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Littérature scientifique sur le sujet « Peripheral arterial obliterative disease »

Auteur : Grafiati
Publié le 9 mars 2023
Mis à jour le 10 mars 2023

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Articles de revues sur le sujet "Peripheral arterial obliterative disease"

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Montron, Armelle, Eric Guignard, Alain Pelc et Sylvie Comte. « Peripheral Arterial Obliterative Disease ». PharmacoEconomics 13, no 1 (1998) : 51–59. http://dx.doi.org/10.2165/00019053-199813010-00005.

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Landi, Anna, et István Jassó. « Peripheral arterial obliterative disease and physical activity ». Orvosi Hetilap 148, no 23 (1 juin 2007) : 1059–65. http://dx.doi.org/10.1556/oh.2007.28141.

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Az arteriosclerosis obliterans az atherothrombosis egyik karakterisztikus klinikai manifesztációja. Előfordulása 2–3%, tehát Magyarországon 2–300000 beteggel kell számolni. Gyakori az együttes előfordulása a coronariasclerosissal és a carotisrendszer atherothromboticus megbetegedésével. A perifériás obliterativ verőér-megbetegedés terápiájában a rendszeres fizikai tréning alapvetően fontos. Az arteriosclerosis obliterans kezelése a társult atheroscleroticus betegségek előfordulását, illetve kimenetelét is befolyásolja. A rendszeres fizikai tréning fő célja a perifériás érbetegek életminőségének javítása, az alsó végtagok funkcionális kapacitásának növelése. A reguláris, egyénre szabott járatás, tornagyakorlatok több olyan folyamatot indítanak el a szervezetben, melyek az atherosclerosis kialakulását, tovahaladását gátolják. Tréning alatt számolni kell a stenoticus érszakasz nyomásgrádiens-növekedéséből és a kollaterálisok megnyílásából álló hemodinamikai változásokkal, az endothel diszfunkció javulásával, a terhelésre jó irányba módosuló vascularis válasszal. A kórképet jellemző diszlipidémiát kedvezően befolyásolja; az LDL-koleszterint csökkenti, a HDL-t növeli. Jótékonyan befolyásolja a vér reológiai tulajdonságait is. A vázizomzatban strukturális változásokat hoz létre, az anyagcsere oxidációs folyamatainak enzimkoncentrációját növeli, és fokozza a célzott vázizomzat rostjainak kapilláris ellátottságát. Az eddig publikált adatok szerint a claudicatio intermittens kezelésében legelőnyösebben legalább heti 3 alkalommal végzett, 30–60 percen át tartó, 5–5 perces bemelegítést és levezetést is tartalmazó, szakember által irányított 3–6 hónapos, járásgyakorlatok formájában kivitelezett tréningkurzus ajánlatos. Az otthon végzett gyakorlatok hasznossága is figyelemre méltó.
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ROSSI, M., et A. CARPI. « Skin microcirculation in peripheral arterial obliterative disease ». Biomedecine & ; Pharmacotherapy 58, no 8 (octobre 2004) : 427–31. http://dx.doi.org/10.1016/s0753-3322(04)00114-3.

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Rossi, M., et A. Carpi. « Skin microcirculation in peripheral arterial obliterative disease ». Biomedicine & ; Pharmacotherapy 58, no 8 (octobre 2004) : 427–31. http://dx.doi.org/10.1016/j.biopha.2004.08.004.

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Coccheri, S., G. Palareti et G. Fortunato. « Antithrombotic Drugs in Peripheral Obliterative Arterial Diseases ». Pathophysiology of Haemostasis and Thrombosis 24, no 2 (1994) : 118–27. http://dx.doi.org/10.1159/000217091.

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Materazzi, M., L. Ralli, A. Bianciardi, L. Domini, A. Monaci, D. Pieragalli, A. Acciavatti, C. Galigani, S. Forconi et T. DiPerri. « Arterial-venous differences in metabolic and rheological parameters in peripheral obliterative arterial disease patients ». Clinical Hemorheology and Microcirculation 7, no 2 (9 décembre 2016) : 253–60. http://dx.doi.org/10.3233/ch-1987-7209.

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Darius, H., V. Hossmann et K. Schrör. « Antiplatelet effects of intravenous iloprost in patients with peripheral arterial obliterative disease ». Klinische Wochenschrift 64, no 12 (juin 1986) : 545–51. http://dx.doi.org/10.1007/bf01735317.

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Despotovic, Nebojsa, et Mihajlo Zdravkovic. « Multiple arterial disease in clinical practice ». Srpski arhiv za celokupno lekarstvo 130, no 9-10 (2002) : 316–19. http://dx.doi.org/10.2298/sarh0210316d.

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There is a significant correlation among obliterate lesions of coronary carotid and peripheral arteries of the lower arteries at the same time. This pointed out that whenever clinical manifestations of obliterate disease of peripheral arteries are present. There is also need for routine examination of existent coronary artery disease. In the case of concomitant significant coronary and carotid vascular disease there is a question what should be operated first. The most vascular centres prefer carotid endarterectomy before aortocoronary bypass, and if there is nonstable coronary disease simultaneous carotid endarterectomy and aortocoronary bypass should be carried out.
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Skórkowska-Telichowska, Katarzyna, Rajmund Adamiec, Dominika Tuchendler et Kazimierz Gąsiorowski. « Susceptibility to apoptosis of lymphocytes from patients with peripheral arterial disease ». Clinical & ; Investigative Medicine 32, no 5 (1 octobre 2009) : 345. http://dx.doi.org/10.25011/cim.v32i5.6922.

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Purpose. To determine, in vitro, the susceptibility to apoptosis of lymphocytes from patients with peripheral arterial disease (PAD) in the presence of a low culture medium serum concentration, and to evaluate the correlation of the degree of apoptosis and the serum lipid levels. Methods. Lymphocytes were isolated from the venous blood of PAD patients with lower limb ischemia secondary to obliterative atherosclerosis of Fountain stage IIb. None of the patients had received hypo-lipemic therapy. The lymphocytes were incubated for 48 hr in media containing reduced concentrations of fetal calf serum. The study group consisted of 10 patients (7 men and 3 women), with a mean age of 67.0 ± 4.0 yr. The control group consisted of ten healthy volunteers, of the same mean age and sex proportion as the study group. Results. The percentage of non-apoptotic lymphocytes was lower (by 17%) and the percentage of late apoptotic lymphocytes was higher (by 33%) in the PAD patients than in the healthy donors when comparing the slopes of regression lines describing the relation between frequency of apoptotic lymphocytes in culture media containing reduced concentration of fetal calf serum The percentage of late apoptotic lymphocytes was correlated with the levels of total cholesterol (rs=0.93; P < 0.01) and LDL cholesterol (rs=0.80; P < 0.01) , and negatively correlated with the level of triglycerides (rs=-0.71; P < 0.05). Conclusion. The results of this study of lymphocyte apoptosis are important in understanding of the disease pathogenesis and should be taken into account in elaboration of treatment strategies.
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Rosato, Maria Laura, Luca Schiaffino, Margherita Luongo, Luigi Mascolo, Silvana Mattera et Marco Mainini. « Oxygen-ozone therapy effects on PaO2 value in a diabetic patient suffering from chronic peripheral obliterative arteriopathy ». Ozone Therapy 1, no 1 (5 avril 2016) : 21. http://dx.doi.org/10.4081/ozone.2016.5843.

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We define chronic occlusive arterial disease of the extremities (COAD) as the aging process of the arterial vessel wall, characterized by the formation of atherosclerotic plaques. Patients suffering from COAD often refer induced pain exercise. Previous studies described benefic effects of oxygen-ozone (O<sub>2</sub>-O<sub>3</sub>) therapy in treatment of COAD. We describe a case of a 69-year old man, suffering from COAD, treated with O<sub>2</sub>-O<sub>3</sub> therapy. The aim of our report was to evaluate not only the effects of the oxygen-ozone therapy on the patient, but also the influence of this method on the arterial partial pressure of oxygen value.
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Thèses sur le sujet "Peripheral arterial obliterative disease"

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TOLVA, VALERIO STEFANO. « A successful experimental model for intimal hyperplasia prevention using a resveratrol delivering balloon ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/76760.

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Restenosis due to intimal hyperplasia is a major clinical problem that compromises the success of angioplasty and endovascular surgery. The pathogenesis of restenosis is multifactorial, involving such events as endothelial injury, inflammation, platelet activation, and hyperplasia of the intima, primarily due to vascular smooth muscle cell replication (vSMC). The incidence of intimal hyperplasia varies in different risk populations, e.g., diabetic patients, up to 35% of whom require bare metal stent implantation; clinical evidence has shown that this value is reduced but continues to cause problems after the implantation of drug-eluting stents (DES). Overall, however, despite many years of clinical experience with drug-eluting balloons (DEB), the number of large, high-quality, randomised clinical trials is low, and further data are urgently needed across the spectrum of clinical indications. Taxol and other cytostatic drugs destroy a cell's ability to use its cytoskeleton in a flexible manner, and, considering the clinical results, further research on a more physiologic mechanism of action should be pursued. Antioxidants are currently under investigation due to their protective activity within the vessels. Rosenbaum et al. showed that the endothelialisation of prosthetic grafts was significantly reduced, and anastomotic hyperplasia, significantly increased in rabbits on a high cholesterol diet. Treatment with an antioxidant improves endothelial cell coverage, decreases intimal hyperplasia and reduces oxidative stress, promoting the patency of prosthetic grafts. Resveratrol is a polyphenolic phytoalexinic antioxidant that is produced by grapes and other plants in response to injurious infections. The molecular structure of RSV, unfortunately, reduces its immediate clinical application for three main reasons: 1) its status as a highly lipophilic molecule; 2) its fast drifting from the TRANS- to CIS-phase, representing an oxidised and inactive state, respectively; and 3) its low circadian bioavailability for rapid hepatic metabolism. As consequence of these features, the oral bioavailability of RSV is negligible since it is rapidly conjugated to improve the solubility of the compound. The disposition of 14C-labeled RSV, as orally and intravenously administered in normal, healthy volunteers, was evaluated to estimate the extent of the oral dose absorbed, the bioavailability of the unchanged drug, and the drug’s metabolic phase. RSV demonstrated a high oral absorption but a rapid and extensive metabolism, resulting in only trace amounts of unchanged RSV remaining until systemic circulation. Five major metabolites were detected in the urine samples14, plasma and colo-rectal cancer tissues, although all were only measured qualitatively due to a lack of available reference materials. Metabolite 1 (M1) was a RSV monoglucuronide, and metabolite 2, an isomeric RSV monoglucuronide (M2), was found in greater abundance. M3 was a dihydroresveratrol monoglucuronide, whereas M4 and M5 were two poorly resolved RSV sulphates, i.e., a resveratrol monosulphate (M4) and a dihydroresveratrol sulphate (M5). Despite the controversial results on the efficacy of RSV reported in the literature, very recent data obtained in colon cancer cells have supported the notion that RSV, in spite of its low bioavailability, is able to act through its metabolites, mainly the sulpho-conjugate but also the combination of sulphate/glucuronide derivatives. Despite the wide literature on RSV, only few preclinical studies have demonstrated the efficacy of RSV in an animal model or investigated the possibility of locally administering this antioxidant by eluting stents. Based on our experience, we decided to set up a sterile, injectable, and hydrophilic RSV-containing compound (RSV-c). This solution was locally administered in the common iliac artery of adult male New Zeeland white rabbits using a dedicated device.
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Sigvant, Birgitta. « Epidemiological aspects of peripheral arterial disease ». Stockholm : Department of Molecular Medicine and Surgery, Karolinska Institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-670-5/.

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Askew, Christopher D. « Exercise intolerance in peripheral arterial disease ». Thesis, Queensland University of Technology, 2002. https://eprints.qut.edu.au/15869/1/Christopher_Askew_Thesis.pdf.

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Patients with Peripheral Arterial Disease have a reduced capacity for exercise, the exact causes of which are poorly understood. This thesis investigated alternative testing procedures that aim to provide a more complete and precise description of the exercise capacities of these patients. Furthermore, the potential roles of gastrocnemius muscle fibre morphometry, capillary supply and glycogen stores in the exercise tolerance of PAD patients were studied. Study one aimed to determine the effect of test repetition on maximal exercise performance and test-to-test variability in PAD patients using an incremental treadmill walking test (T) (n=5), an incremental cycle test (C) (n=5), and incremental endurance (PF-endurance) and maximal strength (PF-strength) plantar flexion tests (n=5). Tests were conducted once per week for eight weeks. Performance was stable on the T (~530 s) and C (~500 s) tests across the eight weeks. Test-to-test variance on T decreased from 16%CV (CV: coefficient of variation) to 6%CV (p=.21,NS), and from ~8%CV to 2%CV on C (p<.05) over the eight week period. Variance of peak gas exchange variables tended to decrease with performance variance on both tests; however, other physiological variables, and the associated variance levels, were stable throughout the study. PF strength (635-712N) gradually increased over the initial 2-3 weeks (p<.05) which was accompanied by a reduction in variance from ~8%CV to ~3%CV (p<.05). Similarly, PF endurance increased over the first two weeks (~32,000 to 41500 N.s-1) while variance of this measure fell from ~21%CV to ~10%CV (p<.05) over the study duration. It is concluded that the implementation of familiarisation sessions leads to a reduction in whole body and local calf muscular performance variance in patients with PAD. Using a randomised crossover design, study two aimed to compare performance and the physiological and symptomatic responses between a T test and a C test in 16 patients with PAD. Peak exercise time on C (690 s) was greater than that on T (495 s); however the two were significantly correlated (n=16, r=.69, p<.05). Peak HR (120 bpm), VO2 (~1.22 l.min-1) and rate pressure product (~20') did not differ between the two tests, nor did the post exercise ankle pressure (T: 56; C: 61 mmHg). In two subjects with lower back pain during C, the ankle pressure of their "worst" limbs failed to fall by >10mmHg. Performance on both the T and C tests was closely related to the onset of leg symptoms; however the site of pain during C was much more variable than during T. Incremental cycle testing would overcome some of the limitations of treadmill testing (e.g. measurement of mechanical work), and it appears to be an acceptable alternative for measuring the exercise capacity and physiological exercise responses in known claudicants. Use of cycle ergometry for the diagnosis of PAD requires testing in the general population. Study three aimed to compare whole body (T test and C test) and local calf muscular (PF strength and endurance) exercise performance between 16 PAD patients (age: 63 ± 2; BMI: 25.9 ± 1.1) and 13 healthy, sedentary control (CON) subjects (age: 62 ± 1; BMI: 25.9 ± 0.4), and to describe relationships between the whole body and local calf muscular exercise capacities within the two groups. Furthermore, this study aimed to compare several histochemical characteristics of the medial gastrocnemius muscle fibres between PAD and CON, and to establish whether these factors were related to the exercise capacities of both groups. Maximal performance on T was 59% lower in the PAD group compared with the CON group, as was performance on C (50%), PF strength (25%), and PF endurance (58%). Compared with CON, PAD patients had a lower estimated calf muscle mass and a slight reduction (10%) in muscle fibre size (p=.14, NS). They also had a lower proportion of type I fibres (PAD: 49%; CON: 62%) that was offset by a greater proportion of type IIA fibres (PAD: 27%; CON: 16%), and a reduction in the capillary contacts per muscle fibre (PAD: 1.63; CON: 2.12) compared with CON. When expressed relative to fibre area there were no differences in capillarisation between PAD and CON; however this index was significantly related to resting and post exercise ABI in the PAD patients. There were no differences in the mixed muscle [glycogen], nor the optical density of glycogen in the individual fibres, between the two groups. PF endurance was poorly predictive of walking performance, and did not correlate with any of the morphological variables in both groups. Calf muscle mass correlated with PF strength (r=.59 - .62), and strength was correlated with T performance (r= .61 - .63) in both groups. In the PAD patients, T performance was correlated with the cross sectional area (n=12, r=.72, p<.05), capillary contacts (n=10, r=.81, p<.05) and glycogen density (n=9, r=.81, p<.05) of type I fibres. This study confirms that a reduction in calf strength, which appears to be mediated through muscle atrophy, plays some role in the reduced exercise capacity of claudicants. While both fibre area and capillary supply seem to be of relevance to the exercise capacity of PAD patients, these two factors are closely linked and further research is required to establish the determinants, and relative importance of both. An important, and possibly limiting role of carbohydrate oxidisation in PAD patients is supported by the strong relationship between type I glycogen stores and whole body exercise capacity.
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Askew, Christopher D. « Exercise intolerance in peripheral arterial disease ». Queensland University of Technology, 2002. http://eprints.qut.edu.au/15869/.

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Patients with Peripheral Arterial Disease have a reduced capacity for exercise, the exact causes of which are poorly understood. This thesis investigated alternative testing procedures that aim to provide a more complete and precise description of the exercise capacities of these patients. Furthermore, the potential roles of gastrocnemius muscle fibre morphometry, capillary supply and glycogen stores in the exercise tolerance of PAD patients were studied. Study one aimed to determine the effect of test repetition on maximal exercise performance and test-to-test variability in PAD patients using an incremental treadmill walking test (T) (n=5), an incremental cycle test (C) (n=5), and incremental endurance (PF-endurance) and maximal strength (PF-strength) plantar flexion tests (n=5). Tests were conducted once per week for eight weeks. Performance was stable on the T (~530 s) and C (~500 s) tests across the eight weeks. Test-to-test variance on T decreased from 16%CV (CV: coefficient of variation) to 6%CV (p=.21,NS), and from ~8%CV to 2%CV on C (p<.05) over the eight week period. Variance of peak gas exchange variables tended to decrease with performance variance on both tests; however, other physiological variables, and the associated variance levels, were stable throughout the study. PF strength (635-712N) gradually increased over the initial 2-3 weeks (p<.05) which was accompanied by a reduction in variance from ~8%CV to ~3%CV (p<.05). Similarly, PF endurance increased over the first two weeks (~32,000 to 41500 N.s-1) while variance of this measure fell from ~21%CV to ~10%CV (p<.05) over the study duration. It is concluded that the implementation of familiarisation sessions leads to a reduction in whole body and local calf muscular performance variance in patients with PAD. Using a randomised crossover design, study two aimed to compare performance and the physiological and symptomatic responses between a T test and a C test in 16 patients with PAD. Peak exercise time on C (690 s) was greater than that on T (495 s); however the two were significantly correlated (n=16, r=.69, p<.05). Peak HR (120 bpm), VO2 (~1.22 l.min-1) and rate pressure product (~20') did not differ between the two tests, nor did the post exercise ankle pressure (T: 56; C: 61 mmHg). In two subjects with lower back pain during C, the ankle pressure of their "worst" limbs failed to fall by >10mmHg. Performance on both the T and C tests was closely related to the onset of leg symptoms; however the site of pain during C was much more variable than during T. Incremental cycle testing would overcome some of the limitations of treadmill testing (e.g. measurement of mechanical work), and it appears to be an acceptable alternative for measuring the exercise capacity and physiological exercise responses in known claudicants. Use of cycle ergometry for the diagnosis of PAD requires testing in the general population. Study three aimed to compare whole body (T test and C test) and local calf muscular (PF strength and endurance) exercise performance between 16 PAD patients (age: 63 ± 2; BMI: 25.9 ± 1.1) and 13 healthy, sedentary control (CON) subjects (age: 62 ± 1; BMI: 25.9 ± 0.4), and to describe relationships between the whole body and local calf muscular exercise capacities within the two groups. Furthermore, this study aimed to compare several histochemical characteristics of the medial gastrocnemius muscle fibres between PAD and CON, and to establish whether these factors were related to the exercise capacities of both groups. Maximal performance on T was 59% lower in the PAD group compared with the CON group, as was performance on C (50%), PF strength (25%), and PF endurance (58%). Compared with CON, PAD patients had a lower estimated calf muscle mass and a slight reduction (10%) in muscle fibre size (p=.14, NS). They also had a lower proportion of type I fibres (PAD: 49%; CON: 62%) that was offset by a greater proportion of type IIA fibres (PAD: 27%; CON: 16%), and a reduction in the capillary contacts per muscle fibre (PAD: 1.63; CON: 2.12) compared with CON. When expressed relative to fibre area there were no differences in capillarisation between PAD and CON; however this index was significantly related to resting and post exercise ABI in the PAD patients. There were no differences in the mixed muscle [glycogen], nor the optical density of glycogen in the individual fibres, between the two groups. PF endurance was poorly predictive of walking performance, and did not correlate with any of the morphological variables in both groups. Calf muscle mass correlated with PF strength (r=.59 - .62), and strength was correlated with T performance (r= .61 - .63) in both groups. In the PAD patients, T performance was correlated with the cross sectional area (n=12, r=.72, p<.05), capillary contacts (n=10, r=.81, p<.05) and glycogen density (n=9, r=.81, p<.05) of type I fibres. This study confirms that a reduction in calf strength, which appears to be mediated through muscle atrophy, plays some role in the reduced exercise capacity of claudicants. While both fibre area and capillary supply seem to be of relevance to the exercise capacity of PAD patients, these two factors are closely linked and further research is required to establish the determinants, and relative importance of both. An important, and possibly limiting role of carbohydrate oxidisation in PAD patients is supported by the strong relationship between type I glycogen stores and whole body exercise capacity.
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Barker, Glenn A. « Carbohydrate metabolism in peripheral arterial disease ». Thesis, Queensland University of Technology, 2003. https://eprints.qut.edu.au/36790/1/36790_Digitised%20Thesis.pdf.

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Peripheral arterial disease results in varying degrees of functional disability. Although principally a disease of the vascular tree, evidence demonstrates a significant contribution from metabolic alterations within ischaemically affected skeletal muscle. This thesis was concerned with better characterising the nature of these metabolic alterations, and their contribution to the functional disability in PAD patients. It also examined the efficacy of dietary carbohydrate supplementation as a therapeutic intervention in PAD. The activity of the pyruvate dehydrogenase complex (PDH) is an important determinant of carbohydrate metabolism, experiment I examined the possibility that the active fraction of PDH (PDHa) is lower than normal in skeletal muscle of patients with intermittent claudication (IC) or patients with chronic limb ischaemia and rest pain (RP). A resting muscle biopsy was taken from the medial gastrocnemius of 11 patients with IC, seven patients with RP and eight healthy control subjects (CON). Biopsies were analysed for PDHa, acetylcarnitine, glycogen and phosphocreatine. In the RP group resting PDHa was 60 percent lower than CON (0.19 ± 0.21 versus 0.53 ± 0.27 mmol.min·1.kg·1 wet wt), but not significantly different (p = 0.09) from IC (0.42 ± 0. i 7 mmol.min·1.kg·1 wet wt); PDHa was not different between IC and CON (p = 0.54). There was no difference in muscle acetylcarnitine and glycogen between the groups, nor were there any associations between PDHa and resting acetylcamitine. Further work is warranted in determining the significance of the reduction in PDHa in the RP group, its relationship to symptoms and amenability to treatment. Study two examined the extent to which resting metabolic changes within ischaemic muscle account for the exercise intolerance in PAD patients with intermittent claudication. Specifically, study two tested the hypothesis that walking intolerance in intermittent claudication (IC) is related to both slowed whole body V02 kinetics and depressed activity of the active fraction of pyruvate dehydrogenase (PDHa) in skeletal muscle. Ten patients displaying IC and eight healthy controls performed two familiarisation and then three maximal incremental walking tests. From these tests averaged estimates of walking time, peak V02 and the time constant of V02 ('t) during submaximal walking were obtained. A muscle sample was taken from the medial gastrocnemius muscle at rest and analysed for PDHa and several other biochemical variables. Walking time and peak V02 were -50 percent lower in IC than controls, and 't was 2-fold higher (p < 0.05). 't was significantly correlated with walking time (r = - 0.72) and peak V02 (r = -0.66) in IC; but not in controls. Resting muscle PDHa tended to be correlated with 't (r = -0.56; p = 0.09) in IC; but not in controls (r = -0.14). A similar correlation was observed between resting ABI and 't (r = -0.63, p = 0.05) in IC. This data demonstrates that impaired V02 kinetics contribute to the reduced walking capacity in IC, and that slowed V02 kinetics may result from both haemodynamic and metabolic factors in claudicants. The final experiment examined the effects of a three-day dietary carbohydrate supplementation regime on walking capacity in claudications and in healthy control subjects. Previous work has demonstrated an ergogenic effect of CHO loading in claudicants, but failed to accurately quantify the magnitude of the improvement in walking capacity, or potential mechanisms involved in the effect. Continuing from study II, eleven PAD patients with intermittent claudication and eight control subjects performed a further two maximal treadmill tests, each preceded by a three day supplemental period. In a randomised blinded fashion, all subjects consumed a total of 700g of glucose polymer dissolved into 6 L of water (CHO), or an equal volume of artificially sweetened water (PLAC) (2Uday with meals). From baseline, walking time was significantly improved in the IC group (660 ± 331 s to 697 ± 313 s) and significantly reduced in the CON group (1335 ± 264 s to 1290 ± 250 s) following CHO. In the IC group the improvement in walking capacity was inversely associated with the initial walking capacity of the patient (r = -0.73, p < 0.05) such that for patients with an initial walking capacity of less than 400 s (n=4) there was a 23% improvement following CHO. Resting, steady state, peak V02 and the kinetics of the transitional response ('t) were unaffected by CHO, however there was an association between the change in walking time and change in 't in the IC group only (r = -0.70, p < 0.05). Resting, steady-state and maximal RER was significantly elevated following CHO in both groups. In the CON group the reduction in walking time was strongly associated with increases in body weight (r = 0.87, p < 0.05). There was no association between the change in walking performance and any muscle measure in the CON group, but in IC the improvement in walking time was inversely associated with resting PDHa (r = -0.65, p < 0.05). This data demonstrates the benefits of CHO supplementation are mainly confined to those patients with greater functional impairments and may be mediated via improvements in V02 uptake kinetics resulting from metabolic alterations within the exercising musculature.
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Bauer, Timothy Alan. « Oxygen uptake kinetics in peripheral arterial disease ». Diss., Manhattan, Kan. : Kansas State University, 2005. http://hdl.handle.net/2097/125.

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Welten, Gijs. « Prognosis of patients with peripheral arterial disease ». [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/13949.

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Widener, Jeanne Malcom. « Disease Severity and Disability in Persons with Peripheral Arterial Disease ». The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1204652303.

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Cleanthis, T. M. « Platelet function in lower limb peripheral arterial disease ». Thesis, University of Newcastle upon Tyne, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432504.

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Koelemay, Mark Jan Wilhelm. « Non-invasive assessment of peripheral arterial occlusive disease ». [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2001. http://dare.uva.nl/document/85398.

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Livres sur le sujet "Peripheral arterial obliterative disease"

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Coffman, Jay D., et Robert T. Eberhardt. Peripheral Arterial Disease. New Jersey : Humana Press, 2002. http://dx.doi.org/10.1385/1592593313.

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Dieter, Robert S. Peripheral Arterial Disease. New York : McGraw-Hill, 2009.

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R, Mohler Emile, Jaff Michael R et American College of Physicians, dir. Peripheral arterial disease. Philadelphia : American College of Physicians, 2008.

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1970-, Dieter Robert S., Dieter Ray A. 1934- et Dieter Raymond A. 1962-, dir. Peripheral arterial disease. New York : McGraw-Hill, 2009.

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Kramer, Christopher M., dir. Imaging in Peripheral Arterial Disease. Cham : Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-24596-2.

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Svante, Horsch, et Vleeschauwer Philippe de, dir. Topics in peripheral arterial disease. München : W. Zuckschwerdt Verlag, 1989.

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David, McManus, et Fisher Daniel Z, dir. Dx/Rx peripheral arterial disease. Sudbury, Mass : Jones and Bartlett Publishers, 2011.

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1928-, Coffman Jay D., et Eberhardt Robert T. MD, dir. Peripheral arterial disease : Diagnosis and treatment. Totowa, N.J : Humana Press, 2003.

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Yost, Mary L. Peripheral arterial disease : Underestimated, underdiagnosed, and undertreated. Atlanta, Ga.] : Sage Group, 2000.

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Shammas, Nicolas W. Saving legs, saving lives-- : Peripheral vascular disease made simple. Davenport, Iowa : Midwest Cardiovascular Research Foundation, 2010.

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Chapitres de livres sur le sujet "Peripheral arterial obliterative disease"

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Bomba, Giovina Lara, et Jonathan L. Halperin. « Peripheral Arterial Disease ». Dans Essential Cardiology, 781–96. New York, NY : Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6705-2_47.

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Rodríguez-Mañas, Leocadio, Marta Castro Rodríguez et Cristina Alonso Bouzón. « Peripheral Arterial Disease ». Dans Cardiovascular Disease and Health in the Older Patient, 345–65. Chichester, UK : John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118451786.ch14.

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Giri, Jay, et Emile R. Mohler. « Peripheral Arterial Disease ». Dans Comprehensive Cardiovascular Medicine in the Primary Care Setting, 311–23. Totowa, NJ : Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-963-5_16.

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Kanthi, Yogendra M., Christos Kasapis et Hitinder S. Gurm. « Peripheral Arterial Disease ». Dans Inpatient Cardiovascular Medicine, 126–37. Oxford : John Wiley & Sons Inc, 2013. http://dx.doi.org/10.1002/9781118484784.ch10.

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Ma˜nas, Leocadio Rodríguez, Marta Castro Rodríguez et Cristina Alonso Bouzón. « Peripheral Arterial Disease ». Dans Pathy's Principles and Practice of Geriatric Medicine, 517–27. Chichester, UK : John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781119952930.ch43.

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Kobayashi, Taisei, Jay Giri et Emile R. Mohler. « Peripheral Arterial Disease ». Dans Contemporary Cardiology, 337–47. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-97622-8_17.

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Sotoda, Yoko, et Ichiro Wakabayashi. « Peripheral Arterial Disease ». Dans Interdisciplinary Concepts in Cardiovascular Health, 115–45. Cham : Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-01074-8_6.

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Baker, Julien S., Fergal Grace, Lon Kilgore, David J. Smith, Stephen R. Norris, Andrew W. Gardner, Robert Ringseis et al. « Peripheral Arterial Disease ». Dans Encyclopedia of Exercise Medicine in Health and Disease, 697–700. Berlin, Heidelberg : Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_284.

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Watson, Lorna, et Gerry Fowkes. « Peripheral Arterial Disease ». Dans The Metabolic Syndrome, 263–77. Chichester, UK : John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470025131.ch10.

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Mañas, Leocadio Rodríguez, Cristina Alonso Bouzon et Marta Castro Rodríguez. « Peripheral arterial disease ». Dans Diabetes in Old Age, 55–66. Chichester, UK : John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781118954621.ch6.

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Actes de conférences sur le sujet "Peripheral arterial obliterative disease"

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Hossmann, V., H. J. Schäfer, H. Auel et H. Etti. « TREATMENT OF ADVANCED STAGES OF PERIPHERAL OBLITERATIVE DISEASE WITH THE THROMBOXANE RECEPTOR ANTAGONIST BM 13.177 : A PLACEBOCONTROLLED DOUBLE BLIND STUDY ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643471.

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Twenty patients (67.2 ± 12.3 yrs; aged 39-86 yrs, 10 males, 10 females) with stage IV of peripheral obliterative arterial disease received at random either a) BM 13.177, a thromboxane receptor antagonist, at a dose of 6 g/24 hrs for 7 days i.v., followed by oral treatment of 6.4 g/day in four doses for 2 weeks and a subsequent placebo week, or b) placebo alone with the same protocol. The clinical course was followed by measurement of blood pressure (by Riva-Rocci on the left brachial artery and by Doppler of the ankle artries), blood flow at restand after 3 min of tourniquet ischemia (by venous occlusion plethysmography), TcpCf2 at the wrist of the affected limb, and by subjective estimation of pain with visual analog scale before, at the end of the infusion period, as well as on day 7 and 14 of oral treatment, and 7 days after treatment while patients of both groups were on placebo. In addition spontaneous platelet aggregation by PAT III, induced platelet aggregation in whole blood by collagen and in PRP by ADP at different doses on the same days were measured on the same days as described above.Results: BM 13.177 completely inhibited aggregation in whole blood induced by collagen 0.3 (ig/ml, however one week after treatment a rebound phenomenon was observed with 16.0 ± 3.8 OHM compared to pretreatment value of 11.0 ± 3.8 OHM (p < 0.01). At a higher dose of 1.2 |ig/ml the same inhibiting effect on platelet aggregation was observed. Spontaneous platelet aggregation as measured by PAT III was evident in only 2/10 pat. pre-treatment, was abolished in all patients on i.v. BM 13.177, returned in 1/10 pat. during oral treatment, but in 4/10 pat. on day 7 after treatment, while being on placebo, again indicating a rebound phenomenon (p < 0.03) ADP induced platelet aggregation was not significantly affected by BM 13.177. In the placebo group, too, no significant differences were observable between the different treatment regimens. Clinical data did not show any significant alteration in either verum or placebo group during the six week period, indicating no benificial effect of thromboxane receptor antagonists in advanced stages of peripheral obliterative arterial disease, although platelet inhibiting effects were clearly demonstable.
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Palareti, G., P. Torricelli, M. Poggi, G. Fortunato, G. Oca et G. Coccheri. « LONG TERM EFFECTS OF TICLOPIDINE ON FIBRINOGEN AND HAEMORHEOLOGY IN PATIENTS WITH PERIPHERAL ARTERIAL DISEASES ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644211.

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Fibrinogen (Fgn) and haemorheologic parameters were serially measured in 44 pts (38 males, age 59+/−7) with claudicatio intermittens due to peripheral arterial obliterative disease (PAOD) treated for 24 months with Ticlopidine (T group, 250 mg b.i.d. p.os), or placebo (P group), in a double blind randomized controlled study, part of a larger clinical trial. Fgn (immunodiffusion), haematocrit (Ht, micromethod), whole blood viscosity (BV, Contraves LS 30, at 37 C) at high (94.5) and low (0.2 sec-1) shear rates (s.r.) and plasma viscosity (PV, Contraves LS 30) were measured three-monthly. The data were evaluated by means of ANOVA and Student's t test. The values in groups T and P did not differ at baseline except for greater BV at high s.r. in group P (p< 0.05). During the observation period circannual variations appeared especially in group T, where summer-time values for most parameters (Fgn, Ht, PV, low s.r. BV) were lower (significance from p<0.05 to <0.01) than the correspondent winter-time values, while a similar pattern was observed in group P only for PV (p<0.01). Fgn (p<0.05), Ht (p<0.01), and low s.r. BV (p<0.001) were significantly lowered in group T versus group P but only in the summer months (after about 1 year of treatment). In conclusion, this study proves that long-term Ticlopidine treatment in PAOD is associated with significant lowering of fibrinogen and “improvement” in haemoreologic tests although limited to the summer observations. Ticlopidine while positively interfering with haemorheology in PAOD may not counteract other mechanisms of rheologic deterioration probably occurring during winter. Long-term evaluation of drug effects should therefore take into account spontaneous or drug-enhanced seasonal changes of the investigated values.
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Torres-Sánchez, Irene, Marie Carmen Valenza, Francisco Manuel Cano Egea, Roberto Cruz-Ramírez, Isabel López-Torres et Irene Cabrera-Martos. « Peripheral arterial disease in COPD patients ». Dans Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa972.

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Makovec, Matej, Uros Aljancic, Danilo Vrtacnik et Borut Pecar. « Evaluation of peripheral arterial occlusive disease with arterial oscillograph prototype ». Dans 2018 41st International Convention on Information and Communication Technology, Electronics and Microelectronics (MIPRO). IEEE, 2018. http://dx.doi.org/10.23919/mipro.2018.8400059.

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Henry, Michel, Max Amor, Gerard Ethevenot, Isabelle Henry, Claude Amicabile, Richard Beron, Bernard Mentre et Mohamed Allaoui. « PALMAZ stent in the treatment of peripheral arterial disease ». Dans Europto Biomedical Optics '93, sous la direction de Kazuhiko Atsumi, Cornelius Borst, Frank W. Cross, Herbert J. Geschwind, Dieter Jocham, Jan Kvasnicka, Hans H. Scherer, Mario A. Trelles et Eberhard Unsoeld. SPIE, 1994. http://dx.doi.org/10.1117/12.169115.

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Sudarev, Alexey, et Evgeny Korotich. « The Method and Apparatus for Peripheral Arterial Disease Treatment ». Dans 15th International Conference on Biomedical Electronics and Devices. SCITEPRESS - Science and Technology Publications, 2022. http://dx.doi.org/10.5220/0010828100003123.

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Choi, Seok Cheol, Kyung Mo Oh, Hwa-Sik Choi et Kyung Yae Hyun. « The Physiological Factors affecting Peripheral Arteriosclerotic Index : Predictors of Peripheral Arterial Disease Risk ». Dans Bioscience and Medical Research 2014. Science & Engineering Research Support soCiety, 2014. http://dx.doi.org/10.14257/astl.2014.68.13.

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Terzikhan, Natalie, Lies Lahousse, Katia Verhamme, Oscar Franco, Guy Brusselle et Bruno Stricker. « Increased risk of peripheral arterial disease in individuals with COPD ». Dans ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa1567.

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Rasmussen, John C., Banghe Zhu, Aaron D. Sahihi, Melissa B. Aldrich, Susan M. Pouliot, Stuart A. Harlin, Kristofer M. Charlton-Ouw, Caroline E. Fife, Thomas F. O'Donnell et Eva M. Sevick-Muraca. « Visualizing lymphatic abnormalities in peripheral venous and arterial disease (Conference Presentation) ». Dans Biomedical Applications in Molecular, Structural, and Functional Imaging, sous la direction de Barjor Gimi et Andrzej Krol. SPIE, 2018. http://dx.doi.org/10.1117/12.2293589.

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Khaw, Kathryn, Susan M. Schultz, Mustafa Mohammed, Zhen Chen, Khalid Ashi et Chandra M. Sehgal. « Photoacoustic Imaging for Assessing Flow-Mediated Oxygenation for Peripheral Arterial Disease ». Dans 2018 IEEE International Ultrasonics Symposium (IUS). IEEE, 2018. http://dx.doi.org/10.1109/ultsym.2018.8580057.

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Rapports d'organisations sur le sujet "Peripheral arterial obliterative disease"

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Alshammari, Mohammed Kanan. Efficacy of Complementary and Alternative Medicine in Peripheral Arterial Disease : A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, mars 2023. http://dx.doi.org/10.37766/inplasy2023.3.0001.

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Review question / Objective: To explore various CAM therapies available and to generate evidence that these therapies are effective for managing the disease. Condition being studied: Peripheral arterial disease (PAD) is described as the atherosclerotic process of arteries other than cerebral and coronary arteries i.e. the abdominal aorta, iliac, and arteries of the lower limb which leads to the narrowing and blocking of arteries. Information sources: An online systematic literature search will be done from the time of database inception from 5 electronic databases namely PubMed, Cochrane Central Register of Controlled Trials (CENTRAL), Ovid SP, ISI Web of Science, Elsevier Science Direct, and Wiley Online Library.
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Smolderen, Kim, John Spertus, Dave Safley, Mehdi, Shishehbor, Mansoor Qureshi, Peter ,. Soukas, Dawn Abbott et al. Treatment and Patient Characteristics Affecting the Health Status of Patients with Peripheral Arterial Disease ‐‐ The PORTRAIT Study. Patient‐Centered Outcomes Research Institute (PCORI)., avril 2019. http://dx.doi.org/10.25302/4.2019.ce.13046677.

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Drug coated balloons have some short-term benefits for peripheral arterial disease. National Institute for Health Research, janvier 2017. http://dx.doi.org/10.3310/signal-000358.

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Rivaroxaban plus aspirin may reduce heart attack and strokes in people with peripheral arterial disease, but with an added risk of bleeding. National Institute for Health Research, février 2018. http://dx.doi.org/10.3310/signal-000554.

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