Summary:The effects of physical training on hemostatic parameters were evaluated in 56 postmyocardial infarction (MI) patients before and after one month of systematic physical training and in 30 control post-MI patients, who did not undergo such training. There were no significant changes in prothrombin time (PT) and alphal-antitrypsin (alAT) at the beginning and end of the study in either group. Levels of fibrinogen, Factor VIII: C (V1II:C) and von Wildebrand antigen (vWf Ag), and activities of ATIII and plasminogen (Plg) were significantly decreased in the group with physical training (pe 0.09, while values were unchanged in the control group. Hematocrit, platelet counts, and alpha2-plasmin inhibitor (a2PI) activities also decreased in the physical training group (pe 0.05). In contrast, these variables increased in the control group (p ~0 . 0 5 ) .Activated partial thromboplastin time (aP'lT) tended to be prolonged in the group with physical training, while it was shortened in the control group. In a subset of 20 patients with physical training, resting levels of plasmin-a2PI complex (PIC), thrombin-antithrombin I11 complex (TAT), protein-C (P-C:Ag), plasminogen activator inhibitor-1 (PAI-l), VII:C, and P-C activities had significantly decreased after one month of physical training (pc0.05), although tissue plasminogen activator activities remained unchanged. Physical training appeared to sup- press coagulability as indicated by the decrease in fibrinogen, VIII:C, vWf:Ag, VII:C, and TAT, and prolongation of aPTT. The decrease in plasminogen, t-PA:Ag, a2P1, PAI-1, and PIC after physical training may result from the decreased coagulability. In conclusion, physical training appears to induce a suppression of the coagulation system in patients in the recovery phase of MI.

We studied the effects of calcium, cyclic nucleotides, and protein kinase C on albumin transfer, electrical resistance, and cytoskeletal actin filaments in cultured human umbilical vein endotheiiai cells. The endotheiiai monoiayer grown on collagentreated filters markedly restricted the transfer of albumin relative to Its transfer across the filter alone. Both Ca ++ lonophore A23187 and ethyleneglycol tetraacetlc acid disrupted the Integrity of the endotheiiai monoiayer, thereby Increasing endotheiiai albumin transfer and decreasing electrical resistance In a concentration-dependent manner. Neither W-7, a calmodulln antagonist, nor TMB-8, an intracellular Ca suggest that the pathogenesis of atherosclerosis involves endotheiiai damage, which reduces the effectiveness of these cells as a barrier.The development of EC culture has allowed the study of permeability in EC monolayers in porous-bottom dishes.3 Such in vitro models have the advantage over in vivo studies of permitting direct measurement of EC permeability. Transendothelial movements of several macromolecules of different molecular weights and radii have been investigated. 45 We chose to study albumin because it is one of the most important physiologic macromolecules, determining the balance of osmotic pressure across the endothelium and acting as a carrier of various substances, including hormones and drugs.Although it is known that ECs can be targets of thrombogenic and inflammatory mediators, which disrupt the EC monoiayer and thereby increase its permeability, the initial transmembrane events that activate EC functions remain unclear. Calcium, cyclic nucleotides, and degradation products of phosphatidyl inositol are important intracellular second messengers and are involved in

No abstract

Summary:The present study was undertaken to determine whether the extent of Factor VII elevation correlated with the severity of coronary artery disease and whether zymogen or activated Factor VII was responsible for this elevation. A group of 69 patients with coronary artery disease with old myocardial infarction was compared with 28 control subjects. The patient groups showed elevated levels of Factor VII procoagulant activity (FVI1:C) and more markedly elevated Factor VII antigen (FV1I:Ag) levels than the control group; therefore they had a decreased FVI1:C to FV1I:Ag ratio. The increased Factor VII level in the patient groups was caused by elevated Factor VII zymogen levels, and not by activated Factor VII. Since FVI1:C levels strongly correlated with the titer of thrombin-antithrombin I11 complexes in all patients, the hypercoagulable state accompanying severe coronary atherosclerosis seems to underlie the increase of FVII and TAT in the stable phase of myocardial infarction.

The clinical significance of beta-thromboglobulin (ƒÀ-TG) and platelet factor 4 (PF-4) levels were evaluated in 26 patients with atrial fibrillation (af) complicated by valvular heart disease (VHD), 73 patients with of but without valvular heart disease and 57 normal subjects. The ƒÀ-TG level was significantly higher in af patients without VHD than in normal subjects (49.4•}35.8ng/ml vs 31.2•} 14.0ng/ml, p<0.01) and in af patients with VHD than in normals (64.1•}52.8ng/ml vs 31.2•}14.0ng/ml, p<0.01). Af patients with or without VHD tended to show high levels of PF4 compared with normals (af patients without VHD: 34.1•}45.5ng/ml, af patients with VHD: 18.6•}27.2ng/ml, normals: 11.6•}8.2ng/ml). There was no correlation between ƒÀ-TG levels and age in af patients without VHD or in normals. There was also no correlation between ƒÀ-TG levels and heart rate in af patients without VHD.