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)

Certain clinical and autopsy findings are described in 13 patients who had both aortic dissection (AD) and fusiform abdominal aortic aneurysm (AAA). All 13 patients had severe and extensive aortic atherosclerosis. The AAA was diagnosed clinically in 9 patients, and 5 had the AAA resected. The AD was diagnosed clinically in 5 patients, and 2 underwent attempted operative repair. Two patients who had the AAA resected because of suspected rupture were found later to have ruptured a more proximal AD. Thus, AD occurs occasionally in patients who have AAA. In older persons with suspected rupture of an AAA, a more proximal rupture of an AD should be ruled out. When both AAA and AD are present in the same patient, the AD is more likely the cause of cardiovascular collapse than is rupture of the AAA.
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PMID:Combined thoracic aortic dissection and abdominal aortic fusiform aneurysm. 843 Oct 87

Atherosclerosis was diagnosed on necropsy in 21 dogs in a 14-year period. Nine dogs died and 12 were euthanatized because of complications associated with the disease. The mean age was 8.5 +/- 0.5 years; 18 dogs were male. Three breeds (Miniature Schnauzer, Doberman Pinscher, and Labrador Retriever) had a higher prevalence of the disease than other breeds in the canine necropsy population of The Animal Medical Center. Most common clinical signs were lethargy, anorexia, weakness, dyspnea, collapse, and vomiting. Hypercholesterolemia, lipidemia, and hypothyroidism were common in affected dogs tested, and protein electrophoresis revealed high values for alpha 2 and beta fractions in all dogs tested. Electrocardiography indicated conduction abnormalities and myocardial infarction in 3 of 7 dogs. Necropsy revealed that affected arteries (including coronary, myocardial, renal, carotid, thyroidal, intestinal, pancreatic, splenic, gastric, prostatic, cerebral, and mesenteric) were yellow-white, thick and nodular, and had narrow lumens. Myocardial fibrosis and infarction also were observed in the myocardium. Histologically, affected arterial walls contained foamy cells or vacuoles, cystic spaces, mineralized material, debris with or without eroded intima, and degenerated muscle cells.
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PMID:Clinical and pathologic findings in dogs with atherosclerosis: 21 cases (1970-1983). 374 84

An association of alcoholic cirrhosis of the liver, hepatoma, extensive aortic thrombosis, and chronic bleeding peptic ulcer of the duodenal bulbus in a patient who survived only three days after hospitalisation is reported. An explanation of each disease is given and the fact that a basically hypocoagulative situation (cirrhosis) can give rise to thrombosis of the aorta is stressed. Production and release into the circulation of thromboplastins by the hepatoma (paraneoplastic syndrome), leading aortic atherosclerosis and slow circulation due to haemorrhagic cardiocirculatory collapse was the most likely explanation.
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PMID:[Association of liver cirrhosis, hepatoma, extensive aortic thrombosis and chronic duodenal peptic ulcer in the same patient]. 626 18

An observation of adrenergic myocarditis with clinical and electrical signs of coronary failure is reported. The patient had electrical and enzymatic manifestations of acute anteroseptal necrosis, complicated at the acute stage by complete atrioventricular block and fatal vasoplegic circulatory collapse. Post-mortem examination showed obstructive atherosclerosis of the anterior interventricular artery without anatomic signs of infarction. Pathogenesis of this coronary failure is discussed. In this case, functional coronary insufficiency produced by catecholamine release was associated with coronary atherosclerosis.
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PMID:[Early coronary atherosclerosis in a malignant pheochromocytoma. Apropos of a case]. 632 81

Morphologic changes in the subendocardial myocardium that appeared to be caused by severe, chronic subendocardial ischemia were studied in patients with fatal ischemic heart disease admitted to the Specialized Center of Research for Ischemic Heart Disease at the University of Alabama in Birmingham in the period 1970--1977. Thirteen patients were selected for this report on the basis that they had the lesions in the subendocardial myocardium we believe to have been caused by subendocardial ischemia and had no evidence of acute or remote myocardial infarction or other conditions that may have contributed to their terminal illness or death. Clinical findings were unstable angina, congestive heart failure, usually no increase in plasma enzymes indicative of myocardial damage, and electrocardiographic changes consistent with subendocardial ischemia. All 13 patients had 75% or greater stenosis of the three major coronary arteries; none had acute thrombotic or embolic coronary artery occlusion. The left ventricle in all cases was hypertrophied. The subendocardial myocardium showed circumferential pallor, hyperemia, or focal fibrosis without perceptible loss of volume in papillary muscles or trabeculae carneae. Microscopically, acute lesions showed one to two layers of preserved myofibers adjacent to the endocardium, vacuolar change in the deeper fibers, and focal areas of coagulation necrosis of variable size in the myocardium external to the fibers with vacuolar change. Coagulation necrosis was extensive in some cases and usually was not associated with infiltration of neutrophils. The repair reaction involved removal of necrotic sarcoplasm by mononuclear phagocytes, resulting in a reticular-appearing tissue without evidence of stromal collapse. Granulation tissue was not seen. Collagen fibers appeared to be deposited within the area of previous sarcolemmal sheaths. The distribution and morphology of subendocardial myocardial lesions associated with severe coronary atherosclerosis are distinctive and can be distinguished from myocardial necrosis or fibrosis associated with acute total occlusion of a coronary artery.
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PMID:Subendocardial ischemic myocardial lesions associated with severe coronary atherosclerosis. 736 50

Nourishment of arteries is accomplished by diffusion from the lumen of the vessel and from vasa vasorum. Most normal arteries have an extensive network of vasa in the adventitia that arise from branch points of parent arteries. When the thickness of arteries exceeds the ability of simple diffusion of nutrients from the lumen (larger muscular of atherosclerotic arteries), vasa extend into the media and intima. Vasa in the intima-media arise predominantly from adventitial vasa, but can arise from the lumen in vascular grafts and recanalized arteries after thrombosis. Vasa respond to vasoactive stimuli, and can regress after they vascularize arterial grafts and in response to regression of the atherosclerotic lesions. Therefore, vasa can increase blood flow to the artery wall by dilation of existing arteries or by formation of new vessels (neovascularization). Conversely, vasa can reduce blood flow to the artery wall by active constriction or by regression (involution) of existing vasa. The pathophysiological significance of vasa vasorum in normal and diseased arteries is related to their structure. Vasa in the intima-media are thin-walled endothelial cell tubes with thin or absent medial smooth muscle cells. Therefore, they are prone to collapse and rupture in response to arterial pressure, mechanical forces in the artery, necrotic substances found in diseased arteries, and vasospasm. Vasa also provide the artery with a vast absorptive endothelial surface that may have important implications for arterial lipid kinetics, and delivery and removal of neurohumoral agents from the artery wall. These properties have lead to speculation about their role in the pathogenesis of atherosclerosis, plaque rupture and thrombosis, medial ischemia leading to arterial dissection and aneurysm, restenosis after angioplasty, and post-stenotic dilatation. Finally, larger veins also have an extensive network of vasa that have been implicated in the pathogenesis of venous thrombosis and varicose veins.
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PMID:[The vasa vasorum of the arteries]. 898 46

To better characterize the heavy proteinuria occasionally described in cholesterol atheroembolic renal disease (CAE), we reviewed the clinical features and histological findings of 24 patients found at renal biopsy to have CAE. Twelve (50%) had a typical clinical presentation soon after an invasive vascular procedure. Eight (33%) underwent biopsies to evaluate proteinuria and four (17%) with insidiously developing renal failure to exclude rapidly progressive glomerulonephritis. All had usual and similar risk factors for CAE; 71% were male, 96% had peripheral vascular disease, 79% had recently undergone an invasive vascular procedure, 74% were hypercholesterolemic, and all were hypertensive. Proteinuria was higher and serum creatinine lower in the proteinuria group. In the nine (38%) nephrotic patients, serum creatinine measurements were lower (2.7 +/- 1.2 v 5.6 +/- 2.4 mg/dL), duration of renal disease to biopsy longer, and time from biopsy to dialysis greater (23.5 +/- 14.8 v 0.03 +/- 0.098 mo, P < 0.05 for all). Focal segmental glomerulosclerosis (FSGS) was observed in 15 (63%) of the biopsy specimens. Although FSGS itself did not occur more commonly in nephrotic patients, these patients did have a higher fraction of segmentally sclerosed glomeruli (0.158 +/- 0.097 v 0.026 +/- 0.050, P < 0.01). A variant of FSGS, the cellular lesion with epithelial cell prominence and capillary loop collapse, was observed in 7 of 9 (78%) patients with nephrotic-range proteinuria, but in only 3 of 12 (25%) patients with lesser degrees of protein excretion (P < 0.05). The cellular lesion was accompanied by higher mean proteinuria, 7.6 +/- 4.3 versus 2.1 +/- 2.4 g/24 hr (P < 0.01). In a larger group of patients with a similar age range as the CAE group who were identified by search of a computerized biopsy database, membranous nephropathy was the only other form of idiopathic glomerulonephritis that occurred with CAE. One of 82 (1.2%) patients with membranous nephropathy also had CAE, compared with 20 of 102 (19.6%) with FSGS (P < 0.0002, chi2). Thus, the finding of FSGS with CAE was not coincidence. Mean follow-up was 20 +/- 26 months (range, 0 to 103 months). Six patients (25%) were followed-up at least 3 years after renal biopsy. These findings indicate that extended survival in CAE is not rare and that heavy proteinuria occurs as part of a chronic disorder with distinctive histological features. Cholesterol atheroembolism with FSGS should be considered in the differential diagnosis of nephrotic syndrome in elderly patients with advanced atherosclerosis.
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PMID:Focal segmental glomerulosclerosis associated with nephrotic syndrome in cholesterol atheroembolism: clinicopathological correlations. 904 Dec 8

The incidence of unilateral blindness and ophthalmoplegia after aneurysm surgery is very rare, but if it occurs, it is mainly caused by intra-operative nerve injury. We experienced 6 cases of unilateral blindness immediately after surgery for 3 recent years. These patients were classified into Hunt-Hess grade I to II except for one patient with III. All patients complained of visual loss with varying degree of lid oedema and ophthalmoplegia ipsilateral to the site of surgery. Angiographic examination of these patients revealed that the aneurysm was located at the internal carotid artery bifurcation in one case and the middle cerebral artery bifurcation in five cases. All of them were relatively far from the optic nerve. The aneurysm was clipped easily with minimal brain retraction via standard pterional craniotomy since the brain was slack in all cases. In all cases, injuring the optic nerve during surgery was remote. All patients showed evidence of retinal ischaemia on fundoscopy with or without fluorescein angiography. The pathophysiology of this ischaemic event is unknown. In our patients, we could exclude possible aetiological factors such as abnormal systemic and ocular conditions, causing ischaemia in intra-orbital structures, increased intracranial pressure, intra-operative hypotension, carotid atherosclerosis, and ocular vasospasm etc. Accordingly we speculate that the complications seen in our cases were most likely related to intra-orbital ischaemia initiated by a collapse of the arterial and venous channels in the orbit and/or to direct or indirect contusion on the intra-orbital structures. These situations could be produced by inadvertent pressure placed on the eyeball with a bulky retracted frontal skin flap. Visual acuity in these patients ranged from no light perception to the ability to see objects and detect colour. Their conditions were irreversible. The degree of visual recovery seems to be dependent on the duration and severity of retinal ischaemia by orbital compression. Unfortunately there is no satisfactory treatment. We recommend the use of an eye shield to protect ipsilateral eyeball just before aneurysm surgery.
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PMID:Sudden unilateral blindness after intracranial aneurysm surgery. 914 88

Measurement of arterial compliance is of interest in evaluating patients with atherosclerosis and other diseases which affect the vessels. Arterial compliance is the relation between changes in transmural pressure and volume of an arterial segment, where a high compliance signifies large changes in volume per change in transmural pressure. The relation between changes in transmural pressure and volume is far from linear as compliance increases progressively with decreases in blood pressure. A change in compliance could indicate static changes in arterial wall composition, i.e. the relation between elastic and collagen fibres and accumulation of disease related deposits or dynamic changes caused by alterations in muscular tone. The most used method reflecting arterial compliance is the measurement of pulse wave velocity. However, the pulse wave velocity method measures compliance at ambient transmural pressures and is affected both by the actual blood pressure and the rate of pressure change. Another commonly used method employs the echo-tracking technique to measure the arterial diameter simultaneously with continuous blood pressure monitoring. By this method it is possible to calculate arterial compliance for continuous pressure values between the diastole and the systole. The volume-oscillometry method is based on the fact that the artery can be made to collapse at the end of the diastole by an occlusive cuff while it remains open in a pressure dependent manner during the rest of the cardiac cycle. Changes in the arterial volume is transmitted to the cuff, where it induces a measurable change in pressure, and hence the volume of the artery can be calculated at different values of transmural pressures. Using this method on normal subjects has shown that the arterial compliance decreases with increasing age and that females have lower compliance than males primarily due to a smaller diameter of their arteries. It has also been shown that patients with essential (diastolic) hypertension have compliances which are higher or equal to those of normal subjects, and that patients with systolic hypertension have lower arterial compliances than normal subjects. The former finding is in contrast with pulse wave velocity measurements, where diastolic hypertension was associated with low arterial compliance.
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PMID:Measurement of arterial compliance in vivo. 1097 6

Cardiogenic shock developed in a 72-year-old Japanese woman during combination therapy with verapamil and atenolol for recurrent supraventricular arrhythmia. She had coronary atherosclerosis, liver cirrhosis and bradycardia-tachycardia syndrome. Despite of the high-dose catecholamines and counterpulsation, she progressively deteriorated. Bolus administration of intravenous calcium chloride (CaCl2) immediately resolved her hemodynamic collapse.
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PMID:Cardiogenic shock triggered by verapamil and atenolol: a case report of therapeutic experience with intravenous calcium. 1111 Apr 38


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