Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “hypercoagulable state”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,081 records · Page 60Linked to original sources
PubMed2003

Complications related to off-pump bypass grafting.

Surgical myocardial revascularization is a technique undergoing critical reevaluation in an attempt to reduce operative morbidity and mortality. As the age and number of comorbidities in the surgical population presenting for bypass increases, improved strategies to lessen operative risk have evolved. The use of off-pump bypass grafting to avoid the detrimental effects of extracorporeal circulation demonstrates great promise in reducing operative complications. However, with new techniques come new challenges. Avoidance of the cardiopulmonary bypass circuit has been linked to the development of a hypercoagulable state postoperatively. Complications related to the unique management of the ascending aorta and target vessels during the performance of beating heart surgery are also being reported. Moreover, despite increasing experience in a number of centers, hemodynamic collapse does occur during off-pump bypass, thereby requiring rapid institution of cardiopulmonary bypass. Continued scientific investigation and research should provide the tools to manage the unique obstacles encountered with off-pump coronary artery bypass.

Aortic Dissection↗
PubMed2002

Catheter-directed thrombolysis in deep venous thrombosis with use of reteplase: immediate results and complications from a pilot study.

PURPOSE: To prospectively determine the thrombolytic success and complication rates of catheter-directed thrombolytic infusions in deep vein thrombosis (DVT) with use of reteplase. MATERIALS AND METHODS: After approval by the institutional review board, prospective, detailed data were obtained for 25 consecutive patients with acute and chronic DVT of the upper or lower extremity (seven upper extremity; 14 lower extremity; four vena cava). Infusion rates were 1.0 U/h in five patients and 0.5 U/h in the remaining 20. Subtherapeutic heparin doses of 300-400 U/h were administered. Thrombolytic success was defined as 95% thrombolysis with return of antegrade flow. Data, including complications such as bleeding, need for transfusions, and laboratory values (fibrinogen, platelets, hematocrit, hemoglobin, and prothrombin time) were obtained throughout the infusions. RESULTS: The total dose of reteplase administered ranged from 2.5 to 42 U (median, 16.5 U). The total infusion time ranged from 0.3 to 84 hours (median, 29 h). Thrombolytic success was achieved in 92% of patients. Endovascular stent placement and/or percutaneous transluminal angioplasty were required in 52% of patients to ensure maintenance of patency. Pre- and postprocedural average fibrinogen levels were 340 mg/dL and 315.3 mg/dL, respectively. The lowest mean fibrinogen levels for the two dose groups were 265.86 mg/dL for the 0.5 U/h group and 314.18 mg/dL for the 1.0 U/h group. The lowest fibrinogen level during the procedure was 252.3 mg/dL (range, 35 to >700). There were only two instances of fibrinogen levels that decreased to below 90 mg/dL: 35 mg/dL and 43 mg/dL. Thrombolytic failures occurred in two patients: one with acquired immune deficiency syndrome in a hypercoagulable state and one with a major bleeding complication. This was the only patient with a bleeding complication (4%). Hemorrhage occurred from the site of a previous mediastinal biopsy-which should have rendered her ineligible for the study-performed 18 hours before the thrombolysis. If thrombolysis had not been attempted in this patient, the complication rate would have been 0%. CONCLUSION: Although there are reports of thrombolytic therapy in peripheral vascular occlusive disease, this study is one of the first to evaluate thrombolytic drugs in the deep venous system exclusively. Reteplase was found to be effective in the thrombolytic treatment of acute and chronic DVT.

Adolescent↗
PubMed1992

Vena caval occlusion after Simon nitinol filter placement: identification with MR imaging in patients with malignancy.

The prevalence of inferior vena caval occlusion associated with the Simon nitinol filter (SNF) was studied at two institutions in the follow-up of filters placed over a 13-month period. Twenty-four consecutive patients with defined indications (contraindication to anticoagulation with pulmonary embolism or deep venous thrombosis [DVT], recurrent pulmonary embolism despite anticoagulation, or extensive DVT [eg, iliofemoral]) underwent placement of a SNF. This patient group includes a high proportion with pelvic or renal malignancy (54%, 13 of 24) or a history of other malignancy. Of these 24, physical examination at follow-up identified 10 symptomatic patients with unilateral or bilateral leg swelling. Of these 10, magnetic resonance imaging, with spin-echo and gradient-echo techniques, demonstrated IVC occlusion in five patients (50%). These data suggest that vena caval occlusion following SNF placement occurs more commonly than previously recognized. Possible contributing factors include reduced venous inflow in patients with prior nephrectomy or pelvic neoplasms, pelvic venous compression by tumor mass, and hypercoagulable states.

Adult↗
PubMedDate not supplied

Transcatheter regional urokinase therapy in the management of inferior vena cava thrombosis.

PURPOSE: To study the efficacy of local infusion of urokinase (UK) in the treatment of symptomatic inferior vena cava (IVC) thrombosis. MATERIALS AND METHODS: Eight patients (five men and three women) who ranged in age from 19 years to 75 years (mean, 56 years) with symptomatic IVC thrombosis underwent local catheter-directed infusion of UK with use of up to three access sites. Infrarenal IVC thrombus and iliac vein thrombus was identified in all patients. Four patients had extension of thrombus proximal to the renal veins. Seven of eight patients had at least one risk factor for IVC thrombosis: hypercoagulable state (n = 3), IVC filter (n = 3), malignancy (n = 2), recent surgery (n = 2), and oral contraceptive use (n = 1). No serious procedure-related complications were encountered, although one patient died 5 days after UK therapy of pulmonary failure due to advanced lung cancer. UK was infused for an average of 79 hours (range, 24-140 hours) and a mean total dose of 7.4 million U of UK (range, 2.9-14.4 million U). Adjunctive balloon angioplasty was performed in three patients. No vascular stents were placed. Clinical and/or radiographic follow-up was obtained in all eight patients. RESULTS: Thrombolysis was successful in seven of eight (88%) IVCs with no or minimal residual thrombus. The remaining seven patients had no lower extremity swelling 2-24 months (mean, 11 months) after the procedure. Three of seven patients had computed tomographic or venographic follow-up (mean, 9 months; range, 1.5-15 months), demonstrating unchanged or improved IVC patency. CONCLUSIONS: Transcatheter regional infusion of UK for re-establishing venous patency in acute IVC thrombosis appears to be effective with good short-term and mid-term clinical benefit.

Adult↗
PubMed1997

Changes in platelet count, coagulation and fibrinogen associated with elective repair of asymptomatic abdominal aortic aneurysm and aortic reconstruction for occlusive disease.

BACKGROUND: Mortality and morbidity following aortic surgery, particularly repair of ruptured abdominal aortic aneurysm (AAA), is frequently associated with the development of coagulopathy. OBJECTIVES: To examine changes in platelet count (PC), fibrinogen, and coagulation in patients undergoing elective repair of asymptomatic abdominal aortic aneurysm (AAA) and aortic surgery for occlusive disease. DESIGN: Prospective clinical study in a University Department of Vascular Surgery. PATIENTS: Thirty-three patients undergoing elective repair of asymptomatic AAA and 19 patients undergoing aortic surgery for occlusive disease. METHODS: Full blood count (FBC), clotting screen, and fibrinogen measured pre-operatively; 6, 12, 24, 48 h postoperatively; and thereafter as clinically indicated in 23 consecutive patient's undergoing AAA repair (Group 1). Pre- and postoperative PC measured weekly for 4 weeks following operation in a further 10 consecutive patients undergoing AAA repair (Group 2) and perioperative PC measured in 19 consecutive patients undergoing aortic surgery for occlusive disease (Group 3). RESULTS: Group 1: Preoperative haematological parameters were normal. There was no mortality. Postoperatively, 21 (91%) patients developed thrombocytopenia (PC < 150 x 10(9)/l). The postoperative fall in PC (median 90, range 12-160 x 10(9)/l) was significantly related to the duration of aortic cross-clamp (median 46, range 20-127 min, r2 = 0.33, p < 0.01). At 10 days all patients had developed thrombocytosis (PC > 350 x 10(9)/l) Postoperatively, by 48 h, 17 (74%) patients had developed hyperfibrinogenaemia. One patient suffered a myocardial infarction associated with a PC of 105 x 10(9)/l and a fibrinogen of 7.2 g/l. GROUP 2: In a further 10 patients undergoing AAA repair postoperative thrombocytosis was found to persist for several weeks in five of nine survivors. GROUP 3: Patients undergoing aortic surgery for occlusive disease had significantly higher preoperative PC than AAA patients (median 292, range 179-251 x 10(9)/l vs. median 204, range 140-293 x 10(9)/l, p < 0.01). CONCLUSIONS: Patients undergoing elective repair of AAA demonstrate similar, albeit less dramatic, changes in platelet count to those we have previously reported in patients undergoing repair of ruptured AAA. Aortic clamping leads to platelet sequestration and thrombocytopenia in the early postoperative period. Later, patients develop hyperfibrinogenaemia and thrombocytosis which may persist for several weeks. Similar changes are seen in patients undergoing aortic surgery for occlusive disease. These changes may represent a hypercoagulable state that predisposes these patients to thrombotic complications.

Aged↗
PubMed1996

Myocardial infarction as the presenting manifestation of systemic lupus erythematosus with antiphosphatidylserine antibodies.

BACKGROUND: The presence of antiphospholipid antibodies has been associated with thrombotic events in systemic lupus erythematosus and other diseases. Antiphosphatidylserine antibodies have been shown more recently to have clinical implications being noted in thrombocytopenia, positive VDRL test, prolonged partial thromboplastin time, and recurrent fetal loss. OBJECTIVE: To report a patient with systemic lupus erythematosus who presented with a myocardial infarction resulting from a single clot in the distal left anterior descending coronary artery and to discuss the merits of evaluating such patients for the presence of antiphospholipid antibodies. METHODS: Case report and review of the literature. RESULTS: A 55-year-old woman with no risk factors for coronary artery disease presented with a myocardial infarction. A distal left anterior descending coronary artery clot was seen on angiography. Evaluation for the presence of a hypercoagulable state revealed evidence for systemic lupus erythematosus. Although lupus anti-coagulant and anticardiolipin antibody titers were negative, antiphosphatidylserine IgA antibodies were detected. CONCLUSION: Because antiphosphatidylserine antibodies of the IgA isotype have been shown to be associated with thrombosis and other manifestations of systemic lupus erythematosus, a complete evaluation for antiphospholipid antibodies should include testing for all three isotypes.

Antibodies, Antiphospholipid↗
PubMed2002

Platelets and cancer.

The presence of platelets in association with cancer deposits has been recognised for over 100 years; however, the recognition of a two-way interaction has been more recent. The link between cancer spread and platelet stimulation is pivotal to understanding of the hypercoagulable state found in most cancer patients. The assistance of platelets in cancer spread may provide opportunities to interrupt this relation, thus inhibiting metastasis.

Animals↗
PubMed2004

Pancreatic cancer and thromboembolic disease.

Thromboembolic disease is a common complication of pancreatic cancer and is causally associated with the generation of an intrinsic hypercoagulable state. Pancreatic-cancer cells activate platelets and express several procoagulant factors, including tissue factor and thrombin. The activation of coagulation is not simply an epiphenomenon, but might also be related to enhanced tumour growth and angiogenesis. Clinical manifestations of thromboembolic disease in pancreatic cancer include deep venous thrombosis, pulmonary embolism, disseminated intravascular coagulation, portal vein thrombosis, and arterial thromboembolism. Reported incidences of disease range from 17% to 57%. Treatment options include warfarin and low-molecular-weight heparins. Studies over the past decade suggest that long-term use of these heparins in both primary and secondary prevention of venous thromboembolic disease improves outcomes in comparison with warfarin. Further research is needed to understand better the morbidity and mortality associated with this disease in pancreatic cancer and to optimise strategies of prevention and treatment.

Anticoagulants↗
PubMed2003

Risk factors for thrombosis in pregnancy.

Pregnancy is a hypercoagulable state affecting both the coagulation and the fibrinolytic systems. Any exacerbation of the pre-disposing factors for coagulation may well lead to a thrombotic event more often in pregnant women than in the general population. Arterial thrombosis is very rare in pregnancy. Pre-eclampsia may be a risk factor for the development of arterial disease in later life. Venous thromboembolism (VTE) in pregnancy, although still rare, is a major cause of maternal mortality. Risk factors, such as older age, increased weight and emergency Caesarean section, as well as acquired and genetic thrombophilia, often coexist and reinforce each other. Appropriate thromboprophylaxis needs to be considered and applied on an individual basis. Uteroplacental thrombosis provides a common pathophysiological link between various poor pregnancy outcomes, including recurrent miscarriage, stillbirth, placental abruption, fetal growth restriction and pre-eclampsia. Its significance depends on the gestational age. Acquired and genetic thrombophilia may be associated with such conditions, particularly in early-onset disease. More data are required to assess the significance of such thrombophilias in obstetric practice. Any treatment should be in the context of clinical trials.

Female↗
PubMed2003

Acquired thrombophilias and pregnancy.

Acquired thrombophilias are hypercoagulable states secondary to various aetiologies. In particular, during pregnancy the risks are exaggerated due to the underlying physiological changes. The commonest cause of acquired thrombophilia in pregnancy is antiphospholipid syndrome. Antiphospholipid syndrome (APS) is a complex multisystem disorder that has been associated with varied medical and obstetric complications. The pathogenesis of APS has been further elucidated in recent studies. The two most clinically significant antiphospholipid antibodies that are associated with recurrent pregnancy loss and thromboembolism are anticardiolipin antibodies (aCL) and lupus anticoagulant (LA). The laboratory diagnosis is based on the presence of moderate to high positive aCL and/or LA antibodies. It is crucial that APS is not inappropriately diagnosed as this has implications for counselling and management with thromboprophylaxis during pregnancy. Over the last decade there have been significant changes in the laboratory and clinical criteria for the diagnosis of APS. National and international collaborations have made efforts to standardize the laboratory methods. There have been very few randomized placebo-controlled trials of drug therapy and so not all drug treatment strategies have a strong evidence base. With current management strategies, using low-molecular-weight heparin and aspirin, a greater than 70% live birth rate may be achieved in affected pregnancies. A multidisciplinary approach in the management of these women is vital.

Anticoagulants↗
PubMed2006

Activation of endothelial cells by antiphospholipid antibodies--a possible mechanism triggering thrombosis in patients with antiphospholipid syndrome.

Antiphospholipid syndrome (APS) is an antibody-mediated hypercoagulable state characterized by recurrent venous and arterial thromboembolic events. The presence of serum antibodies are collectively termed as antiphospholipid antibodies (aPL) and is the hallmark of the disease. Interest in the pathogenesis has mostly been focused on the blood coagulation factor. However, endothelial cells might play an important role. When stimulated, cell membrane would flip to expose negatively charged phospholipids and activation markers such as adhesive molecules may appear. We consider that these changes may play an important role in the initiation of the thrombotic process when endothelial cells encounter a PL. In this study, we incubated human umbilical vein endothelial cells (HUVECs) with IgG isolated from patients with APS and found that the HUVECs were activated by the expression of negatively charged phospholipids, as shown by high annexin V binding and negative propidium iodide staining and by an increase in the level of intracellular cell adhesion molecule-1 on the cell surface. The above findings indicate that endothelial cells can be activated on exposure to aPL and trigger the thrombotic event.

Adult↗
PubMed1996

Spontaneous internal jugular vein thrombosis and recurrent laryngeal nerve palsy: a rare simultaneous presentation of an occult malignant neoplasm.

Internal jugular vein thrombosis is an uncommon potentially life-threatening disorder caused by various conditions. Non-spontaneous internal jugular vein thrombosis is an uncommon condition associated in the pre-antibiotic area with deep-neck infections. Currently iatrogenic trauma to the internal jugular vein from catheterisation and repeated intravenous injections by drug abusers are the leading causes of thrombosis. Spontaneous internal jugular vein thrombosis may occur when there are no apparent pre-disposing mechanical or inflammatory causes although a few of these patients may harbour an occult malignant neoplasm. Hence, careful investigation and follow-up are vital. Thrombosis in Trousseau's syndrome is usually confined to the vascular system of the extremities and the viscera. However, secondary to the paraneoplastic hypercoagulable state, thrombosis can occur in the large veins of the head and neck region. We understand this to be the first case where spontaneous internal jugular vein thrombosis and ipsilateral recurrent laryngeal nerve paralysis were the only initial manifestations of an occult malignancy.

Aged↗
PubMed2002

Idiopathic free-floating thrombus of the common carotid artery.

BACKGROUND: The observation of an intraluminal common carotid artery thrombus overlying a wall defect at ultrasonography or angiography is unusual. To our knowledge, there are no previous reports of a free-floating thrombus in the common carotid artery. CASE REPORT: A 45-year-old woman who was previously healthy and on no medications presented with acute hemiparesis and aphasia. Following testing that included carotid duplex and transcranial Doppler ultrasonography, diffusion-weighted magnetic resonance imaging, and digital subtraction angiography, the patient underwent emergency open embolectomy. No underlying wall defect was seen at the time of imaging or surgery. No obvious hypercoagulable state could be identified. Her NIH Stroke Scale score improved from 26 at admission to 2 at three months and 1 at one year. CONCLUSIONS: Multimodal imaging may have improved diagnosis and management in this patient with a unique finding. The source of the thrombus remains obscure.

Carotid Artery Diseases↗
PubMed1997

Thrombophilia in Patients with Hypertriglyceridemia.

Objectives: To investigate a possible relationship between hypertriglyceridemia and the coagulation system, a Cardiovascular Risk Factor Two-township Study was conducted in Taiwan. Design: A case-control study. This longitudinal, prospective study focused on the evolution of cardiovascular disease risk factors with emphasis on haemostatic factors. Subjects: Hypertriglyceridemic subjects (triglyceride <2.26 mmoll+1, n = 327) and age-matched normal controls from a population screening program. Main outcome measures: Haemostatic parameters measured in this study included prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, factors VIIc and VIIIc, and antithrombin-III and plasminogen levels. Results: In our male hypertriglyceridemic subjects, aPTT was not significantly reduced, while significant elevations of factor VIIIc, factor VIIc, and plasminogen and antithrombin-III levels were noted. In the female hypertriglyceridemic subjects, the elevation of factor VIIc, factor VIIIc, and plasminogen and antithrombin-III levels was highly-significant, whereas aPTT was not significantly reduced. Unexpectedly, the levels of the established coronary risk factor, fibrinogen, did not show a statistically different change. Similar to previous data, our hypertriglyceridemic subjects also presented with hyperinsulinemia, glucose intolerance, upper body obesity, and elevated blood pressure. Conclusions: Despite the fact that in population studies, triglycerides do not consistently appear to be an independent risk factor for coronary heart disease, our data suggest that a pronounced increase in triglycerides warrants aggressive therapy, because this increase may be associated with a hypercoagulable state. This phenomenon contributes another perspective to the study of higher cardiovascular mortality in hypertriglyceridemic subjects.

Journal Article↗
PubMed2000

Decrease in protein C inhibitor activity and acquired APC resistance during normal pregnancy.

BACKGROUND: Since protein C inhibitor (PCI) inhibits activated protein C (APC) and a number of proteases, one would expect lower concentrations of PCI in a hypercoagulable state due to increased consumption of the inhibitor. Normal pregnancy is associated with a state of activated hemostasis, where response to APC is depressed. We aimed to study whether PCI function varies during normal pregnancy, and assess the relationship between this inhibitor and acquired APC resistance. METHODS: PCI activity in plasma was tested during pregnancy and postpartum in 28 healthy pregnant women without factor V Leiden Arg(506) - Gln mutation and in 14 non-pregnant female controls. The PCI levels determined in the present study was compared to the APC ratio (APC-r), we investigated previously, in the same samples. RESULTS: The levels of PCI in the pregnant group, as compared to that in the control group (4.74 +/- 0.48), gradually decreased from the first to the third trimester, i.e., 3.30 +/- 1.31 microg/mL in week 12 (p < 0.001), 2.66 +/- 1.44 microg/mL in week 20 (p < 0.001), 1.92 +/- 1.18 microg/mL in week 28 (p < 0.001), 1.30 +/- 0.94 microg/mL in week 32 (p < 0.001) and 1.49 +/- 1.12 microg/mL in week 37 (p < 0.001). After delivery, they rose to 5.02 +/- 1.93 microg/mL, similar to that in the controls (p > 0.05). The values of APC-r showed the same tendency during gestation and postpartum. CONCLUSION: With advance of normal pregnancy, decreasing PCI function corresponds to increasing APC resistance, probably due to that activated hemostasis acts as a link connecting the two variables.

Activated Protein C Resistance↗
PubMed2000

Emerging concepts in the diagnosis and management of venous thromboembolism during pregnancy.

Multiple changes in the coagulation system occur during pregnancy and account for the hypercoagulable state of pregnancy. Consequently, pregnant women are five times more likely to experience venous thromboembolism than non-pregnant women. Although the estimated rates of such events are low, venous thromboembolic disease is a leading cause of maternal death. The administration of intravenous or subcutaneous unfractionated heparin is the treatment and prophylaxis of choice. Warfarin is safe and efficacious following delivery, but should be avoided during pregnancy. LMWH is a promising alternative for treatment and prophylaxis, but further clinical experience is required.

Anticoagulants↗
PubMed1997

Elevation of platelet activating factor, inflammatory cytokines, and coagulation factors in the internal jugular vein of patients with subarachnoid hemorrhage.

The aim of the present study was to examine the changes of inflammatory and coagulation factors in blood of the internal jugular vein, not of peripheral vein, in patients with subarachnoid hemorrhage (SAH). The results show that while interleukin-6 (IL-6) and platelet activating factor (PAF) concentrations increased within first 4 days after SAH and remained elevated up to 14 days, interleukin-1 beta (IL-1 beta) showed a transient increase between 5-9 days after SAH and tumor necrosis factor-alpha (TNF-alpha) remained unchanged. Also different coagulation factors were increased between 5-9 days after SAH. Moreover, patients with delayed ischemic neurological deficits (DIND) displayed the highest levels of PAF and the coagulation factors, von Willebrand factor (vWF) and thrombin-antithrombin III complex (TAT). These results suggest that elevation of PAF and other inflammatory cytokines following SAH may cause the hypercoagulation state that is associated with cerebral vasospasm and internal jugular vein may be more adequate vessel for sampling blood to examine these factors.

Adult↗
PubMed2002

Congenital thrombophilia associated to obstetric complications.

During pregnancy there are hemostatic changes that result in a hypercoagulable state and can have thrombotic consequences. This condition can be aggravated in women who are carriers of congenital thrombophilic factors. This thrombotic tendency can manifest as thrombotic lesions in the placenta with compromise of utero-placental circulation, which are common characteristics present in obstetric complications, such as preeclampsia/eclampsia, miscarriage, fetal loss, intrauterine growth retardation, and abruptio placentae. In this paper we review data concerning about the association of congenital thrombophilia in pregnancy with obstetric complications, mainly preeclampsia and fetal loss, focusing in factor V Leiden and its related activated protein C resistance, prothrombin mutation G20210A and hyperhomocysteinemia related with C677T mutation of methylenetetrahydrofolate reductase. Although factor V Leiden has been the thrombophilic factor most studied, all three thrombophilic mutations have been related with obstetric complications; however, contradictory results about the specific association of each mutation with each type of obstetric complication are described. These discrepancies could obey to the ethnic difference of the studied groups, or to the fact that some studies were performed in closed populations with few migratory movement, where the genetic pool is relatively homogeneous, as well as the different inclusion and exclusion criteria. Even though this variability is present, the significance of recognizing true associations between these thrombophilic mutations and obstetric complications is essential in order to determine the likelihood of routinely screening for these conditions in pregnant women with risk factors for thrombosis and for carrying out specific prophylactic measures.

Female↗