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PubMed2005

[Advances of study on the relationship between vascular endothelial growth factor and ischemic cerebral vascular disease].

Vascular endothelial growth factor is a potent inducer of angiogenesis identified in recent years, and its relationship with ischemic cerebral vascular diseases is a hotspot for many investigators at present. In this review, we focus on the recent evidence for VEGF expression, biological effect and its role in the treatment and prognostication of ischemic cerebral vascular disease.

Angiogenesis Inducing Agents↗
PubMed2004

Smooth muscle progenitor cells in vascular disease.

Vascular smooth muscle cells have long been described as phenotypically diverse, with some populations possessing the potential for monoclonal expansion within the adult vessel wall. Recent experimental and human data suggest a potential role in atherosclerotic plaque, transplant arteriopathy, and angiogenesis biology for putative smooth muscle progenitor cells in the circulation, adult tissues, and the perivascular adventitia. The location, mobilization, and function of such progenitors is still poorly understood, but may include reparative or alternatively proliferative consequences for plaque development and progression. These observations provide a platform for re-evaluation of smooth muscle cell heterogeneity and progenitor biology in atherosclerosis, with implications for diagnosis and therapy of vascular disease.

Animals↗
PubMed2006

Plasminogen activator system and vascular disease.

Vascular diseases, such as atherosclerosis, thromboembolic disorders and stroke, in addition to surgical procedures such as restenosis, all share the plasminogen activator system as a central component in the pathogenesis of vascular injury. Since the development of plasminogen deficient mice our knowledge of the effects of this proteolytic system in cardiovascular disease has vastly increased. The plasminogen activator system plays a key role in vascular homeostasis and constitutes a critical response mechanism to cardiovascular injury. The central components of the PA system are the proteolytic activators, urokinase-plasminogen activator (u-PA) and tissue-type plasminogen activator (t-PA), plasminogen (plg) and its degradation product, plasmin, together with the major inhibitors of this system, plasminogen activator inhibitor-1 and -2 (PAI-1, PAI-2). An extensive network of additional proteases, inhibitors, receptors and modulators directly associate and are influenced by the PA system, the largest group being the Matrix Metalloproteinases (MMPs) and their respective inhibitors the Tissue inhibitors of MMPs (TIMPS).

Animals↗
PubMed1999

Heart allograft vascular disease: an obliterative vascular disease in transplanted hearts.

More than 30 years have passed since the first human heart transplantation was performed. Since then, short-term survival after heart transplantation has been markedly improved, but this development has not been paralleled with a similar improvement in long-term survival. One of the major reasons for this is the subsequent development of heart allograft vascular disease, an obliterative disease in the coronary arteries of the transplanted heart. The dubious effect of re-vascularization in this disease, the less favorable outcome after repeat heart transplantation, and the low donor supply have called for intensified research for new and efficient prophylactic therapies against heart allograft vascular disease. This research has lead to improved knowledge about diagnosis, etiology, pathogenesis, prophylaxis, and treatment possibilities. The most important among these seem to be: (i) the introduction of intravascular ultrasound for early detection of the disease; (ii) evidence to suggest that hyperlipidemia, insufficient immunosuppressive therapy, human leukocyte antigen (HLA)-mismatch, and infection with cytomegalovirus (CMV) all may promote allografts vascular disease; and (iii) the introduction of at least two promising prophylactic therapies in humans namely 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors and calcium entry blockers, and others potentially promising e.g. angiotensin-converting enzyme-inhibitors, angiopeptin, mycophenolate mofetil and rapamycin. This review summarizes present knowledge on the possibilities of inhibiting or treating heart allograft vascular disease incorporating evidence from both human and experimental studies.

Animals↗
PubMed2003

Exercise considerations in coronary artery disease, peripheral vascular disease, and diabetes mellitus.

Physical inactivity is a risk factor for cardiovascular disease. Regular aerobic and resistance training increases exercise capacity and plays a role both in the primary and secondary prevention of cardiovascular disease. Patients with coronary artery disease, peripheral vascular disease, or diabetes mellitus must be considered individually when prescribing exercise because their clinical status can vary greatly. In addition, a majority of these patients have multiple comorbid disorders such as renal, neurologic, and retinal disease that may affect their ability to exercise safely. Therefore, a preparticipation medical evaluation is required. An exercise prescription should be tailored to each person's unique set of circumstances and reflect an effort to maximize the anticipated benefits while minimizing the risks.

Clinical Laboratory Techniques↗
PubMed1984

Vascular disease and vascular function in the lower limb in diabetes.

This review examines the pathology, clinical effects and physiological disturbances produced by vascular disease and autonomic neuropathy in the lower limb in diabetic subjects. Atherosclerosis is a major factor in causing foot lesions in diabetics. The distribution of the disease frequently makes vascular reconstructive surgery difficult or impossible but an aggressive approach to reconstruction is justified because the results of major amputations are bad. Arterial calcification probably has no significant effect on the blood supply to the foot. There is some evidence that disease of arteries in the foot may be associated with the development of ulcers or gangrene. Disease of the arterioles and capillaries is frequent, but there is little evidence that this microangiopathy causes lesions. Autonomic neuropathy affecting the limb is also common, and although there are several mechanisms by which this might predispose to ulcers or gangrene, there is little evidence of such a direct relationship. In a patient presenting with ulceration or gangrene of the foot it is often impossible to determine the relative roles of vascular disease, affecting large or small vessels, and neuropathy, either somatic or autonomic, in the development of the lesion. Further progress depends on the development of more direct methods for assessing microvascular and autonomic nervous function.

Arteriosclerosis↗
PubMed1989

Unusual manifestations of brachiocephalic vascular disease.

Vascular problems involving the brachiocephalic vessels may occur from atherosclerosis, trauma, vasculitis, infection, and procedures for congenital heart disease. A wide variety of symptoms and signs may result from such disorders. This study is a report of five unusual manifestations of brachiocephalic vascular diseases. Diagnosis, management, and previous surgical experience is discussed relating to each case illustrating the complexity and variability of brachiocephalic vascular pathology.

Adult↗
PubMed1994

Southwestern Internal Medicine Conference: endothelial dysfunction and vascular disease.

Vascular endothelial cells, critically situated at the blood-tissue interface, exert important effects on vascular tone and permeability, regulate the coagulation and fibrinolytic systems, mediate translocation of inflammatory cells to the tissue compartment, and modulate proliferation of vascular smooth muscle cells. As the physiology of the endothelium has been defined, defects in endothelial function have been identified in association with human disease, and a syndrome of dysfunctional endothelium has been described. Although it remains debatable whether a coherent syndrome of endothelial dysfunction exists, disordered endothelial biology appears to contribute to the pathophysiology of human vascular disease. Identification of specific molecular mechanisms offers potential targets for novel therapeutic interventions, including genetic modification of endothelial cells in vivo.

Blood Coagulation↗
PubMed1985

Intraoperative color flow mapping by real-time two-dimensional Doppler echocardiography for evaluation of valvular and congenital heart disease and vascular disease.

We have developed real-time two-dimensional Doppler echocardiography, which can display color flow mapping on a two-dimensional echocardiogram. Intraoperative two-dimensional Doppler echocardiography was performed during cardiovascular operations before and after the definitive procedure in 33 patients, 14 with valvular disease, eight with congenital heart disease, and 11 with vascular disease. Its clinical usefulness was evaluated. In patients with valvular heart disease, 13 valve replacements, 10 valvuloplasties, and four untouched lesions were assessed. No paravalvular leakage and three instances of minimal physiological transvalvular leakage from St. Jude Medical valves in the mitral position were noticed. Regurgitation after valvuloplasty was graded by extent of the regurgitant flow. This grading, comparable to postoperative grading, indicated no need for an additional procedure. In congenital heart disease, preoperative diagnoses were confirmed. The effect of the corrective operation was evaluated and no significant leakage or stenosis was found. Interatrial shunt flow was shown to increase after operative balloon atrial septostomy in a patient with dextro-transposition of the great arteries. In 11 patients with dissecting aortic aneurysm, the aneurysm was totally visualized in the operative field, including the structure and flow dynamics. In two patients, the preoperative cineangiographic diagnosis regarding involvement of dissection was corrected. After the vascular procedure, sufficient flow in the major aortic branches was confirmed in all patients and minimal leakage at the suture line was noticed in four patients. In conclusion, intraoperative color flow mapping by two-dimensional Doppler echocardiography has enabled the precise diagnosis and the necessary operation to be determined before cardiopulmonary bypass. It has also allowed the effects of the operation to be assessed before chest closure.

Adult↗
PubMed2003

Molecular strategies to treat vascular diseases: circulating vascular progenitor cell as a potential target for prophylactic treatment of atherosclerosis.

Atherosclerosis is responsible for more than half of all deaths in Western countries. Numerous studies have reported that accumulation of smooth muscle cells (SMCs) plays a principal role in atherogenesis, post-angioplasty restenosis and transplantation-associated vasculopathy. Although much effort has been devoted to targeting the migration and proliferation of medial SMCs, effective therapy to prevent occlusive vascular remodeling has not been established. Recently, it was suggested that bone marrow-derived precursors can give rise to vascular cells that contribute to the repair, remodeling, and lesion formation of the arterial wall under certain circumstances. This review highlights the recent findings on circulating vascular precursors and describes the potential therapeutic strategies for vascular diseases, targeting mobilization, homing, differentiation and proliferation of circulating progenitor cells.

Animals↗
PubMed1994

[Autoantibodies in the diagnosis of vascular diseases].

Vascular abnormalities are frequent in connective tissue disease. In this kind of patients a lot of autoantibodies are observed. To screen them a strategy must be selected according to the connective tissue disease that is suspected. When the diagnosis is unknown the tests must screen a great number of autoantibodies and this is the case for indirect immunofluorescence assays, at the opposite when the diagnosis is known antibodies specific for the disease should be screened. Some antibodies are specific for a disease this is the case for antibodies directed against double stranded DNA, centromere, extractable nuclear antigens Sm, RNP, Scl-70, Pm-Scl, Jo1, neutrophil cytoplasmic antigen proteinase 3, and beta 2-glycoprotein I the cofactor of anti-cardiolipin antibodies. Anti-SS-A(Ro) antibodies are very frequent in autoimmune diseases and they are not specific for anyone of them. Some autoantibodies are frequent in autoimmune and also in non autoimmune diseases and this is the case for antibodies directed against phospholipids, single stranded DNA, histones, rheumatoid factor. The detection of antibodies depends on the assays used for screening, that is why results should mention the assay used for their detection. The standardization of the detection of the autoantibodies especially when quantitative results are requested, is not yet performed enough. So to obtain reproducible results when monitoring a patient the screening must be done by the same assay in the same laboratory.

Antibody Specificity↗
PubMed2000

Protein kinase C activation and its pharmacological inhibition in vascular disease.

Vascular complications in diabetes mellitus are known to be associated with the activation of the protein kinase C (PKC) pathway through the de novo synthesis of diacylglycerol (DAG) from glycolytic intermediates. Specific PKC isoforms, mainly the beta- and delta-isoforms, have been shown to be persistently activated in diabetic mellitus. Multiple studies have reported that the activation of PKC leads to increased production of extracellular matrix and cytokines, enhances contractility, permeability and vascular cell proliferation, induces the activation of cytosolic phospholipase A2 and inhibits the activity of Na+-K+-ATPase. These events are not only frequently observed in diabetes mellitus but are also involved in the actions of vasoactive agents or oxidative stress. Inhibition of PKC by two different kinds of PKC inhibitors - LY333531, a selective PKC-beta-isoform inhibitor, and vitamin E, d-alpha-tocopheron - were able to prevent or reverse the various vascular dysfunctions in vitro and in vivo. Clinical studies using these compounds are now ongoing to evaluate the significance of DAG-PKC pathway activation in the development of vascular complications in diabetic patients.

Animals↗
PubMed2000

Affective behavioural disturbances in Alzheimer's disease and ischaemic vascular disease.

OBJECTIVES: To investigate affective change in Alzheimer's disease and ischaemic vascular disease and examine the contribution of white matter disease to psychopathology in these dementias. Based on earlier studies, it was predicted that: (1) depression would be more prevalent and severe in ischaemic vascular disease; (2) psychomotor slowing would be more prevalent in ischaemic vascular disease; (3) apathy would be more prevalent in ischaemic vascular disease; and (4) The degree of white matter disease would be positively correlated with the severity of psychomotor slowing. METHODS: Ratings of affective/behavioural states and white matter disease were compared in 256 patients with Alzheimer's disease and 36 patients with ischaemic vascular disease or mixed dementia with an ischaemic vascular component using analysis of variance (ANOVA) and linear regression models. RESULTS: The findings were: (1) decreased affect/withdrawal was more prevalent and severe in patients with ischaemic vascular disease and patients with white matter disease; (2) psychomotor slowing was more severe in patients with ischaemic vascular disease and patients with white matter disease; and (3) differences between Alzheimer's disease and ischaemic vascular dementia groups in the degree of psychomotor slowing were independent of the severity of white matter disease. CONCLUSIONS: Future studies using structural and functional neuroimaging techniques would be helpful for examining the relation between neurobiological factors and affective/behavioural disturbances in dementia.

Adult↗
PubMed1995

Redox status and protein binding of plasma homocysteine and other aminothiols in patients with early-onset peripheral vascular disease. Homocysteine and peripheral vascular disease.

Elevated total homocysteine (Hcy) in plasma is an independent risk factor for early-onset vascular disease in the coronary, cerebral, and peripheral arteries. Different forms of Hcy, and their relation to other aminothiols in plasma, have not been investigated in patients with vascular disease. We therefore investigated 65 patients (35 men and 30 women) operated on for peripheral arterial disease at < 50 years of age and 65 age- and sex-matched control subjects. Total, reduced, oxidized, and protein-bound Hcy, cysteine (Cys), and cysteinylglycine (CysGly) were measured 0 to 11 years (mean, 6 years) postoperatively, in the fasting state, and after a standard methionine loading dose that caused a transient increase in reduced, oxidized, and protein-bound Hcy. All forms of Hcy and Cys, except reduced Cys, were higher in fasting patients than fasting control subjects. A similar difference between the groups was observed after methionine loading. The levels of most Hcy forms both during fasting and after methionine loading were related to smoking, but multivariate analysis showed that the difference between patients and control subjects could not be explained by smoking alone. Notably, reduced Cys and the reduced/total ratio for Cys were significantly higher in control subjects than in patients, both during fasting and after methionine loading. In both groups, the redox status and protein binding of the various aminothiols in plasma were interactive, as demonstrated by positive correlations between their reduced/total ratios and by a decrease in protein-bound Cys when protein-bound Hcy was elevated during methionine loading.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Epidemiology of peripheral vascular disease: a predictor of systemic vascular disease.

It is estimated that peripheral vascular disease (PVD) affects 30 percent of the adult population, and two-thirds of all cases are asymptomatic. Detecting PVD can be relatively easy and inexpensive, and based either on subjectively supplied historical information (claudication) or upon physical examination findings [ankle-brachial index (ABI)]. The ABI may serve as a marker for increased risk for systemic vascular disease as an abnormally low ABI has been shown to be associated with systemic vascular disease. Epidemiology of and risk factors for PVD are in similar to coronary heart disease. PVD is uncommon until middle age and then increases dramatically. Prevalence of PVD is slightly higher in men than women, yet this tends to diminish with age. Cigarette smoking is probably the most important risk factor for PVD. Hypertension, hypercholesterolemia, and diabetes are also risk factors for the development of symptomatic PVD. Conversely, the presence of a high degree of physical activity and higher levels of HDL-cholesterol as well as a lower body mass index (BMI) are protective. Patients who have vascular disease in one organ system often exhibit evidence of vascular disease elsewhere. Presence of coronary artery disease among patients with symptomatic PVD is between two and four times higher than those without PVD, and PVD is also associated with cerebrovascular disease.

Adult↗