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)

100 patients (median age 79 years) were given anticoagulant therapy (ACT) for a period of time averaging 5 years 3 months (522 follow-up years).--Out of 3 522 Quick tests, converted into prothrombin times and all carried out in the same laboratory, the prothrombin time was at or less than 32% in 60.5%, and 34% in 69.6% of the tests.--The mean therapeutic doses were less than 27% of those for adults, and were decreased by 3 mg of phenindione per year over the age of 75, only the actively treated cases being retained.--The risks are the same as those for the middle-aged adult. They depend more on the quality of the investigations than upon age. In the group which has been studied, slight or frank haemorrhagic complications (0.05/year/patient) were the result of a demonstrable overdosage in only one case in four. They were not responsable for any deaths in this series.--because of the referral patterns, the patients studied consisted of 79 with ischaemic heart disease, 27 with peripheral vascular disease, 9 cerebrovascular accidents, and 6 with thrombo-emoblic problems, not counting the 23 complications during the course of the study. In those patients with ischaemic heart disease, well-regulated anticoagulant treatment was associated with a favourable clinical course, and the correlation was significant.--there is not argument against the administering of a full and prolonged course of ACT to a patient of more than 75 years of age.
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PMID:[Long-term anticoagulant therapy in subjects over 75 years of age. 100 cases]. 40 65

The present studies were undertaken to elucidate the pathophysiological effects of postalimentary lipemia(PAL) induced by the intake of much animal fat in patients with ischemic heart disease(IHD) and the preventive measures against them. Results obtained were as follows: 1) Occurrence of augmentation of ischemic changes in ECG was demonstrated after fat intake. 2) After fat intake, lowering of arterial oxygen tension and heparin-induced increase in arterio-venous difference of oxygen tension in the forearm were observed. 3) PAL resulted in an acceleration of platelet adhesiveness as well as a shortening of plasms recalcification time and that of plasma prothrombin time. 4) It was revealed that red blood cells adsorbed fat on their membrane and then readily agglutinate together. 5) Removal of chylomicrons from the blood stream was accelerated by the intravenous injection of glucose. These results lead to the following conclusions: 1)PAL exerts a deleterious effect on the oxygen supply to the myocardium in patients with IHD and it is probably due to the disturbance of pulmonary function and that of oxygen diffusion and blood flow in the myocardium. 2) As one of preventive measures against the concurrent intake of carbohydrate in an appropriate quantity appears to be of use.
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PMID:Studies on pathophysiological effects of postalimentary lipemia in patients with ischemic heart disease. 111 85

To study factor VII (F VII) hyperactivity in chronic dialysis patients, we measured the plasma levels of F VII activity (F VII c) and antigen (F VII Ag), prothrombin activation fragments 1 + 2 (F1 + 2), thrombin-antithrombin III complexes (TAT), and thrombomodulin in 28 patients on hemodialysis. Marked elevation of F VII c was found in long-term dialysis patients (185 +/- 30%). This hyperactivity was accompanied by both elevation of the F VII Ag level (153 +/- 28%) and enhanced activation of F VII zymogen, expressed as the F VII c/F VII Ag ratio (1.23 +/- 0.23), but pseudocholinesterase activity was decreased. The 6 patients with ischemic heart disease had slightly higher F VII c (200 +/- 25%) than those without ischemic heart disease (181 +/- 30%), although the difference was not significant. Increased F VII c was accompanied by factor Xa hyperactivity (a high plasma F1 + 2 level) in the long-term dialysis patients, but there was no significant elevation of plasma TAT levels when compared with controls matched for age, sex, and the presence or absence of diabetes mellitus. Plasma TAT levels were significantly correlated with plasma thrombomodulin levels, suggesting that thrombin generation in blood as a result of hemodialysis could induce systemic endothelial cell injury.
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PMID:Factor VII hyperactivity in chronic dialysis patients. 133 12

It has been suggested that unstable angina at rest, like acute myocardial infarction, might be associated with a thrombotic process. In order to study the hypothesis that myocardial ischemia during exercise could also be associated with an activation of blood coagulation and/or fibrinolysis, we investigated the presence of plasma markers of a prethrombotic or thrombotic state (thrombin-antithrombin III complexes TAT, prothrombin fragment F1 + 2, and D-dimers DD) in 100 consecutive patients with confirmed or suspected coronary artery disease during ergometric test with myocardial thallium-201 scintigraphy. Symptoms and scintigrams allowed to define three groups of patients: those showing no ischemia (n = 79) and those with symptomatic (n = 8) or silent myocardial ischemia (n = 13). Before exercise, DD and TAT levels were not significantly different among the three groups. On the other hand, the F1 + 2 levels were slightly albeit significantly higher in the patients without ischemia than in the patients with symptomatic or silent ischemia. After exercise, no significant difference was found between the three groups. Exercise induced a significant and parallel increase in both the TAT and the F1 + 2 levels (but not of the DD levels) in the three groups. Thus, our study does not support the hypothesis that myocardial ischemia, silent or symptomatic, is associated with an activation of plasma coagulation and fibrinolysis that can be distinguished from the exercise-induced thrombin generation.
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PMID:Effects of exercise test on plasma markers of an activation of coagulation and/or fibrinolysis in patients with symptomatic or silent myocardial ischemia. 160 40

In our present placebo-controlled study on recombinant tissue-type plasminogen activator (rt-PA) and heparin treatment of patients with acute ischaemic heart disease (IHD), we studied the extent of fibrin resolution and generation of coagulant activity. In rt-PA treated patients the lysis of fibrin in vivo (median 60 nmol of fibrin--estimated as fibrinogen equivalents) was significantly higher (p less than 0.02) than can be accounted for solely by lysis of a coronary thrombus (approximately 2 nmol) and circulating soluble fibrin (median 15 nmol). We observed a 200% increase of plasma concentrations of both prothrombin fragment 1 + 2 (p less than 0.001) and thrombin-antithrombin III complexes (p less than 0.001) as a consequence of rt-PA treatment, indicating that the coagulant activity is primarily caused by a physiological activation of the coagulation system. We conclude that an important contribution to the activation of coagulation in patients undergoing coronary thrombolysis is lysis of fibrin deposited widespread on the vascular intima, and that this process causes an intimal-dependent activation of the coagulation system.
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PMID:Possible role of vascular intima for generation of coagulant activity in patients undergoing coronary thrombolysis with recombinant tissue-type plasminogen activator. A randomized, placebo-controlled study. 181 18

An increase in factor VII coagulant activity is known to be an important risk factor for ischaemic heart disease. Four hundred and eight healthy male Post Office workers were screened in an occupational survey. Sixty eight (16.5%) of these had values of factor VII coagulant activity greater than 1.0 SD above the age related mean. A randomised double-blind crossover study was undertaken to investigate the effect of a fixed daily minidose of warfarin (1 mg) on the high activities of factor VII in these men. Forty two agreed to enter the study and 40 completed it. Their mean factor VII coagulant activity before warfarin treatment was 135.9%. Treatment with a fixed minidose of warfarin significantly reduced factor VII coagulant activity to 124.6%; there was no change on placebo. The prothrombin time was also significantly prolonged on active treatment although all the results remained within the normal range. These findings suggested a fixed minidose warfarin regime might be useful in the primary prevention of ischaemic heart disease by reducing high activities of factor VII.
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PMID:Reduction of factor VII coagulant activity (VIIC), a risk factor for ischaemic heart disease, by fixed dose warfarin: a double blind crossover study. 218 69

Cardiovascular complications were examined in a 31-year-old woman with homozygous familial hypercholesterolemia (FH) (LDL receptor defective type), who had had no clinical symptoms of coronary artery disease. She had delivered 2 children without any cardiac complications, and her exercise electrocardiogram showed no positive findings for ischemic heart disease. Coronary angiography showed no significant arterial lesions, and left ventriculography revealed good contraction of the left ventricle (ejection fraction: 67%). This is considered to be a very rare case of homozygous FH without significant lesions in the coronary arteries. This might be attributed at least in part to her dietary regimen consisting of a very low fat and low calorie diet, to the residual LDL receptor activity or to the low value of prothrombin time.
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PMID:A 31-year-old woman with homozygous familial hypercholesterolemia without significant lesions in the coronary arteries. 380 Oct 79

Twenty of approximately 1000 patients attending the arteriosclerosis clinic at MIT during a 13 year period were treated simultaneously with aspirin and warfarin for symptomatic atherosclerotic (19) or rheumatic (1) heart or vascular disease. The average duration of therapy was 5.8 years. Thirteen patients suffered from familial hyperlipoproteinemia; only one patient had none of the major risk factors for arteriosclerosis. Refractory symptoms were related to the central nervous system in 13, peripheral vascular system in 5 and the heart in 2. All twenty patients became asymptomatic or showed marked clinical improvement on aspirin plus warfarin therapy. While on this therapy, complications, both thrombotic and hemorrhagic, occurred in 7 of the 20 patients (graft embolus in 1, and bleeding in 6; with one death as a result of intracranial bleeding) and sudden death, probably from acute myocardial ischemia, in a further 2 patients. We conclude that when alternative therapies are impossible or have proven to be of no avail in patients suffering from the complications of advanced atherosclerosis, the simultaneous administration of aspirin and warfarin may be a therapeutic alternative, although very close and careful followup of the patients' prothrombin times and clinical status is essential.
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PMID:Simultaneous therapy with antiplatelet and anticoagulant drugs in symptomatic cardiovascular disease. 387 67

This literature review was conducted to determine: (a) the rate of bleeding (major, minor and fatal) during long term oral anticoagulant therapy (greater than 4 weeks) in various disorders (ischaemic cerebrovascular disease, prosthetic cardiac valves, chronic atrial fibrillation, ischaemic heart disease and venous thrombosis); and (b) the clinical and laboratory risk factors which predispose such patients to bleeding. Using strictly defined methodological criteria, 167 studies were evaluated and classified into 1 of 5 categories based on the strength of the study design, with level I (randomised trials) representing studies which provided the most reliable information and level V (cases series) the least reliable. The risk of bleeding was substantial, and was most marked in patients with ischaemic cerebrovascular disease (29%), ischaemic heart disease (19%) and venous thromboembolism (23%). Major bleeding in venous thrombosis and cerebrovascular disease was frequently associated with an underlying risk factor. In venous thromboembolism these coexisting conditions (cancer, recent surgery and paraplegia) were also predisposing factors for thrombosis. In cerebrovascular disease major bleeding was almost always intracerebral, possibly because of associated hypertension or the cerebrovascular disease per se. We were unable to determine whether bleeding events were concentrated soon after commencing anticoagulant therapy. Haemorrhagic episodes frequently occurred when the prothrombin time (or thrombotest) was within the targeted therapeutic range, but the relationship between bleeding and the level of anticoagulant therapy was properly evaluated in only 1 study (in venous thrombosis) which demonstrated that the risk of bleeding was reduced by using a less intense anticoagulant regimen. In conclusion, the risk of bleeding during oral anticoagulant therapy is substantial. Our analysis was limited by the lack of concise reporting of clinical and laboratory information and we would suggest that future clinical studies report these in greater detail.
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PMID:Risk of haemorrhage associated with long term anticoagulant therapy. 390 38

Protein C, an antithrombotic protein, was measured immunologically in 299 patients with clinical conditions associated with a high frequency of venous or arterial thromboembolism. The mean protein C antigen (PC:Ag) level was high for 48 patients with ischemic heart disease and, to a lesser extent, for 95 diabetics. In 28 patients with thrombotic strokes, 48 patients with proximal deep-vein thrombosis and in 80 patients with localized or metastatic tumors, mean PC:Ag was normal. Comparison of the pattern of changes of PC:Ag levels with those of fibrinogen, orosomucoid and prothrombin in 21 patients during the postoperative period and in 20 patients with active rheumatoid arthritis ruled out the possibility that high PC:Ag is non-specific, acute-phase reaction to inflammation, tissue injury or neoplastic growth. Therefore, high PC:Ag might be specifically related to the thrombotic tendency of these patients, but the mechanism of such a relationship remains to be clarified.
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PMID:Protein C antigen is not an acute phase reactant and is often high in ischemic heart disease and diabetes. 654 16


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