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PubMed1989

Phlegmasia cerulea dolens and its association with hypercoagulable states: case reports.

Six patients who developed phlegmasia cerulea dolens are described. All patients had associated hypercoagulable states: heparin-induced thrombocytopenia (2 patients), congenital deficiency of protein C (1 patient), and antithrombin III deficiency (3 patients). Their clinical course and management are discussed. Previous reports have failed to show a definite correlation between phlegmasia cerulea dolens and hypercoagulable states because of an unavailability of appropriate diagnostic techniques. Phlegmasia cerulea dolens is a life- and limb-threatening complication. An appreciation of underlying hypercoagulable states is essential to proper management, prophylaxis, and treatment of this disorder.

Adult↗
PubMed1986

Mitral valve prolapse in women with oral contraceptive-related cerebrovascular insufficiency. Associated persistent hypercoagulable state.

We examined a group of former oral contraceptive (OC) users, who had experienced cerebrovascular insufficiency, for the presence of hypercoagulable states. We found hypercoagulability in this group in the form of decreased plasma antithrombin III activity, increased platelet coagulant activity, and elevated plasma beta-thromboglobulin level. Certain characteristics (cigarette smoking, vascular headache, hyperlipidemia, and mitral valve prolapse) were encountered with increased frequency among former OC users who had experienced cerebrovascular insufficiency. The association of mitral valve prolapse with OC-related cerebrovascular insufficiency was particularly striking. We propose that preexisting hypercoagulable states, such as may exist in a subset of individuals with mitral valve prolapse, will magnify the risk of OC-related cerebrovascular morbidity.

Adult↗
PubMed1990

Superficial thrombophlebitis. I. Primary hypercoagulable states.

This review concentrates on those disorders in which superficial thrombophlebitis can be a significant or presenting clinical sign. Primary hypercoagulable states are those conditions associated with an increased risk of thrombosis caused by a specific measurable defect in the proteins of coagulation and/or fibrinolytic systems. These disorders are frequently inherited and include deficiencies of antithrombin III, heparin cofactor 2, protein C, protein S, abnormal fibrinolytic activity, dysfibrinogenemia, and Hageman trait. Patients with a lupus anticoagulant and anticardiolipin antibody syndrome with thrombotic episodes are also considered to have a primary hypercoagulable state. The physiology, pathophysiology, clinical characteristics, and treatment of primary hypercoagulable states are reviewed.

Blood Coagulation↗
PubMed1991

Does ovarian stimulation for in-vitro fertilization induce a hypercoagulable state?

Effects on blood coagulation and fibrinolytic activity during ovarian stimulation for in-vitro fertilization (IVF) were examined in 12 women. Blood samples were taken prior to hormonal stimulation (days 2-3 of the menstrual cycle, mean serum oestradiol concentration 0.16 nmol/l) and the day after ovulation induction with human chorionic gonadotrophin (HCG) (days 10-12, mean serum oestradiol concentration 5.35 nmol/l). We measured whole blood clotting time, whole blood clot lysis time, plasma fibrinogen, factor VII and antithrombin III. The whole blood clotting time was slightly, but not significantly shortened after ovarian stimulation. A significant rise in plasma fibrinogen (P less than 0.001) and reduction in antithrombin III (P less than 0.001) were observed, whereas no change in factor VII was found. The blood fibrinolytic activity was significantly reduced as evaluated by an increase in the clot lysis time (P less than 0.02). These results indicate that ovarian stimulation for IVF may create a state of hypercoagulability.

Adult↗
PubMed1989

Hypercoagulable states and lower limb ischemia in young adults.

This study prospectively evaluates hypercoagulable states in patients under 51 years of age undergoing lower extremity revascularization for ischemia and assesses early outcome after operation. Twenty patients whose ages range from 23 to 50 years (mean 40.8 years) were identified prospectively who underwent lower extremity revascularization and evaluation of hypercoagulability. Fifteen patients were male (75%), 10 were black (50%), six had hypertension (30%), and four were diabetic (20%). All but two were cigarette smokers (90%). Seven aortoiliac procedures and 13 infrainguinal procedures were performed. Six patients had one or more abnormalities of regulatory proteins (protein S deficiency, four; protein C deficiency, three; presence of lupus-like anticoagulant, three; plasminogen deficiency, two). Eight of 17 patients in whom platelet aggregation profiles were obtained showed increased reactivity (47%). Only 4 of 17 patients (24%) were normal when tested for all parameters. Arterial or graft thrombosis developed in four of the 20 patients within 30 days after operation. Hypercoagulability was found in all four patients whose revascularizations failed. A high incidence of hypercoagulable states was found in patients under 51 years of age with lower limb ischemia requiring revascularization. Hypercoagulability may have contributed to early postoperative thrombosis of the vascular procedure.

Adult↗
PubMed1990

Hypercoagulable state after thrombolytic therapy in patients with acute myocardial infarction (AMI) treated with streptokinase.

Fibrinogen activity was studied in 70 patients with AMI who were treated with an intravenous infusion of SK (800,000 U/30 min or 1.5 mill U/60 min). Patients received a continuous infusion of heparin after thrombolytic therapy was completed. 800,000 U and 1.5 mill U SK recanalized infarct-related arteries at a rate of 78%. Early re-infarction occurred in 6% in each group. Upon admission to the hospital patients showed a hypercoagulable state that may be related to an elevated level of fibrinogen and HMW fibrinogen (70.5 +/- 2 vs 65 +/- 2% in patient and normal plasmas, respectively) that changed to a transitory hypercoagulable state indicated by decreased fibrinogen levels after SK treatment. Forty-eight hours after SK, a new fibrinogen hyperfunction, related to an increase in fibrinogen level and especially HMW synthesized fibrinogen (82 +/- 1 or 81 +/- 1%, 800,000 and 1.5 mill U SK, respectively) was observed, which was neutralized by heparin therapy (1,660 U/h with continuous infusion). The elevated levels of fibrinogen (363 +/- 21 vs 240 +/- 8 mg/dl in patient and normal plasmas, respectively) and HMW fibrinogen (70 +/- 3% with both SK hypercoagulable state that is not neutralized by the heparin dose were compared with those whose arteries recanalized. The former group had a higher concentration of fibrinogen (197 +/- 31 vs 147 +/- 18 mg/dl), HMW fibrinogen (78 +/- 0.5 vs 74 +/- 0.3%, respectively), and FPA (130 +/- 3 vs 6 +/- 4 pmol/ml) and more extensive fibrin gel formation kinetics (gelation rate 3.3 +/- 1.4 vs 1.1 +/- 0.2 OD/s x 10(-4), respectively) than the second group. The hypercoagulable state found in patients with acute myocardial infarction undergoing thrombolytic therapy may be related mainly to the progression of HMW fibrinogen and fibrinogen levels.

Adult↗
PubMed1989

Application of thrombin-antithrombin III complex for detecting a latent hypercoagulable state in patients with coronary artery disease.

It is thought that a hypercoagulable state contributes to the pathogenesis of coronary artery disease (CAD), but few sensitive markers have been available for detecting the state. In the present study the plasma level of thrombin-antithrombin III complex (TAT), a specific indicator of thrombin generation in blood, was investigated before and after a submaximal exercise test in 18 patients with CAD and in 12 healthy controls. The mean (+/- SEM) value of plasma TAT before the exercise was 3.30 (0.81) ng/ml in the patient group and 1.49 (0.08) ng/ml in controls, and its level increased to 29.22 (5.74) ng/ml and 12.07 (2.89) ng/ml after the exercise, respectively. Thus, the TAT value in the patient group was higher than that in the controls both before and after the exercise. However, no differences could be found between the groups in the following parameters; prothrombin time, activated partial thromboplastin time, antithrombin III, fibrinogen, FDP, plasminogen, alpha 2-plasmin inhibitor, and alpha 2-macroglobulin. Through these results it was concluded that plasma TAT level could be a sensitive marker for latent activation of blood coagulation, and also that the results of these experiments showed that patients with CAD were in a latent hypercoagulable state.

Adolescent↗
PubMed1996

Mechanisms, markers and management of hypercoagulable states.

Information on hypercoagulability can be achieved through the measurement of peptides that are generated when zymogens are activated, of the active enzymes, or of the complexes that form in the circulation when enzymes are inactivated by their plasmatic inhibitors. These assay methods have dramatically improved our understanding of the mechanisms which regulate coagulation in health and disease. However, their choice and use as predictors of thrombotic events and to monitor anticoagulant treatment still need to be defined in prospective clinical trials.

Biomarkers↗
PubMed1997

[Hypercoagulable state in Duchenne muscular dystrophy].

Pulmonary and cerebral infarctions have come to be noticed as life-threatening complications of Duchenne muscular dystrophy (DMD). In order to elucidate the underlying mechanism of hypercoagulable state, was studied following markers of coagulation and fiblinolysis in 69 DMD and 50 control patients showing no signs of thrombosis: prothrombin time, activated partial thrombin time, thrombotest, fibrinogen, fibrinogen degradation product, thrombin-antithrombin III complex (TAT), alpha 2-plasmin inhibitor plasmin complex (PIC), D-dimer, protein C activity, protein S, antithrombin III, XII factor, thrombomodulin and plasminogen activity. 66 out of 69 patients (96%) showed abnormal results in more than one of these studies, among which abnormally low thrombotest (78%), high TAT (61%) and high PIC (40.3%), were very frequently observed. The results were not correlated to the age, the activity of daily living and the respiratory of cardiac functions. Significantly smaller number of the control patients suffering from other neuromuscular diseases showed abnormal results, while the ambulatory DMD patients not infrequently showed hypercoagulable state. These results strongly suggest that unknown inherent factor(s) as well as inevitable immobilization and cardiac dysfunction play(s) an important role in the development of hypercoagulable state in this intractable disorder.

Adolescent↗
PubMed1990

Screening for hypercoagulable states in vascular surgical practice: a preliminary study.

The prevalence and importance of hypercoagulable states in the general vascular surgical population is unknown. Antithrombin III, protein C, protein S, plasminogen, lupus-like anticoagulant, and heparin-induced platelet activation were determined prospectively in 158 patients with aneurysmal (27), renovascular (1), cerebrovascular (28), aortoiliac (31), or infrainguinal (71) disease. Sixteen abnormal test results were obtained in 15 patients (9.5%) as follows: deficiencies of antithrombin III (2), protein C (4), and protein S (1) and presence of lupus-like anticoagulant activity (5) and heparin-induced platelet activation (4). Reconstructive surgery was performed in 137 of the study patients. Five reconstructions, all infrainguinal bypass grafts, suffered thrombosis within 30 days. Early graft thrombosis occurred in three (27%) of 14 patients with abnormal preoperative test results compared to two (1.6%) of 123 patients with normal testing (p less than 0.01). Of the three patients with abnormal test results and graft thrombosis, lupus-like anticoagulant was detected in two and heparin-induced platelet activation in one. This preliminary study supports routine preoperative screening for lupus-like anticoagulant and heparin-induced platelet activation in patients undergoing infrainguinal reconstruction. Hypercoagulable states appear to be sufficiently common and important in the general vascular surgical population to warrant further investigation.

Adult↗
PubMedDate not supplied

Hypercoagulable states: molecular genetics to clinical practice.

Several physiological antithrombotic proteins--including antithrombin, protein C, protein S, tissue factor pathway inhibitor, and components of the fibrinolytic system--act as inhibitors at strategic sites in the coagulation cascade to maintain normal blood fluidity under normal circumstances. The molecular basis of specific inherited hypercoagulable states has been recently elucidated. With the description of resistance to activated protein C, which is the commonest coagulation defect associated with thrombophilia, a specific primary hypercoagulable state can be identified in over 50% of patients with thrombophilia. Although the prevalence in the normal population of some "prothrombotic" mutations is remarkably high, most affected individuals do not have clinical thrombotic complications, so it is likely that clinically apparent hypercoagulable states result from multigene interactions, and that clinical episodes of thrombosis are precipitated by acquired prothrombotic insults in patients with an inherited predisposition to thrombosis.

Antithrombins↗
PubMed1990

Assessment of hypercoagulable states by measurement of activation fragments and peptides.

Broad spectrum assays which measure a range of fibrinogen/fibrin derivatives (FDPs) in serum have become an established means of identifying activation of blood coagulation and/or fibrinolysis, such as occurs in disseminated intravascular coagulation (DIC). There is considerable interest in the application of these assays to the diagnosis of other hypercoagulable states, such as recurrent deep venous thrombosis and myocardial infarction. In recent years, more sensitive and specific FDP assays (e.g. for fragment E, fragment E neoantigen, D-dimer, fragment D neoantigen, fibrinopeptide A and fibrin fragment beta 15-42) have been devised, some of which allow measurement in plasma of FDPs without interference from fibrinogen or certain of its derivatives. It was predicted that these assays would both avoid the possibility of artifacts introduced as a consequence of serum preparation and improve detection of hypercoagulable states. In the light of these expectations we have reviewed data published on the use of assays to detect clinical hypercoagulability, giving prominence to assays of crosslinked fibrin derivatives and nothing particularly certain studies that have compared the performance of different assays on the same samples. The accumulating evidence indicates that all of the assays are adequate for detection of DIC. The same cannot be said for other hypercoagulable states. Here much variation is evident between different studies of similar patients in the ability of a particular marker to discriminate between a normal control group and patients determined to be hypercoagulable by an independent method. This variability would seem to be a function of patient group heterogeneity and selection, as assays that detect different antigenic determinants produce results on the same plasma samples that are well correlated. It appears that the precise antigenic determinant does not critically affect detection of hypercoagulability. Additionally, some studies have indicated that use of serum need not introduce artifacts. Despite there being no other obvious advantage, the convenience of some of the plasma assays may well encourage their widespread use. Assays have also been developed for measuring activation fragments of coagulation proteins (e.g. prothrombin fragment F1 + 2 and protein C activation peptide) and for proteinase inhibitor complexes (e.g. thrombin-antithrombin complex) generated during activation of coagulation. The latter assays have been useful in providing a biochemical definition of a 'prethrombotic state'.

Blood Coagulation Disorders↗
PubMed1989

Primary hypercoagulable states in general and vascular surgery.

Primary hypercoagulable states are increasingly recognized as causes of venous and arterial thromboembolism in surgical patients. Herein, we describe 10 patients with this syndrome who were diagnosed during a recent 1-year period. A family history and past medical history of thromboembolism and an unusual site of thrombosis are emphasized for accurate diagnosis. Although antithrombin III deficiencies were the most common abnormality found, we describe three patients with hypofibrinolytic syndromes and increased levels of tissue plasminogen activator inhibitor. The effectiveness of anticoagulation therapy in preventing recurrent thromboembolism is stressed.

Adolescent↗
PubMed1994

An evaluation of 200 consecutive patients with spontaneous or recurrent thrombosis for primary hypercoagulable states.

Two hundred consecutive patients who were referred for evaluation of spontaneous or recurrent thrombosis were investigated for possible hypercoagulable states to determine the relative frequencies of these conditions in the Australian population and to identify features that would indicate which patients should be investigated with the expensive battery of tests for hypercoagulable states. Thirty-two percent were found to have prolongation of the postvenous occlusion euglobulin clot lysis time (PVO-ELT), 32% were found to have elevated levels of plasminogen activator inhibitor-1 (PAI) and 66% were found to have reduced release of tissue plasminogen activator (tPA). Antiphospholipid antibodies were found in 12%. Hereditary antithrombin III deficiency was found in 2%. Hereditary deficiency of the naturally-occurring anti-coagulant factors protein C and protein S was found in 2%. Age, sex, site of thrombosis (venous or arterial), or presence of a family history was not helpful in predicting a group more likely to have abnormal investigation results. Reduced fibrinolytic activity and the presence of antiphospholipid antibodies are the most common findings in patients with thromboembolic disease. Further prospective studies are required to assess the natural history and appropriate management of patients with these abnormalities.

Adolescent↗
PubMed1995

Clinical and laboratory evaluation of the hypercoagulable states.

In summary, every patient presenting with a new (or recurrent) thromboembolic event should be carefully assessed for potential predisposing factors. This starts with a thorough patient history and complete physical examination. If indicated, the clinical assessment is then used to guide the clinical laboratory evaluation for a potential hypercoagulable state. Identification of a specific hypercoagulable state, primary or secondary, is extremely important in the prognosis and therapeutic management of the individual patient.

Blood Coagulation Disorders↗
PubMed1993

Management and prevention of thromboembolic events in patients with cancer-related hypercoagulable states: a risky business.

OBJECTIVE: To determine the optimal strategy for managing and preventing thromboembolic events in malignancy-associated hypercoagulable states. DESIGN: A Markov-based decision and cost-effectiveness analysis was performed. The authors explicitly considered consequences of embolic and bleeding events, filter complications, and cancer-related excess mortality. Data were drawn from the current literature. The main outcome measure for each strategy was the quality-adjusted life expectancy and the total average variable costs. SUBJECTS: Patients with advanced malignancies prone to develop thromboembolic events, patients with acute proximal deep venous thrombosis (DVT), and patients who have survived a first episode of pulmonary embolism (PE). INTERVENTIONS: The authors considered three different interventions: 1) OBSERVATION, in which neither anticoagulant therapy nor filter placement is pursued, 2) ANTICOAGULATION, in which long-term anticoagulant therapy is started immediately, and 3) VENA CAVAL FILTER. MAIN RESULTS: Vena caval filter was the preferred strategy for every malignancy studied, yielding an 11% gain in quality-adjusted life expectancy, compared with observation, for patients with acute DVT, and an 18% gain for patients having survived a PE. Anticoagulant therapy yielded gains of 9% and 16%, respectively. Compared with anticoagulant therapy, filter was less costly due to the avoidance of additional expenses incurred by bleeding events. Prophylactic therapy was the least effective of the three strategies examined. CONCLUSIONS: Vena caval filter placement and long-term anticoagulation therapy yield similar outcomes in the setting of cancer-related hypercoagulable states. However, filter insertion is less expensive than anticoagulation. Given the short life expectancy and morbidity of patients with end-stage malignancy, patient preferences for health states must be considered in the decision-making process. If active treatment is pursued, vena caval filter should be used as a primary therapy. Prophylactic therapy is not warranted in any circumstance.

Aged↗
PubMed1997

Hypercoagulable state in a hypobaric, hypoxic environment causes non-bacterial thrombotic endocarditis in rats.

High-altitude hypoxia causes polycythaemia and a hypercoagulable state in humans and animals. This study examines the effects of a hypobaric, hypoxic environment (HHE) on the blood coagulation system in rats. A total of 170 male Wistar rats were housed in a chamber at the equivalent of 5500 m in altitude for 1-12 weeks. After 2 weeks of exposure to HHE, platelet counts decreased significantly; after 4 weeks, the prothrombin and activated partial thromboplastin times were significantly prolonged, compared with those of control rats. In addition, individual coagulation factors (VII, IX, X, XI, and XII) were significantly decreased at 8 weeks (P < 0.05). Levels of anti-thrombin III and alpha 2-plasmin inhibitor also decreased (between 4 and 8 weeks). After 4-12 weeks of exposure to HHE, 30 of 56 rats (54 per cent) developed (i) non-bacterial thrombotic endocarditis (NBTE) or (ii) infarction of the myocardium or kidney, or both (i) and (ii). The incidence of NBTE increased from 33 per cent (5/15 rats) at 4 weeks to 100 per cent (7/7 rats) at 12 weeks. Electron microscopy showed detached endothelial cells in the mitral valves at 1 week; platelets adhered to the subendocardial matrix and platelet aggregation with thrombus formation was seen at 2 weeks of exposure. The results suggest that exposure to HHE induces a hypercoagulable state and causes an NBTE in rats that may result in consumption coagulopathy.

Altitude Sickness↗
PubMed1994

Hypercoagulable states as an evolving risk for spontaneous venous and arterial thrombosis.

This study of 49 patients with spontaneous venous and arterial thrombosis identified 27 with hypercoagulable states: 13 had only venous thrombosis (VT), six had episodes of VT followed by arterial thrombosis (AT) and eight had AT only. All 27 patients were less than 42 years of age; 22 had specific natural anticoagulant or fibrinolytic deficiencies: antithrombin III (nine patients), protein C (eight patients), protein S (three patients), heparin cofactor II (two patients), tissue plasminogen activator release (one patient) and mixed antithrombin III and protein S (one patient). The remaining five patients had recurrent thrombotic events associated with resistance to heparin anticoagulation, but no established laboratory diagnosis. Clotting complications included recurrent VT, pulmonary embolism, multiple failed arterial procedures and lower extremity amputation. The remaining 22 patients (mean age of 53 years, range of 46 to 63 years), 12 with VT and ten with AT, did not have laboratory evidence of hypercoagulability and none had recurrent vascular occlusions. All these patients were successfully treated by conventional therapy without any additional thrombotic events during the follow-up period. Young adults with spontaneous thrombotic events should be screened for possible hypercoagulable states. Additionally, these young patients need further evaluation and treatment of cardiovascular risk factors. Those with premature atherosclerosis have an especially poor prognosis despite surgical intervention and anticoagulant therapy.

Adult↗