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At least 955 records · Page 53Linked to original sources
PubMed1979

Severe pulmonary vascular disease in systemic lupus erythematosus.

A young woman with systemic lupus erythematosus (SLE) had clinical evidence of acute cor pulmonale. Autopsy disclosed vascular lesions in the lungs resembling those seen in advanced pulmonary hypertension. This case illustrates that severe pulmonary vascular disease may complicate SLE and mimic pulmonary thromboembolic disease.

Acute Disease↗
PubMed1990

A clinical trial of laser thermal angioplasty in patients with advanced peripheral vascular disease.

A 3-year prospective trial of laser thermal-assisted balloon angioplasty in 28 patients included 27 who had advanced peripheral vascular disease (severe tissue loss, gangrene, infection, and rest pain), 7 who were failures of previous therapy (surgery and thrombolysis), and 4 who were high risk for operation (myocardial infarction within 6 weeks and/or ejection fractions of less than or equal to 20%). Laser angioplasty was performed in the operating room via a groin incision by a surgeon-radiologist team. In the 27 patients with advanced peripheral vascular disease (ankle-brachial systolic pressure index [ABI] 0.27 +/- 0.2 in 10 nondiabetic, and 0.46 +/- 0.1 in 17 diabetic patients), recanalization of the native vessel was successful in 16, and patency was restored in 2 chronically occluded polytetrafluorethylene (PTFE) grafts. In these 18 (67%) successfully recanalized patients, however, five amputations were required within 1 month, and another six were needed between 8 and 12 months. Early amputations were caused by a failure of wound healing, even through angioplasty sites were patent. Late amputations were caused by reocclusion of the treated site in five of six patients. In the remaining seven patients in whom laser angioplasty alone was successful, five had healed limbs at 6 to 24 months and two remain incompletely healed but functional. The patency for successful procedures ranged from 48 hours to 25 months (5.6 +/- 6.4 mean months, +/- SD), with cumulative patency by life-table analysis of 55.5% at 3 months, 38.8% at 6 months, and 11.1% at 12 months. There were no procedure-related deaths. Complications included seven arterial wall perforations by the laser probe. We conclude that laser angioplasty has a limited role in advanced peripheral vascular disease but may provide an interval patency, thus allowing postponement of operation for high-risk patients until their medical conditions permits surgery, or to correct local tissue necrosis or infection in the operative field before reconstruction, and to restore patency to thrombosed PTFE grafts.

Aged↗
PubMed1975

Smoking and other factors affecting the conservative management of peripheral vascular disease.

Three hundred and ninety patients with peripheral vascular disease, who were neither eligible for, nor fit to undergo, surgery, have been studied in a prospective trial to assess the effectiveness of adequate active conservative therapy. These patients were followed up from 4 to 72 months, the duration of the average follow-up being 24 months. There was a 72% over-all improvement rate. The most striking feature of the trial was the correlation between smoking and failure to improve.

Adult↗
PubMed2000

Paraoxonase (PON1) phenotype is a better predictor of vascular disease than is PON1(192) or PON1(55) genotype.

The paraoxonase (PON1) PON1-Q192R and PON1-L55M polymorphisms have been inconsistently associated with vascular disease. Plasma PON1 activity phenotypes vary markedly within genotypes and were, therefore, expected to add to the informativeness of genotype for predicting vascular disease. The case-control sample included 212 age- and race-matched men (mean age 66.4 years). The 106 carotid artery disease (CAAD) cases had >80% carotid stenosis, and the 106 controls had <15%. Two PON1 substrate hydrolysis rates (paraoxon [POase] and diazoxon [DZOase]) were significantly lower in cases than in controls and were significant predictors of CAAD by use of logistic regression (POase, P=0.005; DZOase, P=0.019). DZOase predicted vascular disease independently of lipoprotein profile, high density lipoprotein subfractions, apolipoprotein A-I, and smoking. PON1-192 and PON1-55 genotypes or haplotypes did not predict case-control status unless the activity phenotype was also included as a predictor by use of logistic regression. When phenotype was included as a predictor, PON1-192 and PON1-55 genotypes or combined haplotypes were significant predictors (P<0.05). In conclusion, examining PON1-192 and/or PON1-55 genotypes alone may mistakenly lead to the conclusion that there is no role of PON1 in CAAD. These results support the benefit of a "level crossing" approach that includes intervening phenotypes in the study of complexly inherited disease.

Aged↗
PubMed2005

Soluble bio-markers in vascular disease: much more than gauges of disease?

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.

Arteriosclerosis↗
PubMed1989

A population-based case-control study of temporal arteritis: evidence for an association between temporal arteritis and degenerative vascular disease?

The first population-based incident case-control study of temporal arteritis (TA) in the US was conducted using the unique data resources of the Rochester Epidemiology Project. During the period 1950-1985, 88 newly diagnosed cases of biopsy-proven TA were identified among residents of Olmsted County, Minnesota. Cases were each matched to four Olmsted County community controls on age, sex and duration of community medical record. Odds ratios (OR) were calculated for marital status, education, Quetelet index, pregnancy, age at menopause, thyroid disease, diabetes, smoking, hypertension, angina, myocardial infarction, peripheral vascular disease, and stroke. Multivariable conditional logistic regression analysis identified statistically significant adjusted OR for smoking (2.3, 95% CI = 1.3-4.1). Elevated ORs which were not statistically significant were noted for angina, myocardial infarction, and peripheral vascular disease. These data suggest that TA and arteriosclerosis may share a common causal pathway. Alternatively, histopathological misclassification of temporal artery biopsies may have resulted in the observed association. Due to the limited power of this population-based study, multicentre collaboration should be encouraged to more precisely define the epidemiology of TA.

Aged↗
PubMed2001

Patients with atherosclerotic vascular disease: how low should plasma homocyst(e)ine levels go?

Plasma homocyst(e)ine level is a strong independent risk factor for vascular disease. The spelling of homocyst(e)ine reflects that what is measured, and what constitutes the risk factor; it includes homocysteine, homocystine (the dimer of homocysteine) and mixed cysteine-homocysteine disulfide. Homocyst(e)ine levels above 10.2 micro mol/L are associated with a doubling of coronary risk, and levels above 20 micro mol/L are associated with a 9.9-fold increase in risk compared with levels below 9 micro mol/L. The mechanisms by which homocyst(e)ine promotes vascular disease include increased thrombosis, consumption of nitric oxide, endothelial injury, and reduced thrombolysis. Homocyst(e)ine is an independent predictor of carotid atherosclerosis. Vitamin therapy with folate, pyridoxine (vitamin B(6)), and cyanocobalamin (vitamin B(12)) reduces blood levels of homocyst(e)ine, improves endothelial function, reduces levels of fibrinogen and lipoprotein(a), improves thrombolysis, and in uncontrolled clinical observation, leads to regression of carotid plaque. These lines of evidence support a causal relationship between homocyst(e)ine and atherosclerosis, and suggest that in patients with vascular disease, an appropriate target level for therapy may be below 9 or 10 micro mol/L. Randomized controlled studies are under way to determine whether vitamin therapy is effective in secondary prevention of myocardial infarction and stroke.

Arteriosclerosis↗
PubMed2004

Homocysteine, vitamins, and prevention of vascular disease.

Within the past four decades, the efforts of investigators worldwide have established the amino acid homocysteine as an important factor in arteriosclerosis and diseases of aging. After its discovery in 1932, homocysteine was demonstrated to be an important intermediate in the metabolism of amino acids. However, little was known about the broader biomedical significance of homocysteine until 1962, when children with mental retardation, accelerated growth, dislocated ocular lenses, and frequent vascular thrombosis were found to excrete homocysteine in the urine. My study of two patients with homocystinuria caused by different inherited enzymatic disorders in 1968 disclosed advanced widespread arteriosclerotic plaques in both cases. This discovery led to the conclusion that homocysteine causes vascular disease by a direct effect on the cells and tissues of the arteries. This interpretation suggests that homocysteine is important in the pathogenesis of arteriosclerosis in persons with hereditary, dietary, environmental, hormonal, metabolic, and other factors predisposing them to hyperhomocysteinemia. Within the past decade, many major clinical and epidemiological studies have proven that hyperhomocysteinemia is a potent independent risk factor for vascular disease. According to the homocysteine theory of arteriosclerosis, insufficient dietary intake of the B vitamins, folic acid and pyridoxine, caused by losses of these nutrients during processing of foods, leads to elevation of blood homocysteine and vascular disease in the general population. The dramatic decline in cardiovascular mortality since the 1960s in the United States is attributed to fortification of the food supply by synthetic pyridoxine and folic acid. The recent Swiss Heart Study showed that B vitamins slowed restenosis in patients with coronary arteriosclerosis treated with angioplasty. Currently, more than 20 prospective, worldwide, interventional trials involving at least 100,000 participants are examining whether lowering plasma homocysteine levels with supplemental B vitamins will prevent mortality and morbidity from arteriosclerotic vascular disease.

Animals↗
PubMed1990

Effects and limitations of pentoxifylline therapy in various stages of peripheral vascular disease of the lower extremity.

One hundred one patients with peripheral vascular disease of the lower extremity were entered into a study of the efficacy of oral pentoxifylline to determine if the response to therapy varied with the severity of disease. Ninety-three patients were evaluated before and after 8 weeks of therapy with pentoxifylline, while 8 did not complete the entire course due to adverse drug reactions. Resting and post-stress ankle/arm Doppler indices (AAIs) were measured and, in those patients who could walk on a treadmill, treadmill walking distances were measured. Patients were classified according to pretreatment clinical and treadmill measurements and according to pretreatment resting AAIs. Resting and post-stress AAIs, as well as treadmill walking distances, increased in patients with moderately severe claudication. Patients in this group responded better to therapy than did patients with rest pain or ischemic ulcers, severe claudication, or mild claudication. Patients with a pretreatment resting AAI greater than or equal to 0.5 responded better than those with an AAI less than 0.5. Only 5% of patients reported satisfaction with the results of treatment. These results support the findings that pentoxifylline may be useful only in selected patients with moderately severe peripheral vascular disease of the lower extremity and may not be useful in those with severe or mild disease.

Diabetes Complications↗
PubMed1980

Pulmonary vascular disease in total anomalous pulmonary venous drainage.

Pulmonary vascular disease (PVD) was assessed by a qualitative and quantitative histopathologic analysis of lung specimens of 40 patients (age at autopsy 5 days to 12 years, median 3 months) with total anomalous pulmonary venous drainage. A PVD index was derived by counting the number of vessels with each Heath-Edwards grade of PVD (PVD index = [0 (Normal) +1 (N grade 1) +2 (N grade 2)....+6 (N grade 6)]/number of vessels graded, where N = the number of patients) in randomly selected pulmonary resistance vessels 30-300 mu in diameter. Patients with pulmonary venous obstruction died earlier and had a higher PVD index as a group than patients with unobstructed venous drainage. A remarkable degree of advanced pulmonary vascular changes was found in the entire group, even young infants. Pulmonary vascular obstructive disease is an important factor in the pathophysiology of this lesion. Careful attention to the prevention and management of increased pulmonary vascular resistance in the postoperative period may improve survival.

Blood Pressure↗
PubMed1994

High-resolution CT and pulmonary function tests in collagen vascular disease: comparison with idiopathic pulmonary fibrosis.

To estimate whether the lung abnormalities seen in collagen vascular diseases (CVD) were similar or distinct to those seen in idiopathic pulmonary fibrosis (IPF), and to ascertain whether the extent of the abnormalities on high-resolution CT (HRCT) correlated with pulmonary function, we reviewed HRCT findings and pulmonary function test results of 64 patients with either CVD (n = 55) or IPF (n = 9). Response to corticosteroid treatment was also evaluated in 20 of the 64. High incidence of honeycomb lesion was observed in IPF (9/9, 100%) and in progressive systemic sclerosis (PSS) (11/14, 79%). CVD, except for PSS, had a low incidence of honeycomb lesion (27%). On the other hand, incidence of ground-glass shadow in CVD (47/55, 85%) was the same as that in IPF (8/9, 89%). Diffusing capacity significantly correlated with the extent of all parenchymal abnormalities in all CVD and IPF, with honeycomb lesion in PSS, and with ground-glass shadow or air-space consolidation in CVD except for PSS (r < -0.7, P < 0.001). In all 15 cases in which corticosteroid therapy was effective, no honeycomb lesions were seen. Collagen vascular disease, except for PSS, had a different pattern of disease than IPF. The morphologic changes seen on HRCT correlated well with pulmonary function in CVD.

Collagen Diseases↗