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)

Plasma fibrinogen and plasminogen levels were measured in 122 male and 56 female healthy adult subjects and in 64 men with ischaemic heart disease. Plasma fibrinogen levels were found to rise markedly and progressively with age in both male and female healthy subjects; plasminogen showed only a slight rise with age. No sex differences were found for either fibrinogen or plasminogen. The correlation between plasminogen and fibrinogen levels was low, reaching the 5% level of significance only in men. Patients with ischaemic heart disease were found to have significantly increased fibrinogen and plasminogen levels in the 31-45 years age group only.
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PMID:Plasma fibrinogen and plasminogen levels in health and in ischaemic heart disease. 592 37

Lipoprotein(a) or Lp(a) is similar to low density lipoproteins (LDL), but also contains a large glycoprotein molecule called apo-lipoprotein(a) or apo(a). The lipid composition of Lp(a) is nearly identical to that of LDL. The structure of apo(a) is similar to that of plasminogen. Several genetic polymorphisms have been described for apo(a). The increasing interest in Lp(a) is due to the positive correlation which exists between the plasma level of Lp(a) and the incidence of ischaemic heart disease. Plasma Lp(a) level varies greatly from one individual to another and is basically dependent on genetic factors, especially for the isoforms of apo(a). A level above 30 mg.dl is associated with increased risk of atherosclerosis-related diseases. There are few treatments which are effective in significantly reducing raised levels of Lp(a).
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PMID:[Lipoprotein (a)]. 782 70

Substantial experimental evidence now implicates lipoprotein (a) as an independent risk factor for premature cardiovascular disease. Both plasma Lp(a) levels and apo(a) phenotype are strong predictors of risk for ischaemic heart disease. The accumulation of apo(a) in vascular wall tissue and in atherosclerotic plaques and the potential inhibition of fibrinolysis by Lp(a) underlie the enhanced risk of premature cardiovascular disease associated with this cholesterol-rich particle. Recent studies of the capacity of purified Lp(a) isoforms to inhibit fibrinolysis in an in vitro system have revealed that small isoforms of Lp(a) (< or = 500 kDa) are efficient inhibitors of plasminogen activation and bind with high affinity to fibrin. Conversely, large isoforms exert little or no inhibitory effect in this system (> 500 kDa). These data suggest that the potential, high affinity interaction of Lp(a) particles containing small isoforms with fibrin introduces a new, third dimension to the atherothrombotic risk associated with these cholesterol-rich particles.
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PMID:Lipoprotein (a): implication in atherothrombosis. 785 88

The relationship of ischaemic heart disease (IHD) to seasonal and latitude variation has prompted speculation that exposure to the ultraviolet component of solar radiation may reduce IHD risk. This hypothesis was partially tested by exposing 14 post-myocardial infarction patients to a 6 week course of artificial whole-body ultraviolet radiation (UVR). Serum lipoprotein and plasma coagulation factor concentrations were measured before and after the course of UVR. Results were compared with similar measurements from a placebo-controlled group of 13 post-myocardial patients. Despite a more than two-fold rise in mean serum 25-OHD, serum lipoprotein and plasma fibrinogen, antithrombin III and plasminogen concentrations did not change significantly in the UVR group. Significant but minor change in prothrombin time and thrombin time in the placebo group appear unlikely to be of biological significance. Seasonal and latitude variation in these IHD risk factors appear unrelated to corresponding variation in solar UVR exposure.
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PMID:Artificial ultraviolet whole-body radiation does not modify serum lipoprotein, plasma fibrinogen, plasminogen or antithrombin III concentrations in post-myocardial infarction patients. 794 60

Fatty fish was included for 7 months into diet of 11 male patients with early stages of ischemic heart disease. Effects of this diet modification on serum fatty acids, lipids and some variables of hemostasis were studied. After control period, patients ate 120-160 g/day of canned Pacific sardine (about 5 g omega-3 polyunsaturated fatty acids) per day. Two patients refused to participate after 2 months and 1 was lost for follow-up. After 7 months of diet, the proportion of eicosapentaenoic acid (EPA) in blood lipids increased from 0.67 + 0.26 to 4.7 + 1.5% (p < 0.015) and of docosahexaenoic acid (DHA) from 2.3 + 1.1 to 4.3 + 1.1% (p < 0.015). Ratio of EPA to arachidonic acid (AA) rose from 0.1 + 0.02 to 0.9 + 0.4 (p < 0.015). Mean serum triglyceride concentration fell after first month from 179.5 + 79.0 to 99.1 + 30.0 mg/dl (p < 0.015) and remained at this level throughout the study. No significant changes were observed in serum total and high-density lipoprotein cholesterol. Plasma activities of tissue-type plasminogen activator inhibitor, contents of plasminogen, alpha 2-antiplasmin, antithrombin III and protein C also did not change. Plasma fibrinogen moderately decreased. Its decrease became statistically significant at month 5 (from 3.8 + 0.5 to 3.0 + 0.7, p = 0.021). Thus, the regimen used in this study led to a substantial and steady increase in plasma EPA, DHA and EPA/AA ratio. This was accompanied by sustained decrease in plasma triglycerides. There were no profibrinolytic changes in the parameters studied.
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PMID:[The effect of the long-term use of a diet enriched with omega-3 polyunsaturated fatty acids on the fatty acid composition, fibrinolytic system indices and lipid spectrum of the blood in patients with ischemic heart disease]. 813 73

Defective fibrinolysis may constitute a risk for the development of myocardial infarction in patients with ischaemic heart disease. We studied prospectively the factor XII-dependent plasminogen proactivator system in 49 survivors of an acute myocardial infarction. Blood samples were collected 8 weeks after hospital discharge. The factor XII-dependent fibrinolytic activity in the specimens was determined on fibrin plates after complete immuno-inhibition of the urokinase-like and the t-PA related fibrinolytic systems. During the subsequent follow-up period of 2.4 years, 10 patients developed recurrent myocardial infarction, whereas the remaining 39 patients did not. The reinfarction group of patients had a significantly lower median factor XII-dependent fibrinolytic activity (24.9 blood activating units (BAU).ml-1) than the patients without a relapse (41.9 BAU.ml-1, P < 0.02). Plasma concentrations of factor XII did not deviate significantly between the groups (P > 0.05), whereas the median plasma concentrations of prekallikrein was slightly lower in the reinfarction group (90%) than in the non-reinfarction group of patients (105%, P < 0.02). These observations point to an association between a depressed factor XII-dependent fibrinolytic activity and an enhanced risk of reinfarction in patients with a previous episode of acute myocardial infarction.
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PMID:Depression of factor XII-dependent fibrinolytic activity in survivors of acute myocardial infarction at risk of reinfarction. 832 6

Lipoprotein (a) is a subspecies of low-density lipoprotein which possesses as part of its protein moiety a mutant form of plasminogen termed apolipoprotein (a), and which may be closely related to the risk of ischaemic heart disease and cerebral infarction. We have investigated the serum concentrations of lipoprotein (a) and other lipoproteins in 24 male patients on CAPD and compared them to healthy men (n = 100) and to age-matched healthy controls (n = 38). The most striking finding was a substantial elevation of serum lipoprotein (a) in CAPD patients in whom it was 46.9 (2.2-168) mg/dl (median and range) compared to 9.0 (< 0.6-87.4) mg/dl in healthy control group and 6.7 (< 0.6-84.2) mg/dl in age-matched controls (both P < 0.001). Patients, when compared to healthy men, also had significantly increased serum triglycerides (median and range, 1.94 (0.55-8.00) versus 1.24 (0.36-4.40) mmol/l; P < 0.001), very-low-density lipoprotein cholesterol (median and range, 0.98 (0.10-3.71) versus 0.46 (0.10-1.17) mmol/l; P < 0.001), and lower-high-density lipoprotein cholesterol (mean +/- 1 SD, 1.26 +/- 0.29 versus 1.35 +/- 0.31 mmol/l). Of these, however, only the difference in very-low-density lipoprotein cholesterol remained statistically significant (P < 0.001) in comparison to age-matched controls. The marked elevation of serum lipoprotein (a) in patients on CAPD may be due to increased hepatic synthesis as a consequence of the substantial amounts of plasma proteins lost in the dialysate. Elevated serum lipoprotein (a) concentrations in CAPD patients may contribute to their risk of coronary artery disease.
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PMID:Serum lipoprotein (a) concentrations in patients undergoing continuous ambulatory peritoneal dialysis. 838 41

Plasminogen activator inhibitor-1 plays a major role in the fibrinolytic system as the main physiological inhibitor of both tissue-type and urinary-type plasminogen activators. The inhibitor is present in plasma in small amounts and derives mainly from endothelial cells. Positive correlations have been reported between plasma levels and different parameters, such as serum triglycerides, insulin plasma levels and body mass index. Moreover, high plasma inhibitor concentrations have been observed in different disease states, but it must be stressed that plasminogen activator inhibitor-1 behaves as an acute-phase reactant and measurement of plasma levels is not significant in the acute phase of the disease. A possible predictive value of inhibitor levels for thrombotic events such as deep vein thrombosis and ischemic heart disease has been studied. On the basis of available studies, the predictive value is not clear for venous thrombosis, whereas plasminogen activator inhibitor-1 levels can predict some coronary events, at least in subgroups of young patients with a first myocardial infarction. It remains to be established if treatments able to reduce plasma inhibitor levels lead to a decrease in the risk of thromboembolic events.
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PMID:Predictive value for thrombotic disease of plasminogen activator inhibitor-1 plasma levels. 851 17

The potential long-term impact of danazol on coronary risk hinges on its effect on lipoprotein metabolism rather than its influence on total plasma lipids. Danazol may exert a regulatory influence on three key processes in lipoprotein metabolism: hepatic lipase activity; low-density lipoprotein receptor function; and lecithin:cholesterol acyl-transferase activity. Danazol decreases plasma fibrinogen and lipoprotein (a) levels, promotes fibrinolysis and causes a rise in plasminogen. Such changes are beneficial as they inhibit the process of thrombosis. Androgenic properties of danazol produce effects of plasma lipids and lipoproteins which oppose estrogen-induced changes. The usual recipients of danazol therapy are premenopausal females, in whom the absolute risk of ischemic heart disease is low. If the drug were shown to increase ischemic heart disease risk, detrimental factors must be weighted against its considerable and proven clinical benefits.
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PMID:Danazol and plasma lipoprotein metabolism. 852 71

The aim of this study was to evaluate plasma levels of lipoprotein (a) [LP(a)] and plasminogen in patients affected with atherosclerotic disease and to understand the mutual relationships. Eighty-four patients affected with atherosclerosis were examined and divided as follows: group I, 24 patients with peripheral arteriopathy; group II, 40 patients with ischemic heart disease (myocardial infarction and/or angina pectoris); group III, 20 patients with multi-infarct dementia; group IV (control group) with 20 healthy young subjects. The results show that Lp(a) plasma levels, in atherosclerotic patients, are higher than 30 mg/dl, while the plasminogen levels are lower than 80 mg/dl. There is an inverse correlation between these two data. Moreover, a different behaviour of Lp(a) and plasminogen rate related to age of patients, to number of atherosclerotic lesions or to acuteness of ischemic heart disease, was observed.
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PMID:[Lipoprotein (a) and plasminogen in atherosclerosis]. 901 33


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