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PubMed2005

Is hypertension a prothrombotic state?

Hypertension is complicated by thrombosis-related events (such as myocardial infarction and stroke), and despite the high vascular pressures, these thrombotic occlusive events paradoxically occur more often than hemorrhagic episodes. The predisposition for thrombogenesis is increased in hypertension, which leads to changes in the platelets, endothelium, and matrix metalloproteinases and their inhibitors, as well as the coagulation and fibrinolytic pathways, which help promote the induction and the maintenance of this prothrombotic or hypercoagulable state. Other cardiovascular diseases, such as atrial fibrillation, congestive heart failure, and left ventricular hypertrophy, which may occur as a result of untreated hypertension, can also activate the prothrombotic state. These changes can, to a certain degree, be reversed by the treatment of hypertension, although the effects may be inconsistent. The evidence for antithrombotic therapy is less consistent, but in "high risk" hypertensive patients, antiplatelet therapy is useful.

Antihypertensive Agents↗

PubMed1998

Relation of left atrial spontaneous echo contrast with prethrombotic state in atrial fibrillation associated with systemic hypertension, idiopathic dilated cardiomyopathy, or no identifiable cause (lone).

To investigate the association of left atrial (LA) spontaneous echo contrast with the hemostatic state in nonrheumatic atrial fibrillation (AF), we examined the plasma levels of prothrombin fragment 1+2 and fibrinopeptide A in 73 patients with chronic nonrheumatic AF undergoing transesophageal echocardiography and 38 age-matched normal subjects. The results support the theory that LA spontaneous echo contrast in nonrheumatic AF is associated with a hypercoagulable state, especially in patients with marked LA spontaneous echo contrast.

Adult↗

PubMed1999

Hairy cell leukemia with an associated lupus-type anticoagulant.

Hairy cell leukemia is a rare, lymphoproliferative disorder usually of B-cell origin. It affects men more often than women by a ratio of 4:1, with approximately 600 cases per year in the United States. Leukemias in general are known to be associated with coagulopathies; however, the case reported here represents only the fourth reported case of hairy cell leukemia with an associated lupus anticoagulant. The lupus anticoagulant is unusual in that it is not truly a coagulation-preventing entity, but rather may result in a hypercoagulable state. The nomenclature for this manifestation derives from its ability to interfere with in vitro phospholipid-dependent tests of coagulation. This report includes a review and discussion of the case presented, as well as a review of both hairy cell leukemia and the lupus anticoagulant.

Aged↗

PubMed1994

Interactions amongst insulin, lipoproteins and haemostatic function relevant to coronary heart disease.

Interest has increased considerably in the past few years in the possible interactions amongst insulin, plasma lipoproteins and several components of the haemostatic system. There is now consistent epidemiological, clinical and experimental evidence that hypertriglyceridaemia, in particular, may represent a procoagulant state involving derangements of both blood coagulation and fibrinolysis. Imbalance in the haemostatic system secondary to increased clotting activity, impaired fibrinolytic function, or a combination thereof, should influence the growth and final size of evolving thrombi and predispose to arterial occlusion. This might be of particular significance in the coronary circulation, where a hypercoagulable state is likely to promote thrombosis at the site of a suddenly ruptured atherosclerotic plaque. In addition, there is accumulating experimental evidence that the haemostatic system plays a part in plaque formation and plaque growth. Basic research on the link between haemostasis and atherosclerosis should be given high priority, because modulation of haemostatic function will probably be a potent complementary approach to the prevention of coronary heart disease.

Blood Coagulation↗

PubMedDate not supplied

Mesenteric venous thrombosis in a patient with prothrombin 20210A mutation and antithrombin III deficiency: challenges to conventional anticoagulation--a case report.

Mesenteric venous thrombosis presents as vague abdominal pain in patients with a medical or family history suggestive of a hypercoagulable state. Classic computed tomography findings will often confirm the diagnosis, and the presence of persistent abdominal pain or tenderness will determine the need for surgical intervention. Expeditious anticoagulation is the treatment of choice. This case demonstrates the CT findings for mesenteric venous thrombosis and discusses the challenges of anticoagulation in a patient with 2 hypercoagulable disorders.

Abdominal Pain↗

PubMed1999

Urinary thromboxane A2/prostacyclin balance reflects the pathological state of a diabetic.

Levels of the stable urinary metabolites of thromboxane A2 and prostacyclin, 11-dehydro-thromboxane B2 (11-dehydro-TXB2) and 2,3-dinor-6-keto-prostaglandin F1alpha (2,3-dinor-6-keto-PGF1alpha) were measured in diabetics to elucidate the relation between the thromboxane A2/prostacyclin (TX/PGI) balance and pathological states of diabetes mellitus. 11-Dehydro-TXB2 and 2,3-dinor-6-keto-PGF1alpha were derivatized to methyl ester-propylamide-dimethylisopropylsilyl ether and methyl ester-methoxime-dimethylisopropylsilyl ether derivatives, respectively, and applied to a gas chromatography/selected ion monitoring. The TX/PGI ratios of diabetics were higher than those of healthy volunteers, suggesting the hypercoagulative states of this disease. The ratios showed positive correlations with the levels of blood glucose. The levels of hemoglobin A1c and triglyceride were correlated weakly with the ratio. Some of the patients who had relatively low levels of blood glucose also showed high TX/PGI ratios. Furthermore, the ratio increased in the order of the groups 1, 2, and 3; group 1 contained patients who did not take medicine for diabetes, group 2 contained those who took oral hypoglycemic agents, and group 3 contained those who received insulin therapy. These observations indicate that the TX/PGI ratio reflects the pathological conditions of diabetes and is a useful marker, having few different features from other markers that are presently used.

6-Ketoprostaglandin F1 alpha↗

PubMed1999

Acquired protein S deficiency with multiple thrombotic complications after orthotopic liver transplant.

BACKGROUND: Orthotopic liver transplantation (OLT) is frequently complicated by thrombotic events that may threaten the viability of the allograft and severely compromise the overall outcome in these patients. Although multiple prothrombotic pathogenic mechanisms may be involved, a role for inadequate natural anticoagulant levels in the early postoperative period has been postulated. METHODS: We describe a case of a woman who suffered multiple thrombotic complications after a second OLT. Prospective assays of procoagulant and natural anticoagulant factor levels, in addition to screening tests for a variety of inherited and acquired hypercoagulable states, were carried out. RESULTS: Serial studies confirmed an acquired, isolated deficiency of Protein S associated with the second transplanted liver. Protein S levels were normal after the patient's first and third OLTs. There was no laboratory evidence of other underlying prothrombotic conditions. CONCLUSIONS: This unusual case of acquired Protein S deficiency demonstrates that the hypercoagulable phenotype may develop in the recipient of a liver from a heterozygous deficient donor. Furthermore, isolated low Protein S may be causally associated with hepatic artery thrombosis after OLT.

Adult↗

PubMedDate not supplied

Arterial thrombosis and embolism in malignancy.

In most reviews of arterial embolism or thrombosis the source of emboli or the cause of thrombosis can reasonably be established in over 90% of patients. Still about 10% remain without demonstrable cardiac or intraarterial sources. Although hypercoagulability induced by malignancy has been alluded to as a cause of unexplained intravascular thrombosis reports of arterial thromboembolism with such association are rare. Seven patients with unequivocal thromboembolism are presented. Two distinct clinical patterns are observed, one with in situ thrombosis of small arteries and the other with occlusion of large arteries causing limb ischemia or fatal organ infarction. The various pathogenetic mechanisms of arterial thrombosis or embolism in malignancy include sustained spasm of arteries, precipitation of cryoglobulins or other abnormal proteins in small arteries, direct tumor invasion of arteries, fragmentation and embolization of intracardiac or intraarterial metastases and spontaneous arterial thrombosis due to hypercoagulability. The hypercoagulable state can be recognized by the observation of shortened bleeding and clotting times, partial thromboplastin and prothrombin times, elevation of coagulation factors, platelets and yield stress index and resistance to anticoagulation. Patients presenting with arterial thromboembolic events with out demonstrable source should be investigated for malignancy. Conversely patients with malignancy should be searched for evidence of hypercoagulability in an attempt to prevent arterial thromboembolic complications.

Adenocarcinoma↗

PubMed1977

Detection of thrombin-induced fibrinogen derivatives in thrombotic states.

Affinity chromatographic studies using insolubilized fibrinogen (fibrinogen-agarose) revealed that fibrin monomer present in plasma is selectively adsorbed to fibrinogen-agarose and may be quantitatively estimated following desorption. Analysis of plasma samples from patients with myocardial infarction, cirrhosis of the liver malignant diseases and DIC confirmed the presence of considerable amounts of fibrin monomer revealing concentrations between 3 and 15 mg/100 m1 plasma as compared to normal plasma (1.96 +/- 0.37 mg/100 m1, = 27). The method is suitable for the assessment of hypercoagulable states. Standard conditions for the procedure were evaluated using 3H-labelled fibrinogen and fibrin monomer.

Blood Coagulation↗

PubMed1993

Adequate iron stores and the 'Nil nocere' principle.

There is a need to change the policy of unselective iron supplementation during periods of life with physiologically increased cell proliferation. Levels of iron stores to be regarded as adequate during infancy and pregnancy are still not well established. Recent data support the view that it is not justified to interfere with physiological adaptations developed through millions of years by sophisticated and precisely coordinated regulation of iron absorption, utilization and storage. Recent data suggest that the chelatable intracellular iron pool regulates the expression of proteins with central importance in cellular iron metabolism (TfR, ferritin, and erythroid 5-aminolevulinic synthetase) in a coordinately controlled way through an iron dependent cytosolic mRNA binding protein, the iron regulating factor (IRF). This factor is simultaneously a sensor and a regulator of iron levels. The reduction of ferritin levels during highly increased cell proliferation is a mirror of the increased density of TfRs. An abundance of data support the vigorous competition for growth-essential iron between microbial pathogens and their vertebrate hosts. The highly coordinated regulation of iron metabolism is probably crucial in achieving a balance between the blockade of readily accessible iron to invading organisms and yet providing sufficient iron for the immune system of the host. The most evident adverse clinical effects of excess iron have been observed in immunodeficient patients in tropical countries and in AIDS patients. Excess iron also increases the risk of initiation and promotion of malignant processes by iron binding to DNA and by the iron-catalysed release of free radicals. Oxygen radicals were shown to damage critical biomolecules leading, apart from cancer, to a variety of human disease states, including inflammation and atherosclerosis. They are also involved in processes of aging and thrombosis. Recent clinical trials have suggested that the use of iron-chelators, natural and synthetic antioxidants, and anti-TfR monoclonal antibodies can contribute in retarding malignant cell proliferation. Hypoferraemia during pregnancy is--like haemodilution--an adaptation to the risks involved in the natural hypercoagulable state of pregnancy. It may also serve to prevent the risk of infections and mutagenicity in the highly proliferating tissues of the foetus. Blunted erythropoiesis has been revealed during the first 30 weeks of pregnancy by the use of the newly developed method of determining the soluble serum transferrin receptor. The lack of increase in erythropoietin levels proves that there is no hypoxia. Decreases in Hb and iron levels are parts of a physiological adaptation. As a consequence they should neither be treated nor prevented. It is stressed that whenever a widespread and ingrained routine medical intervention has to be changed it is essential to first monitor the potential health effects of the recommended change in a national policy.

Adult↗

PubMed2006

A head-to-head comparison of the in vitro coagulation effects of saline-based and balanced electrolyte crystalloid and colloid intravenous fluids.

Both fluid composition (e.g., type of hydroxyethyl starch) and formulation (e.g., saline or balanced salt carrier solution) may alter whole blood coagulation. We therefore enrolled 10 healthy volunteers to test ex vivo, thrombelastograph-based blood coagulation differences of eight crystalloid and colloid solutions at 20%, 40%, and 60% dilutions. Saline and lactated Ringer's solution produced a hypercoagulable state at 20%-40% dilutions. Saline, hetastarch in saline, pentastarch in saline, tetrastarch in saline, and human albumin solutions all produced a hypocoagulable state at 60% dilution. Hetastarch in saline also produced a hypocoagulable state at 40% dilution. The larger molecular weight starches produced more intense coagulation abnormalities than the medium molecular weight compounds formulated similarly (i.e., suspended in saline or balanced salt solution). The balanced salt solutions caused fewer coagulation abnormalities, especially pentastarch in balanced salt solution. This balanced salt pentastarch preparation produced the least derangement of coagulation of the colloid solutions at all dilutions, causing hypercoagulability at the lower dilutions and minimal coagulation derangement at 60% dilution. These data support the theory that smaller molecular weight hydroxyethyl starches and colloids suspended in balanced salt solutions preserve coagulation better than large molecular weight starches and saline-based colloids, as judged by thrombelastography.

Analysis of Variance↗

PubMed1995

L-asparaginase in acute lymphoblastic leukemia treatment: the role of human antithrombin III concentrates in regulating the prothrombotic state induced by therapy.

It is well known that L-asparaginase (L-Ase) treatment may cause thrombotic events in patients with acute lymphoblastic leukemia (ALL). The mechanism of this effect is not well understood although a reduction in plasma antithrombin III (AT III) levels is observed. In our study, a group of patients treated with L-Ase received AT III concentrates as adjuvant treatment. This adjuvant treatment reduced the levels of plasma D-dimer and thrombin-antithrombin complex, which are considered as early markers of a hypercoagulability state. These preliminary data suggest that large randomized trials will have to be conducted to improve our understanding of the role of AT III concentrates in ALL therapy.

Adolescent↗

PubMed2002

Protein C, S and antithrombin III levels in patients with acute mechanical valve thrombosis.

BACKGROUND: Mechanical prosthetic heart valve thrombosis is a serious complication with an incidence of 1-6%. The reduction in active vitamin-K dependent protein C and S levels caused by warfarin treatment also results in a prothrombotic state. This study was conducted to investigate the connection between protein C (PC), protein S (PS), antithrombin III (ATIII) deficiency and prosthetic mechanical valve thrombosis. METHODS: Twenty-nine of the 283 patients who underwent valve replacement with St. Jude medical prosthesis had mechanical valve thrombosis (group 2). The rest were considered as group 1. Twelve of the 29 patients (41.4%) had isolated aortic valve replacement, 12 had isolated mitral valve replacement (41.4%) and 5 patients had double valve replacement (17.2%). Most of the patients had rheumatic valve disease at their 1st operation. The mean time of occurrence for mechanical valve occlusion was 4.1+/-1.0 years following surgery. RESULTS: The values of PC, PS and ATIII were obtained when the mechanical valves stuck or at routine follow-up. PC, PS and ATIII levels were significantly lower in the mechanical valve thrombosis group. PC levels were 75.4+/-37.6% and 49.9+/-32.2% in group 1 and 2, respectively (p=0.001). PC, PS and ATIII values were mostly lower in the 2nd group but this difference only became significant after at least 2 years of warfarin usage. CONCLUSIONS: Natural anticoagulant levels can be low during the use of warfarin. In which case the dose can be increased in order to hold the international normalized ratio (INR) at 3-3.5. However, more frequent follow-up is required and patients should be investigated for hypercoagulation states or deficiency in anticoagulant proteins. Patients referred to hospital with any mechanical valve thrombosis or recurrent thromboembolism should be evaluated for hypercoagulant proteins.

Adult↗

PubMed1982

A thrombotic tendency in patients with infective endocarditis.

An attempt was made to evaluate a thrombotic tendency in cases of infective endocarditis (IE) from the viewpoint of the changes of platelets and coagulo-fibrinolysis. Qualitative changes of platelets by thrombi formation were detected by showing activated responses of platelets to adenosine diphosphate or collagen and by showing a high level of plasma beta-thromboglobulin which is released by platelets during aggregation. A mild hypercoagulable state without acceleration of fibrinolysis was also detected by showing low levels of plasma antithrombin III which is the most potent antithrombin in the blood and normal levels of plasma alpha 2-plasmin inhibitor in the blood. From above findings, it was concluded that a thrombotic tendency in cases of IE was clearly detected by qualitative changes of platelets by thrombi formation and by mild hypercoagulability without acceleration of fibrinolysis.

Adenosine Diphosphate↗

PubMedDate not supplied

Epidural anesthesia prevents hypercoagulation in patients undergoing major orthopedic surgery.

BACKGROUND AND OBJECTIVES: Epidural anesthesia (EA) is known to reduce postoperative thromboembolic complications, but mechanisms are incompletely understood. In this study, we tested the hypothesis that local anesthetics (LA) prevent postoperative hypercoagulability without affecting physiologic aggregation and coagulation processes. METHODS: Clot signature analysis (CSA) was used to assess platelet and clotting function. Venous blood samples were collected pre- and postoperatively from 41 patients undergoing major orthopedic surgery. The effect of surgery on 3 CSA parameters (platelet-mediated hemostasis time [PHT], clotting time [CT], and collagen-induced thrombus formation [CITF]) was determined in patients receiving EA (n = 20) and those receiving general anesthesia (GA) (n = 21). RESULTS: In the GA group, orthopedic surgery induced a hypercoagulable state: PHT was reduced by 39% +/- 8.6% (P <.001), CT by 21% +/- 3.3% (P <.001), CITF by 10.3% +/- 5.9% (P =.06) compared with respective baseline values. In the EA group, by contrast, no parameter was altered significantly, but PHT showed a tendency towards prolongation by 33.2% +/- 15.4% (P =.25). CT changed by 0% +/- 4.4% (P =.89), CITF by 3.8% +/- 7% (P =.78). CONCLUSIONS: Use of EA prevents immediate postoperative hypercoagulability without affecting physiologic aggregation and coagulation processes. Also, CSA appears useful in predicting hypercoagulability and detecting platelet dysfunction. Reg Anesth Pain Med 2001;26:215-222.

Adult↗

PubMedDate not supplied

Activated protein C resistance: the most common risk factor for venous thromboembolism.

BACKGROUND: Venous thromboembolism is a major cause of morbidity and mortality. Although activated protein C resistance (APC-R) is the most commonly recognized inherited risk factor for venous thromboembolism, little is known about its long-term implications on health. METHODS: MEDLINE was searched from January 1989 through August 1999 using the key words "thromboembolism," "thrombosis," "activated protein C resistance," and "factor V Leiden." RESULTS: One in 1000 people in the United States is affected by venous thromboembolism annually. APC-R is now understood to be responsible for up to 64% of these cases. APC-R, which occurs widely in some ethnic groups and is nearly absent in others, is due to a single point mutation in the gene for clotting factor V. As a result, inactivation of factor V by activated protein C is impaired, leading to a hypercoagulable state. This condition creates a lifelong increased risk of thrombosis and, possibly, anticoagulant therapy.. CONCLUSION: Family physicians have a new tool for assessing risks for venous thromboembolism. Recognizing that up to 64% of patients with venous thromboembolism can have APC-R and treating this disorder with prophylactic and therapeutic anticoagulation might reduce patient morbidity and mortality from venous thromboembolism. Screening high-risk patients might now be indicated.

Activated Protein C Resistance↗

PubMed2005

Anti-protein S antibodies following a varicella infection: detection, characterization and influence on thrombin generation.

Postinfectious purpura fulminans is a rare disease. Varicella is one of the precipitating conditions and we recently observed such a case. The 4-year-old child was found to have a severe transient protein S deficiency. By enzyme-linked immunosorbent assay and surface plasmon resonance we first demonstrated that anti-protein S antibodies were present and also transient. Next we characterized the epitopes against which these antibodies were directed and found that they predominantly recognized the N-terminal part of protein S. Finally we showed by thrombography a transient dramatic hypercoagulable state as a result of thrombin being unregulated by the dynamic protein C inhibitory system: in vitro thrombin generation, in response to a low concentration of tissue factor, was almost insensitive to activated protein C up to 25 nmol L(-1) on day 4 while it was normally sensitive on day 42. For the first time, we demonstrated a temporal relationship between protein S deficiency, antibodies to protein S and hypercoagulability, thus supporting the pathogenic role of these antibodies.

Autoantibodies↗

PubMed2003

[Changes in blood coagulation in stress and depression--from evolution to gene regulation].

Mental stress and depression are characterized by a hypercoagulable state, which might mediate the increased coronary risk in individuals who feel stressed or depressed. Changes in blood coagulation and fibrinolysis with stress and depression are largely mediated by the sympathetic nervous system via catecholamine and adrenergic receptor activity. Stress might also affect coagulation activity via an influence on the regulation of genes coding for coagulation and fibrinolysis molecules. There is some evidence that non-selective beta-blocking agents decrease hypercoagulability elicited by acute stress. The selective serotonin reuptake inhibitors appear to normalize increased platelet activity in depression. Prospective studies need to show whether there is an association between coagulation abnormalities in stress and depression with hard cardiovascular end-points and whether such an association is favorably affected by therapeutic interventions (e.g., medication, psychotherapy, stress management).

Animals↗