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PubMed2001

Low adjusted-dose acenocoumarol therapy in sickle cell disease: a pilot study.

Vasoocclusion is a continuous process in sickle cell disease (SCD) and accumulates to significant end organ damage, mostly irrespective of the occurrence of manifest acute vasoocclusive events. As there are indications that reversing the hypercoagulable state may be of clinical benefit in sickle cell patients, we performed a randomized, double blind, placebo-controlled, cross-over pilot study to assess the efficacy and safety of low-adjusted dose acenocoumarol therapy (International Normalized Ratio: 1.6-2.0) in SCD. Treatment consisted of either acenocoumarol or placebo for 14 weeks, after which treatment was discontinued for a period of five weeks. Then, patients initially on acenocoumarol received placebo (and vice versa) for 14 weeks. Therapy efficacy was assessed by comparing the frequency of vasoocclusive complications, the occurrence of bleeding, and clotting activation between acenocoumarol and placebo treatment of each individual patient. Twenty-two patients (14 homozygous [HbSS] and 8 double heterozygous sickle-C [HbSC]; aged 20-59 years) completed the entire study. Acenocoumarol treatment did not result in a significant reduction of acute vasoocclusive events (three painful crises during acenocoumarol, five painful crises during placebo). There was a marked reduction of the hypercoagulable state (depicted by a decrease in plasma levels of prothrombin F1.2 fragments [P = 0.002], thrombin-antithrombin complexes [P = 0.003], and D-dimer fragments [P = 0.001]) without the occurrence of major bleeding. Even though no clinical benefit (pertaining to the frequency of painful crises) was detected in this pilot study, the value of low adjusted-dose acenocoumarol for preventing specific events (such as strokes) and as a long-term treatment of sickle cell patients should be subject of further study.

Acenocoumarol↗
PubMed2005

Sinus vein thrombosis following exposure to simulated high altitude.

A relation exists between high altitude exposure and a hypercoagulable state, the nature of which is not entirely clear. This has been mostly reported in mountain climbers. We report a 19-yr-old female, working as a high-altitude chamber instructor, who presented with severe frontal headaches which persisted for a month following routine high altitude chamber training. The patient was in generally good health and was using oral contraceptives for 3 yr prior to the event. Due to the unremitting nature of the symptoms, the patient was admitted to a neurology department, and computerized tomography (CT) and magnetic resonance imaging (MRI) were performed. Sagittal and transverse sinus vein thrombosis were diagnosed and anticoagulant therapy was initiated (low molecular weight heparin followed by warfarin). Following treatment, a slow symptomatic improvement was observed, and the patient was discharged. On discharge, it was recommended she continue oral anticoagulant therapy (warfarin). A complete coagulation screening panel was performed, which was negative. Although the relation between high altitude exposure and a hypercoagulable state is well known, this is the first time a case of sinus vein thrombosis has been reported after high altitude chamber training. Careful history and closely monitored medical follow-up should be performed on all designated staff exposed to simulated altitude. Even though there is no conclusive evidence regarding it, we suggest, as a matter of caution, that women using oral contraceptives should consider their risks before deciding to undertake exposure to simulated altitude in chambers. Literature review and detailed recommendations for prevention are provided.

Adult↗
PubMed2003

Hemostatic alterations in patients with obstructive sleep apnea and the implications for cardiovascular disease.

STUDY OBJECTIVES: Patients with obstructive sleep apnea (OSA) are at increased risk for coronary artery and cerebrovascular diseases. Numerous studies suggest that a hypercoagulable state is prospectively related to atherothrombotic events. This review explores whether changes in hemostasis may constitute one biological link between OSA and vascular disease. DESIGN: Ten studies on hemostatic variables in OSA were located by electronic library search and descriptively reviewed. Work on hemostatic function with physiologic conditions similar to those found in OSA (hypoxemia and hyperactivity of the sympathetic nervous system) was considered to discuss potential molecular mechanisms of procoagulant disturbances in OSA. MEASUREMENTS AND RESULTS: The reviewed data suggest that, as compared to non-OSA control subjects, patients with OSA have elevated plasma fibrinogen levels, exaggerated platelet activity, and reduced fibrinolytic capacity. Although not consistently shown, severity of OSA (ie, apnea-hypopnea index) and plasma epinephrine were independent predictors of platelet activity, and average minimal oxygen saturation was an independent predictor of fibrinogen. In some studies, treatment with continuous positive airway pressure decreased platelet activity, plasma fibrinogen levels, and activity of clotting factor VII. CONCLUSIONS: There is some evidence for a hypercoagulable state in OSA, which might help explain the increased prevalence of vascular diseases in this population. To further confirm such a notion, future studies need to be performed on sufficiently large samples to be able to control for confounders of hemostatic activity. Prospective studies are needed to examine the association between hemostasis molecules and strong vascular end points.

Blood Platelets↗
PubMed2006

Dural sinus thrombosis in melioidosis: the first case report.

Melioidosis which is infection with Burkholderia pseudomallei, is an important cause of sepsis in India, southeast Asia and northern Australia. Mortality is high and treatment is problematic. Neurological melioidosis is unusual but meningoencephalitis, encephalomyelitis and brain microabscess can occur Dural sinus thrombosis is not an uncommon cerebrovascular disorder with various etiologies. Hypercoagulable state, pregnancy, dehydration, certain blood dyscrasia and contraceptive pills are common causes however meningitis and local head & neck infections may lead to this condition. Dural sinus thrombosis complicating septicemic melioidosis has never been reported. The authors report a 42-year-old Thai man suffering from septicemic melioidosis with dural sinus thrombosis. He had high fever, headache, left hemiparesis, focal seizure and increased intracranial pressure. Diabetes and mild alcoholic cirrhosis were diagnosed in this admission. CT scan, MRI brain and MRV revealed superior saggital sinus thrombosis with complicating venous infarction over right posterior parietal lobe. Hemoculture demonstrated Burkholderia pseudomallei and CSF was acellular Investigations for causes of dural sinus thrombosis were all negative. This patient gradually improved after treatment with ceftazidime, antiepileptic drug and heparin without clinical recurrence. Neuromelioidosis is a rare syndrome that may present as brain abscess, encephalitis or meningoencephalitis. The authors report dural sinus thrombosis associated with septicemic melioidosis. The authors' hypothesis of venous thrombosis in the presented case is sepsis induced hypercoagulable state. Physicians should be aware of cerebral venous thrombosis in case of suspicious melioidosis with neurological involvement. Prompt treatment with intravenous heparin and antibiotic is potentially effective.

Adult↗
PubMed1998

Activated protein C resistance in pediatric inflammatory bowel disease.

BACKGROUND: There is evidence for a hypercoagulable state in inflammatory bowel disease (IBD), and small vessel thrombosis has been identified in the bowel of patients with Crohn's disease, suggesting thrombosis as a possible etiologic factor. Activated protein C (APC) resistance is the most common inherited disorder leading to thrombosis and accounts for 30% to 40% of episodes of idiopathic venous thrombosis. METHODS: The prevalence of APC resistance was studied in 23 patients with IBD (17 with Crohn's disease, 6 with ulcerative colitis) and in 11 control subjects with recurrent abdominal pain or celiac disease, using an APC resistance screening method. RESULTS: One patient with Crohn's disease had a positive screen result, two patients (one with Crohn's, one with ulcerative colitis) had borderline results, and results in all of the control subjects were normal. One patient with Crohn's disease had a history of a thromboembolic event but had a normal screen result. CONCLUSIONS: Activated protein C resistance does not seem to play a major role in the etiology of the hypercoagulable state in inflammatory bowel disease.

Adolescent↗
PubMed2005

Thromboelastographic and hemostatic characteristics in pediatric patients with sickle cell disease.

CONTEXT: Patients with sickle cell disease suffer from a variety of vaso-occlusive events that may be related to activation of the hemostatic system. Thromboelastography assesses the functionality of this system from a global standpoint and has demonstrated some utility in detecting hypercoagulable states in varied clinical settings, but it has not been systematically evaluated in patients with sickle cell disease. OBJECTIVE: To characterize the findings of thromboelastography in patients with sickle cell disease during periods of steady state and illness, to compare these results with those of healthy controls, and to correlate these profiles with other measured hemostatic parameters. DESIGN: In this cross-sectional study, we obtained thromboelastographic and other hemostatic data on specimens from 46 patients with sickle cell disease (35 with hemoglobin SS, 7 with hemoglobin SC, and 4 with hemoglobin S-beta thalassemia) and 20 healthy race-matched controls. Data were obtained from patients with sickle cell disease at baseline conditions (n = 41) and in the setting of acute illness (n = 5). RESULTS: Patients with hemoglobin SS had lower reaction time and higher angle, maximum amplitude, and coagulation index values on thromboelastography than the control group. Hemoglobin SC patients had higher angle, maximum amplitude, and coagulation index values than controls. Hemoglobin S-beta thalassemia patients showed no significant differences compared with controls. Five hemoglobin SS patients with recent or current illness demonstrated increased maximum amplitude and coagulation index compared with hemoglobin SS patients at baseline conditions. CONCLUSIONS: Patients with sickle cell disease demonstrated a significant hypercoagulable state in thromboelastography profiles, with the degree of abnormality dependent on the type of sickle cell disease and perhaps the presence of acute illness. Continued follow-up of this patient cohort, as well as further study of larger and more homogeneous patient groups, is required to adequately assess the utility of thromboelastography in predicting complications of sickle cell disease.

Adolescent↗
PubMed1992

Immunohistochemical identification of tissue factor in solid tumors.

Patients with cancer experience a much higher than expected incidence of thromboembolic disorders, commonly referred as Trousseau syndrome. Although this association has been well documented, the etiology of the hypercoagulable state is not known. The expression on tumor cells of tissue factor (TF), a membrane-bound lipoprotein that functions as a cofactor to factor VIIa in the initiation of the extrinsic pathway of blood coagulation, has been postulated as a possible mechanism. Whereas the distribution of TF in normal tissues is known, no large survey of TF expression in malignant tissues has been reported. In this study a polyclonal, monospecific rabbit anti-human TF IgG was used for immunohistochemical localization of TF antigen in 85 different tumor specimens. In general, cell types which normally express TF continued to do so after malignant transformation (41 of 60 epithelial tumor specimens were positive for TF). Tumors of nonepithelial origin frequently lacked TF, with only 3 of 19 specimens containing evidence of TF antigen. In addition five of six benign tumors did not express TF. Many tumor types commonly associated with Trousseau syndrome, for example lung, pancreatic, breast, colon and gastric carcinomas, stained positively for TF. Based on this survey, it appears that TF expression by tumors may be an important factor in the pathogenesis of a hypercoagulable state in some patients with cancer.

Antigens, Neoplasm↗
PubMed1997

Activation of the hemostatic mechanism after pharmacological cardioversion of acute nonvalvular atrial fibrillation.

BACKGROUND: Given that the restoration of sinus rhythm after chronic atrial fibrillation is associated with embolic events, anticoagulation is prescribed before and after pharmacological and electrical cardioversion. However, the need for anticoagulation in patients with acute atrial fibrillation (lasting <48 hours) who undergo cardioversion is less clear. In addition, it is not known whether cardioversion to sinus rhythm determines a hypercoagulable state in these patients. METHODS AND RESULTS: In 21 patients with acute nonvalvular atrial fibrillation, plasma median concentrations of thrombin-antithrombin complex, a marker of thrombin generation, significantly increased from 2.8 ng/mL (interquartile range, 2.1 to 4.0 ng/mL) on hospital admission to 3.5 ng/mL (interquartile range, 2.9 to 6.0 ng/mL) after cardioversion to sinus rhythm obtained by means of infusion of antiarrhythmic drugs and decreased to 2.5 ng/mL (interquartile range, 2.0 to 3.5 ng/mL) at the 1-month follow-up visit (P=.04). Similarly, the levels of fibrinopeptide A, a marker of thrombin activity, increased from 1.1 nmol/L (interquartile range, 0.7 to 1.5 nmol/L) at baseline to 1.8 nmol/L (interquartile range, 1.1 to 3.0 nmol/L) after cardioversion and returned to 0.8 nmol/L (interquartile range, 0.6 to 1.1 nmol/L) at the 1-month follow-up visit (P=.02). CONCLUSIONS: A significant increase in plasma levels of the markers of thrombin generation and activity was observed in patients with acute atrial fibrillation early after pharmacological cardioversion to sinus rhythm. This is the first biochemical evidence that cardioversion of recent-onset atrial fibrillation determines a hypercoagulable state.

Acute Disease↗
PubMed2003

Ethnic differences in markers of thrombophilia: implications for the investigation of ischemic stroke in multiethnic populations: the South London Ethnicity and Stroke Study.

BACKGROUND AND PURPOSE: The role of hypercoagulable states in the pathogenesis of ischemic stroke in black subjects is not known, and data on normal reference ranges in black populations are lacking. This study estimated ethnic-specific reference ranges in a community population to determine the prevalence of thrombophilic states in a multiethnic stroke population. METHODS: Free protein S, protein C, antithrombin III, activated protein C resistance, IgG anticardiolipin antibodies, and lupus anticoagulant were determined in 130 consecutive ischemic stroke cases < or =65 years of age (50 black Caribbeans, 30 black Africans, 50 whites) and 130 community controls. RESULTS: Black African controls had significantly lower protein S (P<0.001) and protein C (P=0.049) and a trend toward lower antithrombin III (P=0.056) levels compared with white controls. Black Caribbean and African controls had higher diluted Russell's viper venom time ratios compared with whites (P=0.001, P<0.001). Using ethnic-specific reference ranges, 8 controls (6.3%) and 11 cases (8.5%) had thrombophilia abnormalities (odds ratio [OR], 1.39; 95% confidence interval [CI], 0.54 to 3.57; P=0.50). ORs were 0.96 (95% CI, 0.18 to 4.99; P=0.96) for whites, 1.57 (95% CI, 0.41 to 5.94; P=0.51) for black Caribbeans, and 2.07 (95% CI, 0.18 to 24.2; P=0.95) for black Africans. CONCLUSIONS: Failure to account for ethnic differences in the normal reference ranges for thrombophilia markers may lead to inappropriate diagnosis and investigation of hypercoagulable states in black individuals. Protein S and protein C deficiencies and lupus anticoagulant may contribute to stroke risk in a minority of black cases, but they are unlikely to be major contributors to the excess stroke risk seen in young individuals of African and African-Caribbean descent.

Africa↗
PubMed2005

Thromboelastography maximum amplitude predicts postoperative thrombotic complications including myocardial infarction.

Postoperative thrombotic complications increase hospital length of stay and health care costs. Given the potential for thrombotic complications to result from hypercoagulable states, we sought to determine whether postoperative blood analysis using thromboelastography could predict the occurrence of thrombotic complications, including myocardial infarction (MI). We prospectively enrolled 240 patients undergoing a wide variety of surgical procedures. A cardiac risk score was assigned to each patient using the established revised Goldman risk index. Thromboelastography was performed immediately after surgery and maximum amplitude (MA), representing clot strength, was determined. Postoperative thrombotic complications requiring confirmation by a diagnostic test were assessed by a blinded observer. Ten patients (4.2%) suffered a total of 12 postoperative thrombotic complications. The incidence of thrombotic complications with increased MA (8 of 95 = 8.4%) was significantly (P = 0.0157) more frequent than that of patients with MA < or =68 (2 of 145 = 1.4%). Furthermore, the percentage suffering postoperative MI in the increased MA group (6 of 95 = 6.3%) was significantly larger than that in the MA < or =68 group (0 of 145 = 0%) (P = 0.0035). In a multivariate analysis, increased MA (P = 0.013; odds ratio, 1.16; 95% confidence interval, 1.03-1.20) and Goldman risk score (P = 0.046; odds ratio, 2.39; 95% confidence interval, 1.02-5.61) both independently predicted postoperative MI. A postoperative hypercoagulable state as determined by thromboelastography is associated with postoperative thrombotic complications, including MI, in a diverse group of surgical patients.

Adult↗
PubMed2006

Is chronic fatigue syndrome associated with platelet activation?

Chronic fatigue syndrome (CFS) is a debilitating condition that has no known aetiology or pathophysiology. Recent investigations by other workers have suggested that individuals with CFS may have a hypercoagulable state. This study investigated various aspects of platelet activation and function in 17 patients with CFS and in 16 age-matched and sex-matched healthy controls. Platelet aggregation, platelet volume and coagulation tests were performed. Platelet aggregation was investigated by means of the photometric changes using citrated platelet-rich plasma, whole blood aggregation was calculated as the percentage fall in single platelet counts and the coagulation tests were performed on an automatic microcentrifugal analyser.A trend was observed for the patients to have lower aggregation results and a reduced mean platelet volume. However, this only reached statistical significance for one result; the rate of the aggregation slope by 1.0 microg/ml collagen [CFS patients, 18 (9-28) versus controls, 32.5 (19-36); Mann-Whitney U test, P = 0.029]. No significant differences were found for any of the measurements of coagulation. These results are in contrast to previously reported findings. However, due to the heterogeneous nature of the disease, and the resulting lifestyles of the patients, caution should be taken when comparing one group of patients with another. Nevertheless, we certainly found no evidence of increased platelet activation or of a hypercoagulable state in patients with CFS and, on the basis of these results, anti-platelet or anti-coagulant therapy is not warranted.

Adult↗
PubMed2000

Simvastatin attenuates vascular hypercoagulability in cardiac transplant recipients.

BACKGROUND: 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors have been shown to reduce cardiac allograft failure and to lower the incidence of transplant coronary artery disease. These effects result from as yet unknown mechanisms not clearly attributable to lipid lowering. We here report that low-dose simvastatin treatment inhibits excessive expression of monocyte tissue factor (TF) and reduces the persistent hypercoagulability state seen in cardiac transplant recipients. METHODS: Fifteen consecutive heart transplant recipients receiving standard oral immunosuppression were newly assigned to a 10 mg daily simvastatin therapy. Levels of TF activity in both unstimulated and lipopolysaccharide-stimulated peripheral blood mononuclear cells drawn from transplant recipients before and under simvastatin therapy were evaluated by one-stage clotting assay. RESULTS: Monocyte TF activity was found to be significantly increased in cardiac transplant recipients when compared with healthy controls. Excessive monocyte procoagulant activity was reduced in cardiac transplant recipients during simvastatin treatment. This effect occurred independently of the reduction of serum low-density lipoprotein cholesterol. As demonstrated by reverse transcriptase-polymerase chain reaction, monocyte TF reduction by simvastatin, observed in 13 of the 15 transplant recipients investigated, could be ascribed to an inhibition of monocyte TF gene transcription. The reduction of monocyte TF activity during treatment with simvastatin paralleled with the normalization of elevated levels of thrombin-antithrombin complex, prothrombin fragment F1+2, and D-dimer, which are markers of thrombin and fibrin formation indicating coagulation activation after cardiac transplantation. CONCLUSION: Inhibition of monocyte TF expression and attenuation of the persistent hypercoagulable state observed in cardiac transplant recipients during treatment with simvastatin may represent an important mechanism by which HMG-CoA reductase inhibitors protect against the development of transplant coronary artery disease.

Adult↗
PubMed2000

[Pathogenesis of pulmonary thrombosis in Duchenne muscular dystrophy; a consideration from changes in serum CK and LDH levels].

We assessed the hypercoagulative state in patients with Duchenne muscular dystrophy (DMD) by measuring peripheral blood creatine kinase (CK) and lactate dehydrogenase (LDH) levels. In 76 patients with DMD who had no complications during examination, the CK and LDH levels were examined in a total of 173 times. Both enzyme levels were elevated and highly correlated (R = 0.93). We examined the temporal alteration of serum CK and LDH levels during episodes of pulmonary thrombosis experienced in 7 DMD patients who fulfilled the following diagnostic criteria: 1. sudden onset of dyspnea, chest pain, and hypoxia; 2. abnormal coagulation profile or abnormal chest CT findings, such as peripheral wedged shaped shadow and; 3. pneumothorax ruled out from X-ray findings. Throughout the episode of pulmonary thrombosis, CK and LDH levels changed within the range of those from DMD patients who had no complications, however, the CK level was significantly elevated from the basal level (2.12 times, p = 0.0075) on the first day of the episode. The LDH level rose for several days, and subsequently both CK and LDH returned to the basal level. In patients with compartment syndrome, CK levels were reportedly elevated due to muscle fiber necrosis which lead a hypercoagulative state. Therefore, we propose that muscle fiber necrosis is one of causal factors in pulmonary thrombosis. In addition, elevated CK may be helpful in predicting pulmonary thrombosis.

Adolescent↗
PubMed1991

High frequency of antithrombin 3 and protein C deficiency following autologous bone marrow transplantation for lymphoma.

To investigate the possibility that a hypercoagulable state develops during autologous bone marrow transplantation (BMT), we measured levels of circulating natural anticoagulants and fibrinolytic proteins before and weekly during the hospital course of 18 patients undergoing autologous BMT for Hodgkin's and non-Hodgkin's lymphoma. Patients received either weekly (standard dose group) or daily (high dose group) vitamin K supplements with their total parenteral nutrition. By day 14 there had been a significant drop in protein C activity (mean of 95% of normal to 52%), protein C antigen (mean of 105% of normal to 70%), and antithrombin 3 activity (111% of normal to 83%), and an increase in fibrinogen (471-621 mg/dl) and tissue plasminogen activator (6.9-13.8 ng/ml). No changes were seen in free or total protein S, plasminogen activator inhibitor, prothrombin time or partial thromboplastin time. The decreases in protein C and antithrombin 3 persisted through day 28 after transplantation. The drop in protein C correlated strongly with decrease in serum albumin, suggesting impaired synthesis of these proteins by the liver. No differences were seen in any of these parameters between the standard and high dose groups. Deficiencies in anticoagulant proteins antithrombin 3 and protein C and a rise in fibrinogen without a concomitant improvement in fibrinolytic variables create a potentially hypercoagulable state which may contribute to the thrombotic complications of autologous BMT.

Adult↗
PubMed1998

Thrombin-antithrombin III complex in acute retinal vein occlusion.

PURPOSE: To determine whether quantitative differences in systemic hypercoagulable state could be identified among patients with retinal vein occlusion at various sites of occlusion. METHODS: The value of thrombin-antithrombin III complex was determined in 57 patients with retinal vein occlusion within 1 month after the subjective onset of retinal vein occlusion and in 15 age-matched normal controls. RESULTS: Levels of log thrombin-antithrombin III complex were significantly higher in the patients with proximal retinal vein occlusion in which the occlusion site is at the optic disc (mean +/- SD, 0.493 +/- 0.389) than in those with distal retinal vein occlusion in which the occlusion site is away from the optic disc (0.312 +/- 0.150, P = .025) and in the normal controls (0.294 +/- 0.151, P = .020). There was no significant difference between the distal retinal vein occlusion and the normal controls (P = .720). More patients with proximal retinal vein occlusion showed elevated thrombin-antithrombin III complex values more than 3.9 ng/ml than those with distal retinal vein occlusion (8/29 vs 1/28, P = .025). Of nine patients showing an initial value of thrombin-antithrombin III complex of more than 3.9 ng/ml, repeated measurements were obtained in eight patients, who showed reduced value of thrombin-antithrombin III complex in the normal range in several months. CONCLUSIONS: A systemic hypercoagulable state, which could be demonstrated with the elevation of thrombin-antithrombin III complex value, may contribute more to the development of retinal vein occlusion with thrombus at or near the trunk of the central retinal vein than those with thrombus at branch veins away from the optic disc in the retina.

Acute Disease↗
PubMed2002

In vivo effect of haemodilution with saline on coagulation: a randomized controlled trial.

BACKGROUND: Previous studies have shown that 10-30% haemodilution with crystalloid may induce a hypercoagulable state demonstrable by using the Thrombelastograph (TEG). While most are in vitro studies, the few in vivo studies are limited by confounding surgical or 'environmental' factors. We conducted this randomized controlled study to evaluate the coagulation changes associated with in vivo haemodilution. METHODS: Twenty patients undergoing major hepatobiliary surgery were randomly allocated to one of two study groups. Group H (n = 10) had 30% blood volume withdrawn over 30 min and replaced with saline. Group C (n = 10) did not have any blood withdrawn. Blood samples were taken in both groups at 10, 20 and 30 min. Native TEG, complete blood count, coagulation profile, fibrinogen, antithrombin III, protein C and thrombin-antithrombin complex concentrations were measured. RESULTS: Compared with Group C, Group H patients had significantly greater shortening of r-time at 30 min (-30% vs +36%), greater shortening of k-time at all time points (-36% vs +17% at 10 min; -37% vs +44% at 20 min; -45% vs +49% at 30 min), and greater widening of alpha at 30 min (+71% vs +4%). The decrease in antithrombin III and other natural procoagulants and anticoagulants closely followed that of haematocrit, with the exception of thrombin-antithrombin complex. CONCLUSION: In vivo haemodilution of up to 30% with saline can induce a hypercoagulable state. The mechanism remains unclear as disproportionate dilution of natural anticoagulants was not detected. Thrombin-antithrombin complex concentration remained stable despite haemodilution in Group H, which may suggest increased thrombin generation.

Adult↗
PubMedDate not supplied

Association of negative life event stress with coagulation activity in elderly Alzheimer caregivers.

OBJECTIVE: Part of the excess coronary disease rate and overall mortality reported with caregiving stress could relate to a hypercoagulable state. Physiological responses to the chronic distress of caregiving may involve hyperactive sympathetic nervous system responses to superimposed stressors. We wondered whether negative life stress might affect hemostatic function in caregivers. METHODS: The three procoagulant measures thrombin-antithrombin III complex (TAT), fibrin D-dimer (DD), and von Willebrand factor (vWF) antigen were assessed in 54 spousal Alzheimer caregivers (mean age, 73 +/- 6 years). Subjects completed a semistructured interview (Psychiatric Epidemiologic Research Interview, PERI) that assessed for non-caregiving-related life stress (ie, number of negative life events) over the 4-week period before blood sampling. RESULTS: Caregivers reported an average of 2.6 negative life events (range, 0-6). The number of negative life events showed a direct association with plasma DD levels (p =.010). In multiple regression analyses, body mass index (BMI) and life stress were the only significant predictors of DD. Together, BMI, hypertension status, gender, and depression accounted for 23% of the variance in DD (p =.022). After these variables had been controlled for, life stress explained an additional 9% (p =.021) of the variance in DD. On the other hand, the number of life-events did not significantly predict TAT or vWF. CONCLUSIONS: The findings suggest that superimposed life stress on top of the chronic stress of Alzheimer caregiving may elicit a hypercoagulable state that could contribute to coronary disease and to increased overall mortality in this population.

Aged↗
PubMed1993

Thromboembolic complications of polycythemia: polycythemia vera versus smokers' polycythemia.

PURPOSE: This report compares patients with the hypercoagulable state of polycythemia vera to patients with secondary polycythemia caused by tobacco use to determine whether the incidence of thromboembolic events is equivalent. METHODS: The medical records of 146 patients with the diagnosis of polycythemia between 1977 to 1990 were reviewed. Patients with transient, relative, or stress polycythemia were excluded from this study as were patients with polycythemia as a result of cardiac or pulmonary anomalies or both. The diagnosis of polycythemia vera (n = 43) was verified by use of the guidelines of the Polycythemia Vera Study Group. The diagnosis of polycythemia caused by smoking (n = 27) was based on an elevated total red blood cell volume, decreased oxygen saturation on arterial blood gas measurement, evidence of chronic obstructive pulmonary disease, and elevated carboxyhemoglobin levels. RESULTS: Twenty-six patients (60%) with polycythemia vera and 11 patients (41%) with smoker's polycythemia had at least one thromboembolic problem. No significant differences existed between the groups with regard to age, hematocrit, or number of cardiac and cerebrovascular events. Overall, patients with polycythemia vera had a greater number of thromboembolic events per patient (p < 0.05) and more peripheral arterial thromboemboli (p < 0.005) than did patients with polycythemia as a result of smoking (Fisher's Exact Test). CONCLUSIONS: Thus the results of this study demonstrate that smokers' polycythemia does not represent a hypercoagulable state equivalent to that of polycythemia vera.

Analysis of Variance↗