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Vascular disease prevalence in diabetic patients in China: standardised comparison with the 14 centres in the WHO Multinational Study of Vascular Disease in Diabetes.

AIMS/HYPOTHESIS: Rates of vascular complications of diabetes in a cohort of mainland Chinese patients with diabetes, ascertained and examined by similar methodology, are compared with those of the WHO Multinational Study of Vascular Disease in Diabetes (WHO MSVDD). METHODS: The standardised procedures carried out in the WHO MSVDD were followed in assembling and examining a Chinese cohort of 447 diabetic patients recruited in Beijing and Tianjin [2]. RESULTS: Compared with the WHO MSVDD centres, the Chinese cohort was slightly older, had a shorter duration of known diabetes and had fewer insulin-treated patients. Arterial pressure, total blood cholesterol and body mass index were substantially lower. Large vessel disease rate for age, sex and duration adjusted data (17.9 % ) was about half that of the combined WHO MSVDD centres (33.5 % p < 0.001). However, retinopathy (47.4% vs 35.8% p < 0.001) and proteinuria (57.1 vs 24.9 % p < 0.001) rates were significantly higher. CONCLUSION/INTERPRETATION: Relatively low arterial pressures and blood cholesterol are likely contributors to the notably low arterial disease rates in this Chinese diabetic cohort; they reflect low rates in the Chinese mainland general population and resemble the Tokyo and Hong Kong centres of the WHO MSVDD. The high rates of retinopathy and proteinuria could relate to later diagnosis, degree of hyperglycaemia and/or increased susceptibiltiy to microangiopathy.

Adult↗

[Hyperhomocysteinemia--a risk factor for development of occlusive vascular diseases].

INTRODUCTION: Occlusive vascular diseases take the first places on lists of diseases in general population today. In spite of this, all risk factors which contribute to development of these diseases are not yet known. Recent studies have shown that homocysteine plays a critical role in it and is established as a new risk factor. WHAT IS HOMOCYSTEINE?: Homocysteine is a sulfur containing amino acid formed in the metabolism of methionine. Reference values of homocysteine in circulation and different forms in plasma are described. HYPERHOMOCYSTEINEMIA--A RISK FACTOR: Homocysteine was associated with atherosclerosis and occlusive vascular disease in 1960s for the first time. Since then, many studies--prospective and retrospective, have confirmed the role of hyperhomocysteinemia as a risk factor in 42% of patients with cerebrovascular disease, 28% with peripheral vascular and 30% with coronary artery disease. The Physician's Health Study, a prospective study in which 15,000 male physicians took part, revealed that increase in homocysteine concentration of 1.7 mumol/l above normal values was associated by threefold higher risk for myocardial infarction. The risk for carotid artery stenosis also increases with elevation of homocysteine concentration. Hyperhomocysteinemia is associated with poor prognosis in patients with angiographically established coronary disease. Stroke, venous thromboembolism, and atherosclerosis in chronic renal failure are some of the complications of hyperhomocysteinemia. CAUSES OF HYPERHOMOCYSTEINEMIA: Hyperhomocysteinemia has numerous genetic and nongenetic etiologic factors. Cystathionine synthase deficiency, methylenetetrahydrofolate reductase deficiency and defects in the synthesis of cobalamin cofactors are genetically determined. Nutritional factors such as B12, folate or B6 vitamin deficiency, cofactors in homocysteine metabolism, lead to hyperhomocysteinemia. MECHANISMS OF HOMOCYSTEINE ACTION: Atherogenic propensity of homocysteine is related to endothelial dysfunction, blood thrombocyte aggregation changes in factors of coagulation. Oxidative stress is involved, but the exact mechanism is still unknown. CONCLUSION: Hyperhomocysteinemia is established as an important risk factor for occlusive vascular diseases. Reduction in homocysteine concentration can be achieved by supplementation of B-group vitamins, cofactors in homocysteione metabolism. Is it going to be effective in reducing cardiovascular risks remains to be seen.

Arteriosclerosis↗

Genes related to vascular disease (APOE, VLDL-R, DCP-1) and other vascular factors in late-life depression.

OBJECTIVE: The authors asked whether polymorphic variation at three genes related to vascular disease, and other vascular disease risk factors, determine late-life depression. METHODS: A group of 370 participants, representing 57% of survivors of an initial cohort of 1,083 participants in the Medical Research Council treatment trial of hypertension in older adults, had been screened for depression at baseline and were traced and genotyped for genetic analysis 11 years later. Genetic analyses were performed to establish variability at three polymorphisms related to vascular disease: APOE encoding for apolipoprotein-E, VLDL-R encoding for the VLDL cholesterol-receptor, and DCP-1 encoding for angiotensin-converter enzyme. Information on vascular disease and its risk factors (ECG ischemia or arrhythmia, body mass index, serum cholesterol, smoking status, and systolic/diastolic blood pressure) and cognitive functioning was also available from baseline. RESULTS: The authors found no association between the three studied polymorphisms and depression. Female gender, higher diastolic blood pressure, poorer cognitive functioning, and smoking status at baseline were all associated with depression independently of antidepressant and NSAIDs use, age, ECG-established vascular disease, and the remaining vascular disease risk factors studied. CONCLUSIONS: This study found no association between late-life depression and three polymorphisms related to vascular disease. Depression was found to independently associated with smoking, female gender, poorer cognitive functioning, and higher diastolic blood pressure. Taken together, this study does not seem to support the notion of a specific link between the studied vascular risk factors or these vascular-related loci and late-life depression.

Age of Onset↗

Diagnosis and treatment of peripheral arterial disease compared with other atherosclerotic vascular diseases in a university primary care clinic.

BACKGROUND: Despite the fact that peripheral arterial disease (PAD) significantly increases the risk of cardiovascular mortality, it is significantly underdiagnosed and undertreated. The purpose of this study was to evaluate the practice at a northeast Tennessee university primary care clinic regarding the diagnosis and treatment of PAD. METHODS: A retrospective medical record survey was conducted to evaluate practice patterns in diagnosing and treating PAD in a university primary care clinic. A clinic population of 711 patients was selected using International Classification of Diseases-9 codes for coronary artery disease (CAD), cerebovascular disease (CVD), and/or PAD. A sample of 180 patients (25.3%) was randomly selected using a systematic statistical method. Of these, 125 patients met the diagnostic criteria for CAD, CVD, and/or PAD. The study covered a 3-year period, from July 2001 until June 2004. Demographic and other data, including the use of antiplatelet therapy, were collected. RESULTS: One hundred ten patients met all of the inclusion and exclusion criteria. Thirty-nine percent were males, and 61% were females. Overall, 79% had CAD, 53% had CVD, and 25% had PAD. Almost half of the patients had some combination of these. Only about 2% had PAD only compared with 36% with CAD only and 17% with CVD only. Although the prevalence of CAD and CVD (among other atherosclerotic vascular diseases) in our clinic was comparable to national figures, the prevalence of PAD was significantly lower (p = .004). The overall use of any antiplatelet agent was 84.2% for patients with only CAD and 80% for only CVD. There was not an adequate number of patients with only PAD to evaluate the use of antiplatelet therapy in this group. CONCLUSION: The low prevalence of PAD only (most PAD patients had coexisting CAD and CVD) indicates that PAD is underdiagnosed at our clinic. There was suboptimal use of aspirin and other antiplatelet drugs among patients with atherosclerotic vascular disease.

Adult↗

Epidemiology, risk factors, and management of peripheral vascular disease.

Peripheral vascular occlusive disease is initiated with a genetic risk factor component compounded by patient-controlled contributions including obesity, diabetes, hypertension, and smoking. Medical management of these factors may delay or obviate surgical intervention. Angiography may be used to perform angioplasty (+/- stents) or to guide various interventional procedures. The major contribution to pre- and post-operative assessment is the noninvasive laboratory.

Angioplasty↗

Glucose: a continuous risk factor for cardiovascular disease.

The glucose level that defines diabetes mellitus is that level above which patients have a high risk of eye, kidney, and neuronal disease. The risk of these complications rises as glucose levels increase, and decreases as therapy brings the glucose level down. Thus, in patients with diabetes, glucose is a continuous, modifiable risk factor for eye, kidney and peripheral nerve disease. Plasma glucose concentrations in the diabetic range are also a continuous risk factor for cardiovascular disease (CVD). Moreover, epidemiological evidence shows that the relationship between plasma glucose concentration and CVD extends well below the glucose level defined for diabetes and even impaired glucose tolerance. This continuous relationship between glucose and CVD exists in all people, not just in those with a defined metabolic disease, and is therefore similar to the relationship between cholesterol or blood pressure and CVD. It may be secondary to either a direct effect of elevated glucose or to some underlying metabolic abnormality that raises both glucose and cardiovascular risk. Whether interventions that lower glucose will also lower the risk of CVD is still unknown; the results of clinical trials are awaited.

Blood Glucose↗

Gene therapy and vascular disease: potential applications in vascular surgery.

Advances in molecular biology have generated methods that are used to enhance diagnosis and treatment of a variety of human diseases. More recently modification of gene expression in cells by gene transfer has been introduced as a new therapeutic modality. The targeting of vascular cells with this method is appealing not only for anatomical reasons, but also because endovascular techniques provide access to the vasculature and makes site-specific delivery possible. Over the past few years, gene transfer has been widely used to explore the pathophysiology of vascular diseases in experimental models and available data suggests that this method may eventually become a therapeutic alternative for vascular disorders such as restenosis, graft failure, and critical ischaemia. In the following we discuss the methodology of gene transfer, its tentative use in vascular diseases related to vascular surgery, and the problems associated with this new technology.

Animals↗

Open lung biopsies in congenital heart disease for evaluation of pulmonary vascular disease. Predictive value with regard to corrective operability.

For evaluation of pulmonary vascular disease 140 open lung biopsies were performed in 137 patients with congenital heart disease in order to decide whether the state of the lung vessels would allow corrective surgery. As far as possible follow-up was obtained in patients who underwent a cardiac repair. From the study of these biopsy specimens it appeared that medial hypertrophy of pulmonary arteries and changes in pulmonary veins should not be considered an impediment for a corrective operation as long as more advanced changes are absent. The same is true for intimal thickening due to longitudinal smooth muscle, post-thrombotic changes or cellular proliferation. Concentric-laminar intimal fibrosis forms no contra-indication as long as it is mild but, if severe, it is likely that hypertensive pulmonary vascular disease will progress in spite of cardiac repair. In the presence of fibrinoid necrosis or plexiform lesions correction of a cardiac anomaly should not be attempted. The presence of dilatation lesions is more disputable but probably, as long as they are scarce and not accompanied by fibrinoid necrosis or plexiform lesions, corrective surgery may be attempted. This becomes very dubious when they are more numerous.

Adolescent↗

[Congenital heart diseases and obstructive pulmonary vascular diseases in Down's syndrome. Apropos of 142 children with trisomy 21].

Trisomy 21 accounts for 3 p. 100 of reasons for admission to the Paediatric Cardiology unit of the St Luc University Clinics, Brussels. In a series of 142 cardiac children with trisomy 21 evaluated by catheterization between 1969 and 1987, 54 p. 100 of the cardiac malformations observed consisted of persistent common atrioventricular canal (complete in 45 p. 100 of the cases). The other heart diseases were ventricular septal defect (23 p. 100), atrial septal defect of the ostium secundum type (10 p. 100) and tetralogy of Fallot (9 p. 100). In 40 p. 100 of the patients other cardiovascular abnormalities were associated with these predominant intracardiac shunts. These findings were in agreement with those usually reported in the literature. At the time of investigation (mean age 24 months), pulmonary vascular resistance had already reached a pathological level in 88 p. 100 of the cases. Oxygen tests only slightly improved these results, which suggested that the conditions were favourable to the early development of a pulmonary obstructive vascular disease in Down's syndrome, thus darkening the prognosis of congenital heart disease in mongoloid children. In this series to overall mortality rate of corrective surgery was 23 p. 100. The risk was maximum in infants aged less than 3 months with severe and rapidly symptomatic lesions. The outcome in patients successfully operated upon was satisfactory, with benign residual lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Child, Preschool↗

Pathophysiological and metabolic manifestations of pulmonary vascular disease in children.

In children with congenital heart disease pulmonary vascular disease can be fatal for a variety of reasons. Even before the classical changes of advanced pulmonary vascular obstructive disease have developed, a marked increase in pulmonary vascular smooth muscle can be fatal due to pulmonary hypertensive crises. After the Fontan procedure, a modest increase in muscularity can jeopardise the outcome since there is no subpulmonary ventricle to support the pulmonary circulation. Following heart transplantation, a slight increase in muscularity can cause failure of the donor right ventricle unless that heart is already hypertrophied as in the domino procedure. In all children with pulmonary hypertension, either persistent pulmonary hypertension of the newborn or secondary to congenital heart disease the pulmonary vasculature fails to remodel normally after birth. Newborn vessels are characterized by the immaturity of the smooth muscle cells and the paucity of connective tissue. In the hypertensive lung smooth muscle differentiation and connective tissue deposition is accelerated. In children with congenital heart disease intimal changes follow. In these children the potential reversibility of disease following intracardiac repair is determined by the type of pathological change present at the time of repair. However, pulmonary hypertensive crises can occur in young children with potentially reversible disease. Operability is not synonymous with the potential reversibility of pathological lesions. Correlations between structural findings at lung biopsy and haemodynamic findings at cardiac catheterization have improved the accuracy with which the natural and unnatural history of pulmonary vascular disease can be predicted, but is still inadequate because we do not understand the functional implications of the changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Peripheral vascular perfusion scanning. Correlation with the arteriogram and clinical assessment in the patient with peripheral vascular disease.

Peripheral vascular perfusion scan during rest and reactive hyperemia does not necessarily offer the same information as the arteriogram or the clinical assessment of the peripheral pulses. The information obtained from the peripheral vascular perfusion scan offers potentially clinically useful information regarding the physiologic significance of various arterial lesions to the surgeon in selection of his therapeutic approach. The peripheral vascular perfusion scan uniquely and under varied physiologic conditions permits assessment of the effect of arterial disease on the distribution of perfusion within the extremity. The peripheral vascular perfusion scan is not in competition with, but is complementary to, arteriography and clinical assessment of the patient with peripheral vascular disease.

Adult↗

Homocyst(e)ine: an important risk factor for atherosclerotic vascular disease.

Homocysteine is an intermediate compound formed during metabolism of methionine. The results of many recent studies have indicated that elevated plasma levels of homocyst(e)ine are associated with increased risk of coronary atherosclerosis, cerebrovascular disease, peripheral vascular disease, and thrombosis. The plasma level of homocyst(e)ine is dependent on genetically regulated levels of essential enzymes and the intake of folic acid, vitamin B6 (pyridoxine), and vitamin B12 (cobalamin). Impaired renal function, increased age, and pharmacologic agents (e.g. nitrous oxide, methotrexate) can contribute to increased levels of homocyst(e)ine. Plausible mechanisms by which homocyst(e)ine might contribute to atherogenesis include promotion of platelet activation and enhanced coagulability, increased smooth muscle cell proliferation, cytotoxicity, induction of endothelial dysfunction, and stimulation of LDL oxidation. Levels of homocysteine can be reduced with pharmacologic doses of folic acid, pyridoxine, vitamin B12, or betaine, but further research is required to determine the efficacy of this intervention in reducing morbidity and mortality associated with atherosclerotic vascular disease.

Arteriosclerosis↗

Coronary artery stenting in cardiac allograft vascular disease.

Cardiac allograft vascular disease is characterized by diffuse and multifocal heterogeneous myointimal hyperplasia with or without vascular remodeling. Catheter-based interventions are indicated in selected patients. This study documents our experience with percutaneous transluminal coronary angioplasty and coronary stents (n = 48) in a group of 27 patients 5.7 +/- 2.9 years after heart transplantation. Early and intermediate results were controlled by angiography and intravascular ultrasound. Conventional percutaneous transluminal coronary angioplasty resulted in a mild and mostly inadequate gain in luminal dimensions (lumen area: 3.17 +/- 0.92 mm2 to 3.70 +/- 1.21 mm2; minimal lumen diameter: 1.84 +/- 0.23 mm to 2.04 +/- 0.36 mm). Coronary stenting led to a further improvement of luminal gain (lumen area: 3.70 +/- 1.21 mm2 to 5.86 +/- 1.76 mm2; minimal lumen diameter: 2.04 +/- 0.36 mm to 2.53 +/- 0.38 mm). These results were stabilized by application of aspirin and ticlopidine only. There were no stent thromboses or bleeding complications, and early hospital discharge of the patients was possible. At follow-up (mean follow-up period 7.72 +/- 5.45 months (range 0.50 to 23.13 months) all patients were clinically event free. In six of 24 stented vessels (25%) in 16 patients, significant restenosis (>50%) was found by intravascular ultrasound (n = 20) or by angiography (n = 4) 6 months after stent placement. We conclude that in eligible cardiac allograft vascular disease lesions primary stenting may be the method of choice. However, further evaluation of the modalities of stent application and different stent designs with respect to long-term survival is necessary.

Adult↗

Association of autoimmunity to vascular heparan sulfate proteoglycan and vascular disease in the aged.

In the very old, there is an increased prevalence of immunologically mediated vascular disease. Vascular heparan sulfate proteoglycan (vHSPG) is a molecule which plays an important structural and functional role in the vasculature. Autoimmunity to vHSPG may play a role in the pathogenesis of vascular disease. The presence of autoantibodies to vHSPG was investigated in sera from aged nursing home patients who have a high prevalence of vascular disease. The results showed an association of the presence of autoantibodies to vHSPG in the sera from patients in this aged population with vascular disease, particularly cerebrovascular disease, renal disease and diabetes. In addition, autoantibodies to vHSPG protein core were associated with cerebrovascular disease in this frail elderly population. These studies support the hypothesis that autoimmunity may play a role in vascular disease in the aged.

Aged↗

Routine exercise testing to detect coronary artery disease in patients with atherosclerotic vascular disease.

The ability of patients with peripheral vascular disease to perform exercise studies on a conventional treadmill is often hampered by claudication, amputation, ischemic ulceration or rest pain. This study was undertaken to investigate the use of the arm ergometer in these patients. Eighty-three patients admitted with peripheral vascular or carotid artery disease were subjected to electrocardiographic-monitored exercise testing, using both the arm ergometer and conventional treadmill, where possible. Coronary arteriography was performed consecutively on 32 of these patients to establish a control group from which the sensitivity, specificity and predictive accuracy of both methods of exercise testing could be calculated. Nineteen of the 70 arm ergometry tests and 22 of the 48 treadmill tests were positive. Nineteen of the patients with a positive test using either of the methods were asymptomatic for cardiac disease. All five patients who developed cardiac events during surgery had positive exercise tests, preoperatively. The sensitivity of arm ergometry in detecting coronary artery disease was 45.5% and the specificity 100%, while the figures for treadmill testing were 82.4% and 83.3%, respectively. The combined sensitivity for the two tests was 81.8% and the specificity 87.5%. Using a combination of these two tests thus provided a highly specific and adequately sensitive means of detecting the presence of coronary artery disease in patients presenting for peripheral vascular surgery.

Adult↗

Impotence in vascular disease: relationship to vascular surgery.

This review considers diagnosis and treatment of vasculogenic impotence. It describes current information related to normal mechanisms of penile erection and pathophysiology of organic impotence, methods of preoperative diagnosis, quantitative evaluation of penile blood flow and operative techniques to be employed in aneurysmal or occlusive aorto-iliac disease. The importance of preserving internal iliac flow and neural fibres enervating the genitalia is stressed. Large vessel reconstructions have proved practical in maintaining or restoring normal erectile function, but at present reconstructions of isolated pudendal or penile artery occlusions are experimental. Medical therapy can be effective in certain marginal cases of small vessel occlusion.

Aortic Aneurysm↗