Vascular Disease (vascular + disease)

Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Vascular Disease

  • atherosclerotic vascular disease
  • collagen vascular disease
  • peripheral vascular disease
  • retinal vascular disease

  • Selected Abstracts


    NEPHROLOGY, Issue 1 2002
    Dr J Kohlhagen


    Kevin J Woollard
    SUMMARY 1.,In recent years demonstration of a direct association between slightly elevated serum levels of soluble proteins including the acute phase response proteins, selectins and intercellular adhesion molecules and the risk of developing vascular disease have been widely reported. These studies may provide the clinician with an insight into disease diagnosis, prognosis and disease activity. 2.,The simplest interpretation of this data is that soluble proteins are just sensitive markers of inflammation. However, they may in fact be modulating inflammation directly through interaction with circulating cells. 3.,Recent work has shown that these soluble proteins do indeed remain active and can bind to functional ligands expressed by circulating leucocytes. The current review focuses on the soluble proteins C-reactive protein and soluble P-selectin and describes previous studies characterizing their interaction with immune cells to modulate the pathogenesis of vascular disease. 4.,The current review focuses on the soluble proteins C-reactive protein and soluble P-selectin and describes previous studies characterizing their interaction with immune cells to modulate the pathogenesis of vascular disease. [source]

    Vascular Disease in an Expanding World: Seeking Answers Inside and Outside of the Box

    James A. Sloand MD
    No abstract is available for this article. [source]

    Vascular Disease: A Handbook for Nurses

    Gobnait Byrne

    Trafficking of Murine Hematopoietic Stem and Progenitor Cells in Health and Vascular Disease

    MICROCIRCULATION, Issue 6 2009
    ABSTRACT Hematopoietic stem cells (HSCs) possess the unique capacity for self-renewal and differentiation into various hematopoietic cell lineages. Here we summarize the processes that underlie their mobilization and directed migration from bone marrow into peripheral tissues and back to the bone marrow compartment. We specifically focus on the potential role of hematopoietic stem and progenitor cell (HSPC) migration in vascular diseases and review data from recent studies on mice. A better understanding of the mechanisms that guide HSPCs to vascular tissues will be critical for the development of novel therapeutic strategies to prevent or reverse cardiovascular diseases. [source]

    Glycemic Targets for Patients with Type 2 Diabetes Mellitus

    Ole-Petter R. Hamnvik MB
    Abstract Cardiovascular disease is the predominant cause of death in diabetic patients, and reducing the risk of cardiovascular disease in diabetics has recently been the focus of several highly publicized large trials, including ACCORD (Action To Control Cardiovascular Risk in Diabetes), ADVANCE (Action in Diabetes and Vascular Disease: Preterax and Diamicron MR Controlled Evaluation), and VADT (Veterans Affairs Diabetes Trial). These studies randomized high-risk diabetic patients into either intensive treatment or standard treatment. The glycemic control arm of ACCORD was terminated 17 months before the planned end of the study because of a finding of significantly increased all-cause and cardiovascular mortality in the intensive treatment group. These findings were not duplicated in either ADVANCE or VADT. Multiple possible explanations have been brought forward, including a higher incidence of death from unrecognized hypoglycemia, effects due to increased exposure to particular antidiabetic medications, adverse effects of rapid correction of hyperglycemia, weight gain, and differences in baseline characteristics. None of these were validated in post hoc analyses of the trial data, and the cause of the increased mortality remains elusive. Subgroup analyses suggest that those who start off with better control of their diabetes or without preexisting cardiovascular disease may have the most to gain from tight glycemic control. Reducing the risk of macrovascular disease and death in diabetic patients requires not only attention to glucose control but also meticulous attention to control of nonglycemic risk factors, including hypertension, hyperlipidemia, smoking, lack of exercise, and unhealthy diet as well as timely prescription of medications with proven preventative benefits, such as aspirin and statins. Mt Sinai J Med 76:227,233, 2009. 2009 Mount Sinai School of Medicine [source]

    A Simple Noninvasive Test to Detect Vascular Disease in Patients with Erectile Dysfunction: A Novel Method

    MSc (Urol.), Shawket Alkhayal MB ChB
    ABSTRACT Introduction., The association between erectile dysfunction (ED) and cardiovascular disease (CVD) is becoming increasingly evident. Both conditions are thought to share a common denominator, which is endothelial dysfunction. Therefore, testing endothelial function in ED patients may serve to detect vascular disease in this cohort of patients. Aims., To investigate whether measuring the reactive hyperemic response (RHR) of the forearm vessels through a simple noninvasive method could identify vascular disease in patients with ED. Patients and Methods., Forty-eight male subjects were recruited into the study, 35 of whom presented to the sexual dysfunction clinic with a complaint of ED, and 13 healthy subjects served as a control group. The ED patients were subdivided into two groups, according to the presence or absence of CVD or its risk factors. The RHR of the forearm vessels was measured noninvasively in all subjects by using a handheld Doppler device. Results., Significant reduction in the peak systolic velocity ration was observed in ED patients with concomitant CVD or risk factors in comparison with the other ED patients with no CVD or risk factors and the control group. Results were highly significant on both occasions (P < 0.001). The 50% recovery time was not significantly different between any of the groups (P > 0.05). Conclusion., Our results suggest that those patients with impaired RHR have an abnormality in their vascular system, which is likely to be the cause of their ED and CVD. Using this simple noninvasive method can help to identify vascular disease in ED patients. It can also be used to suggest vascular disease in any patient, where further tests might be indicated. Alkhayal S, Lehmann V, and Thomas P. A simple noninvasive test to detect vascular disease in patients with erectile dysfunction: A novel method. J Sex Med 2006;3:331,336. [source]

    Treatment by Mycophenolate Mofetil of Advanced Graft Vascular Disease in Non-Human Primate Recipients of Orthotopic Aortic Allografts

    Jochen Klupp
    Failure to control chronic graft dysfunction [e.g. graft vascular disease (GVD)] is the primary cause of immunologic graft failure. This is the first study of mycophenolate mofetil (MMF) for the treatment of GVD in non-human primate recipients of aortic allografts. Abdominal aortic allografts were exchanged between mixed leukocyte reaction (MLR) -mismatched, blood-group-compatible cynomolgus monkeys. Six control recipients were untreated. Individualized treatment with frequent dose adjustments of MMF insured that treatment was close to the maximum tolerated dose (mean 99.2 mg/kg/day). Immune-mediated injury proceeded unhindered until day 45, after which MMF treatment began. Changes in intimal volume (IV) were quantified by intravascular ultrasound (IVUS) and compared to histology on day 105. Serial IVUS measurements of IV (mm3) in controls showed progressive GVD. In four out of six animals, MMF was well tolerated, thus enabling optimum treatment; in all these animals, IV was significantly less than in the control animals (p = 0.02). In the two remaining animals, high doses were not tolerated; at day 105, there was no significant difference in IV between them and the controls. We found a significant correlation between the mean MMF tolerated dose and the inhibition of progression of IV (r = ,0.88, p = 0.015). When high MMF doses were tolerated, MMF slowed progression of GVD. [source]

    Translational Mini-Review Series on Immunology of Vascular Disease: Accelerated atherosclerosis in vasculitis

    J. W. Cohen Tervaert
    Premature atherosclerosis has been observed during the course of different systemic inflammatory diseases such as rheumatoid arthritis and sytemic lupus erythematosus. Remarkably, relatively few studies have been published on the occurrence of accelerated atherosclerosis in patients with vasculitis. In giant cell arteritis (GCA), mortality because of ischaemic heart disease is not increased. In addition, intima media thickness (IMT) is lower in patients with GCA than in age-matched controls. In contrast, IMT is increased significantly in Takayasu arteritis, another form of large vessel vasculitis occurring in younger patients. In Takayasu arteritis and in Kawasaki disease, a form of medium-sized vessel vasculitis, accelerated atherosclerosis has been well documented. In small vessel vasculitis because of anti-neutrophil cytoplasmic autoantibodies-associated vasculitis, cardiovascular diseases are a major cause of mortality. IMT measurements reveal conflicting results. During active disease these patients experience acceleration of the atherosclerotic process. However, when inflammation is controlled, these patients have atherosclerotic development as in healthy subjects. Several risk factors, such as diabetes and hypertension, are present more often in patients with vasculitis compared with healthy controls. In addition, steroids may be pro-atherogenic. Most importantly, many patients have impaired renal function, persistent proteinuria and increased levels of C-reactive protein, well-known risk factors for acceleration of atherosclerosis. Enhanced oxidation processes, persistently activated T cells and reduced numbers of regulatory T cells are among the many pathophysiological factors that play a role during acceleration of atherogenesis. Finally, autoantibodies that may be relevant for acceleration of atherosclerosis are found frequently in elevated titres in patients with vasculitis. Because patients have an increased risk for cardiovascular events, vasculitis should be treated with as much care as possible. In addition, treatment should be considered with angiotensin-converting-enzyme inhibitors and/or angiotensin receptor-1 blockers, statins and acetylsalicyl acid. Finally, classical risk factors for cardiovascular disease should be monitored and treated as much as possible. [source]

    Translational Mini-Review Series on Immunology of Vascular Disease: Inflammation, infections and Toll-like receptors in cardiovascular disease

    J. R. Ward
    Summary Cardiovascular disease, in which atherosclerosis is the major underlying cause, is currently the largest cause of death in the world. Atherosclerosis is an inflammatory disease characterized by the formation of arterial lesions over a period of several decades at sites of endothelial cell dysfunction. These lesions are composed of endothelial cells, vascular smooth muscle cells, monocytes/macrophages and T lymphocytes (CD4+). As the lesions progress some can become unstable and prone to disruption, resulting in thrombus formation and possibly a myocardial infarction or stroke depending upon the location. Although the exact triggers for plaque disruption remain unknown, much recent evidence has shown a link between the incidence of myocardial infarction and stroke and a recent respiratory tract infection. Interestingly, many reports have also shown a link between a family of pattern recognition receptors, the Toll-like receptors, and the progression of atherosclerosis, suggesting that infections may play a role in both the progression of atherosclerosis and in inducing the more severe complications associated with the disease. [source]

    Reducing the Risk of Vascular Disease: Antiplatelet Therapy in the New Millennium

    Spencer B. King III M.D.
    No abstract is available for this article. [source]

    Vascular disease and affective disorders.

    2002., Edited by Chiu E. Ames D., Katona C. Martin Dunitz Limited, London
    No abstract is available for this article. [source]

    Long-term streptozotocin-induced diabetes alters prostanoid production in rat aorta and mesenteric bed

    H. A. Peredo
    Summary 1 Vascular disease is a major cause of mortality and morbidity in chronic diabetes mellitus. 2 Prostanoids, metabolites of arachidonic acid, include vasoactive substances produced and released from the vascular wall. Alterations in prostanoid production have been reported in the vasculature of diabetic humans and experimental animals. 3 The aim of the present work was to study the influence of three different periods of long-term streptozotocin-induced diabetes, 30, 120 and 180 days in the production of prostanoids in the thoracic aorta and in the mesenteric vascular bed of the rat. The prostanoids released to the incubation medium by the tissues were extracted and measured by reversed-phase HPLC. 4 In the diabetic groups, body weight was reduced and glycaemia was increased when compared with the corresponding non-diabetic controls. 5 In the aorta, 30 days of diabetes did not modify the prostanoid release pattern, meanwhile 120 and 180 days of incubation decreased prostacyclin (PGI2) production. In the mesenteric bed, at 30 days the release of the vasodilators PGI2 and prostaglandin (PGE2) and the vasoconstrictor thromboxane (TXA2) was reduced. At 120 days the vasodilators were reduced and at 180 days such reduction was joined by an increase of the release of vasoconstrictor metabolites. 6 Thirty days of diabetes did not modify the PGI2/TXA2 ratio in the aorta or mesenteric bed. On the other hand, 120 and 180 days of diabetes reduced significantly the ratio when compared with the corresponding controls. 7 In conclusion, the mesenteric bed, a resistance vascular bed, seems to be more sensitive than the aorta, a conductance vessel, to the effects of diabetes on prostanoid production. The observed effects contribute to a displacement of the balance of prostanoid release in favour of the vasoconstrictor metabolites, a phenomenon that could be related to the vascular complications of diabetes mellitus. [source]

    Endothelial cell expression of adhesion molecules is induced by fetal plasma from pregnancies with umbilical placental vascular disease

    Xin Wang
    Objective To test the hypothesis that local production with spill into the fetal circulation of factor(s) injurious to endothelium is responsible for the vascular pathology present when the umbilical artery Doppler study is abnormal. Expression of adhesion molecules is a feature of endothelial cell activation. Design Case,control study. Setting University teaching hospital. Samples Fetal plasma was collected from 27 normal pregnancies, 39 pregnancies with umbilical placental vascular disease defined by abnormal umbilical artery Doppler and 11 pregnancies with pre-eclampsia and normal umbilical artery Doppler. Methods Isolated and cultured human umbilical vein endothelial cells from normal pregnancies were incubated with fetal plasma from three study groups. mRNA expression of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and platelet-endothelial cell adhesion molecule-1 (PECAM-1) were assessed by reverse transcription-polymerase chain reaction. To confirm the occurrence of this in vivo, we measured the levels of soluble fractions of sICAM-1, sVCAM-1 and sPECAM-1 in the fetal circulation in the fetal plasma used for endothelial cell incubation. Results The mRNA expression of ICAM-1 [median 1.1 (interquartile range 0.5,1.9) vs 0.7 (0.3,1.2), P < 0.05] and PECAM-1 [2.1 (1.2,3.0) vs 1.5 (0.7,2.1), P < 0.05] was significantly higher following incubation with fetal plasma from umbilical placental vascular disease compared with the normal group. There was no difference in the expression of VCAM-1 [1.2 (0.9,1.8) vs 1.1 (0.8,1.6), ns]. The group with maternal pre-eclampsia and normal umbilical artery Doppler did not differ from the normal group. In the umbilical placental vascular disease group, the results were similar in the presence or absence of pre-eclampsia. For soluble fractions of the adhesion molecules released into the fetal circulation, we found the levels (ng/mL) of sICAM-1 [median 248.5 (interquartile range 197.3,315.7) vs 174.2 (144.5,212.9), P < 0.05] and sPECAM-1 [9.3 (6.2,11.1) vs 6.1 (5.4,7.7), P < 0.05] in fetal plasma to be significantly increased in the presence of umbilical placental vascular disease compared with the normal. Conclusions Vascular disease in the fetal umbilical placental circulation is associated with an elevation in mRNA expression by endothelial cells of ICAM-1 and PECAM-1. Our study provides evidence for endothelial cell activation and dysfunction in umbilical placental vascular disease. We speculate that the plasma factor(s) affecting the vessels of the umbilical villous tree is locally released by the trophoblast. The occurrence of the maternal syndrome of pre-eclampsia appears to be independent of this. [source]

    Pulmonary Hypertension in Patients after Repair of Transposition of the Great Arteries

    Ellen Chan MD
    ABSTRACT One well-documented complication of unrepaired d-transposition of the great arteries (d-TGA) is progressive pulmonary vascular disease. It is generally accepted that pulmonary vascular disease will not develop if d-TGA repair is performed early in life. Herein, we report a number of repaired d-TGA, especially in older patients with Mustard/Senning procedures, in whom pulmonary vascular disease developed years after their original repair. The etiology of this phenomenon is unknown, warranting further investigation. Our case reports highlight an overlooked, possible long-term complication following d-TGA repair. From this experience, we recommend that evidence of progressive pulmonary vascular disease may need to be regularly sought during the follow-up of patients after d-TGA repair, especially Mustard/Senning repairs, as early treatment of pulmonary hypertension may improve long-term clinical outcomes. [source]

    Mesotherapy and Phosphatidylcholine Injections: Historical Clarification and Review

    BACKGROUND Mesotherapy was originally conceived in Europe as a method of utilizing cutaneous injections containing a mixture of compounds for the treatment of local medical and cosmetic conditions. Although mesotherapy was traditionally employed for pain relief, its cosmetic applications, particularly fat and cellulite removal, have recently received attention in the United States. Another treatment for localized fat reduction, which was popularized in Brazil and uses injections of phosphatidylcholine, has been erroneously considered synonymous with mesotherapy. Despite their attraction as purported "fat-dissolving" injections, the safety and efficacy of these novel cosmetic treatments remain ambiguous to most patients and physicians. OBJECTIVE To distinguish mesotherapy from phosphatidylcholine injections by reviewing their history and the relevant experimental or clinical findings. METHODS A comprehensive search of Medline indexed literature and conference proceedings. RESULTS All the published studies evaluating the clinical efficacy of traditional mesotherapy currently originate from Europe. These reports focus primarily on musculoskeletal pain and vascular disease, rather than cosmetic applications. Although experimental data suggest that a number of traditional mesotherapy ingredients may theoretically reduce fat, these effects have not been supported in peer-reviewed studies. An increasing number of reports demonstrate that subcutaneous injections of a formula containing phosphatidylcholine combined with its emulsifier, deoxycholate, are effective in removing small collections of adipose tissue. Cell lysis, resulting from the detergent action of deoxycholate, may account for this clinical effect. CONCLUSIONS Mesotherapy is distinct from a method of treating adipose tissue with subcutaneous injections of deoxycholate alone or in combination with phosphatidylcholine. Additional clinical and experimental studies are necessary to more definitively establish the safety and efficacy of these treatments. [source]

    Renal vascular disease in neurofibromatosis type 2: association or coincidence?

    Nuno JV Cordeiro MBChB MRCPCH
    Neurofibromatosis type 2 (NF2) remains a challenging diagnosis in childhood where there may be no neurological involvement. A 12-month-old male in whom NF2 was suspected because of characteristic ophthalmological and cutaneous lesions is reported. Cranial MRI showed no tumours. A pathogenic mutation was identified on NF2 gene analysis. The child developed hypertension due to renal vascular disease. Although renal vascular disease is a recognized complication of neurofibromatosis type 1 (NF1), it has not been reported in NF2. [source]

    A cardiologist view of vascular disease in diabetes

    Christopher J. Lockhart
    Diabetes mellitus is a potent risk factor for the development of a wide spectrum of cardiovascular (CV) complications. The complex metabolic milieu accompanying diabetes alters blood rheology, the structure of arteries and disrupts the homeostatic functions of the endothelium. These changes act as the substrate for end-organ damage and the occurrence of CV events. In those who develop acute coronary syndromes, patients with diabetes are more likely to die, both in the acute phase and during follow-up. Patients with diabetes are also more likely to suffer from chronic cardiac failure, independently of the presence of large vessel disease, and also more likely to develop stroke, renal failure and peripheral vascular disease. Preventing vascular events is the primary goal of therapy. Optimal cardiac care for the patient with diabetes should focus on aggressive management of traditional CV risk factors to optimize blood glucose, lipid and blood pressure control. Targeting medical therapy to improve plaque stability and diminish platelet hyper-responsiveness reduces the frequency of events associated with atherosclerotic plaque burden. In patients with critical lesions, revascularization strategies, either percutaneous or surgical, will often be necessary to improve symptoms and prevent vascular events. Improved understanding of the vascular biology will be crucial for the development of new therapeutic agents to prevent CV events and improve outcomes in patients with diabetes. [source]

    Pomegranate flower: a unique traditional antidiabetic medicine with dual PPAR-,/-, activator properties

    Yuhao Li
    PPARs are transcription factors belonging to the superfamily of nuclear receptors. PPAR-, is involved in the regulation of fatty acid (FA) uptake and oxidation, inflammation and vascular function, while PPAR-, participates in FA uptake and storage, glucose homeostasis and inflammation. The PPARs are thus major regulators of lipid and glucose metabolism. Synthetic PPAR-, or PPAR-, agonists have been widely used in the treatment of dyslipidaemia, hyperglycaemia and their complications. However, they are associated with an incidence of adverse events. Given the favourable metabolic effects of both PPAR-, and PPAR-, activators, as well as their potential to modulate vascular disease, combined PPAR-,/-, activation has recently emerged as a promising concept, leading to the development of mixed PPAR-,/-, activators. However, some major side effects associated with the synthetic dual activators have been reported. It is unclear whether this is a specific effect of the particular synthetic compounds or a class effect. To date, a medication that may combine the beneficial metabolic effects of PPAR-, and PPAR-, activation with fewer undesirable side effects has not been successfully developed. Pomegranate plant parts are used traditionally for the treatment of various disorders. However, only pomegranate flower has been prescribed in Unani and Ayurvedic medicines for the treatment of diabetes. This review provides a new understanding of the dual PPAR-,/-, activator properties of pomegranate flower in the potential treatment of diabetes and its associated complications. [source]

    The metabolic syndrome in type 2 diabetes: When does it matter?

    J. Wong
    Aims:, Young adults with type 2 diabetes (T2Dm) present the clinician with the problem of when to start therapies for the primary prevention of vascular disease and how to identify those at most vascular risk. We examine whether the metabolic syndrome (MetS) can be a useful clinical tool to stratify vascular risk in this context. Methods:, Data were collected from 5928 subjects with T2Dm, and subjects were categorized as having MetS by World Health Organization criteria (body mass index criteria modified for Asians using >23 kg/m2). The prevalence of macrovascular disease was examined by MetS status and age. Results:, The overall MetS prevalence was 72.3%. MetS was associated with an increased prevalence of ischaemic heart disease (IHD) (17.2% MetS vs. 11.6% no MetS, p < 0.0001), coronary artery bypass graft (7.6 vs. 4.7%, p < 0.0003), peripheral vascular disease (PVD) (4.7 vs. 3.7%, p = 0.08) and stroke (6 vs. 3.9%, p = 0.002) across all age groups. MetS subjects had an IHD prevalence equivalent to that seen in subjects who were one decade older without MetS. The most significant impact of MetS was for the age group of 40,49 years with much lesser impact seen with progressively increasing age [odds ratio (OR) = 2.1 for IHD in MetS compared with no MetS at age 40,50 years, p < 0.05; falling progressively to OR = 1.5 at age >70 years, p > 0.05]. Similar trends were seen for coronary artery by-pass graft (CABG) and PVD. There was a strong relationship between the number of MetS risk factors and IHD prevalence (r = 0.99, p = 0.0001). Conclusions:, These data suggest that MetS is particularly useful in stratifying vascular risk in younger T2Dm patients and in those with a high number of MetS components. For patients with MetS, especially those with a full house of MetS risk factors, commencing risk-lowering interventions 10 years earlier than their MetS-free counterparts could be considered. [source]

    Economic aspects of diabetic foot care in a multidisciplinary setting: a review

    Giovanni A. Matricali
    Abstract Background To evaluate the economic aspects of diabetic foot care in a multidisciplinary setting. Method A review of the English language literature, published from 1966 to November 2005. Results The results of available studies on the cost-of-illness of diabetic foot problems are difficult to compare. Nevertheless trends concerning excess of costs, protraction in time of costs, positive correlation to severity of ulcer and/or peripheral vascular disease, contribution of in-hospital stay and length of stay, and the patient's own contribution to total costs, are obvious. Only a few cost-effectiveness and cost-utility studies are available. Most use a Markov based model to predict outcome and show an acceptable result on long-term. Conclusions Diabetic foot problems are frequent and are associated with high costs. A multidisciplinary approach to diabetic foot problems has proved to be cost saving with regard to cost of treatment itself. Nevertheless, it remained unclear if these savings could offset the overall costs involved in implementing this kind of approach. The few studies that address this issue specifically all show an acceptable cost-effectiveness, but often the profit will be evident after some years only, because long-term costs are involved. Based on these data, policymakers should foresee sufficient reimbursement for preventive and early curative measures, and not only for ,salvage manoeuvres'. Copyright 2007 John Wiley & Sons, Ltd. [source]

    ,Lipoproteins, glycoxidation and diabetic angiopathy'

    Alicia J. Jenkins
    Abstract The chronic vascular complications of diabetes (nephropathy, retinopathy and accelerated atherosclerosis) are a major cause of morbidity and premature mortality. In spite of the more widespread availability of intensive diabetes management, approximately one in three people with diabetes develop aggressive complications and over 70% die of atherosclerosis-related diseases. Genetic and acquired factors are likely to be contributory. Potential mediators of vascular damage may include the interrelated processes of lipoprotein abnormalities, glycation, oxidation and endothelial dysfunction. Lipoprotein abnormalities encompass alterations in lipid concentrations, lipoprotein composition and subclass distribution and lipoprotein-related enzymes. Nonenzymatic glycation and oxidative damage to lipoproteins, other proteins and to vascular structures may also be deleterious. As atherosclerosis is a chronic condition commencing in youth, and because clinical events may be silent in diabetes, surrogate measures of vascular disease are important for early identification of diabetic patients with or at high risk of vascular damage, and for monitoring efficacy of interventions. The increasing array of biochemical assays for markers and mediators of vascular damage, noninvasive measures of vascular health, and therapeutic options should enable a reduction in the excessive personal and economic burden of vascular disease in type 1 and type 2 diabetes. Copyright 2004 John Wiley & Sons, Ltd. [source]

    Prevalence of silent myocardial ischaemia in new-onset middle-aged Type 2 diabetic patients without other cardiovascular risk factors

    DIABETIC MEDICINE, Issue 7 2006
    P. Fornengo
    Abstract Aims Coronary artery disease (CAD) is the leading cause of death in patients with Type 2 diabetes and is often asymptomatic. Silent myocardial ischaemia (SMI) is frequent in diabetic subjects and is responsible for a late diagnosis of CAD; its early detection is important. There are some data about the prevalence of SMI in Type 2 diabetic patients at high risk for cardiovascular disease, while no data are available in subjects at the onset of diabetes without other cardiovascular risk factors. Methods We screened 274 consecutive patients (mean age 64.3 8.4 years, 66% male) at the time of diagnosis of Type 2 diabetes; we enrolled 111 subjects without other cardiovascular disease risk factors (dyslipidaemia, hypertension, peripheral vascular disease, retinopathy, microalbuminuria, history of heart disease) and with normal resting electrocardiogram (ECG). Participants performed a maximal ECG exercise protocol and, if positive, underwent coronary angiography. Results The ECG exercise test was positive in 19 patients (17.1%); of those 14 (13%) had angiographic coronary disease (one with three-vessel disease, three with two vessels and 10 with one vessel involved). The positive predictive value of the exercise ECG for predicting angiographic coronary disease was 73%. Conclusions The prevalence of SMI was 17% and angiographic coronary disease was found in 13% of middle-aged subjects with new-onset Type 2 diabetes without other cardiovascular risk factors. This prevalence is similar to that observed in studies of subjects with long duration diabetes who have additional cardiovascular risk factors. [source]

    Increased prevalence of cardiovascular disease in Type 2 diabetic patients with non-alcoholic fatty liver disease

    DIABETIC MEDICINE, Issue 4 2006
    G. Targher
    Abstract Aims, To estimate the prevalence of cardiovascular disease (CVD) in Type 2 diabetic patients with and without non-alcoholic fatty liver disease (NAFLD), and to assess whether NAFLD is independently related to prevalent CVD. Methods, We studied 400 Type 2 diabetic patients with NAFLD and 400 diabetic patients without NAFLD who were matched for age and sex. Main outcome measures were prevalent CVD (as ascertained by medical history, physical examination, electrocardiogram and echo-Doppler scanning of carotid and lower limb arteries), NAFLD (by ultrasonography) and presence of the metabolic syndrome (MetS) as defined by the World Health Organization or Adult Treatment Panel III criteria. Results, The prevalences of coronary (23.0 vs. 15.5%), cerebrovascular (17.2 vs. 10.2%) and peripheral (12.8 vs. 7.0%) vascular disease were significantly increased in those with NAFLD as compared with those without NAFLD (P < 0.001), with no differences between sexes. The MetS (by any criteria) and all its individual components were more frequent in NAFLD patients (P < 0.001). In logistic regression analysis, male sex, age, smoking history and MetS were independently related to prevalent CVD, whereas NAFLD was not. Conclusions, The prevalence of CVD is increased in patients with Type 2 diabetes and NAFLD in association with an increased prevalence of MetS as compared with diabetic patients without NAFLD. Follow-up studies are necessary to determine whether this higher prevalence of CVD among diabetic patients with NAFLD affects long-term mortality. Diabet. Med. (2006) [source]

    Recent concepts in non-alcoholic fatty liver disease

    DIABETIC MEDICINE, Issue 9 2005
    L. A. Adams
    Abstract Non-alcoholic fatty liver disease (NAFLD) is present in up to one-third of the general population and in the majority of patients with metabolic risk factors such as obesity and diabetes. Insulin resistance is a key pathogenic factor resulting in hepatic fat accumulation. Recent evidence demonstrates NAFLD in turn exacerbates hepatic insulin resistance and often precedes glucose intolerance. Once hepatic steatosis is established, other factors, including oxidative stress, mitochondrial dysfunction, gut-derived lipopolysaccharide and adipocytokines, may promote hepatocellular damage, inflammation and progressive liver disease. Confirmation of the diagnosis of NAFLD can usually be achieved by imaging studies, however, staging the disease requires a liver biopsy. NAFLD is associated with an increased risk of all-cause death, probably because of complications of insulin resistance such as vascular disease, as well as cirrhosis and hepatocellular carcinoma, which occur in a minority of patients. NAFLD is also now recognized to account for a substantial proportion of patients previously diagnosed with ,cryptogenic cirrhosis'. Diabetes, obesity and the necroinflammatory form of NAFLD known as non-alcoholic steatohepatitis, are risk factors for progressive liver disease. Current treatment relies on weight loss and exercise, although various insulin-sensitizing medications appear promising. Further research is needed to identify which patients will achieve the most benefit from therapy. [source]

    New and experimental approaches to treatment of diabetic foot ulcers: a comprehensive review of emerging treatment strategies

    DIABETIC MEDICINE, Issue 11 2004
    R. Eldor
    Abstract Diabetic foot ulcers occur in up to 15% of all diabetic patients and are a leading cause of nontraumatic amputation worldwide. Neuropathy, abnormal foot biomechanics, peripheral vascular disease and external trauma are the major contributors to the development of a foot ulcer in the diabetic patient. Therapy today includes repeated debridement, offloading, and dressings, for lower grade ulcers, and broad spectrum antibiotics and occasionally limited or complete amputation for higher grades, requiring a team effort of health care workers from various specialties. The large population affected by diabetic foot ulcers and the high rates of failure ending with amputation even with the best therapeutic regimens, have resulted in the development of new therapies and are the focus of this review. These include new off loading techniques, dressings from various materials, methods to promote wound closure using artificial skin grafts, different growth factors or wound bed modulators and methods of debridement. These new techniques are promising but still mostly unproven and traditional approaches cannot be replaced. New and generally more expensive therapies should be seen as adding to traditional approaches. [source]

    Effects of diabetes on plasma nitrotyrosine levels

    DIABETIC MEDICINE, Issue 6 2004
    X. L. Wang
    Abstract Background Oxidative stress plays a major role in disease processes such as atherosclerosis and diabetes. Peroxynitrite is a reaction product of nitric oxide (NO) and superoxide and a potent oxidant. The peroxynitrite-mediated tyrosine nitration, which forms nitrotyrosine (NT), is associated with several pathological conditions. Methods We measured plasma NT levels using the HPLC method in 40 Mexican Americans with diabetes, but not taking medications, and 40 age- and sex-matched euglycaemic controls. Results Plasma-free NT levels were not different between subjects with diabetes (11.0 1.7 nmol/l, n = 40) and with non-diabetes (10.4 1.5 nmol/l, n = 40). There was also no association with levels of fasting glucose (r = ,0.049, P = 0.663) or 2-h glucose (r = ,0.099, P = 0.390). However, females had significantly lower free NT level (7.6 1.4 nmol/l, n = 40) than males (13.8 1.7 nmol/l, n = 40, P = 0.005), which were not affected by age, smoking status, BMI and glucose levels. Conclusions In contrast to some earlier reports, our study shows that diabetes has no effect on plasma NT levels in Mexican Americans. We have also demonstrated lower free NT levels in females than males, which may partly explain the lower risk profile to vascular disease in women. [source]

    Brachial-ankle pulse wave velocity measured automatically by oscillometric method is elevated in diabetic patients with incipient nephropathy

    DIABETIC MEDICINE, Issue 11 2003
    H. Yokoyama
    Abstract Aims To examine whether brachial-ankle pulse wave velocity (baPWV), a possible early marker of atherosclerotic vascular damage, is associated with albuminuria in patients with Type 2 diabetes. Methods BaPWV was measured by automatic oscillometric method in 346 Type 2 diabetic patients with normoalbuminuria (a mean level of three times measurements of albumin-to-creatinine (ACR) < 30 g/mg creatinine; n = 200), incipient nephropathy (a mean level of ACR , 30 and < 300 g/mg creatinine; n = 119), and clinical nephropathy (a mean level of ACR , 300 g/mg creatinine; n = 27), and without peripheral vascular disease. Results BaPWV (cm/s) was significantly higher in patients with incipient nephropathy (1722 382) and clinical nephropathy (1763 322) than in patients with normoalbuminuria (1559 343, P < 0.0001, respectively). By univariate analysis it correlated significantly with age (r = 0.44, P < 0.0001), systolic blood pressure (r = 0.55, P < 0.0001), diastolic blood pressure (r = 0.42, P < 0.0001), albuminuria (r = 0.24, P < 0.0001) and HbA1C (r = 0.11, P < 0.05). Albuminuria revealed an independent significant association with baPWV (P < 0.01) after adjustment for age, sex, smoking, BMI, HbA1C, hyperlipidemia, and hypertension. Multiple regression analysis showed age, diastolic blood pressure and albuminuria were independently associated with baPWV (adjusted R2 = 0.42, P < 0.0001). Conclusions The results might indicate a possible link between the pathogenesis of atherosclerosis and diabetic nephropathy. Future studies are needed to clarify the usefulness and its predictable value. [source]

    Peripheral blood level alterations of TIMP-1, MMP-2 and MMP-9 in patients with Type 1 diabetes

    DIABETIC MEDICINE, Issue 10 2001
    P. R. Maxwell
    Abstract Aim To determine the plasma levels of enzymes and inhibitors involved in extracellular matrix turnover in patients with Type 1 diabetes with normal renal function. Methods Plasma levels of matrix metalloproteinases 2 and 9 (MMP-2, MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) were measured in 43 Type 1 diabetic subjects and age- and sex-matched controls. Results No significant difference in plasma MMP-2 between diabetic patients and controls was observed. MMP-9 was detected in the plasma of 15 diabetic patients (35%), but undetectable in all control subjects (P < 0.015). Plasma TIMP-1 concentrations were significantly elevated (P < 0.001) in diabetic patients compared to controls. There was no correlation observed between MMP-2, MMP-9 and TIMP-1 and similarly between MMP-2, MMP-9 and TIMP-1 and age, duration of diabetes, blood pressure and glycated haemoglobin (HbA1c). Conclusions This study has demonstrated alterations in several plasma extracellular matrix modulators in the absence of significant vascular disease. Diabet. Med. 18, 777,780 (2001) [source]

    Blindness following a diabetic foot infection: a variant to the ,eye,foot syndrome'?

    DIABETIC MEDICINE, Issue 7 2000
    K. C. J. Yuen
    SUMMARY Aims The ,eye,foot syndrome' was initially described by Walsh et,al. to highlight the important association of foot lesions in patients with diabetic retinopathy. We present a case of a 58-year-old patient with Type 2 diabetes mellitus who developed blindness following endogenous staphylococcal endophthalmitis from an infected foot ulcer. Results Our case describes the link between the eye and the foot but is somewhat different to the association as described by Walsh et,al. Endogenous endophthalmitis is rare with diabetic patients being especially at risk, and we report the first case of endogenous staphylococcal endophthalmitis related to a diabetic foot lesion. Conclusions Our case illustrates several important issues in the management of diabetic patients admitted to hospital with infection; the need to thoroughly examine the feet to ascertain any foot lesions and any underlying peripheral vascular disease or peripheral neuropathy, to treat aggressively any infected foot lesions to prevent serious complications of septicaemia and to consider rare conditions like endogenous endophthalmitis in any diabetic patient presenting with acute visual impairment and septicaemia. [source]