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PubMed2003

Hypercoagulable States in patients with patent foramen ovale.

A patent foramen ovale (PFO) is a risk factor for stroke with the presumed mechanism being paradoxical embolism. Hypercoagulable states have been associated with the propensity to develop venous thromboses and have been separately associated with the risk for ischemic stroke. A PFO could provide the missing link. Having a PFO and a hypercoagulable state may place a person at an increased risk for paradoxical embolism. However, the prevalence of PFO in patients with hypercoagulable states and vice versa is unknown, and the best therapeutic strategy for these patients is unelucidated. This review assesses the literature, provides some insight on these topics, and identifies areas for further investigation.

Blood Coagulation Disorders↗
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↗
PubMed2003

Hypercoagulable states and antithrombotic strategies in recurrent vascular access site thrombosis.

Vascular access site thrombosis is a major cause of morbidity in patients receiving hemodialysis. The role of hypercoagulable states in recurrent vascular access site thrombosis remains poorly understood. Data are limited regarding systemic anticoagulation to improve access graft patency, because of concern about hemorrhagic complications. We determined the prevalence of hypercoagulable states and clinical outcome (thrombotic and hemorrhagic) after initiation of antithrombotic therapy in a series of patients with recurrent vascular access site thrombosis. We evaluated 31 patients who had sustained 119 thrombotic events that resulted in vascular access graft failure during the year before evaluation. Sixty-eight percent of patients tested had elevated concentrations of antibody to anticardiolipin or topical bovine thrombin, and 18% of patients tested had heparin-induced antibodies. More than 90% of patients had elevated factor VIII concentration, 62% had elevated fibrinogen concentrations, and 42% had elevated C-reactive protein concentrations. Twenty-nine patients were given antithrombotic therapy: 13 with warfarin sodium, 12 with unfractionated heparin (UFH), and 11 with low molecular weight heparin (LMWH). Seven patients received more than one antithrombotic agent, sequentially. Nineteen patients have had no thrombotic events since beginning antithrombotic therapy (10 with warfarin, 3 with UFH, 6 with LMWH). Mean follow-up was 8.6 months (median, 7 months). Eight patients sustained 10 bleeding complications (5 with warfarin, 3 with UFH, and 2 with LMWH). In conclusion, hypercoagulable states are common in patients with recurrent vascular access site thrombosis. Antithrombotic therapy may increase vascular access graft patency, but is associated with significant risk for hemorrhage. Prospective studies are needed to evaluate the role and safety of antithrombotic agents in improving vascular access graft patency.

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↗
PubMed2002

Is the hypercoagulable state in atrial fibrillation mediated by vascular endothelial growth factor?

BACKGROUND AND PURPOSE: Tissue factor (TF; an initiator of coagulation) and vascular endothelial growth factor (VEGF; a marker of angiogenesis) are involved in the hypercoagulable state associated with malignancy. We investigated their roles in chronic atrial fibrillation (AF), a condition also associated with increased risk of stroke and thromboembolism, as well as a prothrombotic or hypercoagulable state. METHODS: We studied 25 patients with AF (20 men; mean+/-SD age, 62+/-13 years) who were compared with 2 control groups in sinus rhythm: 30 healthy control subjects (17 men; mean age, 60+/-9 years) and 35 patient control subjects with coronary artery disease (CAD; 27 men; mean age, 60+/-12 years). Plasma levels of TF, VEGF, and the VEGF receptor sFlt-1 were measured by enzyme-linked immunosorbent assay. RESULTS: VEGF, sFlt-1, and TF were significantly different between the 3 groups, with abnormal levels in AF and CAD patients compared with control subjects (P<0.001, P=0.022, and P=0.008, respectively). Among the AF patients, TF levels were significantly correlated with VEGF (Spearman's r=0.65, P<0.001) and sFlt (r=0.54, P=0.006) levels. Only TF and VEGF levels were significantly correlated in CAD patients (r=0.39, P=0.02). There were no significant correlations among the healthy control subjects. CONCLUSIONS: Patients with chronic AF have high TF levels, in keeping with the prothrombotic state associated with this arrhythmia. The relationships between TF and VEGF and its receptor sFlt-1 in AF suggest a possible role for VEGF in the hypercoagulable state found in AF, as seen in malignancy and atherosclerosis.

Anticoagulants↗
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↗
PubMed1998

Hypercoagulable states in patients with retinal venous occlusion.

BACKGROUND AND PURPOSE: The pathogenesis of thrombus formation in the retinal vein resulting in retinal vein occlusion is not well understood. This study was carried out to ascertain the role of hypercoagulable states in patients with retinal vein occlusion. METHODS: Fifty seven consecutive patients with acute retinal vein occlusion (mean age 48 +/- 11.5 years) were investigated for possible hypercoagulable states. Levels of antithrombin III (AT III), protein C (PC), Protein S (PS), factor XII, and fibrinogen as well as the presence of antiphospholipid antibodies (APAs) were investigated. The APAs and fibrinogen results obtained in these patients were compared to those of healthy controls. RESULTS: We detected APAs in 15 out of 57 patients compared to 3 out of 74 controls (p = 0.0002). Fibrinogen levels were significantly higher in patients compared with the controls (p < 0.001). Deficiencies in the naturally occurring anticoagulant proteins including AT III (4 out of 54 patients tested), PC (8 out of 42 patients tested), and PS (12 out of 56 patients tested) were detected. Seven patients out of 32 patients tested had reduced levels of factor XII. Subgroup analysis of the thrombophilic differences between patients who aged 45 years or less and older patients and patients with major trunk vein occlusion and patients with branch vein occlusion revealed no significant differences. CONCLUSION: Hypercoagulable states are common in patients with retinal vein occlusion and may contribute to the etiology of the disease.

Adult↗
PubMed2001

[Clinical manifestations and prevalence of hypercoagulable states in patients with venous thromboembolic disease].

BACKGROUND: Blood flow stasis, an alteration in the coagulation process or endothelium injury the most common mechanisms involved in venous thromboembolic diseases (TED) and constitute the so-called hypercoagulable states (HS). The HS have been classified into two groups: primary and secondary and several of them can be measured. Our purpose was to investigate the prevalence in Spain of measurable HS in patients with venous TED and to know the clinical picture of pulmonary embolism in these patients. PATIENTS AND METHOD: Sixty of 175 consecutive patients diagnosed with deep venous thrombosis and pulmonary embolism fulfilled criteria to study a HS. The study was performed 1 month after anticoagulant therapy was finished. RESULTS: Seventeen (28%) of the 60 patients had one HS that was a primary disorder in 14 and a secondary one in 3. The increase of PAI-1 level was the most common; recurrence of thrombotic events and familial history were frequent in these selected patients. CONCLUSIONS: The prevalence of hypercoagulable states in venous thromboembolic disease was high in this series. The clinical picture was similar to those to be expected and PAI-1 was the most frequent marker of hypercoagulable states.

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↗
PubMed1998

Hemorheological alterations and hypercoagulable state in deep vein thrombosis.

Deep vein thrombosis (DVT) seems to be related to a hypercoagulation and definite hemorheological alterations, but the importance of these alterations in the development of thrombotic events in the deep vein system has not been established. The present study examines both aspects in a group of 55 patients with DVT; the presence of a hypercoagulable state was assessed by quantifying the prothrombin fragment 1+2 (F1+2) and the thrombin-antithrombin III complex (T-AT), and the main hemorheological parameters were evaluated in the acute state and 6 and 12 months later. The results show marked hemorheological, F1+2, and TAT alterations in the acute phase. After 12 months the pattern shows a modest improvement, but erythrocyte aggregation, fibrinogen, F1+2 and T-AT remain increased with respect to the control group (8.51 +/- 1.43; 331 +/- 81 mg/dl; 1.33 +/- 0.60 nmol/l; 3.54 +/- 1.71 ng/ml vs. 8.10 +/- 1.40; 230 +/- 38; 0.94 +/- 0.40; 1.56 +/- 0.59, respectively). These data suggest that the thrombotic event could be influenced by the previous rheological situation and hypercoagulable state.

Acenocoumarol↗
PubMed2004

Blood levels of nitric oxide, C-reactive protein, and tumor necrosis factor-alpha are upregulated in patients with malignancy-associated hypercoagulable state: pathophysiologic implications.

Endogenous generation of nitric oxide (NO) plays an important role in the regulation of cardiovascular and inflammatory responses. This mediator is synthesized by a family of enzymes collectively known as NO synthase. Several isoforms of this enzyme have been identified and can be grouped as constitutive or inducible. Increased production of NO is reported in several inflammatory disorders, such as sepsis, arthritis, thrombotic thrombocytopenic purpura (TTP), and antiphospholipid syndrome. In addition, NO upregulates cyclo-oxygenase-2 and synthesis of several other inflammatory cytokines. Inflammation and thrombotic complications are usually associated with malignancy. Earlier reports indicate the upregulation of tumor necrosis factor-alpha (TNF-alpha), C-reactive protein (CRP), and tissue factor (TF) in patients with malignancy. To determine the relationship between inflammatory cytokines and NO in cancer patients with hypercoagulable states, baseline plasma samples from 160 patients with confirmed malignancy and hypercoagulable state were analyzed for NO levels. A chemical method based on a chemiluminescent reaction between NO and ozone using a highly sensitive gas phase NO analyzer was used. CRP, TF, and TNF-alpha were measured using enzyme-linked immunosorbent assay methods. Of the 160 patients who were plasma tested, the baseline NO levels ranged from 13.7 to 98.6 microM (63.1+/-15.9 microM, mean+/-SD) in contrast to age-matched control, which ranged from 9.1 to 34.6 microM (19.8+/-6.2 microM, mean+/-SD, n=138). Cancer patients also showed marked variations in the NO levels. Eighteen of 60 cancer patients exhibited greater than 60 microM NO levels. The CRP, TNF-alpha and TF were also significantly elevated. A correlation between CRP (r(2)=0.73) and NO levels was noted in cancer patients with hypercoagulable state. These data suggest that the pathogenesis associated with malignancy/hypercoagulable state is associated with an inflammatory component. In addition, the observed hemodynamic changes in some of the cancer patients may be due to increased NO production.

Biomarkers↗
PubMed1998

Does hypertension confer a hypercoagulable state?

Although the blood vessels are exposed to high pressures in hypertension, the main complications of hypertension (stroke and myocardial infarction) are paradoxically thrombotic rather than haemorrhagic. In keeping with Virchow's triad, patients with hypertension do demonstrate abnormalities of vessel wall (endothelial dysfunction or damage), blood constituents (abnormal levels of haemostatic factors, platelet activation and fibrinolysis) and blood flow (rheology and flow reserve), suggesting that hypertension does confer a prothrombotic or hypercoagulable state. These abnormalities appear to be related to target organ damage and long-term prognosis and are altered by treatment. The observation that satisfactory blood pressure reduction with non-drug intervention and with various classes of antihypertensive drugs does not lead to an equal reduction in heart attacks and strokes may be due in part to unfavourable effects on the hypercoagulable state in hypertension. Antihypertensive agents with particular benefits in reducing this hypercoagulable state would be likely to have additional advantages in reducing the occurrence of stroke and other thromboembolic events.

Antihypertensive Agents↗
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↗
PubMed1999

Determination of hypercoagulable state in acute bronchospasm.

The issue of hypercoagulability in acute asthmatic attacks is controversial. This may be due to lack of an appropriate test to monitor overall coagulation. Current hematologic tests do not account for the cellular fraction of blood that has procoagulant activity. Our study uses a clotting assay called the modified recalcification time test that is performed with whole blood to ensure the contribution of all chemical and cellular mediators in the coagulation process, particularly tissue factor. Venous blood samples were obtained from 12 adult patients with acute exacerbation of asthma or chronic obstructive pulmonary disease and compared with samples from 12 age-matched healthy control subjects. By use of the modified recalcification time, the presence of a relative hypercoagulable state was demonstrated in patients with acute bronchospasm. Furthermore, there is an identifiable difference in modified recalcification time value between the patients with acute attacks who required hospital admission versus those discharged from the emergency department.

Adult↗