Peripheral Arterial Disease
Original Editors - Students from Glasgow Caledonian University's Cardiorespiratory Therapeutics Project.
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Definition/Description[edit | edit source]
Definition of the disease or condition
Epidemiology[edit | edit source]
In the United Kingdom, an estimated 500-1000 new cases of PAD are diagnosed per million each year[1][2]. Patients at high risk of PAD are those with cardiac disease, diabetes mellitus, older than 70 years or 50 years old with multiple cardiovascular factors[3]. These factors include smoking, dyslipedmia, dysglycemia, hypertension, family history of atherosclerotic vascular disease. In lower socioeconomic areas, PAD is more frequent as a result of increased incidence of smoking [4]. Some studies report no difference in prevalence between the sexes [3], however, other studies have found a 3:1 ratio comparing men to women[4][1]. A few studies have suggested that black non-Hispanics have an increased prevalence of PAD, with a reported 2.39 to 2.83 odd ratio. Although, a study that controlled for atherosclerotic risk factors found a small difference between whites and African Americans; 1.54 and 1.89, respectively[5]. The majority of cases are asymptomatic..
Aetiology[edit | edit source]
Atherosclerosis accounts for the majority of PAD, whereas uncommon vascular symptoms, such as vasculitis, thromboangiitis obliterans, popliteal entrapment syndrome, and fibromuscular dysplasis, account for less than 10% of cases [3]. Atherosclerosis is the formation of lipid deposits in the tunica media and associated with damage to the endothelial lining [6].The endothelial cells become swollen with lipids and create a gap between in the linings. Platelets stick to the exposed collagen fibers, forming a localized clot that restricts arterial blood flow, leading to inadequate tissue perfusion. This and other complex interactions can lead to progression from asymptomatic PAD, Intermittent Claudication, Critical Limb Ischemia, Acute Limb Ischemia [3].
Investigations[edit | edit source]
A tool used to gain a diagnosis of PAD is Ankle Brachial Pressure Index (ABI), a simple and inexpensive test that measures the ratio between blood pressure in the legs to the blood pressure in the arms[3]. The lower the pressure in the legs illustrates that PAD is present. An ABI of 0.9- 1.0 is normal, 0.70-0.89 is a mild disease, 0.40- 0.69 is a moderate disease, and less than .40 is a severe PAD[3]. When measuring for ABI, make sure the patient is calm and in a rested position [7]. It is also important to assess individuals if they have diabetes, non-healing wounds on their legs and feet, unexplained pain in their peripherals, and check for femoral and popliteal pulses[7].
Clinical Manifestations[edit | edit source]
[7]
non-healing wounds on legs or feet
unexplained leg pain
pain on walking that resolves when stopped
pain in foot at rest made which worsens with elevation
ulcers
gangrene
dry skin
cramping
aching
Physiotherapy and Other Management[edit | edit source]
One method of treating PAD is to reduce cardiovascular risk factors by quitting smoking, managing diabetes mellitus, treating dyslipidemia and hypertension [3]. Another method is to treat PAD symptoms to improve quality of life through pharmacotherapy, exercise rehabilitation program, revascularization, thrombolysis and surgical procedures [3]. The least invasive and most appropriate treatment conducted by Physiotherapists would be by prescribing an exercise program. The recommended parameters of physical exercise are a 6 month program of 30-35 minutes walking sessions at a frequency of 3-5 times a week at near-maximal pain tolerant [3]. NICE recommends PAD patients to exercise at near-maximal pain for a total of 2 hours per week for 3 months to improve quality of life [7].
Prevention[edit | edit source]
Brief consideration of how this pathology could be prevented and the physiotherapy role in health promotion in relation to prevention of disease or disease progression.
Resources
[edit | edit source]
http://www.nhs.uk/conditions/peripheralarterialdisease/Pages/Introduction.aspx
http://www.circulationfoundation.org.uk/help-advice/peripheral-arterial-disease/
Recent Related Research (from Pubmed)[edit | edit source]
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Extension:RSS -- Error:Not a valid URL: <channel> <title>pubmed: peripheral arterial ...</title> <link>http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Search&db=PubMed&term=peripheral%20arterial%20disease</link> <description>NCBI: db=pubmed; Term=peripheral arterial disease</description> <language>en-us</language> <docs>http://blogs.law.harvard.edu/tech/rss</docs> <ttl>1440</ttl> <image> <title>NCBI pubmed</title> <url>http://www.ncbi.nlm.nih.gov/entrez/query/static/gifs/iconsml.gif</url> <link>http://www.ncbi.nlm.nih.gov/sites/entrez</link> <description>PubMed comprises more than 24 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.</description> </image> <item>
<title>Time-dependent retinal ganglion cell loss, microglial activation and blood-retina-barrier tightness in an acute model of ocular hypertension.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/26001526?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=26001526%22>Related Articles</a></td></tr></table>
<p><b>Time-dependent retinal ganglion cell loss, microglial activation and blood-retina-barrier tightness in an acute model of ocular hypertension.</b></p>
<p>Exp Eye Res. 2015 May 19;</p>
<p>Authors: Trost A, Motloch K, Bruckner D, Schroedl F, Bogner B, Kaser-Eichberger A, Runge C, Strohmaier C, Klein B, Aigner L, Reitsamer HA</p>
<p>Abstract<br/>
Glaucoma is a group of neurodegenerative diseases characterized by the progressive loss of retinal ganglion cells (RGCs) and their axons, and is the second leading cause of blindness worldwide. Elevated intraocular pressure is a well known risk factor for the development of glaucomatous optic neuropathy and pharmacological or surgical lowering of intraocular pressure represents a standard procedure in glaucoma treatment. However, the treatment options are limited and although lowering of intraocular pressure impedes disease progression, glaucoma cannot be cured by the currently available therapy concepts. In an acute short-term ocular hypertension model in rat, we characterize RGC loss, but also microglial cell activation and vascular alterations of the retina at certain time points. The combination of these three parameters might facilitate a better evaluation of the disease progression, and could further serve as a new model to test novel treatment strategies at certain time points. Acute ocular hypertension (OHT) was induced by the injection of magnetic microbeads into the rat anterior chamber angle (n=22) with magnetic position control, leading to constant elevation of IOP. At certain time points post injection (4d, 7d, 10d, 14d and 21d), RGC loss, microglial activation, and microvascular pericyte (PC) coverage was analyzed using immunohistochemistry with corresponding specific markers (Brn3a, Iba1, NG2). Additionally, the tightness of the retinal vasculature was determined via injections of Texas Red labeled dextran (10 kDa) and subsequently analyzed for vascular leakage. For documentation, confocal laser-scanning microscopy was used, followed by cell counts, capillary length measurements and morphological and statistical analysis. The injection of magnetic microbeads led to a progressive loss of RGCs at the five time points investigated (20.07%, 29.52%, 41.80%, 61.40% and 76.57%). Microglial cells increased in number and displayed an activated morphology, as revealed by Iba1-positive cell number (150.23%, 175%, 429.25%,486.72% and 544.78%) and particle size analysis (205.49%, 203.37%, 412.84%, 333.37% and 299.77%) compared to contralateral control eyes. Pericyte coverage (NG2-positive PC/mm) displayed a significant reduction after 7d of OHT in central, and after 7d and 10d in peripheral retina. Despite these alterations, the tightness of the retinal vasculature remained unaltered at 14 and 21 days after OHT induction. While vascular tightness was unchanged in the course of OHT, a progressive loss of RGCs and activation of microglial cells was detected. Since a significant loss in RGCs was observed already at day 4 of experimental glaucoma, and since activated microglia peaked at day 10, we determined a time frame of 7 to 14 days after MB injection as potential optimum to study glaucoma mechanisms in this model.<br/>
</p><p>PMID: 26001526 [PubMed - as supplied by publisher]</p>
]]></description>
<author> Trost A, Motloch K, Bruckner D, Schroedl F, Bogner B, Kaser-Eichberger A, Runge C, Strohmaier C, Klein B, Aigner L, Reitsamer HA</author>
<category>Exp Eye Res</category>
<guid isPermaLink="false">PubMed:26001526</guid>
</item> <item>
<title>Strategies for Free Flap Transfer and Revascularisation with Long-term Outcome in the Treatment of Large Diabetic Foot Lesions.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/26001322?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=26001322%22>Related Articles</a></td></tr></table>
<p><b>Strategies for Free Flap Transfer and Revascularisation with Long-term Outcome in the Treatment of Large Diabetic Foot Lesions.</b></p>
<p>Eur J Vasc Endovasc Surg. 2015 May 19;</p>
<p>Authors: Kallio M, Vikatmaa P, Kantonen I, Lepäntalo M, Venermo M, Tukiainen E</p>
<p>Abstract<br/>
OBJECTIVE/BACKGROUND: To analyse the impact of ischaemia and revascularisation strategies on the long-term outcome of patients undergoing free flap transfer (FFT) for large diabetic foot lesions penetrating to the tendon, bone, or joint.<br/>
METHODS: Foot lesions of 63 patients with diabetes (median age 56 years; 70% male) were covered with a FTT in 1991-2003. Three groups were formed and followed until 2009: patients with a native in line artery to the ulcer area (n = 19; group A), patients with correctable ischaemia requiring vascular bypass (n = 32; group B), and patients with uncorrectable ischaemia lacking a recipient vessel in the ulcer area (n = 12; group C).<br/>
RESULTS: The respective 1, 5, and 10 year amputation free survival rates were 90%, 79%, and 63% in group A; 66%, 25%, and 18% in group B; and 50%, 42%, and 17%, in group C. The respective 1, 5, and 10 year leg salvage rates were 94%, 94%, and 87% in group A; 71%, 65%, and 65% in group B; and 50%, 50%, and 50% in group C. In 1 year, 43%, 45%, and 18% of the patients in groups A, B, and C, respectively, achieved stable epithelisation for at least 6 months. The overall amputation rate was associated with smoking (relative risk [RR] 3.09, 95% confidence interval [CI] 1.8-5.3), heel ulceration (RR 2.25, 95% CI 1.1-4.7), nephropathy (RR 2.24, 95% CI 1.04-4.82), and an ulcer diameter of >10 cm (RR 2.08, 95% CI 1.03-4.48).<br/>
CONCLUSION: Despite diabetic comorbidities, complicated foot defects may be covered by means of an FFT with excellent long-term amputation free survival, provided that a patent native artery feeds the ulcer area. Ischaemic limbs may also be salvaged with combined FFT and vascular reconstruction in non-smokers and in the absence of very extensive heel ulcers. Occasionally, amputation is avoidable with FFT, even without the possibility of direct revascularisation.<br/>
</p><p>PMID: 26001322 [PubMed - as supplied by publisher]</p>
]]></description>
<author> Kallio M, Vikatmaa P, Kantonen I, Lepäntalo M, Venermo M, Tukiainen E</author>
<category>Eur J Vasc Endovasc Surg</category>
<guid isPermaLink="false">PubMed:26001322</guid>
</item> <item>
<title>MR Angiography at 3 T of Peripheral Arterial Disease: A Randomized Prospective Comparison of Gadoterate Meglumine and Gadobutrol.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/26001243?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=26001243%22>Related Articles</a></td></tr></table>
<p><b>MR Angiography at 3 T of Peripheral Arterial Disease: A Randomized Prospective Comparison of Gadoterate Meglumine and Gadobutrol.</b></p>
<p>AJR Am J Roentgenol. 2015 Jun;204(6):1311-1321</p>
<p>Authors: Loewe C, Arnaiz J, Krause D, Marti-Bonmati L, Haneder S, Kramer U, DALIA study group</p>
<p>Abstract<br/>
OBJECTIVE: This large-scale randomized study aimed to show the noninferiority in terms of diagnostic performance of gadoterate meglumine-enhanced versus gadobutrol-enhanced 3-T MR angiography (MRA) using digital subtraction angiography (DSA) as the reference standard in patients with peripheral arterial occlusive disease (PAOD).<br/>
SUBJECTS AND METHODS: In this prospective international randomized double-blind phase IV trial, 189 patients were enrolled. Of them, 156 could be included in the per-protocol population for on-site assessments and 154 for off-site readings. Subjects underwent peripheral MRA, after injection of 0.1 mmol/kg of either gadoterate meglumine or gadobutrol, and DSA within 30 days. The diagnostic accuracy was evaluated and compared using a noninferiority analysis. Secondary endpoints included sensitivity, specificity, diagnostic confidence, contrast-to-noise ratio, and signal-to-noise ratio evaluations.<br/>
RESULTS: The percentage agreement between MRA and DSA for stenosis detection was similar for on-site readings for both groups (mean ± SD, 80.6% ± 16.1% with gadoterate meglumine vs 77.1% ± 19.6% with gadobutrol; 3.5% difference), and the same was true for off-site readings (73.9% ± 16.9% with gadoterate meglumine vs 75.1% ± 13.8% with gadobutrol; 1.1% difference). The noninferiority of gadoterate meglumine to gadobutrol was shown for both on- and off-site readings. Sensitivity in detecting significant stenosis (> 50%) was 72.3% for gadoterate meglumine versus 70.6% for gadobutrol, whereas specificity (92.6% vs 92.3%), diagnostic confidence (87.0% vs 86.0%), signal-to-noise ratio (165.5 vs 161.0), and contrast-to-noise ratio (159.5 vs 155.3) did not differ statistically significantly between the two groups.<br/>
CONCLUSION: Gadoterate meglumine was found to be not inferior to gadobutrol in terms of diagnostic performance in patients with PAOD undergoing 3-T contrast-enhanced MRA. No statistically significant differences were detected between the two MRA groups.<br/>
</p><p>PMID: 26001243 [PubMed - as supplied by publisher]</p>
]]></description>
<author> Loewe C, Arnaiz J, Krause D, Marti-Bonmati L, Haneder S, Kramer U, DALIA study group</author>
<category>AJR Am J Roentgenol</category>
<guid isPermaLink="false">PubMed:26001243</guid>
</item> <item>
<title>Links between Vitamin D Deficiency and Cardiovascular Diseases.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/26000280?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=26000280%22>Related Articles</a></td></tr></table>
<p><b>Links between Vitamin D Deficiency and Cardiovascular Diseases.</b></p>
<p>Biomed Res Int. 2015;2015:109275</p>
<p>Authors: Mozos I, Marginean O</p>
<p>Abstract<br/>
The aim of the present paper was to review the most important mechanisms explaining the possible association of vitamin D deficiency and cardiovascular diseases, focusing on recent experimental and clinical data. Low vitamin D levels favor atherosclerosis enabling vascular inflammation, endothelial dysfunction, formation of foam cells, and proliferation of smooth muscle cells. The antihypertensive properties of vitamin D include suppression of the renin-angiotensin-aldosterone system, renoprotective effects, direct effects on endothelial cells and calcium metabolism, inhibition of growth of vascular smooth muscle cells, prevention of secondary hyperparathyroidism, and beneficial effects on cardiovascular risk factors. Vitamin D is also involved in glycemic control, lipid metabolism, insulin secretion, and sensitivity, explaining the association between vitamin D deficiency and metabolic syndrome. Vitamin D deficit was associated in some studies with the number of affected coronary arteries, postinfarction complications, inflammatory cytokines and cardiac remodeling in patients with myocardial infarction, direct electromechanical effects and inflammation in atrial fibrillation, and neuroprotective effects in stroke. In peripheral arterial disease, vitamin D status was related to the decline of the functional performance, severity, atherosclerosis and inflammatory markers, arterial stiffness, vascular calcifications, and arterial aging. Vitamin D supplementation should further consider additional factors, such as phosphates, parathormone, renin, and fibroblast growth factor 23 levels.<br/>
</p><p>PMID: 26000280 [PubMed - as supplied by publisher]</p>
]]></description>
<author> Mozos I, Marginean O</author>
<category>Biomed Res Int</category>
<guid isPermaLink="false">PubMed:26000280</guid>
</item> <item>
<title>Emerging therapies for the treatment of ungual onychomycosis.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/25997365?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=25997365%22>Related Articles</a></td></tr></table>
<p><b>Emerging therapies for the treatment of ungual onychomycosis.</b></p>
<p>Drug Dev Ind Pharm. 2015 May 22;:1-7</p>
<p>Authors: Kushwaha A, Murthy RN, Murthy SN, Elkeeb R, Hui X, Maibach HI</p>
<p>Abstract<br/>
INTRODUCTION: Onychomycosis, a common fungal infection in the finger and toe nails, affects approximately 2-8% of the worldwide population. Fungal infection is more complicated in those who suffer from conditions, such as diabetes, peripheral vascular diseases and compromised immune diseases. Area covered: Onychomycosis treatment has been classified on the basis of location of infection in the toes and fingers and infectious agents (dermatophytes fungi, yeast and non-dermatophyte molds). In this review, the available therapies (traditional and device based) and their limitations for the treatment of onychomycosis have been discussed. Expert opinion: The success rate with topical nail products has been minimal. The main reason for this poor success rate could be attributed to the lack of complete understanding of the pathophysiology of the disease and clinical pharmacokinetic data of drugs in the infected nail apparatus.<br/>
</p><p>PMID: 25997365 [PubMed - as supplied by publisher]</p>
]]></description>
<author> Kushwaha A, Murthy RN, Murthy SN, Elkeeb R, Hui X, Maibach HI</author>
<category>Drug Dev Ind Pharm</category>
<guid isPermaLink="false">PubMed:25997365</guid>
</item> <item>
<title>Adventitial layer enlargement correlates with the percentage of medial thickness in peripheral pulmonary arteries from patients with congenital heart defects.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/25991538?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=25991538%22>Related Articles</a></td></tr></table>
<p><b>Adventitial layer enlargement correlates with the percentage of medial thickness in peripheral pulmonary arteries from patients with congenital heart defects.</b></p>
<p>Cardiovasc Pathol. 1997 Jul;6(4):213-7</p>
<p>Authors: Aiello VD, Higuchi Mde L, Gutierrez PS, Ebaid M, Sesso A</p>
<p>Abstract<br/>
Arterial walls undergo modifications during the course of pulmonary hypertension, particularly in the medial and intimal layers, leading to progressive occlusion of the lumen. Adventitial layer enlargement has been described as being present in the experimental hypoxic model and in the persistent pulmonary hypertension of the newborn. It was suggested that this enlargement may be related to stimulating factors derived from the medial smooth muscle cells. This study was designed to verify if different degrees of medial hypertrophy are correlated to the volume density of the adventitial layer in pulmonary hypertension secondary to congenital heart defects. Reviewing 21 lung biopsies from patients with congenital heart defects, we concluded that there is a statistically significant positive linear correlation between the mean percentage of medial arterial thickness and the volume density of the adventitial layer in the biopsies showing isolated medial hypertrophy. On the other hand, in biopsies showing frequent intimal proliferative lesions and irregular medial layer hypertrophy the correlation coefficient was lower. These findings suggest that the adventitial layer participates in the arterial remodeling process in secondary pulmonary hypertension, and that its enlargement depends on the qualitative degree of pulmonary vaso-occlusive disease. <br/>
</p><p>PMID: 25991538 [PubMed]</p>
]]></description>
<author> Aiello VD, Higuchi Mde L, Gutierrez PS, Ebaid M, Sesso A</author>
<category>Cardiovasc Pathol</category>
<guid isPermaLink="false">PubMed:25991538</guid>
</item> <item>
<title>Muramidase: A useful monocyte/macrophage immunocytochemical marker in swine, of special interest in experimental cardiovascular disease.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/25990995?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=25990995%22>Related Articles</a></td></tr></table>
<p><b>Muramidase: A useful monocyte/macrophage immunocytochemical marker in swine, of special interest in experimental cardiovascular disease.</b></p>
<p>Cardiovasc Pathol. 1994 Jul-Sep;3(3):183-9</p>
<p>Authors: Falk E, Fallon JT, Mailhac A, Fernandez-Ortiz A, Meyer BJ, Weng D, Shah PK, Badimon JJ, Fuster V</p>
<p>Abstract<br/>
The reliability of a rabbit polyclonal antibody against muramidase to identify monocytes/macrophages in swine was evaluated by immunostaining of cell smears and formaldehyde-fixed, paraffin-embedded tissue sections. Blood in tissue sections, cell smears (peripheral blood, buffy coat, and isolated mononuclear cells), and cultured mononuclear cells (adherent monocytes) contained positively stained cells with a morphology and in a number corresponding to that expected for a monocyte marker. Polymorphonuclear leukocytes (PMN), lymphocytes, and platelets were negative. In normal organs and tissues, mesenchymal cells with a distribution similar to that expected for macrophages were found to stain positively for muramidase. In pathologic tissues, positively stained inflammatory cells were identified in wounds, infected lungs, recently infarcted myocardium, and acute (variable numbers), organizing (often many), and healed (usually few) arterial thrombi. Enzymatic unmasking of antigenic determinants by trypsinization was necessary to achieve strong and consistent staining of monocytes/macrophages in tissue sections. A variety of epithelial cells of no differential diagnostic significance for monocyte/macrophage identification (e.g., renal proximal tubular cells) also stained positive for muramidase. The staining pattern of muramidase in swine corresponds to that described in humans, in whom muramidase has been shown to be a valuable marker of monocytes/macrophages. Swine PMN were, however, not stained or only weakly stained, whereas human PMN reportedly are strongly positive. As in humans, swine cardiac myocytes, smooth muscle cells, endothelial cells, lymphocytes, and platelets were consistently negative. This antibody against muramidase is a useful immunohistochemical marker for swine monocytes/macrophages in formaldehyde-fixed, paraffin-embedded tissues. <br/>
</p><p>PMID: 25990995 [PubMed]</p>
]]></description>
<author> Falk E, Fallon JT, Mailhac A, Fernandez-Ortiz A, Meyer BJ, Weng D, Shah PK, Badimon JJ, Fuster V</author>
<category>Cardiovasc Pathol</category>
<guid isPermaLink="false">PubMed:25990995</guid>
</item> <item>
<title>Persistently increased expression of the transforming growth factor-β1 gene in human vascular restenosis: Analysis of 62 patients with one or more episode of restenosis.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/25990773?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=25990773%22>Related Articles</a></td></tr></table>
<p><b>Persistently increased expression of the transforming growth factor-β1 gene in human vascular restenosis: Analysis of 62 patients with one or more episode of restenosis.</b></p>
<p>Cardiovasc Pathol. 1994 Jan-Mar;3(1):57-64</p>
<p>Authors: Nikol S, Weir L, Sullivan A, Sharaf B, White CJ, Zemel G, Hartzler G, Stack R, Leclerc G, Isner JM</p>
<p>Abstract<br/>
Transforming growth factor-beta-1 (TGF-β1) is a multifunctional cytokine with both growth-promoting and growth-inhibiting properties. Moreover, there is abundant evidence that TGF-β1 is the principal growth factor responsible for regulating proteoglycan synthesis in human blood vessels. To determine the potential contribution of TGF-β1 to restenosis, the current investigation sought to determine the time course of expression postangioplasty of the TGF-β1 gene. In situ hybridization was performed on tissue specimens obtained by directional atherectomy from 62 patients who had previously undergone angioplasty of native coronary or peripheral arteries and/or saphenous vein bypass grafts. The time interval between angioplasty and atherectomy was 1 hour to 25 months (M ± SEM = 5 ± 4 months) for all 62 patients, 5 ± 4 months for coronary arterial specimens, 8 ± 5 months for vein graft specimens, and 7 ± 3 months for peripheral arterial specimens. TGF-β1 mRNA expression remained persistently increased independent of the site from or time interval following which the specimen was obtained. For saphenous vein by pass grafts, TGF-β1 expression was highest in specimens retreived from patients with multiple versus single episodes of restenosis (16 ± 5 vs. 6 ± 5 grains/nucleus, p < 0.01). TGF-β1 expression did not correlate with patient age, sex, or known risk factors for coronary heart disease. The persistently augmented expression of TGF-β1 observed in the present series of restenosis lesions provides further support for the concept that TGF-β1 influences growth and development of restenosis plaque. <br/>
</p><p>PMID: 25990773 [PubMed]</p>
]]></description>
<author> Nikol S, Weir L, Sullivan A, Sharaf B, White CJ, Zemel G, Hartzler G, Stack R, Leclerc G, Isner JM</author>
<category>Cardiovasc Pathol</category>
<guid isPermaLink="false">PubMed:25990773</guid>
</item> <item>
<title>Vasculopathies of Neurofibromatosis Type 1 (von Recklinghausen Disease).</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/25990068?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=25990068%22>Related Articles</a></td></tr></table>
<p><b>Vasculopathies of Neurofibromatosis Type 1 (von Recklinghausen Disease).</b></p>
<p>Cardiovasc Pathol. 1998 Mar-Apr;7(2):97-108</p>
<p>Authors: Lie JT</p>
<p>Abstract<br/>
Vasculopathies are the least publicized but most important manifestation of neurofibromatosis type 1 (NF1, or, von Recklinghausen disease) as the cause of morbidity and mortality in children and young adults afflicted with the disease. Occlusive or aneurysmal disease of arteries of all sizes may occur almost anywhere in the body. Coarctation or segmental hypoplasia of the abdominal aorta with or without renal artery ostial stenosis is a common cause of renovascular hypertension. Although rare, occlusive coronary artery disease in NF1 may result in myocardial infarction and sudden unexpected death. Visceral vasculopathy causes ischemic bowel disease; and catastrophic retroperitoneal or abdominal hemorrhage has been attributed to spontaneously ruptured arterial aneurysms. Peripheral vascular disease in NF1 with limb ischemia requiring an amputation is described for the first time here. Scanty information exists in the current pathology literature on NF1 vasculopathies, hence the presentation of this review. <br/>
</p><p>PMID: 25990068 [PubMed]</p>
]]></description>
<author> Lie JT</author>
<category>Cardiovasc Pathol</category>
<guid isPermaLink="false">PubMed:25990068</guid>
</item> <item>
<title>Multiple arterial injuries and prolonged cholesterol feeding do not increase percent lumen stenosis: impact of compensatory enlargement in the microswine model.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/25989958?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=25989958%22>Related Articles</a></td></tr></table>
<p><b>Multiple arterial injuries and prolonged cholesterol feeding do not increase percent lumen stenosis: impact of compensatory enlargement in the microswine model.</b></p>
<p>Cardiovasc Pathol. 1998 Jan-Feb;7(1):1-8</p>
<p>Authors: Thorpe PE, Zhan X, Agrawal DK, Hunter WJ, Farb A, Virmani R</p>
<p>Abstract<br/>
While the swine model is frequently utilized in the study of arterial intervention, it has been difficult to create severe peripheral arterial stenosis without total thrombotic occlusion with a single arterial injury and short-term cholesterol feeding. The combination of multiple arterial injuries and prolonged cholesterol feeding was explored in an effort to create lesions with significant luminal compromise. Nineteen microswine were divided into two groups and fed a high cholesterol diet followed by multiple balloon injuries of the iliac arteries. We conclude that repeated balloon injuries and longer cholesterol feeding significantly increase areas of plaque and necrotic core but do not increase percent stenosis because of arterial compensatory enlargement. The microswine iliac arteries enlarge in relation to plaque area and repeated balloon injuries. The compensatory lumen enlargement may be one of the factors resulting in significant angiographic underestimation of plaque area during the early stage of the atherosclerotic disease, but it may functionally delay important lumen stenosis until the lesion occupies 40% of the internal elastic lamina area. This study suggests that repeated injury and longer cholesterol feeding to increase percent stenosis may not be cost effective in this model. However, this model is good for studying an increase in plaque accumulation. <br/>
</p><p>PMID: 25989958 [PubMed]</p>
]]></description>
<author> Thorpe PE, Zhan X, Agrawal DK, Hunter WJ, Farb A, Virmani R</author>
<category>Cardiovasc Pathol</category>
<guid isPermaLink="false">PubMed:25989958</guid>
</item> <item>
<title>Correlation between Patient-Reported Symptoms and Ankle-Brachial Index after Revascularization for Peripheral Arterial Disease.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/25993299?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=25993299%22>Related Articles</a></td></tr></table>
<p><b>Correlation between Patient-Reported Symptoms and Ankle-Brachial Index after Revascularization for Peripheral Arterial Disease.</b></p>
<p>Int J Mol Sci. 2015;16(5):11355-68</p>
<p>Authors: Je HG, Kim BH, Cho KI, Jang JS, Park YH, Spertus J</p>
<p>Abstract<br/>
Improvement in quality of life (QoL) is a primary treatment goal for patients with peripheral arterial disease (PAD). The current study aimed to quantify improvement in the health status of PAD patients following peripheral revascularization using the peripheral artery questionnaire (PAQ) and ankle-brachial index (ABI), and to evaluate possible correlation between the two methods. The PAQ and ABI were assessed in 149 symptomatic PAD patients before, and three months after peripheral revascularization. Mean PAQ summary scores improved significantly three months after revascularization (+49.3 ± 15 points, p < 0.001). PAQ scores relating to patient symptoms showed the largest improvement following revascularization. The smallest increases were seen in reported treatment satisfaction (all p's < 0.001). As expected the ABI of treated limbs showed significant improvement post-revascularization (p < 0.001). ABI after revascularization correlated with patient-reported changes in the physical function and QoL domains of the PAQ. Twenty-two percent of PAD patients were identified as having a poor response to revascularization (increase in ABI < 0.15). Interestingly, poor responders reported improvement in symptoms on the PAQ, although this was less marked than in patients with an increase in ABI > 0.15 following revascularization. In conclusion, data from the current study suggest a significant correlation between improvement in patient-reported outcomes assessed by PAQ and ABI in symptomatic PAD patients undergoing peripheral revascularization. <br/>
</p><p>PMID: 25993299 [PubMed - in process]</p>
]]></description>
<author> Je HG, Kim BH, Cho KI, Jang JS, Park YH, Spertus J</author>
<category>Int J Mol Sci</category>
<guid isPermaLink="false">PubMed:25993299</guid>
</item> <item>
<title>Influence of regular exercise on body fat and eating patterns of patients with intermittent claudication.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/25993298?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=25993298%22>Related Articles</a></td></tr></table>
<p><b>Influence of regular exercise on body fat and eating patterns of patients with intermittent claudication.</b></p>
<p>Int J Mol Sci. 2015;16(5):11339-54</p>
<p>Authors: Leicht A, Crowther R, Golledge J</p>
<p>Abstract<br/>
This study examined the impact of regular supervised exercise on body fat, assessed via anthropometry, and eating patterns of peripheral arterial disease patients with intermittent claudication (IC). Body fat, eating patterns and walking ability were assessed in 11 healthy adults (Control) and age- and mass-matched IC patients undertaking usual care (n = 10; IC-Con) or supervised exercise (12-months; n = 10; IC-Ex). At entry, all groups exhibited similar body fat and eating patterns. Maximal walking ability was greatest for Control participants and similar for IC-Ex and IC-Con patients. Supervised exercise resulted in significantly greater improvements in maximal walking ability (IC-Ex 148%-170% vs. IC-Con 29%-52%) and smaller increases in body fat (IC-Ex -2.1%-1.4% vs. IC-Con 8.4%-10%). IC-Con patients exhibited significantly greater increases in body fat compared with Control at follow-up (8.4%-10% vs. -0.6%-1.4%). Eating patterns were similar for all groups at follow-up. The current study demonstrated that regular, supervised exercise significantly improved maximal walking ability and minimised increase in body fat amongst IC patients without changes in eating patterns. The study supports the use of supervised exercise to minimize cardiovascular risk amongst IC patients. Further studies are needed to examine the additional value of other lifestyle interventions such as diet modification. <br/>
</p><p>PMID: 25993298 [PubMed - in process]</p>
]]></description>
<author> Leicht A, Crowther R, Golledge J</author>
<category>Int J Mol Sci</category>
<guid isPermaLink="false">PubMed:25993298</guid>
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<title>Immunohistochemical analysis of paraoxonases and chemokines in arteries of patients with peripheral artery disease.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/25993297?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=25993297%22>Related Articles</a></td></tr></table>
<p><b>Immunohistochemical analysis of paraoxonases and chemokines in arteries of patients with peripheral artery disease.</b></p>
<p>Int J Mol Sci. 2015;16(5):11323-38</p>
<p>Authors: Hernández-Aguilera A, Sepúlveda J, Rodríguez-Gallego E, Guirro M, García-Heredia A, Cabré N, Luciano-Mateo F, Fort-Gallifa I, Martín-Paredero V, Joven J, Camps J</p>
<p>Abstract<br/>
Oxidative damage to lipids and lipoproteins is implicated in the development of atherosclerotic vascular diseases, including peripheral artery disease (PAD). The paraoxonases (PON) are a group of antioxidant enzymes, termed PON1, PON2, and PON3 that protect lipoproteins and cells from peroxidation and, as such, may be involved in protection against the atherosclerosis process. PON1 inhibits the production of chemokine (C-C motif) ligand 2 (CCL2) in endothelial cells incubated with oxidized lipoproteins. PON1 and CCL2 are ubiquitously distributed in tissues, and this suggests a joint localization and combined systemic effect. The aim of the present study has been to analyze the quantitative immunohistochemical localization of PON1, PON3, CCL2 and CCL2 receptors in a series of patients with severe PAD. Portions of femoral and/or popliteal arteries from 66 patients with PAD were obtained during surgical procedures for infra-inguinal limb revascularization. We used eight normal arteries from donors as controls. PON1 and PON3, CCL2 and the chemokine-binding protein 2, and Duffy antigen/chemokine receptor, were increased in PAD patients. There were no significant changes in C-C chemokine receptor type 2. Our findings suggest that paraoxonases and chemokines play an important role in the development and progression of atherosclerosis in peripheral artery disease. <br/>
</p><p>PMID: 25993297 [PubMed - in process]</p>
]]></description>
<author> Hernández-Aguilera A, Sepúlveda J, Rodríguez-Gallego E, Guirro M, García-Heredia A, Cabré N, Luciano-Mateo F, Fort-Gallifa I, Martín-Paredero V, Joven J, Camps J</author>
<category>Int J Mol Sci</category>
<guid isPermaLink="false">PubMed:25993297</guid>
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<title>Imaging of Small Animal Peripheral Artery Disease Models: Recent Advancements and Translational Potential.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/25993289?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"/><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=25993289%22>Related Articles</a></td></tr></table>
<p><b>Imaging of Small Animal Peripheral Artery Disease Models: Recent Advancements and Translational Potential.</b></p>
<p>Int J Mol Sci. 2015;16(5):11131-11177</p>
<p>Authors: Lin JB, Phillips EH, Riggins TE, Sangha GS, Chakraborty S, Lee JY, Lycke RJ, Hernandez CL, Soepriatna AH, Thorne BR, Yrineo AA, Goergen CJ</p>
<p>Abstract<br/>
Peripheral artery disease (PAD) is a broad disorder encompassing multiple forms of arterial disease outside of the heart. As such, PAD development is a multifactorial process with a variety of manifestations. For example, aneurysms are pathological expansions of an artery that can lead to rupture, while ischemic atherosclerosis reduces blood flow, increasing the risk of claudication, poor wound healing, limb amputation, and stroke. Current PAD treatment is often ineffective or associated with serious risks, largely because these disorders are commonly undiagnosed or misdiagnosed. Active areas of research are focused on detecting and characterizing deleterious arterial changes at early stages using non-invasive imaging strategies, such as ultrasound, as well as emerging technologies like photoacoustic imaging. Earlier disease detection and characterization could improve interventional strategies, leading to better prognosis in PAD patients. While rodents are being used to investigate PAD pathophysiology, imaging of these animal models has been underutilized. This review focuses on structural and molecular information and disease progression revealed by recent imaging efforts of aortic, cerebral, and peripheral vascular disease models in mice, rats, and rabbits. Effective translation to humans involves better understanding of underlying PAD pathophysiology to develop novel therapeutics and apply non-invasive imaging techniques in the clinic.<br/>
</p><p>PMID: 25993289 [PubMed - as supplied by publisher]</p>
]]></description>
<author> Lin JB, Phillips EH, Riggins TE, Sangha GS, Chakraborty S, Lee JY, Lycke RJ, Hernandez CL, Soepriatna AH, Thorne BR, Yrineo AA, Goergen CJ</author>
<category>Int J Mol Sci</category>
<guid isPermaLink="false">PubMed:25993289</guid>
</item> <item>
<title>Endovascular stents and stent grafts in the treatment of cardiovascular disease.</title> <link>http://www.ncbi.nlm.nih.gov/pubmed/25992405?dopt=Abstract</link> <description>
<![CDATA[<table border="0" width="100%"><tr><td align="left"><a href="http://openurl.ingenta.com/content/nlm?genre=article&issn=1550-7033&volume=10&issue=10&spage=2424&aulast=Sun%22><img src="//www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--images.ingentaselect.com-images-linkout-ingentaconnect.gif" border="0"/></a> </td><td align="right"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Link&LinkName=pubmed_pubmed&from_uid=25992405%22>Related Articles</a></td></tr></table>
<p><b>Endovascular stents and stent grafts in the treatment of cardiovascular disease.</b></p>
<p>J Biomed Nanotechnol. 2014 Oct;10(10):2424-63</p>
<p>Authors: Sun Z</p>
<p>Abstract<br/>
Endovascular stents and stent grafts are increasingly used to treat a variety of cardiovascular diseases and these endovascular devices have gained popularity worldwide. The improvement of available endovascular devices is critical for the advancement of patient care in cardiovascular medicine. Problems are still associated with the endovascular treatments, many of which can adversely affect the treatment outcomes, such as the conversion of the patient to conventional open surgery, or resulting in procedure-related complications. This review aims to provide an overview of the commonly performed endovascular procedures including carotid artery stenting, coronary artery stenting, peripheral arterial stenting and endovascular stent grafting with regard to clinical outcomes and imaging assessment. A critical appraisal is given to the novel methods that have been recently developed to deal with these problems and future development of the endovascular devices is highlighted.<br/>
</p><p>PMID: 25992405 [PubMed - in process]</p>
]]></description>
<author> Sun Z</author>
<category>J Biomed Nanotechnol</category>
<guid isPermaLink="false">PubMed:25992405</guid>
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References[edit | edit source]
see adding references tutorial.
- ↑ 1.0 1.1 Patient. Peripheral arterial disease. http://www.patient.co.uk/doctor/peripheral-arterial-disease (accessed 9 May 2015)
- ↑ Peach, G, Griffin, M, Jones, KG, Thompson MM, Hinchliffe, RJ. Diagnosis and management of peripheral arterial disease. BMJ 2012; 345: 1-8. http://www.bmj.com/content/bmj/345/bmj.e5208.full.pdf (acccessed 9 May 2015)
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 Mahameed, AA, Bartholomew, JR, Disease of Peripheral Vessels. In: Topol, EJ, editor. Textbook of Cardiovascular Medicine. 3rd ed. New York: Lippincott Williams &amp;amp;amp;amp;amp;amp;amp;amp; Wilkins, 2007, p.1531-1537
- ↑ 4.0 4.1 Fowkes G. Peripheral vascular disease. 2010. http://www.birmingham.ac.uk/Documents/college-mds/haps/projects/HCNA/09HCNA3D2.pdf (accessed 9 May 2015)
- ↑ Collines, TC, Petersen, NJ, Suarez-Almazor, M, Ashton CM. Ethnicity and peripheral arterial disease. Mayo Clin Proc. 2005; 80(1): 48-54.
- ↑ Martini, FH, Nath, JL, Bartholomew, EF. Fundamentals of anatomy and physiology. San Francisco: Pearson Education, 2015.
- ↑ 7.0 7.1 7.2 7.3 NICE National Institute for Health and Care Excellence. Lower limb peripheral arterial disease: diagnosis and management, 2012. https://www.nice.org.uk/guidance/cg147/chapter/guidance#management-of-intermittent-claudication (accessed 9 May 2015)
