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At least 703 records · Page 39Linked to original sources
PubMed2003

Effects of losartan or atenolol in hypertensive patients without clinically evident vascular disease: a substudy of the LIFE randomized trial.

BACKGROUND: Cardiovascular morbidity and mortality are reduced by treatment with the angiotensin II AT(1)-receptor antagonist losartan compared with conventional treatment with the beta-blocker atenolol in patients with hypertension and electrocardiogram-defined left ventricular hypertrophy, many of whom had known vascular disease. OBJECTIVE: To determine whether losartan reduces cardiovascular event rates in lower-risk hypertensive patients without clinically evident vascular disease. DESIGN: Subgroup analysis of a randomized trial. SETTING: The Losartan Intervention for Endpoint reduction in hypertension (LIFE) study. PATIENTS: 6886 men and women (57% women) 55 to 80 years of age (average, 66 years) with essential hypertension (sitting blood pressure, 160 to 200/95 to 115 mm Hg [average, 174/98 mm Hg]) and electrocardiogram-defined left ventricular hypertrophy who did not have clinically evident vascular disease. INTERVENTION: Patients were randomly assigned to once-daily double-blind treatment with losartan or atenolol. MEASUREMENTS: An end point committee ascertained end points (cardiovascular death, stroke, or myocardial infarction). RESULTS: Blood pressure was reduced similarly by losartan and atenolol. The primary composite end point occurred in 282 losartan-treated patients (17.5 per 1000 patient-years) and 355 atenolol-treated patients (21.8 per 1000 patient-years; relative risk, 0.81 [95% CI, 0.69 to 0.95]; P = 0.008). Cardiovascular death occurred in 103 losartan-treated patients and 132 atenolol-treated patients (relative risk, 0.80 [CI, 0.62 to 1.04]; P = 0.092), stroke (nonfatal and fatal) occurred in 125 losartan-treated patients and 193 atenolol-treated patients (relative risk, 0.66 [CI, 0.53 to 0.82]; P < 0.001), and myocardial infarction (nonfatal and fatal) occurred in 110 losartan-treated patients and 100 atenolol-treated patients (relative risk, 1.14 [CI, 0.87 to 1.49]; P > 0.2). New-onset diabetes occurred less often in patients treated with losartan (n = 173) than in patients treated with atenolol (n = 254) (relative risk, 0.69 [CI, 0.57 to 0.84]; P < 0.001). Benefits of losartan treatment were numerically smaller, but not significantly so, in patients with preexisting vascular disease. CONCLUSION: In hypertensive patients without clinically evident vascular disease, losartan was more effective than atenolol in preventing cardiovascular morbidity and death, predominantly stroke, independent of blood pressure reduction.

Adrenergic beta-Antagonists↗
PubMed2003

Relationship between peripheral vascular disease and high plantar pressures in diabetic neuro-ischaemic patients.

BACKGROUND: It has been shown that high foot pressure in diabetic patients plays a crucial role in plantar ulcer development. The purpose of the study is to analyze the relationship between foot arterial pressures and plantar pressures in diabetic patients with both peripheral neuropathy vascular disease. METHODS: We have evaluated the relationship between foot arterial pressures and plantar pressure parameters (Peak Plantar Pressure, Foot-Floor Contact and Plantar Pressure Integral) in eleven diabetic patients with both peripheral neuropathy and peripheral vascular disease. Peripheral neuropathy was defined as a tuning fork score<4/8 measured at the great toe and internal malleolus with a Tuning fork (Rydel-Seiffer 128 Hz), the absence of both patellar and ankle reflexes and with a temperature discrimination more than +5 degrees C (Thermocross). The peripheral vascular disease (PVD) was evaluated by Doppler technique. Peak Plantar Pressure (PPP) and Foot-Floor Contact (FFC) were measured by Force-Sensing Resistive (FSR 174) sensors under the 1st, 3rd and 5th metatarsal heads as well as under the heel and big toe of both feet. The Plantar Pressure Integral (PPI) was defined by the integral of the pressure over the time. RESULTS: We have found significant relationship between plantar pressure parameters (PPP, FFC, and PPI) under the first metatarsal heads and Doppler arterial pressures of both tibial posterior and dorsalis pedis artery. However, there was no relationship between Doppler arterial pressures and plantar pressure parameters (PPP, FFC, PPI) under 3rd and 5th metatarsal heads or under both the heel and the big toe. CONCLUSION: According to our results, the peripheral vascular disease could contribute to the elevation of plantar pressures and to the prolonged duration of foot floor contact at each step in diabetic patients with both peripheral neuropathy and peripheral vascular disease. In such patients, severe ischaemia could lead to an increased risk of foot ulceration and consecutive lower extremity amputation.

Aged↗
PubMed1992

Not so rapid progression of peripheral vascular disease after diagnostic angiography.

It was recently reported that peripheral vascular disease may progress so rapidly after diagnostic angiography that most likely the diagnostic procedure is in some way responsible. Because flow-limiting arterial stenoses often become complete occlusions within hours or days of the diagnostic procedure, it was recommended that angioplasty be performed immediately after diagnostic angiography to avoid this complication. The authors attempted to confirm these findings before implementing this recommendation. In fact, they did not confirm the findings. Among 96 flow-limiting stenoses considered for angioplasty, the procedure was performed in 31 on the same day. Among the remaining 65 cases, in 64 the stenosis did not occlude and angioplasty was successfully performed. Only one stenosis was discovered to have thrombosed, and this occurred 3 weeks after diagnostic angiography. These results indicate that there is not such rapid progression of peripheral vascular disease after diagnostic angiography. It is not necessary to perform angioplasty of stenotic lesions emergently, and treatment is not impaired by electively scheduling the patient for the next available day.

Angiography↗
PubMed1981

Hypersensitivity to tobacco glycoprotein in human peripheral vascular disease.

One hundred and sixty-four patients with peripheral vascular disease (PVD) were skin tested with a purified tobacco glycoprotein (TGP). A basophil degranulation test (BDT) was also performed to assess in vitro reactivity to TGP. Immediate skin test hypersensitivity to TGP was found in 18 of 164 (11%) patients with radiologically demonstrable PVD. BDT was positive in 25/42 (60%) smokers as opposed to 6/23 (24%) nonsmokers (p less than 0.01). Twenty-one of 49 (43%) skin test-negative and 10/11 (91%) skin test-positive patients wih PVD had a positive BDT (p less than 0.02). Only 1/34 (3%) patients with negative BDT had a positive skin test. Skin test-positive patients had significantly higher BDT at 0.01 and 0.001 microgram/ml TGP in vitro compared to skin test-negative patients (p less than 0.01). When PVD was graded by arteriography, one of 11 patients with "mild," 11/87 with "moderate" and 4/20 with "severe" PVD were skin test-positive to TGP (p less than 0.01 "mild" vs "moderate"; p less than 0.05 "mild" vs. "severe"). These differences could not be attributed to age, sex, atopy or smoking status. Reactivity to TGP exists in a proportion of patients with PVD and may be causally related in such cases to the development of atherosclerotic vascular disease.

Adult↗
PubMedDate not supplied

Preventive treatment of graft coronary vascular disease: the potential role of vasodilator therapy.

The prevention or treatment of graft coronary vascular disease is one of the major challenges facing cardiovascular medicine today. Further investigation is necessary to elucidate the mechanisms by which myointimal hyperplasia develops within the coronary vasculature of heart transplants. Studies of several models of the vascular disease, however, suggest that there is an interaction between vasoactive substances, hemodynamic stimuli, and autocrine/paracrine growth factors that governs the vascular remodeling response to vessel injury. In this review I will focus primarily on the role of vasoactive substances and hemodynamic stimuli as determinants of vascular structure. In addition, this review will provide substantiating evidence that advances the postulate that vasodilator therapy may have an adjunctive role in the prevention and treatment of graft coronary vascular disease. It is hoped that this provocative concept will stimulate further investigation of novel therapeutic strategies in the treatment of this disease.

Coronary Disease↗
PubMed1998

Common methylenetetrahydrofolate reductase gene mutation leads to hyperhomocysteinemia but not to vascular disease: the result of a meta-analysis.

BACKGROUND: The results of retrospective and prospective case-control studies have clearly established that mild elevations of the plasma homocysteine level are associated with increased risk of coronary, cerebral, and peripheral vascular disease. Recently, a mutation (677C-->T) was identified in the methylenetetrahydrofolate reductase (MTHFR) gene that results in reduced folate-dependent enzyme activity and reduced remethylation of homocysteine to methionine. Mutant homozygotes (TT genotype) constitute approximately 12% of the white population and frequently have mildly elevated circulating homocysteine. Therefore, it seems likely that they would also be at increased risk of vascular disease. A number of studies have investigated this during the past 3 years, and the present article evaluates the results in a meta-analysis. METHODS AND RESULTS: We identified 13 studies in which there were measurements of plasma homocysteine in relation to the 3 genotypes (TT, CT, and CC) and 23 case-control studies comprising 5869 genotyped cardiovascular disease patients (mostly coronary artery disease) and 6644 genotyped control subjects. Those bearing the TT genotype had plasma homocysteine concentrations 2.6 micromol/L (25%) higher than those with the CC genotype. However, there was no difference between patients and control subjects either in the frequency of mutant alleles (T) (34.3% versus 33.8%) or the TT genotype (11.9% versus 11.7%). In the analysis of the 23 studies, the relative risk (OR) of vascular disease associated with the TT genotype was 1.12 (95% CI, 0.92 to 1.37). CONCLUSIONS: We conclude that although the C677T/MTHFR mutation is a major cause of mild hyperhomocysteinemia, the mutation does not increase cardiovascular risk. Our findings suggest that the mild hyperhomocysteinemia found frequently in vascular disease patients is not causally related to the pathogenesis of the vascular disease.

Cardiovascular Diseases↗
PubMed1990

Role of oxygen-derived free radicals in acute angiotensin II--induced hypertensive vascular disease in the rat.

Severe experimental hypertension is associated with vascular hyperpermeability and cellular damage in small arteries and arterioles in rats. Oxygen-derived free radical production is also associated with increased vascular permeability and cellular injury in a variety of conditions, including ischemia-reperfusion and inflammation. To determine if free radicals play a role in the pathogenesis of hypertensive vascular disease, the free radical scavengers superoxide dismutase (SOD), catalase, SOD and catalase, and dimethyl sulfoxide (DMSO) were given to rats made acutely hypertensive with angiotensin II infusions. Untreated hypertensive and normotensive control animals were used for comparison. The effects of scavenger treatment were assessed by in vivo observations of intestinal small arteries by use of stereomicroscopy and videotape and light and transmission electron microscopy to identify and quantitate vascular lesions, and tracer particle injections to determine permeability changes. In vivo observations revealed that scavenger treatment did not alter vascular constriction patterns, vessel caliber, or blood pressures. Electron microscopy of arteries from untreated hypertensive rats showed more severe and more extensive endothelial and smooth muscle lesions, increased tracer particle penetration, and greater fibrin deposition than that found in scavenger-treated hypertensive groups. Quantitation of vascular lesions showed approximately equal reductions in smooth muscle necrosis (p less than 0.01) and fibrin deposition (p less than 0.05) in arteries from each of the scavenger-treated hypertensive groups. The results indicate that the free radical scavengers SOD, catalase, SOD-catalase, and DMSO inhibit (but do not prevent) vascular hyperpermeability and cellular damage during acute, angiotensin II--induced hypertension. These findings suggest that free radicals play a role in the pathogenesis of hypertensive vascular disease, probably by exacerbating the vascular changes initially triggered by an acute elevation in blood pressure.

Acute Disease↗
PubMed2006

Meeting report on the Bellagio Conference 'prevention of vascular diseases in the emerging world: An approach to global health equity'.

Representatives from five international organizations (International Society of Nephrology, World Heart Federation, International Diabetes Federation, International Atherosclerosis Federation, and International Society of Hypertension) participated in a strategic planning workshop in December 2005 in Bellagio, Italy sponsored by the Rockefeller Foundation. There were equal representatives from developed and developing countries. Global perspectives on diabetes and cardiovascular and renal diseases were presented, with special emphasis on China, India, Latin America, and Africa. The rationale and effectiveness of preventive measures were discussed. It was apparent that measures for primary prevention and early intervention for all the chronic vascular diseases are similar. The five organizations agreed that an integrated global approach to chronic vascular diseases is needed. They resolved to collaborate and work towards an integrated approach to chronic vascular diseases with the establishment of a 5-year plan for the prevention and treatment of chronic vascular diseases, including public advocacy, advising international and national agencies, and improving education and the practice of established approaches.

Chronic Disease↗
PubMed1998

Low circulating folate and vitamin B6 concentrations: risk factors for stroke, peripheral vascular disease, and coronary artery disease. European COMAC Group.

BACKGROUND: A high plasma homocysteine concentration is a risk factor for atherosclerosis, and circulating concentrations of homocysteine are related to levels of folate and vitamin B6. This study was performed to explore the interrelationships between homocysteine, B vitamins, and vascular diseases and to evaluate the role of these vitamins as risk factors for atherosclerosis. METHODS: In a multicenter case-control study in Europe, 750 patients with documented vascular disease and 800 control subjects frequency-matched for age and sex were compared. Plasma levels of total homocysteine (before and after methionine loading) were determined, as were those of red cell folate, vitamin B12, and vitamin B6. RESULTS: In a conditional logistic regression model, homocysteine concentrations greater than the 80th percentile for control subjects either fasting (12.1 micromol/L) or after a methionine load (38.0 micromol/L) were associated with an elevated risk of vascular disease independent of all traditional risk factors. In addition, concentrations of red cell folate below the lowest 10th percentile (<513 nmol/L) and concentrations of vitamin B6 below the lowest 20th percentile (<23.3 nmol/L) for control subjects were also associated with increased risk. This risk was independent of conventional risk factors and for folate was explained in part by increased homocysteine levels. In contrast, the relationship between vitamin B6 and atherosclerosis was independent of homocysteine levels both before and after methionine loading. CONCLUSIONS: Lower levels of folate and vitamin B6 confer an increased risk of atherosclerosis. Clinical trials are now required to evaluate the effect of treatment with these vitamins in the primary and secondary prevention of vascular diseases.

Adult↗
PubMed2001

Obstructive sleep apnea and vascular disease.

There is emerging evidence linking obstructive sleep apnea (OSA) to vascular disease, including hypertension. This relationship may be independent of co-morbidity, such as obesity. Even apparently healthy OSA patients have evidence of subtle functional vascular abnormalities that are known to occur in patients with hypertension and atherosclerosis. Untreated OSA may possibly contribute to the initiation and/or progression of pathophysiologic mechanisms involved in hypertension, heart failure, cardiac ischemia and stroke. This brief commentary will examine the evidence and mechanisms linking OSA to vascular disease.

Animals↗
PubMed1992

Fasting lipids and anticardiolipin antibodies as risk factors for vascular disease in systemic lupus erythematosus.

Fasting cholesterol, triglyceride, low density lipoprotein cholesterol, high density lipoprotein cholesterol, apoprotein AI, and apoprotein B were measured in 64 patients with systemic lupus erythematosus to assess the risk factors for vascular disease. The relation between the lipid profile, steroid treatment, the presence of anticardiolipin antibodies, and the prevalence of vascular disease was examined. Raised concentrations of triglyceride and apoprotein B were seen in those patients treated with more than the equivalent of 10 mg prednisolone a day in the six months before testing. An increase in vascular disease was found only in the subgroup of patients with increased triglycerides who also expressed anticardiolipin antibodies. This study confirms the association between treatment with high doses of steroids in lupus and the development of an atherogenic plasma lipid profile. The presence of anticardiolipin antibodies compounds the risk of developing vascular disease.

Adult↗
PubMed1994

Raynaud's phenomenon and vascular disease in scleroderma.

Raynaud's phenomenon is the most common sign of vascular involvement in scleroderma. Careful clinical evaluation using a simple definition of Raynaud's phenomenon is the most reliable and reproducible method in the diagnosis. The assessment of microvascular function by laboratory methods is still not specific or sensitive enough for individual patient evaluation. The study of mechanisms involved in the pathogenesis of primary and secondary Raynaud's phenomenon offers the best window for investigation of the early pathogenetic stages in scleroderma. The structural vascular disease in scleroderma is well documented. Still, the impact of endothelial involvement on organ functions is just beginning to be identified and appreciated. Dysregulation of vascular tone control and deficiency of the vasodilatory neuropeptides in scleroderma is proposed as a mechanism in the development of Raynaud's phenomenon. Decreased fibrinolysis and enhanced platelet aggregation is documented and undoubtedly contributes to microvascular thrombosis. The nature of endothelial injury is still elusive, yet markers of endothelial activation and injury continue to be described. Therapy directed toward the vascular disease continues to focus on the alleviation of vascular spasm. Calcitonin gene-related peptide is the newest agent in our therapeutic armamentarium.

Clinical Trials as Topic↗
PubMed2007

Correlation between risk factors for vascular disease and the American Urological Association Symptom Score.

OBJECTIVE: To evaluate the correlation between risk factors for vascular disease and the American Urological Association Symptom Score (AUA-SS), by comparing the presence of these risk factors with the degree of lower urinary tract symptoms (LUTS). PATIENTS AND METHODS: We retrospectively reviewed the medical history, AUA-SS, and prostate volume of men who had a radical prostatectomy. The degree of LUTS in men with and without risk factors for cardiovascular disease was compared. RESULTS: The mean AUA-SS was 7.2 for the entire cohort, 5.6 in men with no risk factors, and 7.9 in men with at least one risk factor (P < 0.05). In men with one to four risk factors, the mean AUA-SS was 6.9, 7.9, 10.7, and 19.5, respectively. There was no correlation between the AUA-SS and prostate size in the entire cohort or among any groups. CONCLUSIONS: Men with risk factors for vascular disease are more likely to have a higher AUA-SS than men without these risk factors. These findings suggest the possibility of an association between vascular disease and the development and severity of LUTS in men.

Adult↗
PubMed2004

Gender issues in pulmonary vascular disease.

Gender differences in pulmonary vascular diseases, as exemplified by primary pulmonary hypertension and scleroderma-related pulmonary hypertension, are not well-explained; however, in general terms, they seem to be related to a combination of genetic predispositions and gender-specific environmental triggers. More information is needed in both areas with respect to mechanisms of disease. More information also is needed about possible gender differences in disease presentation,course, and response to treatments.

Autoimmune Diseases↗
PubMed1993

[Progress in the treatment of atherosclerotic vascular diseases].

The treatment of atherosclerotic vascular diseases has improved greatly. Clinical and epidemiological studies have recently revealed the following data. Changes in lifestyles is extremely effective and should be prevailed widely. Amelioration of atherosclerosis by drugs, including hypolipidemics, antihypertensives and antioxidant agents, is also confirmed. Skills and devices are much improved in PTCA and DCA which face the possibility of restenosis. Control of risk factors is also considered to be important to prevent restenosis.

Angioplasty, Balloon, Coronary↗
PubMed2001

Pulmonary function test abnormalities in pulmonary vascular disease and chronic heart failure.

Diagnostic criteria based on pulmonary function testing for pulmonary vascular disease and CHF are imprecise. Although these tests constitute a necessary part of the work-up of a patient with dyspnea, additional studies are required to obtain a final diagnosis in the setting of cardiopulmonary vascular disease. In contrast, specific pulmonary function tests may offer an objective means of assessing severity of dysfunction resulting from pulmonary hypertension or CHE Serial measurements of pulmonary function offer insight into general and specific patterns of cardiopulmonary vascular disease and are useful in evaluating response to treatment.

Heart Failure↗
PubMed1976

Effect of cardiac, pulmonary, and vascular disease on one-minute oxygen uptake.

A simplified method for estimation of one-minute oxygen uptake (VO2-1) during treadmill grade walking at vertical power requirements of 250, 750, and 1,000 kg-meters/min was devised, where power=weight (kg) X grade (fractional) X walking speed. All subjects were men. There were 29 controls, 34 subjects with coronary arterial disease (of whom 18 had had myocardial infarction), nine subjects with diffuse pulmonary disease, and four subjects with ischemic vascular disease. Abnormally reduced values for VO2-1 were related to these diseases and, more specifically, to a history of myocardial infarction and (in pulmonary subjects) to reduced single-breath diffusing capacity. Lowest values of VO2-1 for a group were found in ischemic vascular disease. Reduced response of VO2-1 may therefore be caused by central defects of oxygen transport.

Adult↗
PubMed2005

ADMA: its role in vascular disease.

Endothelium-derived nitric oxide (NO) is the most potent endogenous vasodilator and, by virtue of its anti-inflammatory and anti-thrombotic effects, it is an endogenous anti-atherogenic agent. Accordingly, impairment of NO synthesis or bioactivity may increase the risk of vascular disease. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of the NO synthase pathway. Plasma levels of ADMA are increased in patients with vascular disease, or with risk factors for vascular disease. Preclinical and clinical studies indicate that ADMA may mediate the adverse effects of traditional risk factors on endothelial vasodilator function. By impairing endothelial function, ADMA may contribute to pulmonary or systemic hypertension, as well as to vascular disease. Several drugs known to treat cardiovascular disease also reduce plasma ADMA levels, such as angiotensin receptor antagonists, converting enzyme inhibitors, and insulin sensitizing agents. Plasma ADMA may be a common mediator of endothelial dysfunction induced by vascular risk factors. Insights into the mechanisms by which plasma ADMA is regulated may lead to new therapeutic knowledge.

Amidohydrolases↗