PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “VASCULAR DISEASES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1994

Long-term survival in patients with coronary artery disease: importance of peripheral vascular disease. The Coronary Artery Surgery Study (CASS) Investigators.

OBJECTIVES: The purpose of this study was to determine the importance of peripheral arterial disease in predicting long-term survival in patients with clinically evident coronary artery disease. BACKGROUND: Patients in the Coronary Artery Surgery Study (CASS) Registry were followed up for > 10 years. METHODS: Survival in 2,296 patients with peripheral arterial disease was compared with that of 13,953 patients without peripheral arterial disease using Kaplan-Meier survival curves. All patients had known stable coronary artery disease. Clinical, electrocardiographic (ECG), chest X-ray film and catheterization variables of the two groups were compared using the chi-square statistic or the two-sample t test. The independent effect of peripheral arterial disease (as well as other variables) on mortality was determined utilizing a Cox proportional hazards model. RESULTS: Patients with peripheral vascular disease were more likely to have hypertension, diabetes, family history of coronary artery disease, previous angina or myocardial infarction, previous coronary bypass surgery or to have smoked. They also had a higher incidence of congestive heart failure, ECG abnormality and modestly increased frequency of three-vessel disease. Independent correlates of long-term mortality for the entire cohort included age, smoking, diabetes, number of diseased coronary vessels, left ventricular function, hypertension, pulmonary disease, anginal class, previous myocardial infarction and peripheral vascular disease (all p < 0.001). At any point in time, patients with peripheral vascular disease had a 25% greater likelihood of mortality than patients without peripheral vascular disease (multivariate chi-square 25.83, hazard ratio 1.25, 95% confidence interval 1.15 to 1.36, p < 0.001). CONCLUSIONS: Peripheral vascular disease is a strong, independent predictor of long-term mortality in patients with stable coronary artery disease. Aggressive attempts at secondary disease prevention are warranted in this high risk group.

Cohort Studies↗
PubMed1998

Pain and powerlessness: the experience of living with peripheral vascular disease.

Peripheral vascular disease (PVD) is a widespread condition, the most common manifestation being a gradual occlusion of the arteries of the legs due to atheroma, which results in symptoms of ischaemia such as intermittent claudication or rest pain, ulceration and gangrene. Treatment of the condition is palliative and reconstructive, and aims to salvage the limb, restore mobility and function, and relieve pain. It usually involves attempts to revascularize the affected limb, either by surgical procedures such as bypass grafting, or by percutaneous transluminal angioplasty or thrombolysis. In some cases, it may be necessary to amputate the limb or part of it. Despite the chronicity of PVD, little is known about the ways in which individuals with vascular disease cope with their condition and about the effect it has on their life. In this context the aims of this study were to explore the lived experience of peripheral vascular disease, in order to identify key themes and categories, using a phenomenological grounded theory approach. A sample of nine individuals was drawn from patients who had had vascular bypass surgery within the past 18 months. Data were collected using audiotaped one-to-one interviews and the researcher's field notes, and were validated with a group of experienced vascular nurses. Transcripts were analysed using open and axial coding techniques, and major and minor categories were identified and related to other data collected. It appeared that vascular patients experienced powerlessness in relation to the direct effects of their condition and in relation to its treatment modalities. The findings suggested that the 'acute' style of management of PVD often led to unrealistic expectations on the patient's part, which gave rise to the experience of powerlessness. The implications of these findings for the management of patients with PVD are discussed.

Activities of Daily Living↗
PubMedDate not supplied

VEGF gene therapy for coronary artery disease and peripheral vascular disease.

Coronary artery disease (CAD) and peripheral arterial disease (PAD) are significant medical problems worldwide. Although substantial progress has been made in prevention as well as in the treatment, particularly of CAD, there are a large number of patients, who despite maximal medical treatment have substantial symptomatology and who are not candidates for mechanical revascularization. Therapeutic angiogenesis represents a novel, conceptually appealing treatment option. Ad(GV)VEGF121.10 (BIOBYPASS) is an adenovector, carrying the transgene encoding for human vascular endothelial growth factor 121 (VEGF(121)). A number of preclinical studies have demonstrated angiogenic activity of BIOBYPASS, not only anatomically but also functionally. Phase I clinical studies have demonstrated that intramyocardial infection of BIOBYPASS in patients with severe CAD as well as intramuscular injections of BIOBYPASS in patients with severe peripheral vascular disease (PVD) was well tolerated; furthermore, these studies provided some intriguing indications of activity, which led to initiation of major randomized Phase II "proof-of-concept" studies. This paper provides a review of the rationale behind BIOBYPASS as well as a summary of pertinent preclinical and early clinical data.

Adenoviridae↗
PubMed2001

Periodontal disease, race, and vascular disease.

Recently, a number of studies have rekindled the possible hypothesis that oral health has repercussions beyond the oral cavity and is associated with systemic diseases. Interestingly, it is a return to an old theory that chronic infections and inflammation played a crucial role in atherosclerosis. This larger theory was advocated by French physicians, among others, at the beginning of the 20th century. In this article, we will review the epidemiologic evidence pointing to a possible association between oral health and vascular diseases and examine the role of race/ethnicity in the interpretation of this association.

Acute Disease↗
PubMed2004

Paediatric pulmonary vascular disease.

Pulmonary vascular disease comprises any congenital or acquired pathology of the intrinsic pulmonary vessels with the unique feature of pulmonary arteries carrying unsaturated blood and pulmonary veins carrying oxygenated blood. Pulmonary hypertension (PH) ensues when pulmonary vascular disease affects at least 50% of the capillary resistance vessels, i.e. pulmonary pre-acinar and intra-acinar arteries (so-called pre-capillary PH), or when pressure in the pulmonary venous system distal to the capillaries rises above a mean of 15 mmHg (so-called post-capillary PH). PH is defined by a mean pulmonary arterial pressure above 25 mmHg at rest. Vasoconstriction, remodelling and thrombosis of small pulmonary arteries lead to an increase in pulmonary vascular resistance. The consequence is failure of the afterload-intolerant right ventricle. In this review, pulmonary vascular disease in children will be addressed according to the 2003 World Health Organisation (Venice) classification of PH.

Child↗
PubMed1991

[Relation of baseline examination results to death from ischemic heart disease, cerebro-vascular disease and sudden death].

The relation of variables obtained from a baseline examination to death from ischemic heart disease (IHD), cerebro-vascular disease (CVD) and sudden death (SUD) was analyzed in a case-control study. From questionnaire survey of approximately 180,000 subjects who underwent baseline health examinations in 1971-1986 at Aichi prefectural center of health care, 148 deaths were selected for this study. The number of cases on IHD, CVD and SUD was 36, 60, and 52, respectively. Mean age of cases was 54.8 years old and the mean follow up interval between baseline examination and death was 3.7 years. Four controls matched according to year of baseline examination, age and sex were chosen arbitrarily for each case, and odds ratios for the three diseases were estimated. In some of the matched sets, odds ratios at a follow up examination were compared with that at the first examination. The results were as follows: 1) Variables showing positive relationships to death from each of the three diseases were hypertension, high fasting blood sugar, abnormality of cardio-thoracic ratio, ST-T abnormality in ECG, left ventricular hypertrophy in ECG. The odds ratio for ST-T abnormality in ECG was significant for all three causes of death. 2) High total cholesterol showed a significant positive relation only to death from IHD. As to death from CVD and SUD, albuminuria and sclerotic changes in fundus oculi were positively and significantly related. Risk factors differed for deaths from the three diseases. 3) In death from IHD and CVD, odds ratio at the second examination was apt to be higher than that at baseline examination. In death from SUD, however, odds ratios at the first and the second examination showed no significant difference.

Adult↗
PubMed1986

Head and neck manifestations of collagen vascular diseases.

Collagen vascular disease is among the least understood entities in medicine. What appears to be a localized process may be a manifestation of a systemic disease with serious sequelae. The otolaryngologist must be aware of the manifestations of these disorders in the head and neck.

Adult↗
PubMed2004

Chymase as a novel target for the prevention of vascular diseases.

In vascular tissues, chymase catalyzes the production of angiotensin II, which plays a crucial role in vascular diseases. Recent clinical studies and animal models of vascular proliferation and atherosclerosis have provided evidence that angiotensin II formed by chymase is involved in these processes. These observations suggest that chymase might promote the development of vascular proliferation and atherosclerosis. Chymase also activates matrix metalloproteinase 9, which promotes aortic aneurysm and angiogenesis, and thus chymase inhibitors might also prevent the progression of abdominal aortic aneurysm and angiogenesis. We propose that chymase is a novel target for preventing vascular diseases.

Animals↗
PubMedDate not supplied

Percutaneous continuous aortic flow augmentation for cardiac recovery in a chronic heart failure patient with peripheral vascular disease.

Peripheral vascular disease is an obstacle to the use of continuous aortic flow augmentation (CAFA). The authors used CAFA in a patient with a 50% stenosis of the left iliac artery. Five hours after initiating therapy, flow rates dropped from 1.47 L/min to 0.2 L/min, possibly due to obstruction around the inflow cannula near the site of the iliac artery stenosis. Flow was stabilized by adequate fluid infusion and successfully restored by slightly withdrawing the tip of the inflow catheter. This finding suggests that peripheral vascular disease is a relative-not an absolute-contraindication for CAFA, but requires close monitoring of flow during CAFA therapy.

Aged↗
PubMed2004

Metabolic inertia in contracting skeletal muscle: a novel approach for pharmacological intervention in peripheral vascular disease.

Peripheral vascular disease (PVD) is generally accepted to result in the failure of skeletal muscle blood flow to increase adequately at the onset of muscular work. There are currently no routine pharmacological interventions towards the treatment of PVD, however, recent Phase III trials in the USA have demonstrated the clinical potential of the phosphodiesterase III inhibitor Cilostazol for pain-free and maximal walking distances in patients with intermittent claudication. PVD is characterized by a marked reliance on oxygen-independent routes of ATP regeneration (phosphocreatine hydrolysis and glycolysis) in skeletal muscle during contraction and the rapid onset of muscular pain and fatigue. The accumulation of metabolic by-products of oxygen-independent ATP production (hydrogen and lactate ions and inorganic phosphate) has long been associated with an inhibition in contractile function in both healthy volunteers and PVD patients. Therefore, any strategy that could reduce the reliance upon ATP re-synthesis from oxygen-independent routes, and increase the contribution of oxygen-dependent (mitochondrial) ATP re-synthesis, particularly at the onset of exercise, might be expected to improve functional capacity and be of considerable therapeutic value. Historically, the increased contribution of oxygen-independent ATP re-synthesis to total ATP generation at the onset of exercise has been attributed to a lag in muscle blood flow limiting oxygen delivery during this period. However, recent evidence suggests that limited inertia is present at the level of oxygen delivery, whilst considerable inertia exists at the level of mitochondrial enzyme activation and substrate supply. In support of this latter hypothesis, we have reported on a number of occasions that activation of the pyruvate dehydrogenase complex, using pharmacological interventions, can markedly reduce the dependence on ATP re-synthesis from oxygen-independent routes at the onset of muscle contraction. This review will focus on these findings and will highlight the pyruvate dehydrogenase complex as a novel therapeutic target towards the treatment of peripheral vascular disease, or any other disease state where premature muscular fatigue is prevalent due to metabolite accumulation.

Acetyl Coenzyme A↗
PubMed1981

Hypomagnesemia and vasoconstriction: possible relationship to etiology of sudden death ischemic heart disease and hypertensive vascular diseases.

In-vitro experiments are presented which indicate that the concentration of extracellular magnesium ions ([Mg2+]o) can exert profound influences on the contractility and reactivity of arteries, arterioles and veins from a number of regional vasculatures in several mammalian species, including man. Hypomagnesemia can potentiate the contractile activity of a variety of neurohumoral substances and induce vasospasm. Hypermagnesemia can do the reverse, i.e., induce hyporeactivity, relaxation and vasodilatation. Data are also presented to indicate that [Mg2+]o can control the entry, distribution and exit of calcium ions (Ca2+) from vascular smooth muscle cells. Arterial and venous smooth muscles excised from rats with alloxan-diabetes mellitus or spontaneous hypertension (SHR) appear to exhibit vascular membranes which have modifications in their Mg-Ca exchange sites. Data are reviewed which suggest that certain vascular diseases (e.g., sudden-death ischemic heart disease, hypertension, eclampsia, diabetes mellitus) are associated with a Mg-deficiency. Overall, it is suggested that [Mg2+]o and membrane [Mg] may play critical roles in regulating vascular tone and homeostasis.

Animals↗
PubMed1983

Endothelial cell damage and tubuloreticular structures in interstitial lung disease associated with collagen vascular disease and viral pneumonia.

Lung tissue showing the light microscopic changes of interstitial inflammation and fibrosis was studied electron-microscopically in 11 patients with collagen vascular disease and 26 patients with viral pneumonia. All patients exhibited progressive respiratory insufficiency and had abnormal pulmonary function test results. Endothelial cell cytoplasmic swelling and intracellular tubuloreticular structures were the dominant ultrastructural change in the lungs of both groups. Tubuloreticular structures were identified in peripheral blood lymphocytes in all patients with collagen vascular disease and in 2 with viral pneumonia. Tubuloreticular structures were not identified in the lung tissue from various control patients and in the lymphocytes from patients with idiopathic interstitial pulmonary fibrosis. We conclude that (1) the ultrastructural changes seen in viral pneumonia and collagen vascular-associated interstitial lung disease are essentially identical; (2) endothelial cell damage may be the primary pathologic change associated with both diseases; (3) tubuloreticular structures are seen in large numbers in lung tissue from patients with viral pneumonia and collagen vascular disease; (4) tubuloreticular structures are present in peripheral blood lymphocytes from all patients with collagen vascular disease.

Adult↗
PubMed1994

Human endothelial cells are defective in diabetic vascular disease.

Diabetic vascular disease is characterized pathologically by endothelial cell (EC) hyperplasia and basement membrane (BM) thickening. One key question regarding the pathogenesis of diabetic vascular disease is whether the EC or BM or both are primarily defective and responsible for these pathological changes. Previous studies, which took the approach of creating artificial diabetic conditions, have been inconclusive. It is known, however, that the extracellular matrix may be altered by glycosylation as a result of hyperglycemia, thereby altering EC function. To begin to address this question and more closely mimic the situation in vivo, we characterized human diabetic EC harvested from insulin-dependent diabetic mothers (IDDM) at the cellular and molecular levels. Human EC were isolated from both normal and IDDM umbilical cords and cellular functions evaluated using standard assays of attachment (% attached cells), proliferation (cpm/cell), resistance to detachment under shear stress (number of cells remaining attached), and glucose uptake (cpm/2 X 10(4) cells). Gene expression of major BM components (collagen type IV, laminin beta 1, and laminin beta 2) was quantified by Northern analysis. Diabetic EC demonstrated increased proliferation (two- to eightfold compared to normals), were 20-40% less resistant to shear stress and took up glucose 10-15% more slowly than normal EC. Furthermore, Northern analysis showed that the expression of major BM components was increased by an average of 10-18% in diabetic cells compared to normal cells. These results were consistent with in vivo observations and previously published data.(ABSTRACT TRUNCATED AT 250 WORDS)

Basement Membrane↗
PubMed2001

Dementia due to subcortical ischemic vascular disease.

Ischemic vascular disease (IVD) is the second most common cause of dementia in the Western world. This article focuses on dementia resulting from subcortical ischemic vascular disease (SIVD), a subtype of IVD, which in many cases may be prevented. Hypertension and diabetes are the leading causes of small-artery disease, subcortical brain ischemia, and stepwise or slowing progressive decline in cognitive function. The pattern of cognitive impairment in SIVD, as compared with Alzheimer's disease, is characterized by greater impairment of executive function but better preservation of recognition memory. Structural neuroimaging studies, such as computed tomography and especially magnetic resonance imaging, are more sensitive than the clinical examination and can enable detection of subcortical lacunes and deep white matter changes that are clinically silent. Often the brain can be protected against SIVD by early diagnosis and management of risk factors. Once end-organ damage has occurred, however, treatment outcome is less satisfactory. The most common risk factors for SIVD--hypertension and diabetes mellitus--are best detected and managed in primary care settings.

Algorithms↗
PubMed2000

Focus on HDL: a new treatment paradigm for athero-thrombotic vascular disease.

Atherosclerotic vascular disease is the leading cause of mortality and morbidity in much of the Western world. Although advances in lifestyle and risk factor modification, pharmacotherapy, endovascular interventions and surgery have considerably improved clinical outcome, 40 - 50% of adverse cardiovascular events continue to occur despite current strategies. A number of new targets for therapeutic exploitation are currently being investigated that include, among others, apolipoprotein A-I, the major structural component of high density lipoprotein (HDL) particle. The strong negative relationship between HDL-cholesterol levels and coronary heart disease in epidemiological studies, as well as data from experimental models suggest that HDL-based therapies could be an important new paradigm for prevention, treatment and reversal of atherosclerotic vascular disease.

Animals↗
PubMed2003

Peripheral vascular disease in Type 2 diabetic Chinese patients: associations with metabolic indices, concomitant vascular disease and genetic factors.

AIMS: Conventional and genetic risk factors have been reported to play a role in the pathogenesis of vascular disease, but do not explain the lower burden of cardiac and peripheral vascular disease (PVD) in Chinese compared with Caucasians. The role of renin-angiotensin system (RAS) gene polymorphisms and conventional vascular risk factors has not been determined. METHODS: A total of 3097 Chinese diabetic subjects were screened for PVD, which was identified in 194 of the 2967 patients with Type 2 diabetes. Biochemical parameters and the genotype and allele frequencies of three RAS gene polymorphisms, the angiotensin-converting enzyme (ACE) insertion/deletion, angiotensinogen (AGT) M235T and angiotensin II type 1 receptor (AT1R) A1166C polymorphisms were then compared between the PVD patients and 1046 age, gender and diabetes duration-matched patients without PVD. RESULTS: PVD identified in 6.5% was associated with significantly worse glycaemic control, lipid profile and renal function. Smoking was more common, as were the other macro- and microvascular diseases. The prevalence of hypertension was similar between the groups, yet diastolic blood pressure was slightly lower in the PVD group. The ACE D allele was significantly more frequent in patients with PVD compared with the matched diabetic controls (38.1 vs. 29.8%, P = 0.039). No differences in the AT1R or AGT polymorphisms were observed. CONCLUSIONS: PVD was associated with a worse metabolic profile and greater concomitant vascular disease than controls. The ACE I/D polymorphism was associated with PVD in these Type 2 diabetic patients.

Aged↗