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PubMed1996

Intracoronary thrombolysis in the treatment of graft closure immediately after CABG.

A patient with a hypercoagulable state underwent coronary artery bypass grafting and was recovering uneventfully until diffuse electrocardiographic changes and cardiogenic shock developed within hours of the operation. Because of severe hemodynamic compromise on high-dose inotropic drugs and intraaortic balloon pump support, she was taken to the catheterization laboratory, where the patient was discovered to have thrombotic occlusion of all grafts, including the left internal mammary artery to the left anterior descending artery. Multiple graft percutaneous transluminal coronary angioplasty and thrombolysis with urokinase successfully opened the grafts, without bleeding complication. Anastomoses were all free of significant anatomic lesion. She has remained free of cardiac symptoms for 3.5 years after operation.

Angioplasty, Balloon, Coronary↗

PubMed1995

The effect of lipid peroxidation and lipolysis on the ability of lipoproteins to influence thromboplastin activity.

High, low and very low density lipoproteins and lipoprotein (a) were prepared from porcine serum. The apolipoprotein components of the lipoproteins were then isolated and resuspended in soybean lecithin. Apolipoprotein B was also resuspended in lipids more representative of those found in LDL and VLDL. Lipid peroxidation was induced in samples of all the lipoproteins and reconstituted apolipoproteins by incubation with either Cu2+ ions or hedgehog 15-lipoxygenase. Furthermore, aliquots of the samples were incubated with a mixture of lipases. The effect of native preparations and the treated samples on the procoagulant activity of thromboplastin was examined. Native HDL, apo A-II, native LDL, reconstituted LDL and apo B inhibited thromboplastin activity, whereas native VLDL and reconstituted VLDL enhanced this activity. While the ability of HDL and apolipoprotein A-II to inhibit thromboplastin was unaltered by either Cu2+ oxidation, lipoxygenase oxidation or lipolysis, VLDL and particles resembling VLDL, which acted cooperatively with thromboplastin lost their activating potential. On the other hand, LDL and particles resembling LDL changed from being inhibitory to enhancing the thromboplastin activity following oxidation, but not after lipolysis. Apolipoprotein B fragments obtained by mild digestion of this protein, expressed an inhibitory effect towards thromboplastin, while extensive degradation of the protein reduced its inhibitory potential. It is suggested that modifications of lipoproteins in vivo can lead to a hypercoagulable state by modulation of the cofactor activity of thromboplastin to factor VII.

Animals↗

PubMed1989

Human fibrinogen heterogeneity. A study of limited fibrinogen degradation.

Different fibrinogen species were examined in normal plasma following urokinase treatment, in isolated high molecular weight fibrinogen treated with plasmin and in plasma samples from patients with acute myocardial infarction receiving thrombolytic therapy. In normal plasmas two main fibrinogen species (Mr = 340,000 and Mr = 320,000) and an intermediate fragment (Mr = 330,000) were observed. The 340,000 fibrinogen was the most sensitive to degradation; it gave rise to 330,000 and 320,000 species. Degradation of isolated 340,000 fibrinogen was similar to plasma fibrinogen degradation. After thrombolytic therapy in acute myocardial infarction patients, when the plasma fibrinogen decreased near to zero, the new synthesized fibrinogen was 340,000 form. 'In vivo' conversion of 340,000 to 320,000 fibrinogen, associated with the transitory 330,000 form, was observed. The coagulation study of plasma fibrinogen showed that when Mr 340,000 fibrinogen decreased (40%), the gelation rate decreased and lag time increased drastically. The high 340,000 fibrinogen content found in acute myocardial infarction patients gave rise to the hypercoagulable state.

Blood Coagulation↗

PubMed1992

Effect of Norplant-2 rods on haemostatic function.

A longitudinal study on one-hundred Singaporean women using Norplant-2 rod implant for contraception and their effects on the haemostatic function was carried out. There was a decrease in vitamin K-dependent Factors II, VII and a tendency towards lowered fibrinolytic activity after prolong use of Norplant-2 rods. The results indicate that the Norplant-2 rod implant system does not contribute towards hypercoagulable state but increased platelets and accelerated platelet aggregation observed will require further study to ascertain whether there is a concomitant increase in platelet activation.

Blood Coagulation Factors↗

PubMed1995

Large increase in plasmatic 11-dehydro-TxB2 levels due to oral contraceptives.

Coagulation factors, 11-dehydro-TxB2 (metabolite of TxA2) and 6-keto-PGF1 alpha (metabolite of PGI2) levels in 87 women who were treated for 9 months with oral contraceptives (OC) containing low doses of oestrogens and progestogens (Triquilar, Trinovum or Cilest) were investigated. In plasma, increases in F I, II, VII, VIII-c and 11-dehydro-TxB2 levels, but no modification of 6-keto-PGF1 alpha were observed. In urine, FPA concentration rose, but no change occurred in 11-dehydro-TxB2 and 6-keto-PGF1 alpha levels. No marked difference between the 3 OC preparations were noted. These data, and particularly the large increase of 11-dehydro-TxB2 (p < 0.01) suggest that a hypercoagulable state persists in low dosage OC users.

6-Ketoprostaglandin F1 alpha↗

PubMed1995

Crohn's disease: pathogenesis and persistent measles virus infection.

The Inflammatory Bowel Disease Study Group at the Royal Free Hospital School of Medicine has tested the hypothesis that the primary pathological abnormality in Crohn's disease is in the mesenteric blood supply. Early morphological studies involved arterial perfusion-fixation and either resin casting and scanning electron microscopy or vascular immunostaining of resected intestine affected by Crohn's disease. Granulomatous and lymphocytic damage to intramural blood vessels, even in macroscopically normal areas, was observed. We put forward possible mechanisms by which a chronic ischemic process might account for many of the idiosyncracies of Crohn's disease. It was proposed that persistent viral infection of the mesenteric microvascular endothelium might underly this vasculitic process; based on certain behavioral characteristics of measles virus, including its tropism for the submucosal endothelium of the intestine, this agent was investigated further. This report reviews the preliminary evidence from both epidemiological and basic scientific data for persistent measles virus in the intestine of patients with Crohn's disease. Possible mechanisms for virus persistence and subsequent reactivation are discussed. In conclusion, we believe that Crohn's disease may be a chronic granulomatous vasculitis in reaction to a persistent infection with measles virus within the vascular endothelium. This granulomatous inflammation, perhaps aggravated by either a hypercoagulable state or mechanical stress, results in the clinical features of Crohn's disease.

Colon↗

PubMed1988

Relationship between sex hormones and haemostatic factors in healthy middle-aged men.

Associations of plasma testosterone and estradiol with some haemostatic factors (factor VII activity, fibrinogen, antithrombin III and alpha 2-antiplasmin) were cross-sectionally examined in 251 healthy, middle-aged men participating in the Paris Prospective Study II on risk factors for ischaemic heart disease. Testosterone levels were negatively correlated to factor VII activity and alpha 2-antiplasmin, the main inhibitor of fibrinolysis. No association was found either between testosterone levels and both fibrinogen and antithrombin III, or between estradiol levels and the set of haemostatic variables. The associations between testosterone and both factor VIIc and alpha 2-antiplasmin were independent of HDL-cholesterol, LDL-cholesterol, triglycerides, smoking, alcohol, body mass index and blood pressure. These results suggest that low circulating testosterone levels might be associated with a hypercoagulability state and therefore could contribute to an increased risk of IHD.

Antigens↗

PubMed1992

The possible role of hemorheology in atherothrombogenesis.

Conventional risk factors predict only about 30-50% of incidental cases in cardiovascular diseases, which are still the leading cause of death in western societies. During the last decade, the importance of thrombosis as an essential mechanism in acute myocardial infarction (AMI) and stroke has been established. The introduction of thrombolysis has led to an impressive reduction in AMI case fatality and possibly also to a substantial amelioration of its prognosis. Evidence from experimental, clinical and epidemiological studies suggest, that several hemostatic and hemorheological factors (e.g., fibrinogen, Factor VII, plasma viscosity, hematocrit, red blood cell aggregation, total white cell count) might not only play an important role in the evolution of acute thrombotic events, but may also take part in the pathophysiology of atherosclerosis. An increasing number of studies reports altered hemostatic and hemorheological parameters to be associated with smoking, hyperlipoproteinemia, and high blood pressure, as well as with adverse dietary habits and other life-style factors. To date, their way of interaction with the atherosclerotic process is poorly understood. Hemorheological or hemostatic mechanisms that might promote thromboatherogenesis include the predisposition to thrombosis via a hypercoagulable state, the enhancement of atherosclerosis by fibrinogen and its metabolites, and finally the reduction of blood flow through various rheological effects (e.g., increase in plasma viscosity and red cell aggregation, or leukocyte activation). Future research should focus in more detail on the interrelationship between accepted risk factors and the hemostatic system as well as hemorheological parameters. Deeper insight into the mechanisms involved might lead to new preventive strategies as well as to therapeutic procedures in the management of atherosclerosis and associated thrombotic events.

Arteriosclerosis↗

PubMed1994

Intestinal necrosis from congenital hypercoagulopathy.

Protein-S deficiency is a rare congenital disorder that results in a hypercoagulable state, typically presenting as recurrent venous thrombosis in adults. Few cases have been reported in children. A 2-year-old girl presented in septic shock. During laparotomy, ischemic necrosis of the intestine was noted, which extended from the gastroesophageal junction to the midjejunum. Total gastrectomy, pancreaticoduodenectomy , and partial resection of the small intestine were performed. She was left with 140 cm of distal small bowel, and had reconstruction with a single limb for the pancreaticojejunostomy, choledochojejunostomy, and esophagojejunostomy to preserve intestinal length. Postoperative evaluation eventually disclosed a previously unrecognized protein-S deficiency. The hypercoagulopathy of protein-S deficiency can be complicated by catastrophic thrombotic events that require surgery. This congenital disorder should be considered in any child who has an unexplained thrombotic episode, because failure to recognize protein-S deficiency may have potentially fatal consequences.

Child, Preschool↗

PubMed1987

An assessment of monocyte procoagulant activity in patients with solid tumors.

Generation of thromboplastin by monocytes has been shown to play a vital role in hypercoagulable states seen in malignancy. The purpose of this study was to compare the procoagulant activity in cancer patients and controls. Recalcification times (RT) of whole blood from 19 normal volunteers, 8 patients with benign polyps, 12 patients previously treated by surgery for head and neck (H&N) or colon cancer, and 13 untreated patients with various stages of H&N or colon cancer were determined. Tests were performed with and without stimulation with Escherichia coli endotoxin. The mean RT in saline (RTS) of untreated patients with early cancer (4.58 +/- 0.83 min) and that of patients with advanced cancer (5.23 +/- 1.16 min) were lower than that of controls (6.55 +/- 0.82 min), P less than 0.01 and P less than 0.05, respectively. The RTS of patients previously treated and of those with benign polyps were no different from those of controls. Activation with endotoxin significantly lowered the recalcification times (RTE) in the early (3.90 +/- 0.58 min) and advanced cancer patients (4.23 +/- 0.66 min) compared to the RTE of controls (5.69 +/- 0.75 min, P less than 0.01 for both groups) as well as compared to those with benign tumors, P less than 0.05. The mean RTE of previously treated patients (4.72 +/- 0.58 min) was also lower than that of controls, P less than 0.05. Our results suggest that RT is significantly reduced in cancer patients compared to that of controls. Furthermore, monocyte activation with endotoxin may enable us to distinguish cancer patients from controls as well as from those with benign tumors.

Adenoma↗

PubMed1996

Hematologic disorders associated with ischemic stroke.

Hematological disorders underlie a small proportion of all ischemic strokes. The association of these coagulation abnormalities with ischemic stroke is not always clear. The etiology of stroke still remains uncertain in a large number of cases and proper screening for coagulation abnormalities and the discovery of new coagulation disorders will probably increase the rate of strokes attributable to these causes. Since large case-control studies with unselected and consecutive stroke patients from different ethnic origins have not yet been performed to determine the role of coagulation abnormalities in ischemic stroke, our knowledge is dependent on case reports and small series of mostly younger patients. Extensive hematologic evaluation of unselected stroke patients will likely yield little useful information and be too expensive. Every stroke patients needs a careful evaluation, and in selected cases, this should include coagulation parameters. Patients with unexplained strokes after a careful evaluation, previous thrombotic episodes, or a positive family history for thrombosis, are good candidates for further coagulation studies. As long as the hypercoagulable state persists, both arterial and venous thromboembolic recurrences can be expected. Many of these patients may benefit from anticoagulants. In patients with hereditary coagulation disorders, studies should be extended to close relatives. Since some coagulation tests are fairly expensive, provide only equivocal data, and are not widely available, we advise a step-by-step approach starting with the patient and family history.

Anemia, Sickle Cell↗

PubMed1989

Fibrinopeptide A levels in maternal and newborn plasma.

Plasma fibrinopeptide A (FPA), a dynamic measure of intravascular coagulation, was determined in 70 healthy Chinese women during normal pregnancy, labour, delivery and the early puerperium and compared to a group of healthy non-pregnant adult controls. In the normal controls the plasma FPA level (mean +/- SD) was 1.43 +/- 0.46 ng/ml. During pregnancy and labour, the FPA levels were 3.05 +/- 0.98 ng/ml and 11.47 +/- 4.43 ng/ml, respectively, and it reached a peak of 32.95 +/- 11.66 ng/ml at parturition, then falling to 6.15 +/- 2.52 ng/ml in the early puerperium. All these levels were significantly higher (p less than 0.001) compared to controls. Fifteen of the 21 mothers with blood sampling during parturition also had umbilical cord blood taken for determination of FPA level. There was no significant difference between the maternal (34.07 +/- 10.12 ng/ml) and cord (31.06 +/- 12.67 ng/ml) plasma FPA levels. It is concluded that the hypercoagulable state in women during pregnancy and the puerperium is associated with increased intravascular coagulation activity, and that increased intravascular coagulation activity also occurs in the fetus during parturition. This observation may account for the increased risk of thrombotic disorders observed in pregnant and parturient women as well as in the newborn.

Female↗

PubMed1992

The influence of labor on thrombotic and fibrinolytic systems.

Plasma fibrinopeptide A, thrombin-antithrombin III complexes, tissue-plasminogen activator and alpha 2-plasmin inhibitor-plasmin complexes were measured early in the first stage of labor, in the second stage of labor and at 15 min after placental separation. Fibrinopeptide A and thrombin-antithrombin III complex levels did not change from the first to the second stage of labor but increased significantly after placental separation. There was a significant increase of the tissue-plasminogen activator level between the early first stage of labor and the second stage of labor, and it remained high after placental separation. A significant increase in the level of plasma alpha 2-plasmin inhibitor-plasmin complexes was observed after placental separation. These findings suggest that activation of the thrombotic system occurs at the time of placental separation and that activation of the fibrinolytic system begins during labor before placental separation to compensate for the hypercoagulable state which develops at the time of delivery.

Adult↗

PubMed1991

An evaluation of procoagulant activity in the peripheral blood of rats treated with monocrotaline pyrrole.

Monocrotaline pyrrole (MCTP), a putative toxic metabolite of the naturally occurring pyrrolizidine alkaloid, monocrotaline, causes pulmonary vascular thrombi that are associated with vascular remodeling, pulmonary hypertension, and right cardioventricular hypertrophy in rats. The thrombi are composed of platelets and fibrin and occur in the absence of vascular necrosis. Since thrombosis may result from excessive procoagulant activity in the systemic circulation, we evaluated the hemostatic system of rats treated with MCTP to determine if a hypercoagulable state developed in the peripheral blood. Male Sprague-Dawley rats received a single, bolus injection of MCTP (3.5 mg/kg) or an equal volume of the N,N-dimethylformamide (DMF) vehicle in the tail vein. Rats were killed at 1, 3, 5, 8, 11, or 14 days after toxin administration, and several markers of lung injury and hemostasis were evaluated. The protein concentration of cell-free bronchoalveolar lavage fluid (BALF) from MCTP-treated rats was slightly elevated at 1 and 3 days. At 5 days the elevation had become more pronounced, and values increased markedly thereafter. The wet lung-to-body-weight ratio and lactate dehydrogenase activity of cell-free BALF from rats treated with MCTP were mildly increased at 3 days. Increases in these markers progressed at 5 days and values reached a plateau thereafter. MCTP-treated rats had moderately increased total nucleated cell counts in BALF at 5 days, and counts increased markedly thereafter. Right cardioventricular hypertrophy was first detected at 8 days in MCTP-treated rats and became more pronounced with time. The prothrombin time and modified prothrombin time of MCTP-treated rats were consistently greater than those of controls. Although statistically different, these values never exceeded the range of normal values. The activated partial thromboplastin time of MCTP and control rats was variable. Only at Day 14 did MCTP-treated rats have significantly longer activated partial thromboplastin times than those of controls, and these values were within the normal range. Rats treated with MCTP had statistically significant elevations in antithrombin 3 activity at Day 8 and of fibrinogen concentration and antithrombin 3 activity at Day 11 that exceeded the normal range. Platelet numbers of both MCTP- and DMF-treated rats were greater than normal on Day 1 but quickly returned to baseline. The plasminogen values of rats treated with MCTP were lower than controls on Day 5 only. These results suggest that the pulmonary vascular thrombi induced by administration of MCTP to rats are not mediated by an excess in procoagulant activity in the peripheral blood.

Animals↗

PubMed1983

The clotting time of whole blood in plastic tubes: the influence of exercise, prostacyclin and acetylsalicylic acid.

An assay for detection of a hypercoagulable state was accomplished by measuring the clotting time of whole blood (without anticoagulant present) in plastic tubes. This assay appeared to be quite sensitive to the activation state of platelets. Thus, acetylsalicylic acid (ASA) or prostacyclin (PGI2) was found to prolong significantly the whole blood clotting time (WBCT), specially under conditions where the platelet might be hyperactive. When the WBCT was carried out before and after exercise, a mean value of 12.95 min was obtained before as compared to 7.48 min after exercise. In the presence of PGI2, the WBCT after exercise was prolonged to 13.91 min. The shorter clotting time after exercise, in the absence of inhibitor, might be explained by the observation in the present study that platelet factor 3 became more readily available upon consecutive stimuli. These results suggest that platelet release may be important for the initiation of prothrombin activation in situations without already available platelet factor 3 activity.

Adult↗

PubMed1984

Involvement of hemostasis during an autoimmune glomerulonephritis induced by mercuric chloride in brown Norway rats.

Mercuric chloride (HgCl2) induces in Brown Norway (BN) rats an autoimmune disease characterized by a biphasic glomerulonephritis (GN). A transient nephrotic syndrome occurs during the third and fourth weeks after the first HgCl2 injection. Related to nephrotic syndrome, an hypercoagulable state develops with decreased factor XII and anti-thrombin III (AT III) levels and increased factor V activity and fibrinogen concentration. Moreover, during the same period, most of the rats were found thrombocytopenic. The presence of soluble fibrin monomer complexes and of fibrin degradation products (FDP) in the plasma of these rats associated with fibrin thrombi in glomerular capillary lumen proved the occurrence of disseminated intravascular coagulation (DIC). DIC was responsible for the death of several rats but most of these survived and clotting abnormalities were no longer found. Numerous factors can explain the occurrence of DIC in this model: anti glomerular basement membrane antibodies, circulating immune complexes, complement activation and/or glomerular endothelial cell detachment. The HgCl2 induced autoimmune disease appears as a good experimental model to study the relation between coagulation process and glomerulonephritis.

Animals↗

PubMed1989

Acute phase reaction, fibrinogen level and thrombus size.

The influence of an acute phase reaction on the size, weight, and fibrin content of experimental venous thrombi was examined in 10 pairs of rabbits. Jugular vein thrombosis was provoked by venous stasis plus mechanical injury 36 hours after one member of each pair received 0.5 ml/kg sterile turpentine in olive oil by subcutaneous injection. Fibrinogen level, factor VIII activity, and antithrombin III activity were significantly higher at the time of thrombus formation in turpentine treated rabbits, as were thrombus size (assessed by visual scoring), dry weight of thrombi, and their fibrin content (derived by measuring 125I-fibrinogen incorporation). In addition, the fibrinogen concentration correlated significantly with size, weight, and fibrin content of thrombi when results from turpentine treated and control animals were pooled, suggesting that plasma fibrinogen concentration at the time of thrombus formation may strongly influence the extent of thrombosis. This effect could help explain observations of a "hypercoagulable state" after injury.

Acute-Phase Reaction↗

PubMed1989

A new index for collagen induced platelet aggregation.

In this paper, we propose a new index of platelet aggregation for optical aggregometry, the "R" value. This represents the rate of change in the half time for platelet aggregation (T1/2) induced by collagen with changes in the platelet concentration and expresses the degree of platelet sensitivity to collagen. The "R" value has been shown to reflect the aggregability of platelets due to activation of the contact factors. The "R" values were significantly different in the acute and chronic phases of occlusive arterial disease, while ordinary platelet aggregation parameters did not change. A decrease in the "R" value appears to indicate a platelet hyperfunction and hypercoagulable state, in other words a prethrombotic state.

Adenosine Diphosphate↗