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PubMed2001

Percutaneous interventions for lower extremity peripheral vascular disease.

Peripheral vascular disease of the lower extremities is an important cause of morbidity that affects up to 10 million people in the United States. The primary care physician can easily identify patients who are at risk for the disease with a questionnaire and a relatively simple test-the ankle brachial index. More than 70 percent of patients diagnosed with the disease remain stable or improve with conservative management. Those who do not improve may undergo contrast angiography or magnetic resonance angiography, which may be used in planning for surgery or percutaneous intervention. Surgical bypass is the gold standard for extensive vascular occlusive disease, but endovascular interventions, including percutaneous transluminal angioplasty and stent placement, are being used more frequently, particularly in patients with significant comorbid conditions.

Angiography↗
PubMed2004

Therapeutic angiogenesis for treatment of peripheral vascular disease.

Peripheral vascular disease (PVD) is characterized by compromised circulation to the limbs. Currently, PVD is treated conservatively and the first-line options include therapy with pain medication and "anti-thrombotic" drugs to prevent blood from clotting. Nonsurgical interventions such as angioplasty and thrombolytic therapy provide alternative treatment modalities. However, in the case of severe symptoms and with progressive deterioration, surgical interventions such as bypass surgery, atherectomy and even amputation may be necessary. Despite major advances in these areas, PVD is challenging, and difficult to manage with the current surgical and conservative medical approaches. In some cases, even short-term results in treated patients with advanced stage disease remain unsatisfactory. Indeed, there is a great clinical need for new treatment options that may stimulate collateral blood vessel growth, increase vascularity and improve skeletal muscle function.

Animals↗
PubMed1994

Rationale for the use of antiplatelet drugs in patients with peripheral vascular disease.

Peripheral vascular disease (PVD) is complicated by progression of atherosclerotic disease of lower limbs and by cardiovascular events occurring in cardiac and cerebral area. Antiplatelet treatment seems to be able to retard the atherosclerotic progression of peripheral vessel. This was demonstrated by angiographic studies and by a clinical trial showing that aspirin reduced the need of surgical intervention in PVD patients. Three large clinical trials have been planned to assess the effect of antiplatelet treatment on cardiovascular complications. By intention-to-treat analysis, no study showed a beneficial effect for this treatment. Conversely, by on-treatment analysis, antiplatelet treatment showed a significant reduction of global cardiovascular events. Until now, no study has had the power to assess the effect of antiplatelet treatment on major cardiovascular events. The evaluation of patients at high risk of major events by antiplatelet treatment should be an important issue of future clinical trials.

Arteriosclerosis↗
PubMed2005

Evidence-based management of peripheral vascular disease.

Peripheral vascular disease (PVD) is very prevalent in the United States and is part of a global vascular problem. PVD patients have a heightened inflammatory state and are at high risk of death from acute cardiovascular problems rather than from progression of PVD. Modifiable risk factors for PVD include smoking, hypertension, diabetes, hyperlipidemia, elevated high sensitivity C-reactive protein, obesity, and the metabolic syndrome. Symptomatic treatment of claudication includes smoking cessation, exercise, cilostazol, statins, and revascularization with percutaneous or surgical therapy. Antithrombotic therapy with aspirin or clopidogrel is important to reduce cardiovascular events but does not affect symptoms of claudication. Patients with rest limb ischemia or ulceration should be revascularized to minimize the chance of limb loss. Percutaneous revascularization is not without significant complications, however, and future research needs to focus on inflammation, thrombosis, and restenosis in the PVD patient. Finally, new devices that tackle difficult lesions, drug-eluting stents, and pharmacologic agents that reduce global atherosclerosis are on the horizon and are likely to become critical components in the management of the PVD patient.

Angioscopy↗
PubMed1993

Apolipoprotein (a) concentrations and susceptibility to coronary artery disease in patients with peripheral vascular disease.

OBJECTIVE: To investigate the relation between apolipoprotein(a) concentrations and angiographically defined coronary artery disease in patients with atheromatous peripheral vascular disease. DESIGN: 40 consecutive patients were recruited at the time of admission for peripheral vascular surgery. All underwent clinical assessment and coronary arteriography. Apolipoprotein(a) concentrations were measured by an immunoradiometric assay. SETTING: Tertiary referral centre. SUBJECTS: Patients requiring surgical intervention for large vessel peripheral vascular disease. MAIN OUTCOME MEASURES: Presence or absence and severity and distribution of angiographically defined coronary artery disease. Measurement of circulating contractions of apolipoprotein(a) and other lipid indices. RESULTS: Coronary artery disease was absent in 11 patients (group 1), mild to moderate in 12 (group 2), and severe in 17 (group 3). The distribution of peripheral vascular disease and of standard lipid indices was similar in these three groups of patients. There was a significant difference in apolipoprotein(a) concentrations between the three groups, with concentrations progressively increasing with the severity of coronary artery disease (mean (95% confidence interval): group 1, 112 U/1 (52 to 242); group 2, 214 U/1 (129 to 355); group 3, 537 U/1 (271 to 1064) (analysis of variance p < 0.005). The prevalence of coronary artery disease was increased 7.4 fold in patients with apolipoprotein(a) concentrations that were greater than the cohort median (206 U/1) (p < 0.01). CONCLUSIONS: The results show an association between apolipoprotein(a) concentrations and angiographically defined coronary artery disease in patients with large vessel peripheral vascular disease. The findings imply differences in the pathogenesis of coronary and peripheral atheroma and suggest that the measurement of apolipoprotein(a) may prove a useful additional tool in the risk factor assessment of patients undergoing peripheral vascular surgery.

Aged↗
PubMed1997

Genes and the development of vascular disease.

Clinical vascular disease occurs as the result of the chronic development of atherosclerosis, often with acute occlusive thrombus formation as the final event. Both atherosclerotic and thrombotic disorders are complex processes resulting from genetic and environmental interactions. We review genes currently implicated as risk factors and the approaches for identifying novel genetic risk factors.

Arteriosclerosis↗
PubMed1998

Sociology of care in patients with severe peripheral vascular disease.

Peripheral vascular disease (PVD) remains a leading cause of limb amputation, resulting in a significant morbidity and disability. This study was undertaken to evaluate whether earlier referral of the patients with severe limb-threatening PVD to a vascular surgeon could result in a higher limb-salvage rate. Seventy-one consecutive patients, 48 men and 23 women, with mean ages of 67.1 and 70.4 years, respectively, were studied; there were 64 blacks (42 men, 22 women). Risk factors included smoking (39 men, 20 women) and diabetes mellitus (31 men, 11 women). The delay in seeking medical attention in patients with rest pain was 9 to 24 weeks (mean, 14.2), and with nonhealing ulcers the delay was 4 to 20 weeks (mean, 6.7). An additional delay of 11.7 weeks was noted if the patient was seen by a primary-care physician, and only 4 weeks if the patient was seen in the Emergency Department. Ten primary amputations were performed; 61 patients underwent limb-salvaging revascularization procedures, with a success rate of 87 per cent; 8 patients had below-the-knee amputation as a result of failed bypass. Delay in referral of patients with severe PVD can cause an increase in limb loss.

Black or African American↗
PubMed1978

Tuberculosis of the liver presenting as peripheral vascular disease.

Peripheral vascular disease in African males may be associated with a tuberculous infection elsewhere in the body. The case history is described of a patient who presented with gangrenous lesions of both feet and was found to have tuberculosis of the liver. The lesions on the feet healed within 2 months of starting anti-tuberculosis chemotherapy.

Adult↗
PubMed2006

Does nutrition have a role in peripheral vascular disease?

Peripheral vascular disease (PVD) is a manifestation of systemic atherosclerosis in the lower limbs, and PVD patients have a 3- to 5-fold increased risk of cardiovascular mortality compared with age-matched controls. Nevertheless, recent reports show how PVD patients are undertreated with regard to CVD risk-factor reduction and the use of lipid-lowering or antiplatelet drugs. There is appreciable evidence that demonstrates the beneficial effects of certain nutrients and dietary habits in the prevention of CVD, but there has been little attention paid to the role of nutrients in PVD. The purpose of the present review is to provide an overview of our understanding of how foods could possibly benefit PVD. In the last few decades, several nutrients have arisen as potentially health-promoting in PVD. While nutritional interventions in PVD show positive clinical effects for fish oil, carnitine or vitamin E, others such as olive oil or vitamin C seem to interact only at a biochemical level by decreasing risk factors. Moreover, only epidemiological associations exist for the potential role of fibre, folates or vitamin B6 in this disease. In all cases, the limited data available provide no clear-cut evidence in favour of the clinical benefit of nutritional interventions aimed at reducing risk factors and ameliorating symptoms in PVD patients. No practical recommendations can be given at this stage, and further studies are clearly needed.

Antioxidants↗
PubMed1986

Nursing intervention in patients with peripheral vascular disease.

Peripheral vascular disease is a chronic progressive disease. Nursing intervention will be aimed at primary prevention through risk factor modification. Quality patient care will be facilitated through the development of an individualized plan of care. An essential element to consider in promoting successful nursing intervention is collaboration of the nurse and patient when developing the plan of care. Overall goals of care for a patient with PVD include promotion of circulation, relief of pain, and prevention of tissue damage or infection.

Behavior Therapy↗
PubMedDate not supplied

Alterations of thrombogenesis, endothelial damage and oxidative stress with reperfusion during femoral artery bypass surgery for peripheral vascular disease.

Peripheral vascular disease (PVD) is a significant cause of cardiovascular morbidity. We hypothesised that there would be significant alterations of thrombogenesis, platelet activation and endothelial damage, which could be associated with abnormal oxidative stress during femoral artery bypass surgery for PVD, where the femoral artery is cross-clamped (causing acute ischaemia) and reperfused (following revascularisation). To test this hypothesis, we measured sequential changes in von Willebrand factor (vWF, and index of endothelial damage/dysfunction), tissue factor (TF, an index of thrombogenesis) and soluble P-selectin (sP-sel, an index of platelet activation) as well as lipid hydroperoxides (LPO, an index of oxidative stress) in 28 consecutive patients undergoing elective peripheral artery bypass surgery. Mean baseline vWF and sP-sel levels in PVD patients (before clamping) were significantly higher compared with age- and sex-matched controls (unpaired t test, both p < 0.05), but there were no significant differences in TF and LPO levels. There was a correlation between TF and vWF (Spearman's, r = 0.374, p = 0.05), as well as between sP-sel and vWF at the start of surgery (r = 0.467, p = 0.012). The patients undergoing peripheral artery bypass surgery had a mean femoral artery clamp time of 28 min (standard deviation 14 min; range 11-65 min). There were no significant overall changes in sP-sel, vWF, TF and LPO with femoral artery cross-clamping and reperfusion (repeated measures ANOVA, p = NS). In conclusion, we found that during ischaemia-reperfusion during peripheral arterial bypass surgery, thrombogenesis (as measured by plasma TF) and oxidative damage (as measured by LPO) within the affected leg does not increase in the immediate perioperative period. Further studies are required to assess the mechanism(s) of ischaemia-reperfusion injury in PVD, and the contributory role(s) of the endothelium and platelets.

Aged↗
PubMed1995

[Pulmonary manifestation of collagen vascular diseases: role of cytokines in interstitial pneumonia associated with collagen vascular diseases].

Although the pathological patterns of interstitial pneumonia associated with collagen vascular disease (CVD-IP) resemble those of usual interstitial pneumonia in idiopathic interstitial pneumonia (IIP), the clinical features of CVD-IP and IIIP are quite different. We evaluated the differences between these conditions, with regard to the expression of genes in cells obtained by bronchoalveolar lavage. The reverse transcription-polymerase chain reaction was used to measure the levels of mRNA for IL-1 beta, TNF-alpha, IL-8, TGF-beta, PDGF-B, and IGF-1, and no significant differences were found between patients with CVD-IP and those with IIP. However, differential display analysis revealed a fragment that can be considered to have been derived from an unknown gene mRNA, and this was found only in patients with pulmonary fibrosis associated with progressive systemic sclerosis. Expression of specific genes may differentiate CVD-IP from IIP.

Adult↗
PubMed2001

Vascular disease in younger-onset diabetes: comparison of European, Asian and American Indian cohorts of the WHO Multinational Study of Vascular Disease in Diabetes.

AIMS/HYPOTHESIS: This study compared the incidence of vascular disease in subjects with younger-onset diabetes from different ethnic groups. METHODS: The incidence of vascular disease endpoints has been studied in a sub-group (n = 994) of participants of the World Health Organization Multinational Study of Vascular Disease in Diabetes (WHO MSVDD) who had younger-onset diabetes (diagnosed before the age of 30 years). The study participants have been divided into European (n = 631), Asian (n = 84) and American Indian (n = 91) cohorts. RESULTS: For Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus, American Indian men had a higher incidence of lower-extremity amputation and renal failure than the other cohorts, whereas European women had a higher incidence of angina than other cohorts. American Indians also had a higher incidence of any retinopathy, clinical proteinuria and albuminuria than the European and Asian cohorts. CONCLUSION/INTERPRETATION: This study confirms the high burden of large and small-vessel disease complications manifest in American Indian people with younger-onset diabetes.

Adult↗
PubMedDate not supplied

From hemobiology to vascular disease: a review of the potential of gliclazide to influence the pathogenesis of diabetic vascular disease.

Patients with type II diabetes commonly die from thrombotic vascular disease. Large vessel occlusion due to thrombosis or atherosclerotic stenosis is a process accelerated by diabetes and results in premature death. Diabetic small vessel disease, with its unique microangiopathic process, underlies many of the large vessel changes as well as causing retinopathy and nephropathy. The microangiopathic changes produce a prothrombotic tendency that has been widely reported in type II diabetes. There is reduced endothelial cell production of prostacyclin and the activators of fibrinolysis, together with increased platelet reactivity. In addition, there is increased lipid peroxidation and oxidative stress due to excess free-radical activity and impaired antioxidant defenses particularly in the presence of microvascular disease. The development of many of these abnormalities is associated with poor long-term glycemic control. However, the changes are also seen in atherosclerosis in nondiabetic patients where the progression of the disease can be modified by antiplatelet agents and antioxidants. The process of vascular damage is accelerated by diabetes, often due to co-existing disease and aging, although it is not clear that improvement in long-term glycemic control by lowering blood glucose levels to near to the nondiabetic state reduces the development of small and large vessel disease. Although the biochemical mechanism underlying this observation remains uncertain, protein glycosylation and increased platelet reactivity are implicated and interrelated. Increased oxidative stress due to excess free-radical activity may be central to diabetic vascular disease as endothelial cell damage, lipoprotein oxidation, modification of both platelet reactivity and arachidonic acid cascade are all properties of free radicals and their reaction products lipid peroxides.(ABSTRACT TRUNCATED AT 250 WORDS)

Antioxidants↗
PubMed2004

Thrombogenesis, atherogenesis and angiogenesis in vascular disease: a new 'vascular triad'.

Amongst the components of the pathophysiology of atherosclerosis are the tendency to thrombus formation (i.e., thrombogenesis) and the loss of endothelial cell integrity. The endothelium is also implicated in atherogenesis, as vasa vasorum are present in the adventitia and media at a higher density in atherosclerotic tissue, and that neovascularisation leading to collateral growth bypassing obstruction and/or stenoses provides important alternative routes to feeding distal tissues. The development of these new blood vessels is the process of angiogenesis. The present 'viewpoint' article will explore the relationships between the three processes. There is considerable evidence that atherogenesis and thrombogenesis are intimately linked, but angiogenesis in cardiovascular disease is a recently developed concept. We propose a new 'vascular triad' of these abnormal pathophysiological processes, leading to an alternative view of the pathogenesis of vascular disease. Indeed, we suggest that angiogenesis is an important aspect of the pathophysiology of cardiovascular disease, impacting with both thrombogenesis and atherogenesis, in a new vascular triad (the 'Birmingham vascular triad').

Arteriosclerosis↗
PubMed1998

Intravenous pulse cyclophosphamide in the treatment of interstitial lung disease due to collagen vascular diseases.

OBJECTIVE: Substantial toxicity limits the use of daily oral cyclophosphamide (CYC) for the treatment of interstitial lung disease (ILD) due to collagen vascular diseases. We examined whether intravenous (i.v.) pulse CYC can be substituted for daily oral therapy. METHODS: Six patients with rapidly progressive ILD due to polymyositis, systemic sclerosis, systemic lupus erythematosus, or primary Sjögren's syndrome received 6-9 cycles of i.v. pulse CYC (0.5 gm/m2 of body surface area), together with an initial course of 50 mg of prednisolone, which was tapered to a maintenance dosage of 5-7.5 mg/day, and their response was measured clinically, by high-resolution computed tomography (HRCT) and by assessment of the bronchoalveolar lavage (BAL) cell profile. RESULTS: All patients showed significant improvement in exercise tolerance and lung function. Elevated BAL neutrophils dropped substantially, whereas the response of BAL lymphocytes was inconsistent. Low-attenuation opacities in the HRCT regressed in 4 patients and remained unchanged in 2, but reticular infiltrates remained largely unaffected. Remission was maintained with hydroxychloroquine, azathioprine, or cyclosporin A. CONCLUSION: I.v. pulse CYC proved to be an effective and well-tolerated treatment in these patients. Since it appears to target mainly the inflammatory component of the disease, it should be reserved for progressive ILD featuring indices of high inflammatory activity.

Adult↗