Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Relations of factor VIII activity, FVIIIC, and von Willebrand factor antigen (vWFAg), with ischaemic heart disease (IHD) were examined in 1393 men aged between 40 and 64 years at entry to the Northwick Park Heart Study (NPHS) who experienced 178 first major episodes of IHD during an average follow-up period of 16.1 years. After allowing for the large factor VIII differences between the main ABO blood groups, FVIIIC was probably associated with IHD incidence, possibly more strongly with fatal than non-fatal episodes. Thus, an increase of 1 standard deviation in FVIIIC raised the risk of fatal IHD by about 28%. vWFAg was also significantly associated with fatal events. The observed relation of FVIIIC with IHD incidence probably underestimates the true strength of the association because of the considerable within-person and laboratory variability in factor VIII measurements. FVIIIC and vWFAg were strongly correlated (r = 0.57) and in statistical terms there may be little to choose between them in long-term studies of IHD. Taking account of evidence that haemophiliacs seem to experience less IHD than expected, high factor VIII levels may contribute to the incidence of IHD by increasing thrombogenic potential. The incidence of IHD was significantly higher in those of blood group AB than in those of groups O, A or B, particularly for fatal events. There was no evidence that the FVIIIC and vWFAg associations with IHD are determined by ABO group. The factor VIII and ABO blood group effects therefore appeared to be independent. Group AB may be a genetic marker of characteristics influencing other indices of IHD risk such as short stature, NPHS men (though not women) of group AB being about 2 cm shorter than those of other groups.
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PMID:Factor VIII, ABO blood group and the incidence of ischaemic heart disease. 781 72

An increased risk of ischemic heart disease has been reported in men with the Lewis blood group phenotype Le(a-b-). We have investigated the relationship between Lewis phenotype and cardiovascular risk factors in 1714 participants in the Coronary Artery Risk Development in Young Adults Study, an ongoing investigation on life-styles and evolution of cardiovascular risk factors. No significant differences were observed among Lewis phenotypes for body mass index, blood lipid levels, blood pressure, or clotting factors VII and fibrinogen. However, in white men with blood groups A, B, or AB, and the Le(a-b-) phenotype, significantly higher levels of factor VIII (p < 0.01) and von Willebrand factor (p < 0.03) were observed than in those with other Lewis phenotypes (Le[a+b-] or Le[a-b+]). Two-way analysis of variance indicated a significant interaction between blood group and Lewis phenotype (p = 0.0053) in terms of relationship to factor VIII. A similar trend was observed in black men with blood type A, B, or AB, and phenotype Le(a-b-) for factor VII/von Willebrand factor and in women with blood type A, B, or AB, and phenotype Le(a-b-) for factor VIII. Our data suggest that the Le(a-b-) phenotype and blood groups A, B, and AB, by virtue of their association with raised levels of factor VIII and von Willebrand factor, may be risk markers for future atherothrombotic disease.
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PMID:Relationship among Lewis phenotype, clotting factors, and other cardiovascular risk factors in young adults. 859 91

Hemostasis was assessed in 115 steady-state heart transplant recipients (HTRs) and compared with that of 23 age-matched healthy controls and 21 age-matched patients with ischemic heart disease (IHD). Compared with the controls, the HTRs had increased levels of fibrinogen (mean and 95% confidence limits of 4.50 [4.32-4.68] g/L versus 3.47 [3.07-3.87] g/L, P < 0.001), factor VIIC (1.16 [0.98-1.21] IU/ml versus 0.99 [0.89-1.10] IU/ml, P < 0.001), and von Willebrand factor antigen (1.72 [1.58-1.88] IU/ml versus 1.00 [0.80-1.26] IU/ml, P < 0.001). HTRs had increased antithrombin III activity (P = 0.002) and protein C activity (P = 0.002), with a decrease in total protein S levels (P < 0.001) but no change in free protein S levels. Stepwise discriminant analysis of hemostatic variables showed that fibrinogen was the best discriminator of the three groups, classifying 55.6% of HTR, 40% of IHD, and 66.7% of the controls. More marked prothrombotic changes were found in HTRs transplanted for IHD than for other causes; this reached significance for prothrombin (P = 0.048), factor IX (P = 0.003), and poor fibrinolytic activity as measured by euglobulin clot lysis time (P = 0.008). The HTRs with accelerated coronary sclerosis (ACS) tended to have the most prothrombotic changes; this reached significance with factor IX (P = 0.03). In conclusion, HTRs have perturbed hemostasis; the net effects of these changes are prothrombotic. The relationship between prothrombotic changes and ACS merits further studies.
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PMID:Hemostatic changes in heart transplant recipients and their relationship to accelerated coronary sclerosis. 843 82

In the past decade the importance of the vascular endothelium in cardiovascular pathophysiology has become more apparent. One substance that is synthesised by and stored in endothelial cells is von Willebrand factor (vWF). When released, vWF seems to mediate platelet aggregation and adhesion to the vascular endothelium. Because the release of vWF is increased when endothelial cells are damaged, vWF has been proposed as an indicator of endothelial disturbance or dysfunction. The availability of such an index of endothelial dysfunction may have clinical value, because measurement of such a marker can be a non-invasive way of assisting in diagnosis or as an indicator of disease progression. The known association between vWF, thrombogenesis, and atherosclerotic vascular disease also suggests that high concentrations of vWF may be an indirect indicator of atherosclerosis and/or thrombosis. In addition, high vWF concentrations have prognostic implications in patients with ischaemic heart disease and peripheral vascular disease.
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PMID:von Willebrand factor and its relevance to cardiovascular disorders. 854 Nov 59

Tissue plasminogen activator antigen (tPA), plasminogen activator inhibitor antigen (PAI-1), soluble P-selectin and von Willebrand factor antigen (vWf) were measured by ELISA in 41 patients with peripheral vascular disease (PVD), 41 with ischaemic heart disease (HD) and in 46 age and sex matched asymptomatic controls. Increased vWf was found in patients with IHD (p = 0.0002) and in patients with PVD (p = 0.0011) relative to the controls but levels did not differ between the two patients groups. Raised tPA found in both PVD (p = 0.0006) and IHD (p = 0.0061) compared to the controls also failed to differentiate the two groups of patients. Soluble P-selectin was also raised in both groups (p = 0.003 in IHD and p = 0.0102 in PVD) with no difference between the groups. There were no differences in levels of PAI-1 between the groups. In the subjects taken as a whole, there were significant Spearman's correlations between tPA and vWf (r = 0.37, p < 0.001), tPA and triglycerides (r = 0.38, p < 0.001), tPA and P-selectin (r = 0.19, p = 0.032), vWf and age (r = 0.25, p = 0.005) and inversely between vWf and HDL (r = -0.25, p = 0.006). These data support the concept that increased levels of tPA may be important in atherosclerosis, and indicate that soluble P-selectin may be useful in further analysis of the role of platelets and the endothelial cell in this disease.
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PMID:von Willebrand factor, soluble P-selectin, tissue plasminogen activator and plasminogen activator inhibitor in atherosclerosis. 858 97

Murine monoclonal antibody E9 recognises a transforming growth factor (TGF) beta receptor, which is expressed in increased amounts by activated endothelial cells. In order to examine the biological role of this molecule in atherosclerosis, we have measured levels of the TGF-beta receptor alongside those of two other endothelial cell products (von Willebrand factor and soluble E-selectin) in the serum of 55 patients with atherosclerosis (29 with ischaemic heart disease and 26 with peripheral vascular disease), and in a cohort of 26 age- and sex-matched asymptomatic controls. There were increased levels of the TGF-beta receptor (P = 0.0079) and von Willebrand factor (P = 0.0001), but not soluble E-selection in patients' serum relative to the controls. In multivariate analysis of the endothelial cell products against total cholesterol, high density lipoprotein cholesterol and low density lipoprotein cholesterol, triglycerides, systolic and diastolic blood pressures, age, sex and smoking, both the TGF-beta receptor and von Willebrand factor correlated with total cholesterol (Spearman's r = 0.37 and r = 0.35, respectively, both P < 0.001). Lack of a correlation with a coarse endothelial damage marker von Willebrand factor or soluble E-selectin (produced by immunologically stimulated endothelial cells) implies other mechanisms are responsible for increased levels of the TGF-beta receptor in serum of patients with atherosclerosis.
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PMID:Serum levels of the TGF-beta receptor are increased in atherosclerosis. 864 63

Increased levels of the endothelial markers soluble E-selectin (P = 0.011), soluble thrombomodulin (P < 0.0001) and von Willebrand factor (VWF, P < 0.0001) were found in 116 patients with ischaemic heart disease compared to an equal number of age- and sex-matched asymptomatic controls. In a multivariate analysis of the markers versus the major risk factors for atherosclerosis, VWF correlated with total cholesterol (P = 0.002) and E-selectin with sex (lower in women, P = 0.004) and triglycerides (P = 0.007). The data point to profound differences in the release mechanisms of these three endothelial cell products and suggests that further studies into the roles of these molecules in coronary artery disease are warranted.
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PMID:Circulating endothelial cell/leucocyte adhesion molecules in ischaemic heart disease. 890 79

The Steno hypothesis suggests that albuminuria reflects widespread vascular damage (proliferative retinopathy and severe macroangiopathy) due to a generalized vascular (endothelial) dysfunction. We assessed this concept in NIDDM (non-insulin-dependent diabetic) patients with (13 female/ 39 male, age 60 +/- 7 years, group 1) and without (12 female /41 male, age 61 +/- 7 years, group 2) diabetic nephropathy compared to matched non-diabetic subjects (7 female/15 male, age 58 +/- 8 years, group 3). A 12-lead ECG was recorded and coded blindly using the Minnesota Rating Scale; the World Health Organization cardiovascular questionnaire was used to assess past and present evidence of myocardial infarction, angina pectoris, stroke, and peripheral vascular disease (digital systolic blood pressure determination). The degree of diabetic retinopathy was scored from fundus photography. The following variables were measured: transcapillary escape rate of albumin (initial disappearance of intravenously injected 125I-labelled human serum albumin), plasma concentrations of prorenin (radioimmunoassay) and serum concentrations of von Willebrand factor (enzyme-linked immunoadsorbent assay). Prevalence of ischaemic heart disease (ECG reading) (49/20/5)% and peripheral vascular disease as indicated by reduced systolic blood pressure on big toe (69/30/ 14)% was significantly higher in group 1 vs group 2 (p < 0.01) and in group 2 vs group 3 (p < 0.01), respectively. The prevalence and severity of retinopathy was higher in group 1 vs 2 (p < 0.01). Transcapillary escape rate of albumin (%/h) was elevated in group 1 and 2 as compared to control subjects: 7.9 (4.3-13.7); 7.4 (3.7-16.4) vs 6.0 (3.4-8.7), (p < 0.005), respectively. Plasma prorenin activity (IU/ml) was raised in group 1 and group 2 as compared to group 3: 272 (59-2405); 192 (18-813), and 85 (28-246), p < 0.001, respectively. Serum von Willebrand factor (IU/ ml) was elevated in group 1 as compared to group 2 and 3: 2.07 (0.83-4.34); 1.60 (0.30-2.99) and 1.50 (1.00-2.38), p < 0.001, respectively. Our study demonstrated that NIDDM patients with and without albuminuria had increased transcapillary escape of albumin and raised prorenin activity, whereas only those with albuminuria had increased von Willebrand factor. Patients with NIDDM may have abnormal endothelial function in the absence of albuminuria.
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PMID:Macro-microangiopathy and endothelial dysfunction in NIDDM patients with and without diabetic nephropathy. 896 Aug 47

We cross-sectionally measured plasminogen activator inhibitor-1 (PAI-1) activity, fibrinogen, factor VII (FVII:C) and VIII (FVIII:C) coagulant activity, and von Willebrand factor antigen (VWF:Ag) in 162 traditional horticulturalists older than 40 years from the tropical island of Kitava, Papua New Guinea, where the intake of western food is negligible and where stroke and ischaemic heart disease appear to be absent. Identical analyses were made in Swedish subjects of comparable ages. Kitavams had markedly lower PAI-1 activity, with 85% of males and 100% of females having PAI-1 activity < or = 5 U/ml, as compared with 22 and 14% in Swedish males and females (p < 0.0001). Surprisingly, Kitavans also had higher FVII:C. FVIII:C and VWF:Ag. Fibrinogen was 10% lower in Kitavan males while 25% higher in Kitavan females. The very low PAI-1 activity in Kitavans may explain some of their apparent freedom from cardiovascular disease and probably relates to their extreme leanness.
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PMID:Haemostatic variables in Pacific Islanders apparently free from stroke and ischaemic heart disease--the Kitava Study. 903 56

The vascular endothelium is involved in the production of many important substances which are involved in a cardiovascular pathophysiology. One such substance which is synthesised by, and stored in, endothelial cells is von Willebrand factor (vWf). When released, vWf appears to mediate platelet aggregation and adhesion. Numerous clinical and experimental reports suggest that high vWf levels reflect damage to the endothelium or endothelial dysfunction. The close association between vWf and the processes of thrombus formation (thrombogenesis) or atherogenesis also suggests that high vWf levels may be a useful indirect indicator of atherosclerosis and/or thrombosis. The availability of a useful marker of endothelial dysfunction may have potential clinical value. The measurement of such a marker can perhaps be a non-invasive way of assisting in clinical diagnosis or as an indicator of disease progression. High vWf levels have also been shown to have prognostic value in patients with ischaemic heart disease, peripheral vascular disease and inflammatory vascular disease. However, there is limited information that increased vWf is actually casual in the progression of vascular disease and that measures aimed at reducing vWf levels will be beneficial. In addition, interpretation of raised plasma vWf levels is complicated by the fact that vWf may be an acute phase reactant. Further research is indicated to explore the predictive value of this marker in population studies and, perhaps, therapeutic approaches in (and the value of) modifying vWf levels or function.
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PMID:von Willebrand factor: a marker of endothelial dysfunction in vascular disorders? 920 37


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