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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The writer discusses the progress of atherosclerosis of the lateral vessels of the tongue and also demonstrates the clinical and diagnostic value of observing these changes. On the lateral undersurface of the tongue, which is uniformly pink in young persons on account of the delicate and rich vascular network, blue and pointed nodules start to appear in the fourth decade. These nodules are pathological and represent venous dilatations and thromboses. In advancing age more and more vessels obstruct, and the reduction of perfusion causes in all individuals a paleness and advancing atrophy. Examination of this region discloses the state of the vascular system. The number, location and severity of the thromboses has an important relevance in the assessment of vitality and biological aging of the individual.
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PMID:[The natural progress of atherosclerosis of the lateral vessels of the tongue (author's transl)]. 119 5

Acute arterial occlusion in an extremity must be treated as a medical-surgical emergency since not only the affected limb is endangered, but the life of the patient as well. The cause of the acute occlusion is an embolism or in situ thrombosis. The most common source of embolism is the heart from which about 30% of the cardiac emboli obliterate the bifurcation of the femoral artery and about 4/5 of all emboli involve the extremities. Arterio-arterial emboli arise from aneurysms or from nonocclusive, ulcerated atheromatous plaques. Acute in situ thrombosis occurs mostly at the site of stenotic arteriosclerotic lesions. Aneurysms and dilated forms of atherosclerosis can be both the cause of in situ thrombosis as well as the source of an embolism. Differentiation between thrombosis and embolism can be extremely difficult but for acute treatment, however, it is of little relevance. There is a peak of both events in the seventh and eighth decades. On complete occlusion without adequate collaterals, the presentation is characterized by "the six Ps": pain, pallor, pulselessness, paresthesia, paralysis and prostration. With acute occlusion of central points such as the aortic bifurcation or the femoral artery bifurcation, there is complete ischemia with onset of rhabdomyolysis after four to six hours which can lead to severe local and generalized symptoms due to the dangerous metabolites released. In contrast, occlusion of isolated lower leg arteries usually only lead to transient symptoms. If arterial occlusion is suspected, prior to transportation to the hospital, 5000 I.E. heparin should be given intravenously. Acute thrombotic occlusion of large arteries is the surgical domain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Therapy of acute peripheral arterial occlusion]. 183 82

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

Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are common diseases in the elderly. The arteritis usually affects medium sized vessels, but large vessel involvement can also occur leading to arm claudication, bruits, loss of pulses and pallor of the upper extremities. The differential diagnosis of large vessel arteritis includes atherosclerosis and Takayasu's disease. Atherosclerosis, which affects patients of similar age to GCA is usually confined to the lower limbs and can be differentiated on the basis of the clinical setting and investigations such as the ESR, arteriography and temporal artery biopsy. Takayasu's arteritis' although histologically and arteriographically indistinguishable from GCA, is predominantly a disease of young women. A patient is described who presented with upper limb ischemia. A clinical examination revealed absence of right radial pulses and presence of murmurs at level of the carotids. The blood pressure was unrecordable in the upper right limb. The ESR was 102 mm/hr and the C-reactive protein was 11.66 mg/dl. A selective arteriography of the aortic arch and its branches revealed a right subclavian artery obstruction with good collateral circulation and a left subclavian artery stenosis. The biopsy of left temporal artery showed a typical GCA in acute stage. Treatment with prednisolone 30 mg/day was started and four weeks later, the ESR had fallen to normal. In addition this case confirms that PMR implies a systemic arteritis.
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PMID:[Giant cell arteritis and polymyalgia rheumatica presenting as subclavian artery obstruction]. 823 15

Central retinal artery occlusion occurs most commonly between the ages of 50 and 70 years, and nearly one-half (45%) of patients also have carotid artery disease. Other causes of vision-threatening vascular disease include atherosclerosis, embolism, hypertension, diabetes mellitus, and valvular disease. Symptoms vary, depending on the ocular structures involved. The patient's symptoms are an important clue to the diagnosis of peripheral or posterior retinal vascular occlusion, macular blood vessel disease, intravitreal hemorrhage, optic nerve ischemia, and ocular ischemic syndrome. The patient's ocular symptoms should lead to investigation for clinical signs of ocular vascular disease (eg, hemorrhage, "hard" or "soft" exudates, neovascularization, retinal edema, pallor, emboli, vessel narrowing, or atriovenous crossing changes).
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PMID:Ocular vascular disease: in-office primary care diagnosis. 843 37

We report a 91-year-old man who had a stroke and died of renal failure. He had been treated for hypertension since 20 years before the onset of the present illness. In addition, he was operated on a gastric cancer 17 years previously. Otherwise he was doing well until May 29, 1991 (when he was 87-year-old) when he had sudden onset of dysarthria and right facial weakness. He was admitted to our hospital. On admission, general physical examination was unremarkable, and neurologic examination revealed a mentally sound man with slight dysarthria, right facial weakness, orolingual dyskinesia, and dysequilibrium in which he showed difficulty in tandem gait; however, no cerebellar ataxia was noted. A cranial CT scan revealed leukoaraiosis with multiple low density areas in the cerebral white matter. His BUN was 37 mg/dl and Cr 2.2 mg/dl. His neurologic symptoms cleared within the next few weeks and he was discharged with ticlopidine 100 mg q.d.. He had been doing well after the discharge except for gradual worsening of his renal function; his BUN was 65 mg/dl and Cr 3.27 mg/dl in April of 1994. On March 10, 1995, he fell down and hit his back; he became unable to walk because of pain, and he was admitted again on March 16, 1995. On admission, his blood pressure was 170/80 mmHg. There was an 1 + pitting pretibial edema; otherwise general physical examination was unremarkable. Neurologic examination revealed an alert and oriented man, however, Hasegawa's dementia scale was 23/30. Higher cerebral functions as well as cranial nerves were intact. He showed some unsteadiness of gait, however, no motor weakness or ataxia was noted. Deep tendon reflexes were diminished, but Chaddock sign was positive bilaterally. Vibration was diminished in the feet, however, pain and touch sensations were intact. Laboratory examination revealed a compression fracture of the twelfth thoracic vertebra. Blood count and chemistries were as follows; Hb 7.6 g/dl, Hct 23.3%, TP 6.0 g/dl, Alb 3.6 g/dl, BUN 87 mg/dl, Cr 4.53 mg/dl, T-Chol 174 mg/dl, HDL-Chol 49 mg/dl, Glu 156 mg/dl, Na 142 mEq/L, K 5.4 mEq/L, Cl 115 mEq/L. A urine specimen contained 1 + protein and 1 + glucose, and the sediments contained hyaline casts. A cranial CT scan was essentially same as that taken four years ago. His hospital course was complicated with pneumonia, congestive heart failure, and progressive renal failure. He was treated with intravenous fluid, chemotherapy, and other supportive measures, however, he expired from respiratory failure on April 30, 1995. He was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had Binswanger's disease in the brain, benign nephrosclerosis from arteriolosclerosis due to hypertension, congestive heart failure, and pneumonia. Opinions were divided regarding the question as to whether or not this patient had Binswanger's disease. Although his cranial CT scan revealed leukoaraiosis, his dementia and gait disturbance was only mild until his fall on March, 1995. Clinical features did not conform to those of Binswanger's disease. Postmortem examination of the right hemisphere revealed wide spread atherosclerosis and arteriolosclerosis. The kidney showed benign nephrosclerosis due to arteriolosclerosis. Sclerotic changes were also seen in the coronary arteries and the left middle cerebral artery with 70% stenosis. Myelin stain showed diffuse myelin pallor of the cerebral white matters with scattered small infarcts. Arterioles in the white matter showed arteriolosclerosis. Small infarcts were also seen in the putamen and in the thalamus. This patient appeared to have had circulatory disturbance of the white matter which is the basic abnormality causing Binswanger's disease. However, white matter changes in this patient were not quite severe enough to make a pathologic diagnosis of Binswanger's disease.
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PMID:[A 91-year-old man with a stroke, hypertension, and renal failure]. 899 Apr 84