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)

Levels of plasma soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), and von Willebrand factor (vWF) increase in patients with peripheral vascular or ischemic heart disease. These factors are related to the progression of atherosclerosis. Furthermore, these substances and thrombomodulin (TM) are indicators for assessing the degree of damage to the endothelium. To evaluate the effect of double filtration plasmapheresis (DFPP) on these molecules, the plasma levels of vWF, sICAM-1, sVCAM-1, and TM were measured in 4 familial hypercholesterolemia (FH) patients who underwent treatment with DFPP at 2 week intervals for more than 3 years. The levels of sVCAM-1 and sICAM-1 in hypercholesterolemia patients with ischemic heart disease as a control was 773 +/- 109 and 334 +/- 82 ng/ml. These values were higher than the normal value. In the FH patients who underwent DFPP treatment, the average sICAM-1 levels were 221 +/- 47 and 197 +/- 36 ng/ml before and after, respectively. The average sVCAM-1 levels were 601 +/- 87 and 486 +/- 60 ng/ml. There were no significant differences between the pre- and post-DFPP values. The activities of plasma vWF before and after DFPP treatment were 158 +/- 23 and 45 +/- 9%. The levels of plasma TM before and after treatment were 3.0 +/- 0.3 and 3.4 +/- 0.5 FU/ml. From these results, it is suggested that DFPP treatment does not damage the endothelium and may prevent the progression of atherosclerosis by removing the substances that induce the production of sICAM-1 and sVCAM-1 due to long-term treatment.
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PMID:Double filtration plasmapheresis maintains normal adhesion molecule levels. 1022 74

The relationships of three measurements of the factor VIII/von Willebrand factor (VWF) complex (factor VIII activity, FVIIIc (one-stage assay); VWF antigen, VWF Ag (ELISA); and VWF activity, VWF act, measured by a recently-developed ELISA) to major ischaemic heart disease (IHD) events were studied in 1997 men aged 49-65 years, in the second phase of the Caerphilly Heart Study. These variables were related using logistic regression analysis to myocardial infarction or IHD death, which occurred in 129 men during an average follow-up period of 61 months. All three measurements were highly correlated (r = 0.63-0.77), and each was significantly associated with incident major IHD on univariate analyses (relative odds in highest fifth compared to lowest fifth, 1.68-1.90; P = 0.028-0.006) and on multivariate analyses adjusting for major IHD risk factors and for baseline IHD. Neither FVIIIc nor VWF act was significantly related to incident IHD following adjustment for VWF Ag. We therefore suggest that the associations between these three measurements of the factor VIII/VWF complex and incident IHD might have at least three explanations: VWF Ag is a marker of arterial endothelial disturbance; VWF act promotes platelet adhesion/aggregation and hence the platelet component of arterial thrombosis; and FVIIIc promotes fibrin formation and hence the fibrin component of arterial thrombosis.
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PMID:Factor VIII, von Willebrand factor and the risk of major ischaemic heart disease in the Caerphilly Heart Study. 1023 72

Increased levels of von Willebrand factor (vWf) and C-reactive protein (CRP) predict cardiovascular mortality in selected populations. It is uncertain whether vWf and CRP predict mortality in a general population and whether vWf and CRP predict mortality through similar pathways. This study investigated the association of vWf and CRP with cardiovascular and all-cause mortality among diabetic and nondiabetic subjects. An age-, sex-, and glucose tolerance-stratified sample (n=631) of a population-based cohort aged 50 to 75 years was followed prospectively for 5 years. After 5 years of follow-up, 58 subjects had died (24 of cardiovascular causes). vWf (>1.56 IU/mL) and CRP (>2.84 mg/L) levels in the upper tertile were associated with, respectively, a 3- and 2-fold increase in cardiovascular mortality after adjustment for age, sex, and glucose tolerance status. Analyses in nondiabetic and diabetic subjects separately gave similar results. After further adjustment for hypertension, levels of HDL cholesterol and triglyceride, smoking habits, ischemic heart disease, and peripheral arterial disease, the relative risks (RRs) were 3.0 (95% CI 1.2 to 7.9) for vWf and 1.4 (95% CI 0.6 to 3.5) for CRP. When both vWf and CRP were included in the latter multivariate analysis, the RRs were 3.0 (95% CI 1.1 to 7.9) for vWf and 1.3 (95% CI 0.5 to 3.4) for CRP. The association between vWf and risk of cardiovascular mortality was independent of blood group (O versus non-O) and, moreover, similar among subjects with different blood groups. Repeating the analyses for all-cause mortality gave similar results for CRP. For vWf, the RR was 2.0 (95% CI 1.1 to 3.5) after adjustment for all other risk factors. Increased levels of vWf are independently associated with cardiovascular and all-cause mortality in both diabetic and nondiabetic subjects. The association between increased levels of CRP and cardiovascular mortality was partly explained by other risk factors. Mutual adjustment of vWf and CRP did not markedly change the results, favoring the hypothesis that vWf and CRP predict mortality through different pathways.
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PMID:von Willebrand factor, C-reactive protein, and 5-year mortality in diabetic and nondiabetic subjects: the Hoorn Study. 1059 89

Atherosclerosis is more extensive and occurs earlier in diabetics compared with the general population. The pathophysiology of atherosclerosis is not fully established. We compared the activity of two blood clotting agents, activated factor VII (VIIa) and von Willebrand factor (vWF), in diabetic and non-diabetic subjects with coronary artery disease. According to clinical features, subjects were placed in one of four groups: Group I, non-insulin-dependent diabetes mellitus (NIDDM) with coronary heart disease (CAD) (n = 16); Group II, NIDDM (n = 15); Group III, CAD with no presence of diabetes (n = 17); and Group IV, healthy volunteers (n = 15). The level of factor VIIa was higher in Group I compared with all other groups, and was significantly higher in Group II compared with Group III and Group IV. Activity of vWF was higher in Group I compared with Group II, Group III and Group IV. There was no statistical difference between Group II and Group III. There was no significant correlation between concentration of blood glucose, total cholesterol or triglyceride, duration of diabetes and either factor VIIa or vWF activity. The results of this study suggest that increased activity of plasma vWF and factor VIIa may be useful markers to identify ischaemic heart disease risk in NIDDM subjects.
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PMID:Activity of factor VIIa and von Willebrand factor in non-insulin-dependent diabetic subjects with coronary artery disease. 1059 31

We have recently shown that fibrin D-dimer, tissue plasminogen activator (tPA) antigen, von Willebrand factor antigen, fibrinogen, plasma viscosity, and white cell count are associated with subsequent ischemic heart disease (IHD) in men aged 49 to 65 years in the Caerphilly Study from South Wales. We now report the contribution of major lifestyle factors to plasma levels of these new risk predictors for IHD. Results were available for up to 2188 men. The contribution of factors associated with lifestyle (smoking, alcohol, body mass index, leisure and work activity, social class, and use of prescribed medicines) to variation in plasma levels of 8 hemostatic variables was examined. All results were adjusted for other lifestyle variables, age, and time of day. Most hemostatic variables increased with age and smoking habit. Increasing levels of alcohol consumption were associated with increases in tPA and plasminogen activator inhibitor (PAI-1) activity and with decreases in fibrinogen and white cell count. tPA, PAI-1, fibrinogen (nephelometric), and viscosity were positively associated with body mass index. Increasing levels of leisure activity were inversely associated with D-dimer, von Willebrand factor, nephelometric fibrinogen, and viscosity. Use of prescribed medicines (a marker for chronic illness) was associated with adverse levels of D-dimer, fibrinogen, plasma viscosity, and white cell count. tPA, PAI-1, and plasma viscosity were associated with blood pressure, cholesterol, and triglycerides but not with lipoprotein(a) or homocysteine. We conclude that several lifestyle factors are associated with hemostatic risk predictors for IHD. Lifestyle modifications may reduce IHD risk partly by altering hemostatic function; large intervention studies are required to test this hypothesis.
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PMID:Lifestyle and hemostatic risk factors for ischemic heart disease : the Caerphilly Study. 1063 29

Endothelial injury plays critical roles in acute and chronic complications after percutaneous transluminal coronary angioplasty (PTCA). We investigated coronary endothelial injury and the release of vasoactive substances induced by PTCA. We examined 44 patients with ischemic heart disease who underwent elective PTCA to isolated stenotic lesions in left coronary arteries. Eleven patients received balloon angioplasty (BA), 14 percutaneous transluminal rotational atherectomy (PTRA), and 19 stent implantation. Blood samples were drawn from the coronary sinus immediately before and after as well as 4 hr and 24 hr after PTCA. Plasma levels of endothelin (ET) 1, angiotensin (ANG) II, von Willebrand factor (vWF), and thrombomodulin (TM) were measured. Seven control subjects who underwent diagnostic coronary angiography (CAG) were used as controls. In all patients, ET-1 levels in the coronary sinus blood significantly increased immediately after PTCA. ANG II levels and vWF activity showed significant increases 4 hr after PTCA. Changes in levels of these markers were similar among the BA, PTRA, and stent groups. TM levels were elevated in all groups of patients, including those simply undergoing diagnostic CAG. Changes in ET-1, ANG II, and vWF levels in the coronary sinus reflect coronary endothelial injury induced by PTCA.
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PMID:Release of endothelin 1 and angiotensin II induced by percutaneous transluminal coronary angioplasty. 1097 17

Moderate and strenuous exercise is known to enhance platelet aggregability in patients with obstructive coronary artery disease (CAD), but the effect of low-grade exercise is not known. We assessed shear-induced platelet aggregability before and after mild exercise (less than or equal to stage III of the modified Bruce protocol) in 27 patients with documented CAD who were receiving aspirin and in 12 subjects without CAD (controls). Ex vivo platelet aggregability was assessed in flowing whole blood as the time to occlude a collagen and adenosine diphosphate-coated ring; shorter times indicated greater aggregability. Aggregability, plasma von Willebrand factor (vWF) antigen, platelet and white cell counts, and hematocrit were measured at baseline, immediately after exercise (peak), and at 30 and 180 minutes after exercise. Exercise of similar workloads induced myocardial ischemia in 14 patients (group 1), but not in the other 13 (group 2) nor in controls. Both patient groups showed a reduction in aggregation time at peak exercise compared with baseline (group 1: 84+/-17 seconds at peak vs 96+/-22 seconds at baseline; group 2: 84+/-20 seconds at peak vs 99+/-20 seconds at baseline; p <0.03 for both comparisons), with a return to baseline values within 180 minutes. No significant variation occurred in controls (89+/-18 seconds at peak vs 85+/-21 second at baseline). Changes in vWF antigen did not differ significantly among groups. Aggregation times did not correlate with hematocrit or platelet and white cell counts. Thus, even low-grade exercise transiently enhances whole blood platelet aggregability in patients with obstructive CAD, but not in controls. The effect is independent of myocardial ischemia, occurs despite aspirin, and is likely dependent on hemodynamic factors interacting with coronary obstructions or dysfunctional endothelium.
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PMID:Low-grade exercise enhances platelet aggregability in patients with obstructive coronary disease independently of myocardial ischemia. 1113 27

Therapeutic angiogenesis achieved either through the use of discreet angiogenic proteins or by gene therapy is fast emerging as a highly attractive treatment modality for ischemic heart disease. Herein we examine a novel method of stimulating myocardial angiogenesis by hypoxic preconditioning at both capillary and arteriolar levels, and the potential role of NF kappa B in mediating such a response. We also investigate the functional relevance of such treatment by assessing whether the induced neovascularization can help preserve left ventricular contractile functional reserve in the setting of developing heart failure secondary to myocardial infarction. Male Sprague-Dawley rats were randomly divided into eight groups: normoxia + sham surgery (NS), normoxia + permanent left anterior descending coronary artery (LAD) occlusion (NMI), hypoxic preconditioning + sham surgery (HS), hypoxic preconditioning + permanent LAD occlusion (HMI), PDTC (NF kappa B inhibitor) + hypoxic preconditioning + LAD occlusion (PHMI), PDTC+normoxia + LAD occlusion (PNMI), PDTC + hypoxic preconditioning + sham surgery (PHS) and PDTC + normoxia + sham surgery (PNS). Rats in the preconditioned groups were subjected to systemic hypoxemic hypoxic exposure (10+/-0.4% O2) for 4 h followed by a 24-h period of normoxic reoxygenation prior to undergoing LAD occlusion. Rats in the normoxia groups were time matched with the preconditioned group and maintained under normoxic conditions for the 28-h period prior to LAD occlusion. The HMI group displayed significant increases in capillary as well as arteriolar density after 2, 4 and 7 days post-operation compared to the NMI. Prior PDTC administration prevented such increases in the PHMI group and effectively abolished the pro-angiogenic effect of hypoxic preconditioning (HP). One week after sham surgery or LAD occlusion, rats underwent a pharmacological stress test with dobutamine in progressively increasing doses which revealed significantly elevated values of dp/dt(max) at each dose point in the HMI group compared to the NMI or PHMI groups. Hypoxic preconditioning also decreases endothelial cell injury as determined by the extent of endothelial cell apoptosis using anti-VWF factor labelling and TUNEL assay. The results suggest that HP stimulates myocardial angiogenesis via redox-regulated transcription factor, NF kappa B-dependent pathway to an extent sufficient to exert significant preservation of contractile functional reserve in a rat model of myocardial infarction progressing to heart failure.
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PMID:Hypoxia/reoxygenation promotes myocardial angiogenesis via an NF kappa B-dependent mechanism in a rat model of chronic myocardial infarction. 1116 33

ABO histo-blood group is a major determinant of plasma levels of factor VIII (FVIII) and von Willebrand factor (vWF). Blood group O individuals have significantly (approximately 25%) lower plasma levels of both glycoproteins. This association is of clinical significance. Low plasma levels of either FVIII or vWF have long been established as causes of excess bleeding. Conversely, there is accumulating evidence that elevated FVIII-vWF levels may represent an important risk factor for ischaemic heart disease and venous thromboembolic disease. In spite of the well-documented association between ABO blood group and FVIII-vWF levels, the underlying mechanism remains unknown. However, it has been established that the ABO effect is primarily mediated through a direct functional effect of the ABO locus on plasma vWF levels. Theoretically, ABO blood group may alter the rate of vWF synthesis or secretion within endothelial cells. Alternatively, ABO group may affect vWF plasma clearance rates. ABH antigenic determinants have been identified on the N-linked oligosaccharide chains of circulating vWF and FVIII, according to the blood group of the individual. It remains unclear whether these carbohydrate structures are responsible for mediating the effect of ABO blood group on plasma vWF levels.
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PMID:The relationship between ABO histo-blood group, factor VIII and von Willebrand factor. 1153 89

Abnormalities of coagulation and fibrinolysis may play an important role in the pathogenesis of ischaemic stroke and vascular dementia. We aimed to determine whether haemostatic function is altered in acute recent-onset or chronic ischaemic cerebrovascular disease. We studied consecutive patients with ischaemic stroke (n = 74) and vascular dementia (n = 42) compared with healthy controls (n = 40) in a case-control study. The ischaemic stroke group was assessed twice, 3-10 days after the acute stroke and at 1-3 months. Fibrinogen, fibrin D-dimer (marker of fibrin turnover) and von Willebrand factor (vWF) (marker of endothelial disturbance) were elevated acutely (P < 0.0001) and in the convalescent phase after ischaemic stroke (P < 0.0001, P < 0.0001, and P < 0.01 respectively, compared with controls). Similar results were seen in the vascular dementia group. Stepwise multivariate regression analyses showed that cerebrovascular disease correlated independently with fibrinogen (P < 0.001) and fibrin D-dimer levels (P < 0.001), while vWF correlated independently with electrocardiograph evidence of ischaemic heart disease (P = 0.004). Changes between acute and convalescent phases in ischaemic stroke were slightly inconsistent. However, in the acute stage there were tendencies for fibrinogen, D-dimer and vWF to be increased, and factor VIII was significantly higher. Abnormalities of haemostasis, including increased fibrin turnover and endothelial disturbance, are found in both acute and chronic cerebral ischaemia. Many of these patients have co-existent ischaemic heart disease and this may contribute to some of these changes. Acute ischaemic stroke is associated with transient changes in haemostatic factors; however, most abnormalities persist into the convalescent phase, and are also demonstrable in subjects with vascular dementia.
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PMID:Haemostasis in ischaemic stroke and vascular dementia. 1173 65


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