[Blood platelets and cardiovascular diseases. III. Diseases with increased platelet consumption and vascular diseases].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
OBJECTIVE: To determine the predictive values of noninvasive tests for the detection of allograft vascular disease. METHODS: We studied 39 patients with mean ages of 48+/-13 years and a follow-up period of 86+/-13 months. The diagnosis of allograft vascular disease was made by cine-coronary arteriography, and it was considered as positive if lesions existed that caused > or =50% obstruction of the lumen. Patients underwent 24h Holter monitoring, thallium scintigraphy, a treadmill stress test, and dobutamine stress echocardiography. Sensitivity, specificity, and positive and negative predictive values were determined in percentages for each method, as compared with the cine-coronary arteriography results. RESULTS: Allograft vascular disease was found in 15 (38%) patients. The Holter test showed 15.4% sensitivity, 95.5% specificity. For the treadmill stress test, sensitivity was 10%, specificity was 100%. When thallium scintigraphy was used, sensitivity was 40%, specificity 95.8%. On echocardiography with dobutamine, we found a 63.6% sensitivity, 91.3% specificity. When the dobutamine echocardiogram was associated with scintigraphy, sensitivity was 71.4%, specificity was 87%. CONCLUSION: In this group of patients, the combination of two noninvasive methods (dobutamine echocardiography and thallium scintigraphy) may be a good alternative for the detection of allograft vascular disease in asymptomatic patients with normal ventricular function.
We wanted to assess habitual snoring as a credible risk factor for acute vascular disease, mainly stroke and myocardial infarction. The patients selected for the study had been admitted to the hospital through the emergency department, and were evaluated by means of multidimensional interviews and clinical records: 164 had acute cerebrovascular disease, and 136 cardiovascular disease; 330 patients with nonvascular disease were the controls. The evaluation showed 48% of vascular disease patients to be habitual snorers, but only 30% of the controls; the difference was statistically significant. Compared with the controls, in the cerebrovascular patients the risk (odds ratio) associated with habitual snoring was significantly increased, and of the same order as the risk associated with age over 65 yrs, male gender, diabetes mellitus, and dyslipidaemia; whilst the risk associated with hypertension was higher. In the cardiovascular patients, the risk associated with habitual snoring was again significantly increased and of the same order as the risk associated with male gender, body mass index > 29 (kg.m-2), dyslipidaemia, heavy smoking, excessive alcohol intake and hypertension. A logistic regression analysis, entering the variables in the following order: age, gender, body mass index, diabetes, dyslipidaemia, smoking, alcohol, hypertension, and habitual snoring, showed that habitual snoring carries a significant risk factor for stroke and myocardial infarction, even after adjusting for other factors. Since habitual snoring carries a definite risk for acute vascular disease, we conclude that inquiring about it should become routine practice.
Acute rejection (AR) and graft vascular disease (GDV) are processes mediated, at least in part, by cellular processes. Therefore, we cultured graft-infiltrating lymphocytes (GIL) from endomyocardial biopsies (EMB) taken during the first year after transplantation, determined their phenotypic composition, and correlated it to AR and GVD. We observed more often GIL growth from EMB with AR than from non-rejection EMB (P = 0.02), but no difference was found between patients with and without GVD 1 year after transplantation. CD4+ cells were always more numerous than CD8+ cells, and no difference in phenotypic composition was found between AR and non-rejection EMB nor between EMB derived from patients with or without signs of GVD. In conclusion, AR is correlated with cell growth of EMB, but the development of GVD is not associated with AR, GIL growth from EMB, or their phenotypic composition.
BACKGROUND: Homocyst(e)ine is reported to increase the binding of lipoprotein(a) [Lp(a)] to fibrin, which may increase the thrombogenic effects of Lp(a) in vivo. The aim of this study was to investigate whether there is a relationship between homocyst(e)ine and Lp(a) levels and vascular disease risk, and if the relationship depends on the apo(a) isoforms. METHODS: A case-control study was performed in 91 Caucasian male subjects with vascular disease due to athersclerosis, and in 100 healthy age- and sex-matched control subjects. RESULTS: Both hyperhomocyst(e)inemia and elevated Lp(a) were significantly more prevalent in patients. Concordant elevated Lp(a) and hyperhomocyst(e)inemia were not associated with increased vascular disease risk (relative odds 2.96; 95% CI: 0.90-9.80), while hyperhomocyst(e)inemia in the absence of elevated Lp(a) was associated with increased vascular disease risk (relative odds 7.20; 95% CI: 2.37-21.91). Hyperhomocyst(e)inemia in individuals with high-molecular weight apo(a) isoforms [smaller apo(a) isoform > S3] was observed to be associated with increased vascular disease risk (relative odds 11.02; 95% CI: 3.54-34.30), while vascular disease risk in subjects with low-molecular weight apo(a) isoforms [smaller apo(a) isoform < S3] was not significantly increased, the relative odds being 1.92; 95% CI: 0.51-7.24. CONCLUSIONS: We conclude that hyperhomocyst(e)inemia is an important risk factor in individuals with high-molecular weight apo(a) isoforms.
Whether the 677C-T polymorphism of the methylene tetrahydrofolate reductase (MTHFR) gene acts as a risk factor for homocysteine-related vascular disease remains a matter of debate. Testing for the 677C-T nucleotide substitution and assay of plasma homocysteine were carried out simultaneously in 69 controls and 113 vascular disease patients from the Paris area. The variant gene frequency as well as the variant homozygous genotype frequency were very similar in controls and patients. Conversely, plasma homocysteine levels were substantially higher in patients than in controls. A slight interaction between the 677C-T MTHFR polymorphism and homocysteinaemia was observed in the patient group only, while a negative correlation between fasting homocysteine and plasma folate levels was found in all individuals homozygous for the 677C-T MTHFR genotype, irrespective of vascular disease. These data suggest that the 677C-T MTHFR polymorphism is not a major determinant of the vascular disease but contributes to increased plasma homocysteine concentration in conjunction with low plasma folate levels.
Abnormal dietary deficiency in Mg as well as abnormalities in Mg metabolism appear to play important roles as risk factors for ischemic heart disease and acute myocardial infarction, namely in hypertensive vascular disease, diabetic vascular disease, insulin resistance, atherosclerosis and vasospasm. Experimental, epidemiological as well as clinical evidence that supports a role for Mg in these risk factors are reviewed. Extracellular Mg ions ([Mg2+]o) exert important actions upon divalent cation metabolism, transport and intracellular release of [Ca2+]i and intracellular free Mg ([Mg2+]i) in both vascular smooth muscle and endothelial cells. Digital imaging microscopy, using molecular fluorescent probes, clearly indicates that both intracellular free Ca2+ and intracellular free Mg2+ are compartmented in both vascular smooth muscle cells and endothelial cells. [Mg2+]o appears to exert important effects on the precise subcellular location and concentration of both [Ca2+]i and [Mg2+]i. Use of specific ion-selective electrodes for [Mg2+]o has revealed that [Mg2+]o can change more rapidly than heretofore believed in cardiovascular pathophysiologic states. The latter new findings therefore suggest that the ionized level of [Mg2+]o is an important determinant of vascular tone, contractility and reactivity.
Peripheral vascular disease (PVD) is a common condition often associated with cardiovascular risk factors and events. With the aid of B-mode ultrasound scanning, evidence is emerging that these risk factors and events are significantly related to an increased carotid and femoral intima-media thickness (IMT). More importantly, treatment of these risk factors is associated with a decrease or a diminished progression of the IMT, paralleled by a reduction in cardiovascular events and an improvement in the symptoms associated with PVD. This evidence is particularly strong for lipid lowering therapy. Additional predictors of cardiovascular risk like the IMT, could now influence the decision to intervene with medication.
Platelet aggregation has been studied in 28 control subjects and 46 patients with peripheral vascular disease. The platelets from the patients with peripheral vascular disease were significantly more sensitive to the aggregating effects of adenosine diphosphate and adrenaline than those from the control group (P less than 0.001). In addition, spontaneous platelet aggregation was observed in vitro in several of the vascular patients; this response was not apparent in the control group. Increased platelet aggregation could add to the vascular impairment in the unoperated subject and might also play a part in premature graft failure. Platelet function studies should perhaps be included as a routine in the assessment of patients with peripheral vascular disease.
The WHO Multinational Study of Vascular Disease in Diabetes was launched in 1975-77 to investigate international variations in the occurrence of different manifestations of vascular disease in subjects with insulin-dependent and non-insulin-dependent diabetes. A morbidity and mortality follow-up extending until January 1, 1988 was carried out in 10 centres, including five European centres (London, Switzerland, Berlin, Warsaw and Zagreb), two East Asian centres (Hong Kong and Tokyo), two Native American centres (Arizona and Oklahoma) and one Caribbean centre (Havana). Of a total of 4714 diabetic subjects (2310 men and 2404 women) aged between 35 and 55 years at baseline who were successfully followed up, 1266 were classified as having insulin-dependent diabetes and 3448 as having non-insulin-dependent diabetes. There was a large variation between the centres in ischaemic heart disease and cerebrovascular disease mortality rates for both insulin-dependent and non-insulin-dependent diabetic subjects, presumably reflecting in part differences between the background populations in mortality rates from these cardiovascular causes. The lowest ischaemic heart disease mortality rates for diabetic subjects were observed in Hong Kong and Tokyo centres, representing industrialized countries which have continued to have low ischaemic heart disease mortality rates. The importance of raised blood pressure and proteinuria as potentially modifiable cardiovascular risk factors in diabetic subjects was confirmed in this study.
OBJECTIVE: To investigate the incidence and clinical features in patients with cytomegalovirus (CMV)-positive antigenemia during high dose corticosteroid therapy for collagen vascular diseases, and risk factors associated with it. PATIENTS AND METHODS: We examined retrospectively 35 consecutive patients for the presence of CMV-positive pp65 antigenemia. The patients were admitted to Saka General Hospital from 2000 to 2003, and were administered more than 0.5 mg/kg of body weight/day of peroral prednisolone for collagen vascular diseases. Characteristics of patients with and without CMV-positive antigenemia were compared. RESULTS: CMV-positive antigenemia was detected in 14 patients (40.0%), including six with microscopic polyangitis, three with rheumatoid arthritis, and five with other conditions. Three patients (8.6%) were diagnosed as having a CMV disease: pneumonitis or encephalitis. Symptoms and laboratory findings, including slight fever and a low increase in levels of hepatic enzymes and cytopenia, were observed in 10 of the 14 patients. Two patients died of CMV diseases refractory to ganciclovir. Ages of more than 70 years old were associated with the presence of CMV-positive antigenemia (relative risk = 4.5, 95% confidence interval = 1.14-17.6). CONCLUSION: CMV infection diagnosed by CMV pp65 antigenemia assay is not rare during high dose corticosteroid therapy for collagen vascular diseases, and advanced age is considered a risk factor for it. It has a variety of symptoms and laboratory findings, which are mild and nonspecific to this type of infection, and they may not be clearly noted as clinical signs of CMV infection, even in patients with CMV diseases whose prognoses can be unsatisfactory. During high dose corticosteroid therapy for collagen vascular diseases, careful attention should be paid to CMV infection.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The occurrence of peripheral vascular disease (PVD) and atraumatic lower-extremity amputations is significantly greater in patients with end-stage renal disease (ESRD) than those with normal renal function. Moreover, the mortality for dialysis patients undergoing atraumatic lower-extremity amputations is far greater. Because PVD requiring amputation is an extreme form of PVD, we tested the hypothesis that mortality and intermediate outcomes for patients with ESRD undergoing lower-extremity revascularization, a less extreme form of PVD, would be equivalent to that for patients without ESRD. This is a retrospective case-control analysis of lower-extremity revascularization in patients with ESRD. Procedures in patients with ESRD were matched with procedures in non-ESRD controls for patient age, sex, race, diabetes mellitus, and hospital setting. Patient survival, graft survival, and limb salvage rates were determined using Kaplan-Meier analysis. Subjective interpretation of functional and symptomatic improvement was determined by telephone interviews with patients or relatives. Thirty-one procedures were performed on 20 patients with ESRD and 64 matched procedures were performed on 57 patients without ESRD. In the ESRD group, median patient survival was 1.72 years compared with 5.17 years for the control group (P < 0.001). Time to 50% limb loss was 1.24 years in the ESRD group and longer than 5.65 years in the control group (P < 0.001). Time to 50% graft patency loss was 0.70 years in the ESRD group and longer than 5.5 years in the control group (P < 0.05). Subjective improvement was less in patients with ESRD. Outcomes of lower-extremity revascularization in patients with ESRD are inferior to those in non-ESRD controls. The mortality rate for patients with ESRD who undergo revascularization is extremely high. Patient-related variables (eg, increased prevalence of hypertension and cardiovascular disease) and/or provider-specific factors (eg, timing of surgery in the course of PVD) may be responsible for poorer outcomes.
To test the hypothesis that psoriasis is associated with an increased incidence of occlusive vascular disease (thrombophlebitis, myocardial infarction, pulmonary embolization, and cerebrovascular accident), the clinical records of 323 psoriatic and 325 non-psoriatic patients admitted to the dermatology service of the Roger Williams General Hospital were examined. The data obtained in this study suggest that (1) the occurrence rate of occlusive vascular disease is significantly greater in the psoriatic than in the non-psoriatic dermatological patient. This is particularly true in the male population; (2) psoriasis predisposes to occlusive vascular disease; and (3) the psoriatic patient with certain predisposing factors is at greater risk of experiencing an occlusive vascular episode than both the non-predisposed psoriatic and the non-psoriatic dermatological patient.
Insufficient blood flow through end-resistance arteries leads to symptoms associated with peripheral vascular disease. This may be caused in part by poor macrocirculatory inflow or impaired microcirculatory function. Dysfunction of the microcirculation occurs in a similar fashion in multiple tissue beds long before the onset of atherosclerotic symptoms. Impaired microcirculatory vasodilatation has been shown to occur in certain disease states including peripheral vascular disease, diabetes mellitus, hypercholesterolemia, hypertension, chronic renal failure, abdominal aortic aneurysmal disease, and venous insufficiency, as well as in menopause, advanced age, and obesity. Microcirculatory structure and function can be evaluated with transcutaneous oxygen, pulp skin flow, iontophoresis, and capillaroscopy. We discuss the importance of the microcirculation, investigative methods for evaluating its function, and clinical applications and review the literature of the microcirculation in these different states.
Low bone mineral density and rapid bone loss of the skeleton are associated with mortality risk from vascular diseases in post-menopausal women. Panoramic radiographic measurements are considered as indicators of skeletal bone mineral density or bone turnover. We hypothesize that such measurements may be associated with vascular disease risk in post-menopausal women. Associations of mandibular cortical shape and width on panoramic radiographs with skeletal bone mineral density and risk factors related to vascular diseases were investigated in 87 post-menopausal women. Cortical shape was associated with skeletal bone mineral density, low-density lipoprotein cholesterol, apolipoprotein B, resting heart rate, and endothelial dysfunction. Cortical width was associated with skeletal bone mineral density, low-density lipoprotein cholesterol, and apolipoprotein A1. Dentists may be able to refer women with increased risk of vascular diseases, as well as low bone mineral density, to medical professionals for further examination by panoramic findings.
Vascular smooth muscle cells (SMCs) exhibit extensive phenotypic diversity and rapid growth during embryonic development, but maintain a quiescent, differentiated state in adult. The pathogenesis of vascular proliferative diseases involves the proliferation and migration of medial vascular SMCs into the vessel intima, possibly reinstating their embryonic gene expression programs. Multiple mitogenic stimuli induce vascular SMC proliferation through cell cycle progression. Therapeutic strategies targeting cell cycle progression and mitogenic stimuli have been developed and evaluated in animal models of atherosclerosis and vascular injury, and several clinical studies. Recent discoveries on the recruitment of vascular progenitor cells to the sites of vascular injury suggest new therapeutic potentials of progenitor cell-based therapies to accelerate re-endothelialization and prevent engraftment of SMC-lineage progenitor cells. Owing to the complex and multifactorial nature of SMC regulation, combinatorial antiproliferative approaches are likely to be used in the future in order to achieve maximal efficacy and reduce toxicity.