Blood Hypercoagulability Research Articles

Prevention and Management of Graft Thrombosis in Pancreatic Transplant

Pancreatic transplant effectively cures type 1 diabetes mellitus and maintains consistent long-term euglycemia. However, technical failure, and in particular graft thrombosis, accounts for the vast majority of transplants lost in the early postoperative period. The pancreas' inherently low microvascular flow state makes it vulnerable to vascular complications, as does the hypercoagulable blood of diabetic patients. Ultimately, the phenomenon is most definitely multifactorial. Prevention, as opposed to treatment, is key and should focus on reducing these multiple risk factors. This will involve tactical donor selection, optimal surgical technique and some form of anticoagulation. Close monitoring and early intervention will be crucial when treating thrombosis once preventative methods have failed. This may be achieved by further anticoagulation, graft salvage, or pancreatectomy with retransplant. This article will explore the multiple factors contributing to graft thrombus formation and the ways in which they may be addressed to firstly prevent, or more likely, reduce thrombosis. Secondly, we will consider the management strategies which can be implemented once thrombosis has occurred.

Outcomes of pregnancy following maternal fontan repair

The Fontan procedure is performed in patients with anatomical or functional single ventricle. Modifications have been made to the original procedure, but in essence it involves diverting blood from the...

MODERN CONCEPTS OF THE MECHANISMS FORMING NORTHERN STRESS IN HUMANS IN HIGH LATITUDES

The extreme climatic and geographical northern conditions cause a human northern stress (“the polar tension syndrome”). The main components of this syndrome are an oxidative stress, failure of detoxication processes and barrier organs, disorders of the northern metabolism, the northern tissue hypoxia, immune insufficiency, blood hypercoagulation, polyendocrine disorders, regenerative and plastic failure, electromagnetic homeostasis disorders, functional dissymmetry of interhemispheric interrelations, desynchronosis, psychoemotional tension, meteopathia. It has been shown that chronic stress caused organism reserve exhaustion leading to development of some dysaptative disorders and pathological states.

Myocardial bridging is a potential risk factor of very late stent thrombosis of drug eluting stent

SummaryDrug eluting stents have been implanted worldwide and used in nearly 90% of percutaneous coronary interventions in China. Although many randomized trials have confirmed the efficacy and safety profile of drug eluting stents, they were not powered to detect or exclude the effect of drug eluting stents on rare events such as stent thrombosis. Several mechanisms of very late stent thrombosis have been postulated, but are not widely accepted. Virchow’s triad describes the 3 main factors of thrombus formation – stasis of blood flow, endothelial injury and hypercoagulability. Myocardial bridging is a common congenital anomaly. Modern anatomy and angiography regard myocardial bridging as widespread, but its pathophysiological response is always ignored. According to Virchow’s triad, myocardial bridging negatively affect endothelial function, and the turbulent shear stress and intimal trauma predispose the vessel toward thrombus formation. Therefore, we question whether a relationship between myocardial bridging and very late stent thrombosis of drug eluting stents exists. Also, we propose that myocardial bridging might be a potential risk factor of very late stent thrombosis of drug eluting stents; coronary artery bypass grafting might be a promising and novel choice in the treatment of myocardial bridging with severe stenosis in the coronary artery.

Treatment of diabetic vasculopathy: an overview

Correspondence: Sayeeda Rahman Department of Clinical Sciences, School of Medical Sciences, University of Bradford, Bradford BD7 1DP, United Kingdom Tel +44 12 7423 6283 Email srahman6@bradford.ac.uk Abstract: Type 2 diabetes is a chronic, degenerative, and noncommunicable disease, and is associated with a high prevalence of cardiovascular morbidity and mortality. The complications of diabetic vasculopathy are commonly grouped into microvascular and macrovascular complications. In diabetes, macrovascular complications are the commonest cause of morbidity and mortality and are responsible for a high incidence of vascular diseases. The aim of this review to provide an overview of current treatment modalities for diabetic vasculopathy and highlight the importance of effective control of blood glucose, blood lipids, and blood pressure, as well as reduction of blood hypercoagulability, in lowering the macrovascular complications of diabetic vasculopathy. A literature review was conducted to retrieve the relevant information using the PubMed, Science Direct, and Google Scholar databases, reports, and books. People with type 2 diabetes are at markedly increased risk for cardiovascular disease and mortality. The initiators of vasculopathy that ultimately develop into long-term diabetic complications can be avoided by a healthy lifestyle and pharmacological intervention. Clinical trials have shown that effective control of blood glucose, blood lipids, blood pressure, and blood hypercoagulability can reduce macrovascular complications in patients with type 2 diabetes. Type 2 diabetes is responsible for premature mortality, predominantly through atherosclerotic vascular disease. Lifestyle modification and pharmacotherapy should be used to prevent or delay development of type 2 diabetes, including adverse cardiovascular outcomes. A multidisciplinary approach involving patients, health professionals, and diabetic educators should be used to combat the type 2 diabetes epidemic and its associated cardiovascular complications.

Puérpera com trombose de prótese mecânica e estenose supravalvar aórtica adquirida

The blood hypercoagulability in pregnancy increases significantly the incidence of thrombosis of mechanical valves. Acquired supravalvular aortic stenosis is extremely rare. We report the case of an immediate postpartum patient with aortic mechanical prostheses and acquired supravalvular aortic stenosis who underwent emergency heart surgery, with severe hemodynamic instability, using adapted surgical technique for correction of supravalvular stenosis with satisfactory clinical and echocardiography results.

Venous Valvular Stasis–Associated Hypoxia and Thrombosis: What Is the Link?

This review focuses on the role of the venous valves in the genesis of thrombus formation in venous thromboembolic disease (VTE). Clinical VTE and the evidence for the valvular origin of venous thrombosis are reviewed. Virchow's triad is then used as a framework for discussion to approach the question posed regarding the link between venous valvular stasis-associated hypoxia and thrombosis. Thus, the effects of blood flow stasis, hypercoagulability of blood, and the characteristics of the vessel wall within the venous valvular sinus are assessed in turn.

Proximal atherosclerotic lesion as a cause of very late stent thrombosis

Very late stent thrombosis is defined as in-stent thrombosis occurring after 1 year of an intra-coronary artery stent placement. Drug eluting stents have lately been criticized for increased reports of very late stent thrombosis. The exact cause of these very late stent thromboses is not clearly understood. Virchow’s triad describes the three main factors of thrombus formation to be stasis of blood flow, endothelial injury and hypercoagulability. Based on Virchow’s triad, we propose the cause of very late stent thrombosis to be formation of a de novo atherosclerotic lesion in the proximal segment of a stented artery. The de novo atherosclerotic lesion narrows the vessel lumen and causes stasis of blood flow in the distal stent. The de novo lesion can also cause myocardial ischemia creating a prothrombotic environment in the stented region. Stasis of blood flow and prothrombotic environment in the stented region can lead to the formation of very late stent thrombosis. Since atherosclerosis is a dynamic aging process in humans, we propose de novo proximal lesions in the coronary arteries can predispose to very late stent thrombosis.

Paraneoplastic vasculitis and paraneoplastic vascular syndromes

Paraneoplastic syndromes are localized or diffuse pathologic manifestations that may occur in subjects affected by neoplastic diseases, even occult ones. Among the many clinical manifestations of paraneoplastic syndromes, cutaneous ones are quite common. It is estimated that skin manifestations may represent the very first diagnostic sign of a neoplastic disease in about 1% of patients. Many paraneoplastic syndromes with skin manifestations are caused by vascular alterations. In case of solid tumors, migrant thrombophlebitis and blood hypercoagulability can be seen, whereas in case of hematological neoplasms, vasculitis, and erythromelalgia can occur. Paraneoplastic vasculitis and paraneoplastic vascular syndromes are challenging issues in dermatology and general medicine. The present article will review the actual knowledge in the argument, together with providing hints for its diagnosis and management.

Genetic repression of mouse VEGF expression regulates coagulation cascade

VEGF is an important growth factor in embryonic development and functional maintenance of adult organs. Single allele inactivation of VEGF leads to embryonic lethality and many conditional disruptions show dramatic phenotypes or reduced viabilities. To overcome this burden, a reversible system, which was used in the regulation of VEGF expression and functional studies of many tissues and organs in adult, was developed. VEGF is known for expression in many tissues and high expression in platelets. Repression of VEGF expression showed significant defect in bleeding time and clotting time. In mouse model of LPS-induced blood hypercoagulation, significant reduction of plasma thrombin-antithrombin formation was observed in VEGF repressed mice, and tissues expressed different modes of damages. These results indicate that VEGF regulates coagulation cascade and may affect sepsis. This is the first genetic evidence of direct link between VEGF transcription and coagulation cascade. Studies using this system may help us to find out how VEGF regulates coagulation cascade and provide new strategies in treating coagulation related diseases.

P-Selectin as a new gender associated biomarker in patients with metabolic syndrome

Metabolic syndrome (MetS) is a cluster of risk factors for atherosclerosis, including abdominal obesity, hypertension, insulin resistance, dyslipidemia with high triglycerides and low high-density lipoprotein cholesterol [ [1] Grundy S.M. Cleeman J.I. Daniels S.R. et al. American Heart Association; National Heart, Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation. 2005; 112: e298 Crossref PubMed Scopus (8736) Google Scholar ]. Affected patients have a significantly increased risk of developing cardiovascular disorders. This is probably due to a blood hypercoagulability as well as to endothelial cell activation [ [2] Ay C. Tengler T. Vormittag R. et al. Venous thromboembolism—a manifestation of the metabolic syndrome. Haematologica. 2007; 92: 374-380 Crossref PubMed Scopus (132) Google Scholar ]. Furthermore, several epidemiological studies, the Framingham in particular [ [3] Ingelsson E. Pencina M.J. Tofler G.H. et al. Multimarker approach to evaluate the incidence of the metabolic syndrome and longitudinal changes in metabolic risk factors: the Framingham Offspring Study. Circulation. 2007; 28: 984-992 Crossref Scopus (149) Google Scholar ], have investigated into the evolution of cardiovascular disease (CVD) hypothesizing the presence of a gender difference in the pathogenetic and progression determinants detectable in men and women. For example, women were found to outlive men and to experience fewer atherosclerotic cardiovascular events, with an incidence lagging behind that in men by 10 to 20 years [ [4] Mølstad P. Coronary heart disease in women: less extensive disease and improved long-term survival compared to men. Scand Cardiovasc J. 2008; 10: 1-7 Google Scholar ]. On these bases, and considering that several risk factors for vascular diseases have been associated with inflammation and platelet activation [ [5] Kyrle P.A. Hron G. Eichinger S. Circulating P-selectin and the risk of recurrent venous thromboembolism. Thromb Haemost. 2007; 9: 880-883 Google Scholar ], a pilot study has been conducted in platelets from a low number of patients with MetS of both sexes. In particular, we focused our attention on P-Selectin protein expression. This is a transmembrane protein present in the alpha granules of platelets that, following activation, is rapidly translocated to the cell surface and then released in the blood flow.

Thrombophilic risk factors in the pathogenesis of non-arteritic anterior ischemic optic neuropathy patients

Non-arteritic anterior ischemic optic neuropathy (N-AION) is caused by acute ischemic infarction of the optic nerve head, supplied by the posterior ciliary arteries. Thrombophilia is the tendency/predisposition to vascular thromboses of arteries and veins, and the existence of thrombophilic risk factors leads to blood hypercoagulability and potentially increased risk for thromboses. To investigate whether there is an association between N-AION and a wide spectrum of thrombophilic risk factors. Seventy-seven consecutive cases of confirmed N-AION and 60 age- and sex-matched consecutive controls constituted the study group. Fibrinogen levels, deficiency of proteins C, S, ATIII, lupus anticoagulant, activated protein C resistance, factor V Leiden, factor V H1299R, factor II G20210A, MTHFR C677T, MTHFR A1298C, GPIIIa A1/A2, and ACE I/D polymorphisms were analysed. Statistical analysis of the plasma proteins in our study demonstrated that the only significant difference was the one concerning protein S levels. In particular, the mean value for N-AION patients was 78.8% +/- 21.2, and for the control group the mean value was 88% +/- 21.2 (p = 0.013). Despite the above-mentioned result, there was not any statistical difference between the two subgroups regarding actual protein S deficiency, as 9/77 (11.7%) patients and 4/60 (6.7%) controls had protein S levels below 60% (p = 0.32). In our study sample, homozygosity for MTHFR C677T polymorphism in the study group as a whole, and the presence of at least one A2 allele of GPIIIa in the subgroup of male patients as compared to healthy male controls, proved to be the most significant thrombophilic risk factors, with odds ratios of 16.78 (95% C.I 0.96-294.42, p = 0.054) and 4.6 (95% C.I 1.52-13.88, p = 0.007) respectively. Screening for these polymorphisms would probably constitute a valuable procedure in N-AION patients, as they may have an important contribution to the pathogenesis of the disease.

Migraine Associated with Patent Foramen Ovale May Be Caused by Reactivation of Cerebral Toxoplasmosis Triggered by Arterial Blood Oxygen Desaturation

ABSTRACTApproximately two billion people worldwide are chronically infected with T. gondii and yet with largely unknown consequences. On the other hand, several authors reported an association between migraine and patent foramen ovale (PFO), and different types of headaches, including migraine, may be precipitated by various diseased states or medications associated with marked immune irregularities, which sometimes cause reactivation of latent cerebral toxoplasmosis (CT). Recently, in a group of 104 subjects with migraine, 46 individuals (44.2%%) were found to be seropositive for T. gondii. PFO, atrial septal defects, as well as pulmonary right-to-left shunts are usually associated with a various degree of arterial blood oxygen desaturation. Hypoxia is associated with an increase in the generation of several proinflammatory cytokines and other inflammation mediators, such as TNF-α, IL-1-β, IL-6, IL-8, chemokines (monocyte chemoattractant protein-1, CC-chemokine receptor 2, macrophage inflammatory protein-1α, intercellular adhesion molecule-1), acute-phase protein gene expressions, COX-2 gene transcription, induction of iNOS, and reactive oxygen species. Moreover, hypoxia markedly decreased T-lymphocyte IL-2 mRNA, a key cytokine responsible for B-cell proliferation and immunoglobulin secretion, and ischemic tissues demonstrated intravascular neutrophil accumulation, vascular damage, and increased vascular wall permeability. Interestingly, T. gondii activates hypoxia-inducible factor 1 already at physiologically relevant oxygen levels and requires HIF1 for growth and survival. These abnormalities may cause imbalance in the host/T. gondii immune system, which finally results in the reactivation of CT. In addition, hypoxia may participate in paradoxical microembolism because arterial oxygen desaturation enhances expression of plasminogen activator inhibitor-1, an important factor which suppresses fibrinolysis, and this effect may be further amplified by a decreased expression of plasminogen activators, finally causing blood hypercoagulability and paradoxical microembolism. In summary, further studies are required to verify the above-presented pathomechanisms probably responsible for the association between PFO and the development of migraine. It is possible that some migraineurs with PFO may benefit from evaluation and treatment of toxoplasmosis in the future once more information is known.

Demonstration of a positive effect of emotional expression on blood coagulation is possible with dark field microscopy

Effects of psychological stress on blood hypercoagulation have been shown by a number of authors. In healthy subjects acute mental stress simultaneously activates coagulation and fibrinolysis within a physiological range. However, in patients with atherosclerosis or in healthy subjects under acute or chronic psychosocial stressors (e.g. exam, earthquake, blood donation, job strain, low socioeconomic status, social isolation) hypercoagulable states reflected by an increased number of procoagulant molecules and by reduced fibrinolytic capacity might develop. There is also evidence that points to hypercoagulability in depression. The aim of this paper was to demonstrate the positive effect of emotional expression on blood coagulation using dark field microscopy. Cases of three patients suffering from psychological stress are presented. Humaniversity therapy was applied for all cases integrating a variety of therapeutic techniques, such as: emotional expression, cognitive change, integrity of a holistic approach, touch and positivity. Dark field microscopy was used before and after the sessions to evaluate the effect of therapeutic work on blood coagulation. The results of three cases showed the immediate effect of emotional release on blood coagulation. After the sessions lasting from 1–1.5 hours, all three cases reported improved emotional well-being with changes in blood clotting from levels 4 and 5 (light severe and severe clotting) to no clotting at all. A positive objective effect of emotional expression on blood coagulation can be demonstrated using dark field microscopy.

Splenectomy Exacerbates the Hypercoagulable State and Causes Significant Organ Dysfunction in Patients with Hemoglobin E/β-Thalassemia.

Abstract 2014Poster Board I-1036 Introduction:Clinical manifestations of blood hypercoagulability, such as pulmonary arterial hypertension (PAH) and ischemic stroke, are well known in patients with thalassemia. We herein present evidence that the hypercoagulable state in β-Thalassemia disease patients is to a significant extent the result of prior splenectomy. Patients and Methods:One hundred and ten clinically stable hemoglobin E/β-Thalassemia outpatients, on no medication aside from folic acid and who received no blood transfusion in the preceding 4 weeks were studied. All gave written informed consent, and study protocol was approved by the institution ethics committee on studies in humans (#0774/2548). Echocardiogram was used to estimate systolic PA pressure (SPAP). Clinical features and laboratory data were stratified according to the presence or absence of the spleen, and statistical analysis was done by STATA version 10 (Stata Corp, Texas), considering a P value <0.05 as statistically significant. Results:Of the 110 patients, 61 were asplenic and females comprised 51% in both groups. Selected statistically significant results are shown in the table.ResultsAsplenic (61 Patients)Non-splenectomized (49 Patients)P valueAge at 1st transfusion (median)4.7 years17 years<0.001Total transfusions (median)35 units PRBC13 units PRBC0.005Systolic pulmonary artery pressure37.1 +/- 14.6 mm Hg28.8 +/- 7.6 mm Hg<0.001Cardiomegaly50.9%27.3%0.013Extramedullary hematopoiesis50.9%27.3%0.013RBC count3.19 +/- 0.57 × 106/μL3.87 +/- 1.09 × 106/μL<0.001Corrected reticulocyte count (median)5.2%1.4%<0.001Nucleated RBC (median)581/100 WBCs5/100 WBCs<0.001Corrected WBC count9.72 +/- 4.2 × 103/μL6.71 +/- 2.3 × 103/μL<0.001Platelet count726 +/- 215 × 103/μL243 +/- 115 × 103/μL<0.001Serum ferritin (median)1,892 ng/mL1,050 ng/mL0.001ALT (median)65.5 u/L44.5 u/L0.004AST (median)64 u/L36 u/L0.001Free hemoglobin (median)4.2 mg/dL2.5 mg/dL0.001C-reactive protein (high sens) (median)2.7 mg/L1.2 mg/L0.012Thrombin-antithrombin complexes3.5 μg/L1.1 μg/L<0.001Soluble P-selectin113.4 +/- 31.2 ng/mL56.4 +/- 32.1 ng/mL<0.001Soluble E-selectin43.3 +/- 21.5 ng/mL29.5 +/- 18.4 ng/mL0.003 Conclusions:In comparison with non-splenectomized hemoglobin E/β-Thalassemia patients, asplenic ones have higher SPAP, more severe hemolysis, more liver impairment and chronic iron overload, significant chronic low grade inflammation, and evidence of coagulation activation. Splenectomy should be more judiciously applied than heretofore, and if performed, measures to blunt or prevent a subsequent hypercoagulable and inflammatory state, which could lead to PAH should be initiated. Disclosures:No relevant conflicts of interest to declare.

Eingriff-spezifische Thromboseprophylaxe beim Erwachsenen

According to the concept of Virchow, alterations of the blood flow, vascular injury and hypercoagulability of the blood (due to inherited or acquired thrombophilia or as a consequence of perioperative coagulation activation) are causally related to the risk of venous thrombosis. The overall risk of venous thromboembolic events in the perioperative setting ranges between <10% and >50%. The risk is highest in patients undergoing major orthopaedic surgery or cancer surgery. The aim of perioperative thrombosis prophylaxis is to reduce perioperative morbidity and mortality. The article discusses patient- and intervention-dependent thromboprophylactic measures. Recent recommendations for non-pharmacological and pharmacological prophylaxis are presented including the information on the beginning and duration of anticoagulation. Management strategies for patients undergoing abdominal and orthopaedic surgery as well as special aspects of the neurosurgical population and of cancer surgery are highlighted.

Aortic Atherosclerosis, Hypercoagulability, and Stroke: The APRIS (Aortic Plaque and Risk of Ischemic Stroke) Study

Our goal was to assess the effect of hypercoagulability on the risk of stroke in patients with aortic plaques.Atherosclerotic plaques in the aortic arch are a risk factor for ischemic stroke. Their relationship with blood hypercoagulability, which might enhance their embolic potential and affect treatment and prevention, is not known.We performed transesophageal echocardiography in 255 patients with first acute ischemic stroke and in 209 control subjects matched by age, gender, and race/ethnicity. The association between arch plaques and hypercoagulability, and its effect on the stroke risk, was assessed with a case-control design. Stroke patients were then followed prospectively to assess recurrent stroke and death.Large (> or =4 mm) arch plaques were associated with increased stroke risk (adjusted odds ratio [OR]: 2.4, 95% confidence interval [CI]: 1.3 to 4.6), especially when ulcerations or superimposed thrombus were present (adjusted OR: 3.3, 95% CI: 1.4 to 8.2). Prothrombin fragment F 1.2, an indicator of thrombin generation, was associated with large plaques in stroke patients (p = 0.02), but not in control subjects. Over a mean follow-up of 55.1 +/- 37.2 months, stroke patients with large plaques and F 1.2 over the median value had a significantly higher risk of recurrent stroke and death than those with large plaques but lower F 1.2 levels (230 events per 1,000 person-years vs. 85 events per 1,000 person-years; p = 0.05).In patients presenting with acute ischemic stroke, large aortic plaques are associated with blood hypercoagulability, suggesting a role for coagulation activation in the stroke mechanism. Coexistence of large aortic plaques and blood hypercoagulability is associated with an increased risk of recurrent stroke and death.

Whole blood hypercoagulability despite anticoagulation during mechanical cardiac assist

We report hypercoagulability despite activated partial thromboplastin time (APTT)-guided heparin treatment during Berlin Heart-supported circulation in a 38-year-old man with heart failure for 19 days. The patient was anticoagulated using unfractionated heparin, acetylsalicylic acid and dipyridamole. Contact and tissue factor-activated thromboelastometry revealed increased clot firmness, although anticoagulation assessed by APTT was in accordance with the treatment protocol. Strength of polymerized fibrin was also increased. We saw no clinical signs of thrombosis. Thromboelastometry normalized after heart transplantation. Our results suggest that hypercoagulability is due to excess fibrin formation. Monitoring anticoagulation using APTT may, therefore, be misleading during mechanical cardiac assist.

Profilassi eparinica nella tromboembolia polmonare: responsabilità professionale e profili giuridici

Early diagnosis of deep vein thrombosis (DVT) is often difficult: DVT can be asimnthomatic and pulmonary thrombo-embolism (PTE) often occur in a sudden and unexpected way. Pharmacological prophylaxis, aiming at reducing the state of blood hypercoagulability, is the elective therapeutic strategy for vein thomboembolism. Pulmonary embolism is not only one of the most common causes of unexpected death in hospitalized patients, but also one of the top diseases leading to medical malpractice lawsuits. This article describes a case where the lack of adequate pharmacological prophylaxis caused the death of a woman for pulmonary thromboembolism. After some clinical and pharmacological considerations about prophylactic measures for PTE, the Authors explore the question of legal liability of medical practitioners in this situation.

Anticipatory Cognitive Stress Appraisal and the Acute Procoagulant Stress Response in Men

Acute mental stress elicits blood hypercoagulability. Following a transactional stress model, we investigated whether individuals who anticipate stress as more threatening, challenging, and as exceeding their coping skills show greater stress reactivity of the coagulation activation marker D-dimer, indicating fibrin generation in plasma. Forty-seven men (mean age 44 +/- 14 years; mean blood pressure [MBP] 101 +/- 12 mm Hg; mean body mass index [BMI] 26 +/- 3 kg/m(2)) completed the Primary Appraisal Secondary Appraisal (PASA) scale before undergoing the Trier Social Stress Test (combination of mock job interview and mental arithmetic task). Heart rate, blood pressure, plasma catecholamines, and D-dimer levels were measured before and after stress, and during recovery up to 60 minutes poststress. Hemodynamic measures, catecholamines, and D-dimer changed across all time points (p values <.001). The PASA "Stress Index" (integrated measure of transactional stress perception) correlated with total D-dimer area under the curve (AUC) between rest and 60 minutes poststress (r = 0.30, p = .050) and with D-dimer change from rest to immediately poststress (r = 0.29, p = .046). Primary appraisal (combined "threat" and "challenge") correlated with total D-dimer AUC (r = 0.37, p = .017), D-dimer stress change (r = 0.41, p = .004), and D-dimer recovery (r = 0.32, p = .042). "Challenge" correlated more strongly with D-dimer stress change than "threat" (p = .020). Primary appraisal (DeltaR(2) = 0.098, beta = 0.37, p = .019), and particularly its subscale "challenge" (DeltaR(2) = 0.138, beta = 0.40, p = .005), predicted D-dimer stress change independently of age, BP, BMI, and catecholamine change. Anticipatory cognitive appraisal determined the extent of coagulation activation to and recovery from stress in men. Particularly individuals who anticipated the stressor as more challenging and also more threatening had a greater fibrin stress response.