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PubMed2003

Folic acid supplements and fortification affect the risk for neural tube defects, vascular disease and cancer: evolving science.

Folic acid supplements reduce the risk of neural tube defects and may be associated with reduced risk for vascular disease and cancer. Research data from both observational and controlled intervention studies provide strong support for the existing public health policies related to folic acid and neural tube defects. However, educational efforts to promote daily intake of folic acid supplements by women of reproductive age have not, in most cases, resulted in increased supplement use. In contrast, food fortification appears to be associated with a reduction in neural tube defects in the United States and Canada but is not practiced universally. The potential for folic acid supplements to reduce the incidence and severity of vascular disease and cancer is the focus of major research efforts including ongoing intervention studies.

Dietary Supplements↗
PubMed1995

Elastase and cell matrix interactions in the pathobiology of vascular disease.

Ultrastructural observations in lung tissue implicated an endogenous vascular elastase (EVE), in the pathobiology of pulmonary vascular disease. In experimental rats, increased activity of a 20 kDa serine proteinase related to adipsin precedes the development of sustained pulmonary hypertension and vascular abnormalities. A further increase in activity is related to malignant progression of the disease. A cause and effect relationship was suggested by studies in which elastase inhibitors successfully prevented or retarded progression of pulmonary hypertension. In vitro studies have shown that both serum and endothelial factors induce EVE via tyrosine kinase intracellular signalling. Induction of EVE can release basic fibroblast growth factor from the extracellular matrix in an active form stimulating smooth muscle cell proliferation. Elastase activity was also observed in the process of smooth muscle cell migration and neointimal formation in coronary arteries following experimental cardiac transplantation. An immune/inflammatory response is observed with increased production of cytokines, tumor necrosis factor-alpha and interleukin (IL)-1 beta, reciprocally up-regulating production of fibronectin, a glycoprotein which mediated smooth muscle cell migration. The action of IL-1 beta in inducing fibronectin is facilitated by the production of elastin peptides generated by increased activity of an elastase in the coronary arteries. Our studies suggest that ligation of the elastin binding protein by elastin peptides unmasks IL-1 receptors. Fibronectin also stimulates transendothelial migration of lymphocytes which perpetuates the inflammatory response leading to neointimal formation in this model. Masking integrins on T cells with a decoy synthetic CS-1 (fibronectin) peptide largely prevented transendothelial migration and coronary neointimal formation following cardiac transplant.

Animals↗
PubMed1995

Peripheral vascular disease: educational concerns for patients with a chronic disease in a changing health-care environment.

Education about vascular disease requires information to change habits related to diet, activity, and personal health. Uncertainty significantly impacts the ability of individuals with a chronic disease to feel secure in treatment programs. A clear understanding of the disease, mutual development of measurable goals, clear communication, and a commitment to change provide the format for a successful education and prevention program. As the health-care system expects each individual to assume more responsibility for health promotion and maintenance, education will be key.

Chronic Disease↗
PubMed2006

Peripheral vascular disease and outcomes following coronary artery bypass graft surgery.

HYPOTHESIS: There is an increased operative risk in patients with a history of peripheral vascular disease (PVD) who undergo coronary artery bypass grafting (CABG). There are also outcome differences associated with these patients. DESIGN: A study from a 10-year hospitalization cohort with prospective data collection. SETTING: Multiple hospitals in the Greater Cincinnati area with 1 surgical group of cardiac surgeons. PARTICIPANTS: Cases were CABG patients with PVD, which was defined as having a history of type 1 neurologic injury, prior vascular surgery, or current vascular disease (n = 1561). Controls were CABG patients without PVD (n = 6328). INTERVENTIONS: The study examined 42 potential confounding risk factors and 16 outcome variables. RESULTS: Twenty-nine potential risk factors were found to be significantly different between CABG patients with and without PVD. Twenty-six confounding risk factors were correlated with 3 factors. Logistic regression analysis showed that even after controlling for sex, significant associative disorders, and other procedures, CABG patients with PVD still experienced more arrhythmias requiring treatment (odds ratio [OR], 1.7; 95% confidence interval [CI], 1.03-1.33; P = .01), neurological complications (OR, 1.7; 95% CI, 1.43-2.07; P<.001), pulmonary complications (OR, 1.4; 95% CI, 1.23-1.62; P<.001), low output (OR, 1.3; 95% CI, 1.09-1.45; P = .001), and intraoperative complications (OR, 1.39; 95% CI, 1.06-1.83; P = .02). CONCLUSIONS: Patients with a PVD history undergoing CABG had more coexistent risk factors. These patients also exhibited higher rates of cardiac, systemic, renal, neurologic, and pulmonary complications.

Aged↗
PubMed1998

Activated protein C resistance in patients with peripheral vascular disease.

PURPOSE: The frequency of activated protein C (APC) resistance, caused by factor V R506Q gene mutation and abnormal APC ratio, in patients with peripheral vascular diseases was analyzed. METHODS: All patients electively admitted to the vascular ward unit of our tertiary care academic medical center from January 1995 through October 1996 (n = 679) were prospectively analyzed using an APC-resistance screening test to determine the frequency of abnormal APC ratio (< or =2.6). Baseline activated partial thromboplastin time (APTT) and its prolongation after the addition of a standard amount of APC were determined. The factor V R506Q gene mutation (Leiden) was analyzed in patients with an APC ratio less than 3.0. Statistical comparisons were made to an age-matched control population (n = 278). RESULTS: The factor V Leiden gene mutation or abnormal APC ratio was detected in 154 of the patients (22.7%), compared with 34 of 278 the control subjects (12.2%; t = 13.65; P < .001). The factor V Leiden gene mutation was found in 102 patients (15.2%), compared with 29 control subjects (10.4%; t = 4.64; P < .05); an abnormal APC ratio was found in 132 patients (19.8%), compared with 26 (9.8%) of controls (t = 14.56; P < .001). The frequency of the factor V Leiden gene mutation was significantly increased in patients with femoro-popliteal occlusive disease (n = 126), to 21.6% (t = 16.94; P< .001), and venous disease (n = 50), to 36.0% (t = 20.93; P< .001). Overall, 63% of the patients with abnormal APC ratios tested positive for the factor V Leiden gene mutation. A significantly increased frequency of APC resistance was demonstrated in patients undergoing aorto-iliac (n = 37) or femoro-crural graft reconstructions (n = 72); it was found in 41% and 35%, respectively (P < .001). In addition, a significantly increased frequency of APC resistance was found in patients who suffered from occlusion after reconstruction; 13 of 41 (32%) had the factor V Leiden gene mutation (P < .001), and 19 of 39 (49%) had an abnormal APC ratio (P < .001). CONCLUSION: The factor V Leiden gene mutation and abnormal APC ratios are significantly increased in patients with lower extremity peripheral vascular disease and failed reconstructions. An abnormal APC ratio was seen without factor V Leiden gene mutation in 37% of patients with peripheral vascular diseases, suggesting additional causes of an abnormal APC ratio, exclusive of gene mutation.

Activated Protein C Resistance↗
PubMed1997

Improvement of limb circulation in peripheral vascular disease using epidural spinal cord stimulation: a prospective study.

Spinal cord stimulation was used in 46 patients for pain associated with lower extremity ischemic vascular disease that was considered to be nonreconstructable. Thirty-nine patients who had a follow-up examination between 2 and 36 months after the procedure form the basis of this report. Thirty (77%) of 39 cases were considered successful. Clinical endpoints indicating failure included amputation, vascular reconstruction, poor pain relief, or hardware malfunction. The transcutaneous partial pressure of oxygen (TcPO2) increased in both target and control feet. In patients with good outcome with a preimplantation TcPO2 of less than 30 mm Hg, TcPO2 increased significantly (p < 0.05). Pulse volume recording improved significantly (p < 0.05) at the thigh, metatarsal, and great toe levels in successfully treated patients. Peak blood flow velocity also showed a significant increase in patients with good outcome (p < 0.05). Patients with a TcPO2 of less than 10 mm Hg following stimulation tended to undergo amputation within the first 3 months. Improvement in pain control, combined with an increase in TcPO2 values that was greater than 10 mm Hg, were significant early predictors of long-term success. An initial increase in peak blood flow velocities (measured in Doppler studies) of greater than 10 mm also signified a good long-term outcome. Spinal cord stimulation appears to be a useful therapeutic modality for controlling pain and improving perfusion in a select group of patients with end-stage ischemic vascular disease considered nonreconstructable. The best results were seen in patients with severe claudication and rest pain without trophic changes in the foot. The mechanism of this beneficial effect is not yet completely understood.

Aged↗
PubMed1991

Infusion of a stable prostacyclin analogue, iloprost, to patients with peripheral vascular disease: lack of antiplatelet effect but risk of thromboembolism.

PURPOSE: Prostacyclin, a potent inhibitor of platelet function and vasodilator, has been used to treat peripheral vascular disease. The aim of this study was to monitor the thrombotic status of patients treated by infusion of a stable prostacyclin analogue, iloprost. PATIENTS AND METHODS: Thirteen patients with peripheral vascular disease underwent iloprost infusion for 3 days (8 hours each day) in a dose ranging from 0.5 to 2 ng/kg/minute. Variable parameters of thrombosis such as platelet reactivity (shear-induced hemostatic plug formation and thrombus formation on a collagen fiber), coagulation, and spontaneous thrombolysis (dislodgment of hemostatic plugs) were measured from non-anticoagulated blood samples by hemostatometry immediately before and 1 hour after the infusion and on the last day, 4 hours after initiation of the infusion. RESULTS: Analysis of data from all patients 1 hour after the infusion showed no changes in platelet reactivity and spontaneous thrombolysis, but coagulation was significantly enhanced. In four patients, significant platelet hyperreactivity was observed after the infusion. Four of the five patients tested while undergoing iloprost infusion showed an enhanced thrombotic reaction and markedly enhanced coagulation. Iloprost employed in vitro in a concentration that corresponds to the therapeutic peak blood level caused no inhibition of platelet function but significantly enhanced coagulation. The threshold in vitro iloprost concentration at which anti-platelet effect and increased spontaneous thrombolysis were observed was twice that of the therapeutic blood level. CONCLUSIONS: These findings challenge the view that antagonism of platelet function is an important factor of iloprost therapy. Furthermore, platelet hyperreactivity in some patients and markedly enhanced coagulation during and after infusion of iloprost in general, represent a risk of thromboembolism, especially as patients are already in a prethrombotic condition.

Adult↗
PubMed2001

[Detection of brain vascular diseases with CT angiography].

OBJECTIVE: To identify the diagnostic effect of spiral CT in brain vascular diseases. METHODS: Sixty four patients underwent CT angiography, including 22 patients with subarachnoid hemorrhage (SAH), 6 patients with oculomotor nerve paralysis, 5 patients with brain substance hemorrhage, 6 patients with arteriovenous malformation (AVM), 4 patients with mass or aneurysm, 5 patients with brain infarction, 16 patients with epilepsy or headache and dizzy. 8 cases also underwent digital subtraction angiography (DSA), 4 cases were performed operation in 64 cases. RESULTS: Spiral computed tomography angiography (SCTA) was all succeeded in 64 cases. 26 aneurysms and 8 AVMs were found by SCTA; in 6 of 8 cases of AVMs, their supply arteries and drainage veins were clearly displayed; SCTAs of 5 cases with substance hemorrhage were normal; in 1 of 5 cases with cerebral hemisphere infarction, its internal carotid obstruction was demonstrated by SCTA; the results of 12 SCTAs were identical with the results of their DSA or operation. CONCLUSION: SCTA is a useful non-invasive inspection method for detecting brain vascular diseases such as aneurysms and AVMs.

Adolescent↗
PubMedDate not supplied

Outcome in patients with failed percutaneous transluminal angioplasty for peripheral vascular disease.

The outcome in 299 patients having 321 percutaneous transluminal angioplasty (PTA) procedures for peripheral vascular disease was analysed. Technical failure occurred in 21 patients (7%) but in none was the limb ischemia made worse by the failed PTA attempt; nine of these (3%) had been considered unsuitable for arterial reconstruction and proceeded to primary amputation, while 12 (4%) did not have subsequent management compromised by the failed PTA attempt. Complications occurred in seven patients (2.3%); four of these (1.3%) had worsening ischemia but were able to be satisfactorily managed by surgical intervention. There were 71 patients (23.7%) who had an initially successful PTA procedure which subsequently failed; 20 of these (6.7%) had been considered unsuitable for arterial reconstruction and proceeded to amputation, while five patients suitable for arterial reconstruction (1.7%) came to amputation, four following failed bypass surgery and one following multiple trauma from a motor vehicle accident. The remaining 46 patients (15.3%) did not have subsequent management compromised by the late failure of PTA. Early and late failure of PTA in patients presenting with peripheral vascular disease does not compromise subsequent management.

Adult↗
PubMed1981

Central retinal vein occlusion and scleroderma: implications for sclerodermatous vascular disease.

A patient with scleroderma (progressive systemic sclerosis) who developed central retinal vein occlusion is described. The aetiology of this condition is discussed and the role of possible sclerodermatous vascular disease is highlighted. It is suggested that studies of fundal vasculature could be useful in the clinical assessment of sclerodermatous vascular disease.

Constriction, Pathologic↗
PubMed2006

Clinical manifestations of noncoronary atherosclerotic vascular disease after moderate dose irradiation.

BACKGROUND: Accelerated atherosclerosis and carotid stenosis are well-established risks occurring after high radiation doses that are used to treat cancers of the head and neck. Noncoronary vascular disease has been observed and may relate to more moderate dose irradiation. METHODS: A search of patients treated for Hodgkin disease, non-Hodgkin lymphoma, or seminoma was performed to identify cases with noncoronary vascular complications after irradiation. These three groups were chosen because of the use of intermediate dose radiation and prevalence of long-term survivors. Individual patient records were reviewed to document the type and presentation of the stenosis and the clinical factors that may have contributed to this risk. RESULTS: Twenty-one patients were identified who developed disease in noncoronary arteries after treatment. The median time from irradiation to diagnosis of vascular stenosis was 15 years. Antecedent risk factors for vascular disease were prevalent. Five patients had disease identified by auscultation of bruits before an adverse clinical event occurred. Five patients died from complications related to their vascular disease, which included three deaths after stroke and two after small bowel infarction. CONCLUSION: Twelve cases arose at an atypically young age for atherosclerotic vascular disease and featured unusual clinical presentations. Nine cases identified occurred at an advanced aged and at a shorter median interval, making a causal relation to irradiation uncertain. Incorporating careful auscultation for bruits in followup evaluation of irradiated patients may identify individuals who are at risk for adverse vascular events. The potential for early vasculopathy in individuals exposed to intermediate dose irradiation suggests a need to manage dyslipidemia and reduce vascular risk factors throughout the posttreatment period.

Adolescent↗
PubMed2004

Unifying concept for Alzheimer's disease, vascular dementia and normal pressure hydrocephalus - a hypothesis.

The three common forms of dementias in the elderly include Alzheimer's disease (AD), vascular dementia (VD) and normal pressure hydrocephalus (NPH). These disorders are distinguished by their specific pathological features. However, overlapping clinical and imaging features in a given case are not too uncommon. Based on alterations in CSF dynamics study, a unifying concept in the pathogenesis of AD and NPH has been proposed recently which may have therapeutic implications. Altered CSF dynamics by affecting the absorptive process may lead to hydrocephalic change. This may also affect clearance of amyloid protein leading to increased amyloid deposition in brain parenchyma resulting in AD pathology. Hence it is likely that a subgroup of patients may have an AD-NPH syndrome who may be benefitted by CSF drainage procedure. The present author attempts to extend this concept to hypothesise a unifying concept to explain the pathophysiology of all the three disorders which may explain overlapping features observed clinically and in neuroimaging studies. It is surmised that altered CSF dynamics and hypoperfusion from vascular disease may be interlinked. The defective clearance of amyloid may also lead to amyloid angiopathy perpetuating hypoperfusion. Hypoperfusion may also affect formation as well as absorption of CSF altering clearance of amyloid and promoting vascular and parenchymal deposition. Thus the pathologies of AD, VaD and NPH get interrelated.

Alzheimer Disease↗
PubMed1999

The effects of peripheral vascular disease with osteomyelitis in the diabetic foot.

BACKGROUND: Osteomyelitis in the diabetic foot is a difficult problem with multiple etiologies. The effects of peripheral vascular disease, neuropathy, and repetitive trauma all interact to produce complex lesions with exposed bone, surrounding cellulitis, and gangrenous changes. METHODS: We performed a retrospective study over a 14-year period at a community hospital looking at osteomyelitis in the diabetic foot. We looked at the contributing factors, organisms involved, most common locations, physical findings, and surgical procedures necessary to treat this condition. The purpose of the study was to determine the incidence and effect of peripheral vascular disease in diabetic patients with foot ulcers. RESULTS: There were a total of 150 patients requiring 278 hospitalizations over the 14-year period who represented 14% of all diabetic admissions. A total of 438 surgical procedures were necessary in these patients, with the most common being debridement (39%) and toe amputation (19%). There were 6 deaths (4%) in this series, and leg amputation was necessary in 21 patients (14%). A vascular bypass was necessary for healing and limb salvage in 36 patients (24%). Most of the bypasses (85%) were with autogenous tissue to the distal leg in order to limit the extent of amputation and to preserve a functional limb. CONCLUSION: Ischemia is often a contributing factor in the diabetic foot ulcer that must be recognized and treated to avoid prolonged hospitalization, spreading infection, and unnecessary amputation.

Adult↗
PubMed1998

Erythrocyte promotion of platelet reactivity decreases the effectiveness of aspirin as an antithrombotic therapeutic modality: the effect of low-dose aspirin is less than optimal in patients with vascular disease due to prothrombotic effects of erythrocytes on platelet reactivity.

BACKGROUND: Aspirin (acetylsalicylic acid, ASA) is widely used for secondary prevention of ischemic vascular events, although its protection only occurs in 25% of patients. We previously demonstrated that platelet reactivity is enhanced by a prothrombotic effect of erythrocytes in a thromboxane-independent manner. This diminishes the antithrombotic therapeutic potential of ASA. Recent data from our laboratory indicate that the prothrombotic effect of erythrocytes also contains an ASA-sensitive component. In accordance with this observation, intermittent treatment with high-dose ASA reduced the prothrombotic effects of erythrocytes ex vivo in healthy volunteers. In the present study, the effects of platelet-erythrocyte interactions were evaluated ex vivo in 82 patients with vascular disease: 62 patients with ischemic heart disease treated with 200 mg ASA/d and 20 patients with ischemic stroke treated with 300 mg ASA/d. METHODS AND RESULTS: Platelet activation (release reaction) and platelet recruitment (fluid-phase proaggregatory activity of cell-free releasates from activated platelets) were assessed after collagen stimulation (1 microg/mL) of platelets, platelet-erythrocyte mixtures, or whole blood. Platelet thromboxane A2 synthesis was inhibited by >94% by ASA administration in all patients. Importantly, platelet recruitment followed one of three distinct patterns. In group A (n=32; 39%), platelet recruitment was blocked by ASA both in the presence and absence of erythrocytes. In group B (n=37; 45%), recruitment was abolished when platelets were evaluated alone but continued in the presence of erythrocytes, indicating a suboptimal effect of ASA on erythrocytes of this patient group. In group C (n= 13; 16%), detectable recruitment in stimulated platelets alone persisted and was markedly enhanced by the presence of erythrocytes. CONCLUSIONS: In two thirds of a group of patients with vascular disease, 200 to 300 mg ASA was insufficient to block platelet reactivity in the presence of erythrocytes despite abolishing thromboxane A2 synthesis. Platelet activation in the presence of erythrocytes can induce the release reaction and generate biologically active products that recruit additional platelets into a developing thrombus. Insufficient blockade of this proaggregatory property of erythrocytes can lead to development of additional ischemic complications.

Adult↗