary hypertension. The wall of the pulmonary artery showed atherosclerosis and cystic medionecrosis.
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PMID:Pulmonary artery rupture in pregnancy complicating patent ductus arteriosus. 146 58

The author reviews findings assembled during the last 20 years on the endothelium-derived relaxing factor (EDRF), and in particular findings assembled the last five years which revealed that EDRF is identical with nitric oxide, NO. The enzyme NO synthetase produces NO from l-arginine with the concurrent formation of citrulline and is present not only in the endothelium of the vascular wall but also in cerebral neurons and other tissues. NO is probably also the effective factor of the vasodilatating action of organic nitrates (nitroglycerol, amyl nitrite, sodium nitroprusside). In recent years these findings are applied also in clinical work. In atherosclerosis of the coronary vessels NO formation is obviously reduced and l-arginine infusion may improve the coronary blood supply in patients with hypercholesterolaemia. Inhalation of NO has been tried in pulmonary hypertension. Antidotes of NO (methylene blue) conversely may prevent hypotension in hepatic failure. Infusion of an antidote of l arginine prevents hypotension in septic shock. This is due to the fact that an excess of NO is formed from macrophages during infections. NO is, however, also mutagenic and there are reports on its participation in the genesis of genetic and neoplastic diseases.
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PMID:[EDRF-NO. The endothelium-derived relaxing factor is nitric oxide]. 150 92

Cardiovascular disease is the third most common cause of death in Tshepong Hospital in the western Transvaal, and the most common cause of death in patients older than 35 years. A prospective study was undertaken which included limited necropsies in 90 of the 167 cardiovascular disease deaths over 1 year. A reliable mortality pattern for cardiovascular deaths is described. Additionally, attention is paid to co-existing conditions. Conditions relating to cardiovascular disease, such as hypertension, benign hypertensive nephrosclerosis, atherosclerosis and obesity, were also evaluated. Cerebrovascular conditions were found in 32% of cardiovascular deaths. Intracerebral haemorrhage was found in 50% and cerebral infarction in 29% of cases. Fifty-seven per cent of cardiovascular deaths were due to cardiac conditions, the most common being pulmonary hypertension (31%), dilated cardiomyopathy and chronic rheumatic valvular disease (17% each) and hypertensive heart disease (14%). Forty-nine per cent of subjects were hypertensive, while 40% exhibited benign nephrosclerosis and only 3% of the examined vessels had signs of severe atherosclerosis. Tuberculosis was present in 13% of cases. The clinical diagnosis was the same as the final necropsy diagnosis in 38% of cases. These results emphasise the importance of performing necropsies to obtain reliable mortality statistics.
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PMID:Cardiovascular causes of death at Tshepong Hospital in 1 year, 1989-1990. A necropsy study. 173 52

When examining survival rates following cardiac transplantation, it is important to examine the risk factors for both early (30-day) and late (greater than 30-day) survival as they may well be different. Factors affecting early survival appear related more to the preoperative condition of the patient (including degree of pulmonary hypertension) as well as advances that have been made in postoperative care. It is not immediately obvious why gender has such a profound effect on early survival and why primary graft failure rates appear higher in this group. Donor organ factors did not appear to relate to this difference. On the other hand, late survival appears to be influenced mainly by immunologic factors such as panel reactive antibody level and immunosuppressive protocol. A less dramatic effect of transpulmonary gradient appears to have a lasting effect on recipients even when they survive the initial 30-day period. Thus, pulmonary hypertension may have prolonged effects on the cardiac allograft which as yet we do not understand completely. The majority of late mortality is still due to graft atherosclerosis, infection, and acute cellular rejection, the latter 2 occurring most frequently within the first year after transplantation whereas death from graft atherosclerosis becomes most prominent beyond 5 years. Despite persistent improvements in 30-day survival, late survival following cardiac transplantation will only improve with the advent of better tissue matching and improved immunosuppression. The results with FK506, for example, are promising.
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PMID:Cardiac transplantation at the University of Pittsburgh: 1980 to 1991. 182 Jan 49

EDRF is a potent, endogenous vasodilator that is produced and released from endothelial cells and subsequently causes the relaxation of VSM through the activation of soluble guanylate cyclase and an increase in VSM cyclic GMP. Structurally, EDRF is likely to be NO or a related nitrogen oxide-containing compound. It is synthesized in endothelial and other cell types from L-arginine by a calcium-calmodulin and NADPH-dependent enzyme. Its action is very similar to the nitrovasodilators that act directly on VSM. EDRF is present in all vascular beds, large and small vessels, and in a wide range of species. Its role in human vascular physiology and pathophysiology is just beginning to be understood. EDRF is a potent endogenous vasodilator and inhibitor of platelet aggregation and adhesion. Its activity is impaired in hypertension and atherosclerosis, and its absence due to endothelial damage may play a role in cerebral and coronary vasospasm. It is a mediator of flow-dependent vasodilation, and its inhibition by hypoxia may contribute to the hypoxic pulmonary vasoconstrictor response. Endothelial cell damage and impairment of EDRF production may also contribute to acute and chronic pulmonary hypertension. A further understanding of the chemical nature and synthetic pathways of EDRF should lead to the production of analogs and antagonists, which may play an important role in future treatments for atherosclerosis, myocardial infarction, angina, hypertension, and other vascular diseases. The recent realization that EDRF serves as the second messenger for guanylate cyclase activation and cyclic GMP production in a variety of cell types outside of the cardiovascular system, including renal and respiratory epithelium, cerebellar neurons, macrophages, and adrenocytes, suggests even broader implications. The importance of EDRF to the anesthesiologist may go beyond an understanding of its role in cardiovascular physiological and pathophysiological states. Initial studies have shown that the endothelium may play a role in mediating the vascular actions of anesthetics, and that anesthetics can inhibit the production, release, or action of EDRF. How are these interactions mediated? Are there significant differences between anesthetics with regard to their effects on EDRF? Is there a clinically significant effect of anesthetics on basal activity of EDRF, or only in response to exogenous stimulation? Conversely, it is important to determine if alterations in endothelial cell function by various disease states such as hypertension, atherosclerosis, adult respiratory distress syndrome, cerebral vasospasm, and others cause changes in the vascular actions of anesthetics. The potential interactions of anesthetics with EDRF production and action in cell types other than the endothelium have not yet been explored.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Endothelium-derived relaxing factor: basic review and clinical implications. 186 89

In the past 3 years at our institution 130 patients have undergone cardiac transplantation for ischemic cardiomyopathy in 49 (38%), idiopathic cardiomyopathy in 42 (32%), viral cardiomyopathy in 9 (6.9%), pulmonary hypertension in 8 (6%), and graft atherosclerosis in 2 (1.5%). Routine preoperative abdominal ultrasonography was performed on 98 (75%) of these patients with specific visualization of the abdominal aorta in 93 (95%). Abdominal aortic aneurysms (all infrarenal) were found before operation in four patients and only in the subgroup undergoing transplantation for ischemic heart disease (10.5%). They measured 3.4, 4.5, 3.6, and 3.8 cm before transplantation. Periodic evaluation by ultrasonography was carried out after transplantation during the 3-year period of this study. One aneurysm that was initially 3.6 cm increased to 4.0 cm and ruptured 2 months after transplantation. The patient died despite emergent surgery. Aneurysms in three patients who demonstrated rapid aneurysm expansion after transplantation were successfully repaired at 5, 20, and 33 months after transplantation when the lesions reached 5.5, 5.9, and 4.8 cm. A fifth patient with an initially normal (1.5 cm) aorta developed a symptomatic aneurysm of 4.1 cm, which was repaired uneventfully. The average expansion rate of these aneurysms after transplantation was 0.74 +/- 0.15 cm/year. This experience suggests that aneurysms are limited to patients undergoing transplantation for ischemic heart disease. Ultrasound examination may be appropriate for preoperative screening. Careful aortic surveillance after transplantation is important in patients having transplantation for ischemic cardiomyopathy because of the apparent rapid expansion rate compared to aneurysms in the population not receiving transplants.
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PMID:Abdominal aortic aneurysm in the patient undergoing cardiac transplantation. 192 Jun 43


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