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)

In a preliminary report from the Caerphilly study four haemostatic factors showed univariate associations with prevalent ischaemic heart disease after adjusting for age. These factors were fibrinogen concentration, plasma viscosity, white cell count, and the heparin-thrombin clotting time. Age and these haemostatic variables were entered into a stepwise multiple logistic regression analysis; after age the white cell count and heparin-thrombin clotting time remained significantly associated with ischaemic heart disease. Further regression analyses indicated that diastolic blood pressure contributed additionally to this association with ischaemic heart disease but that smoking habit did not.
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PMID:Haemostatic factors and ischaemic heart disease. The Caerphilly study. 399 61

Platelet aggregation and its relation to fatty acid composition of platelets, plasma and adipose tissue was determined in 196 randomly selected, free-living, 40-49-year-old men in two regions of Finland (east and southwest) with a nearly twofold difference in the IHD rate. There were no significant east-southwest differences in platelet aggregation induced with ADP, thrombin or epinephrine. ADP-induced platelet secondary aggregation showed significant negative associations with all C20-C22 omega 3-fatty acids in platelets (r = -0.26- -0.40) and with the platelet 20: 5 omega 3/20: 4 omega 6 and omega 3/omega 6 ratios, but significant positive correlations with the contents of 18:2 in adipose tissue (r = 0.20) and plasma triglycerides (TG) (r = 0.29). Epinephrine-induced aggregation correlated negatively with 20: 5 omega 3 in plasma cholesteryl esters (CE) (r = -0.23) and TG (r = -0.29), and positively with the total percentage of saturated fatty acids in platelets (r = 0.33), but had no significant correlations with any of the omega 6-fatty acids. Thrombin-induced aggregation correlated negatively with the omega 3/6 omega ratio in adipose tissue (r = -0.25) and the 20: 3 omega 6/20: 4 omega 6 ratio in plasma CE (r = -0.27) and free fatty acids (FFA) (r = -0.23), and positively with adipose tissue 18:2 (r = 0.23) and 20:4 omega 6 (r = 0.22) in plasma phospholipids (PL). The percentages of prostanoid precursors in platelet lipids, i.e. 20:3 omega 6, 20:4 omega 6 and 20:5 omega 3, correlated best with the same fatty acids in plasma CE (r = 0.32 - 0.77) and PL (r = 0.28 - 0.74). Platelet 20:5 omega 3 had highly significant negative correlations with the percentage of 18:2 in adipose tissue and all plasma lipid fractions (r = -0.35 - -0.44).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Platelet aggregation in Finnish men and its relation to fatty acids in platelets, plasma and adipose tissue. 408 91

Fibrinopeptide A (FPA) concentrations were measured in blood taken by direct cardiac puncture from 31 patients who had died suddenly of ischaemic heart disease (IHD) and from 8 patients who had died suddenly of other causes. Mean FPA concentration in the IHD group was five times higher than that in the non-IHD group. This difference was almost entirely due to the high FPA level in the IHD subjects with a history of the disease. The FPA difference between the IHD and non-IHD groups is unlikely to have been due to differences in methods of resuscitation. A possible interpretation of the findings is that thrombin production causes or aggravates the course of events leading to sudden IHD death, particularly in subjects with a past history of IHD.
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PMID:Fibrinopeptide A and sudden coronary death. 614 43

Platelets are thought to be involved in the initiation and propagation of arterial and venous thrombi. A new formation of platelet thrombus in a coronary artery has been implicated in the genesis and extension of myocardial infarction. Experimental evidence suggests that platelet aggregates may be responsible for occlusion of small coronary arteries and subsequent ischemia. Whether the thrombotic component of myocardial infarction is primary or secondary in a given patient, platelet function alterations can influence many mechanisms - operating at the microenvironment level from which depends if the thrombotic lesion grows or sends platelet emboli to the smaller myocardial vessels. Although myocardial infarction is usually associated with arteriographic evidence of atherosclerotic coronary obstruction, examples of infarction in the absence of coronary artery disease have been reported. ARterial thrombosis, small vessel coronary disease and arterial spasm are several possibilities that have been described. Recently in some cases of myocardial infarction, coronary artery spasm has been demonstrated angiographically; thromboxanes, vasoconstrictive and platelet aggregating substances, are released by platelets; thromboxanes, vasoconstrictive and platelet aggregating substances, are released by platelets during myocardial ischemia as an increase of prostaglandin synthesis, like prostacyclin, is stimulated by ischemia and hypoxia. The local release of these substance may modify the myocardial cell viability and regional blood flow. The aim of the present study was to investigate some changes in platelet function in relation to the time stimulated with thrombin. The tests showed, in the first three days, an augmented release of BTG levels with a platelet "exhaustion", demonstrated by a reduced formation of MDA by platelets changing to a state of hyperactivity, with a maximal production of MDA in 10th-15th day.
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PMID:[MDA formation by platelets and plasmatic BTG levels in patients suffering from acute myocardial infarction (author's transl)]. 617 83

The hypothesis that exercise-induced myocardial ischemia is associated with abnormal platelet activation and fibrin formation or dissolution was tested in patients with coronary artery disease undergoing upright bicycle stress testing. In vivo platelet activation was assessed by radioimmunoassay of platelet factor 4, beta-thrombo-globulin and thromboxane B2. In vivo fibrin formation was assessed by radioimmunoassay of fibrinopeptide A, and fibrinolysis was assessed by radioimmunoassay of thrombin-increasable fibrinopeptide B which reflects plasmin cleavage of fibrin I. Peripheral venous concentrations of these substances were measured in 10 normal subjects and 13 patients with coronary artery disease at rest and during symptom-limited peak exercise. Platelet factor 4, beta-thromboglobulin and thromboxane B2 concentrations were correlated with rest and exercise catecholamine concentrations to determine if exercise-induced elevation of norepinephrine and epinephrine enhances platelet activation. Left ventricular end-diastolic and end-systolic volumes, ejection fraction and segmental wall motion were measured at rest and during peak exercise by first pass radionuclide angiography. All patients with coronary artery disease had documented exercise-induced myocardial ischemia manifested by angina pectoris, ischemic electrocardiographic changes, left ventricular segmental dyssynergy and a reduction in ejection fraction. Rest and peak exercise plasma concentrations were not significantly different for platelet factor 4, beta-thromboglobulin, thromboxane B2, fibrinopeptide A and thrombin-increasable fibrinopeptide B. Peripheral venous concentrations of norepinephrine and epinephrine increased significantly (p less than 0.001) in both groups of patients. The elevated catecholamine levels did not lead to detectable platelet activation. This study demonstrates that enhanced platelet activation, thromboxane release and fibrin formation or dissolution are not detectable in peripheral venous blood of patients with coronary disease during exercise-induced myocardial ischemia.
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PMID:Exercise-induced myocardial ischemia in patients with coronary artery disease: lack of evidence for platelet activation or fibrin formation in peripheral venous blood. 633 91

Lipolytic factors associated with myocardial ischemia and factors which activate phospholipase A2 in cells other than heart cells were tested for their actions on the rhythmicity of cultured heart cells. Exogenous triglyceride lipase was without a significant effect on beating while phospholipase A2 produced concentration-related arrhythmias in concentrations as low as 0.0375 U/ml. Quinacrine, a phospholipase inhibitor, demonstrated concentration-dependent inhibition of reoxygenation-induced arrhythmias. Of the compounds known to activate phospholipase only kallikrein and thrombin produced arrhythmias; only bradykinin, thrombin and trypsin depressed beating. Lysophosphatidylcholine, a reaction product of phospholipase A2 on phospholipids, inhibited reoxygenation arrhythmias in a concentration-dependent manner.
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PMID:Arrhythmogenic and antiarrhythmic effects of lipolytic factors on cultured heart cells. 663 27

Platelet aggregates play an important role in rheology of the blood flow in microcirculation. The formation of platelet aggregates markedly raise the threshold diameter of the vessel at which the inversion of Fahraeus-Lindquist effect takes place. In different diseases (ischemic heart disease, diabetes) thromboxane A2 production by platelets is increased and, as a consequence, platelet aggregate formation is facilitated. Platelet aggregation is modulated by several mechanisms, among which thromboxane A2 and thrombin increase and prostacyclin decrease formation of platelet aggregates. Prostacyclin is able also to increase blood red cells deformability thus it appears one of the most important factors for the control of blood flow rheology in microcirculation. However, prostacyclin production is limited in time, and repeated and close periods of venous stasis induce exhaustion of prostacyclin production and increase the formation of platelet aggregates.
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PMID:Pathophysiological aspects of platelet aggregation in relation to blood flow rheology in microcirculation. 676 41

A stimulant of vascular smooth muscle contraction was generated in fresh, citrated human plasma during activation of the clotting system. Plasma, exposed briefly to thromboplastin and Ca++, induced a contraction of isolated rabbit aorta and dog coronary arteries that was slow in development and persisted after washout. The contractile activity was not blocked by phenoxybenzamine, atropine, or angiotensin inhibitor, but was blocked when heparin or hirudin was incubated with the plasma. The contractile stimulant produced in the plasma was short-lived (less than 3 min) and paralleled the appearance of thrombin in plasma. Purified human alpha-thrombin also induced a sustained contraction in these blood vessels that was not inhibited by phenoxybenzamine, atropine, or angiotensin inhibitor, but was blocked by hirudin. Partial relaxation of the thrombin-treated blood vessel was achieved by the addition of heparin. These results suggest that this vasoactive component of thromboplastin-activated human plasma is alpha-thrombin. Because of its potent and persistent effects, thrombin-induced vasospasm may be an important mechanism in the etiology of ischemic heart disease.
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PMID:Generation of a vasoactive substance in human plasma during coagulation. Evidence of thrombin-induced contraction of rabbit aorta and dog coronary artery. 682 92

We evaluated the consequences of platelet activation within the coronary circulation and determined the contribution of released thromboxanes, the most potent vasoconstrictors known, to the ensuing cardiac ischemia. Human platelets were isolated by sepharose column chromatography from blood of normal donors and added to the crystalloid perfusate of a Langendorff rabbit heart (platelet counts greater than or equal to 10,000/microliters). Following thrombin-induced (1 U/ml) platelet activation, the coronary flow decreased by 30 +/- 10% (mean +/- SEM, P less than 0.02), the mean concentration of thromboxane B2 in the coronary sinus effluent rose to 62 +/- 25 pmol/ml, and immediate, often irreversible cardiac ischemia as monitored by nicotinamide adenine dehydrogenase autofluorescence photography, ensued. However, with high concentrations of the platelet inhibitor and vasodilator, prostaglandin E1 (1.0 mM), the coronary flow increased by 50 +/-= 15%, and the epicardial fluorescence remained unchanged despite a small (10 +/- 3 pmol/ml) increase in coronary sinus thromboxanes. Platelets isolated from donors who ingested aspirin were incapable of thromboxane synthesis (less than 5 pmol/ml) but remained normally responsive to thrombin-induced activation. When these platelets were challenged by thrombin during cardiac perfusion, however, coronary flow and epicardial fluorescence remained unchanged. We conclude that platelet activation within the coronary circulation can induce irreversible cardiac ischemia, which, however, can be prevented by appropriate pharmacologic inhibition of platelet function. Furthermore, the fact that cardiac perfusion was preserved during a thrombin challenge of platelets from aspirin-treated donors establishes a fundamental role for the products of cyclooxygenase activity (e.g., thromboxanes) in the genesis of this form of myocardial ischemia.
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PMID:Mediation of cardiac ischemia by thromboxanes released from human platelets. 704 97

Although platelets have been associated with angina pectoris, myocardial infarction, and sudden death, the platelet's capacity for induction and propagation of cardiac ischemia remains incompletely defined. We therefore evaluated the effects of platelet activation occurring within the coronary circulation and tested the hypothesis that inhibition of platelet function would prevent platelet-induced cardiac ischemia. Human platelets were isolated from blood obtained from normal donors by Sepharose 2B column chromatography, resuspended in Hepes buffer, and added to the perfusate of a Langendorff rabbit heart (platelet counts greater than 10,000/microliters). Without, and with low dose (10 microM) prostaglandin E1 (PGE1), a reversible inhibitor of platelet function, immediate and irreversible global cardiac ischemia, as monitored by NADH fluorescent photography, ensued (N = 4) following platelet activation with thrombin (0.1 to 1 U/ml). Higher concentrations of PGE1 (0.1 to 1 mM, N = 2) or aspirin ingestion (1000 mg taken approximately 12, 4, and 1 hr prior to experiment, N = 2) completely prevented this platelet-induced myocardial ischemia. Aspirin, unlike PGE1, was effective despite its inability to block thrombin-induced platelet aggregation in our in vitro gel-filtered system. We conclude that activation of platelets within the coronary circulation is sufficient for induction of irreversible cardiac ischemia. The efficacy of aspirin, a cyclooxygenase inhibitor, further suggests that the products of arachidonate metabolism (e.g., thromboxanes) have a fundamental role in the genesis of platelet-mediated myocardial ischemia.
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PMID:Platelet-mediated cardiac ischemia. 713 26


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