Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arterial occlusive disease of the upper extremity is most often due to posttraumatic occlusion of the ulnar artery. An embolic source of the ischemia should be considered most strongly when sudden ischemia or vasospasm is associated with atrial fibrillation or follows a myocardial infarction. Connective tissue disorders and several arteridities are infrequent causes of upper-extremity occlusive disease and can usually be detected by a thorough peripheral vascular examination and blood studies. Atherosclerosis of the upper extremity is usually localized to the region of the subclavian artery and can present as a subclavian steal syndrome or arm ischemia. Finally, upper-extremity venous occlusive disease occurs in association with the hypercoagulable state, venous endothelial injury, or arises in otherwise healthy patients because of venous impingement in the thoracic outlet.
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PMID:Occlusive vascular disorders of the upper extremity. 844 72

Arterial occlusive disease (AOD) which is rarely described in patients with inflammatory bowel disease, is mainly associated with Crohn's disease (CD), and its etiology and natural course are unknown. We studied six patients (five women, one man) with CD and major lower extremity AOD who were treated at the Cleveland Clinic between 1985 and 1994. These were relatively young patients (age range 24-48 years) with steroid-dependent Crohn' colitis. On their presentation, five had acute onset of severe ischemic symptoms ("blue toe" syndrome in three) and one had rapid progression of claudication. All the patients had active CD and/or prior extensive bowel resections, and had no evidence of extraintestinal manifestation. Cardiovascular risk factors were smoking (n = 5), dyslipidemia (n = 3), family history of coronary artery disease (n = 3), premature menopause (n = 2), diabetes mellitus (n = 1). Arteriograms showed iliac artery involvement in all six patients and bilateral AOD in three. None of the patients had arteriographic or clinical signs of vasculitis. Five patients required arterial revascularizations, i.e., endovascular (n = 2), surgical (n = 2), and combined in one. Three patients had microscopic evidence of atherosclerosis. Lower extremity AOD in patients less than 50 yr of age and with CD may be partially related to premature atherosclerosis. Prospective screening for cardiovascular risk factors, subclinical disease, and hypercoagulability might be indicated in patients with active CD to prevent major arterial complications.
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PMID:Lower extremity arterial occlusions in young patients with Crohn's colitis and premature atherosclerosis: report of six cases. 906 77

Arterial occlusive disease is one of the leading causes of organic erectile dysfunction (ED). Recent studies have shown that the incidence of cardiovascular disease closely correlates with the prevalence of ED. Also, ED is thought to be an early signal of impending cardiovascular problems. We previously found that the atherosclerosis of iliohypogastric arteries in the rabbit causes ED, down-regulates cavernosal neuronal nitric oxide synthase (nNOS) gene expression, and impairs NO synthesis. The goal of this study was to determine the effect of atherosclerosis-induced ischemia on cavernosal nNOS, endothelial NOS (eNOS), and inducible NOS (iNOS) expression and NO-mediated smooth muscle relaxation in the rabbit. Our study showed that iliac artery blood flow, intracavernosal blood flow, and intracavernosal oxygen tension were unchanged 4 weeks after the induction of arterial atherosclerosis, whereas they were significantly diminished at weeks 8 and 16. Erectile responses to nerve stimulation and cavernosal smooth muscle relaxation were unchanged at week 4 and were significantly diminished at weeks 8 and 16 after the induction of atherosclerosis. Western blotting showed that cavernosal nNOS and eNOS protein levels were unaffected at week 4 but were significantly decreased at weeks 8 and 16 after the induction of atherosclerosis. iNOS protein, however, markedly increased during the course of the induced arterial disease. Immunohistochemical staining showed no change in cavernosal eNOS or nNOS expression at week 4. A dramatic decrease in both was evident at 8 and 16 weeks. iNOS expression progressively increased between 4 and 16 weeks of atherosclerosis. Down-regulation of nNOS and eNOS, along with up-regulation of iNOS, may explain ischemic cavernosal smooth muscle relaxation impairment in the rabbit. Ischemically altered NOS expression may be of great pathophysiologic importance in atherosclerosis-induced ED. These data may provide further insight into the mechanism of arteriogenic ED.
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PMID:Effect of chronic ischemia on constitutive and inducible nitric oxide synthase expression in erectile tissue. 1506 16

Arterial occlusive disease of supraaortic vessels, particularly the subclavian and innominate arteries, is infrequent. Hemodynamically significant proximal lesions of all supraaortic arteries are uncommon and the combination with coronary artery disease is even rarer. So far, the surgical management and operative timing of patients with coexisting severe disease of brachiocephalic and heart vessels is still a matter of debate. We report the case of a patient with severe polydistrectual atherosclerosis treated with single-stage aorto-carotid, carotid-subclavian and aortocoronary bypass.
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PMID:Diffuse atherosclerosis of thoracic aorta involving supraaortic and coronary arteries: single-stage surgical revascularization. 1901 18