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2.
Semin Thromb Hemost ; 41(6): 549-55, 2015 Sep.
Article in English | MEDLINE | ID: mdl-26270112

ABSTRACT

Forming an interface with virtually every other organ, endothelium has a strategic role in modulating vascular homeostasis. While its miscellany of functions includes regulation of vasomotor tone, promotion, and prevention of vascular growth, and modulation of inflammatory and hemostatic processes, it functions critically in maintaining the balance of hemostasis in health. Whereas endothelium has been recognized to influence all stages of hemostasis, new evidence suggests it to have a primary role for thrombin generation. Endothelial dysfunction is being increasingly appreciated in several pathological states and particularly, by virtue of its critical role in hemostasis, in causing thrombosis in a multitude of diseases.


Subject(s)
Endothelium, Vascular/physiology , Hemostasis/physiology , Homeostasis/physiology , Thrombosis/blood , Animals , Antigens, CD/physiology , Endothelial Cells/pathology , Endothelial Cells/physiology , Endothelial Protein C Receptor , Endothelium, Vascular/pathology , Hormones/metabolism , Humans , Lipoproteins/physiology , Paracrine Communication , Receptors, Cell Surface/physiology , Thrombin/biosynthesis , Thrombomodulin/physiology , Thrombophilia/blood , Thrombophilia/etiology , Thrombophilia/pathology , Thromboplastin/physiology , Thrombosis/etiology , Thrombosis/pathology , von Willebrand Factor/physiology
3.
Semin Thromb Hemost ; 41(6): 665-72, 2015 Sep.
Article in English | MEDLINE | ID: mdl-26305235

ABSTRACT

It is well established that inflammation and thrombosis are intricately linked processes, and there is increasing evidence of the importance of their roles in activated complement in the pathogenesis of thromboembolism. The two systems are activated by similar stimuli simultaneously and interact, either directly or through biochemical mediators, to protect the host from microbial invasion. Diseases characterized by complement hyperactivity such as paroxysmal nocturnal hemoglobinuria and atypical hemolytic uremic syndrome have high rates of thrombosis. This review describes how disease processes where there is excessive complement activation leads to thrombosis, and the specific interactions between the complement and coagulation systems that lead to pathological thrombus formation.


Subject(s)
Complement Activation/physiology , Inflammation/blood , Thromboembolism/etiology , Antiphospholipid Syndrome/blood , Antiphospholipid Syndrome/complications , Antiphospholipid Syndrome/immunology , Blood Coagulation Factors/physiology , Cardiovascular Diseases/blood , Cardiovascular Diseases/complications , Hemoglobinuria, Paroxysmal/blood , Hemoglobinuria, Paroxysmal/complications , Hemoglobinuria, Paroxysmal/immunology , Humans , Immunity, Innate , Infections/blood , Infections/immunology , Inflammation/immunology , Inflammation Mediators/metabolism , Models, Biological , Platelet Activation , Thromboembolism/blood , Thromboembolism/immunology , Thrombophilia/blood , Thrombophilia/etiology , Thrombotic Microangiopathies/blood , Thrombotic Microangiopathies/immunology
4.
Blood Coagul Fibrinolysis ; 25(7): 671-4, 2014 Oct.
Article in English | MEDLINE | ID: mdl-24806321

ABSTRACT

Preeclampsia (P-EC) is a multisystem disorder of pregnancy whose cause and pathogenesis remain poorly understood. However, abnormal haemostasis and endothelial dysfunction are thought to be implicated. Women with a past medical history of P-EC have a baseline hypercoagulable state postpregnancy. The aim of this study is to examine the relationship between tissue factor (TF) and TF pathway inhibitor (TFPI) in women who have had P-EC within the last 3 years (more than 6 months postpartum) and their normal counterparts. Blood specimens were collected from women known to have had P-EC within the last 3 years (n = 26) and aged-matched healthy women without past history of P-EC in previous pregnancy (n = 26). Plasma TF and TFPI levels were measured using ELISAs. Women who have had P-EC showed increased TF levels compared with their normal counterparts, whereas TFPI levels were reduced. Neither parameter differed significantly when the groups were tested against each other. Interestingly, the TF/TFPI ratio was significantly increased (P = 0.024) when the two groups were compared. In summary, there was a trend towards increased TF and reduced TFPI levels in the P-EC group. Such a tendency was not statistically significant. However, the TF/TFPI ratio was significantly increased when the groups were compared. Our findings suggest an imbalance between TF/TFPI levels in women with past history of P-EC postpregnancy. This may contribute to the development of maternal hypercoagulable states and may predispose women with a history of P-EC to cardiovascular risks later in life.


Subject(s)
Lipoproteins/blood , Pre-Eclampsia/blood , Thrombophilia/blood , Thromboplastin/metabolism , Adult , Case-Control Studies , Female , Humans , Middle Aged , Pregnancy , Young Adult
5.
J Card Surg ; 28(4): 414-6, 2013 Jul.
Article in English | MEDLINE | ID: mdl-23692692

ABSTRACT

Heyde syndrome (the combination of iron deficiency anemia and aortic stenosis) has been a controversial entity. The proposed mechanisms between aortic valve disease and iron deficiency anemia are examined in this article along with impact valve replacement on iron deficiency anemia.


Subject(s)
Anemia, Iron-Deficiency/surgery , Aortic Valve Stenosis/surgery , Aortic Valve/surgery , Gastrointestinal Hemorrhage/etiology , Heart Valve Prosthesis Implantation , Aged , Anemia, Iron-Deficiency/etiology , Aortic Valve Stenosis/etiology , Bioprosthesis , Female , Humans , Syndrome , von Willebrand Diseases/etiology
8.
Blood Coagul Fibrinolysis ; 22(7): 600-5, 2011 Oct.
Article in English | MEDLINE | ID: mdl-21934489

ABSTRACT

The association between type 2 diabetes and cardiovascular disease is long recognized. Although perturbations of haemostatic markers have been shown to be associated with macrovascular disease in patients with type 2 diabetes, it is unclear whether these are primarily due to endothelial dysfunction or a result of inflammation. The present study was undertaken to elucidate whether elevated levels of factor VIII (FVIII) and von Willebrand factor (vWF) in women with type 2 diabetes represent endothelial dysfunction, inflammation or an alternate mechanism. Sixty-four women with type 2 diabetes were evaluated using ultrasonography Doppler for carotid intima-media thickness (IMT) and were classified as group A--having no (<1  mm), group B - mild (≥1  mm and no plaque) and group C--moderate (≥1 mm and presence of plaque and stenosis) macrovascular disease. Several haemostatic markers including, FVIII, vWF and fibrinogen were assessed. In addition, thrombomodulin, a marker for endothelial damage, and high-sensitivity C-reactive protein (hsCRP), an inflammatory marker, were also measured. A significant association of elevated FVIII was found in group B and C patients (i.e. patients with IMT ≥1 mm and with plaque). Elevated fibrinogen and vWF levels were also found but confined to group C patients. No significant difference among subgroups was found for any other variable evaluated (hsCRP, thrombomodulin and FVII). In conclusion, plasma FVIII levels are elevated in women with type 2 diabetes and macrovascular disease. It also appears that this is not mediated by inflammation or endothelial injury and is likely to be due to an alternate mechanism.


Subject(s)
Cardiovascular Diseases/blood , Diabetes Mellitus, Type 2/blood , Endothelium, Vascular/metabolism , Factor VIII/metabolism , Inflammation/blood , von Willebrand Factor/metabolism , Aged , Biomarkers/blood , C-Reactive Protein/analysis , Cardiovascular Diseases/complications , Cardiovascular Diseases/diagnostic imaging , Cardiovascular Diseases/physiopathology , Carotid Intima-Media Thickness , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/diagnostic imaging , Diabetes Mellitus, Type 2/physiopathology , Endothelium, Vascular/diagnostic imaging , Endothelium, Vascular/physiopathology , Female , Fibrinogen/metabolism , Humans , Inflammation/diagnostic imaging , Inflammation/physiopathology , Middle Aged , Thrombomodulin/blood , Tunica Intima/anatomy & histology , Tunica Intima/diagnostic imaging , Ultrasonography, Doppler, Color
9.
Br J Clin Pharmacol ; 72(4): 593-603, 2011 Oct.
Article in English | MEDLINE | ID: mdl-21752066

ABSTRACT

Conventional anticoagulants have proven efficacy in the management of thromboembolism. Their adverse effects and a narrow therapeutic window, necessitating regular need for monitoring, however, have long been an incentive for the development of safer anticoagulants without compromising efficacy. Over the last decade or so several new parenteral and oral anticoagulants have been launched with efficacy comparable with conventional agents. From fondaparinux to its long acting derivative idraparinux, and the factor Xa inhibitor rivaroxaban to the direct thrombin inhibitor dabigatran, the advent of new anticoagulants is radically changing anticoagulation. For conventional anticoagulants, despite their shortcomings, effective methods of reversing their anticoagulant effects exist. Moreover, strategies to deal with the occurrence of fresh thrombotic events in the face of therapeutic anticoagulation with the conventional agents have also been addressed. Nevertheless, for the new anticoagulants, the optimal management of these complications remains unknown. This review explores these issues in the light of current evidence.


Subject(s)
Anticoagulants/adverse effects , Benzimidazoles/adverse effects , Hemorrhage/chemically induced , Morpholines/adverse effects , Thiophenes/adverse effects , Thromboembolism/drug therapy , Thrombosis/drug therapy , beta-Alanine/analogs & derivatives , Dabigatran , Humans , Rivaroxaban , Treatment Failure , beta-Alanine/adverse effects
11.
Semin Thromb Hemost ; 37(2): 131-6, 2011 Mar.
Article in English | MEDLINE | ID: mdl-21370213

ABSTRACT

Pronounced hemostatic changes occur during pregnancy, and the balance shifts markedly in favor of hypercoagulability. Although primarily a result of a marked rise in the levels of several procoagulants and a fall in some natural anticoagulants, platelet activation also contributes to this prothrombotic tendency. Several studies have confirmed the accentuation of platelet activation in pre-eclampsia (P-EC), which remains an important obstetric complication affecting ~2 to 4% of pregnancies. Although there is still a long way to go, significant inroads have been made in the understanding of this enigmatic condition. Whereas the pathogenesis of P-EC is protean and involves a complex interplay of placental and maternal tissues, platelet activation is likely to contribute to several clinical features. Several techniques have been used to assess platelet activation in P-EC. Detection of aberrations of platelet function and activation appear to have predictive value for its diagnosis. The findings also lend support to the use of antiplatelet agents as prophylaxis in those women with a high risk of developing the condition.


Subject(s)
Blood Platelets/physiology , Pre-Eclampsia/blood , Antigens, CD/blood , Biomarkers/blood , Blood Pressure , Female , Humans , Infant, Newborn , P-Selectin/biosynthesis , Platelet Activation , Platelet Aggregation Inhibitors/therapeutic use , Platelet Membrane Glycoproteins , Pre-Eclampsia/drug therapy , Pregnancy , Tetraspanin 30
12.
Semin Thromb Hemost ; 37(2): 153-7, 2011 Mar.
Article in English | MEDLINE | ID: mdl-21370217

ABSTRACT

A plethora of evidence exists to show that endothelial perturbations underlie many of the clinical features of pre-eclampsia (P-EC), and consequently the markers signifying endothelial disturbance exhibit a rise in plasma. Among others, plasma thrombomodulin (TM) level rises significantly. TM is a transmembrane glycoprotein expressed abundantly on the endothelium of the microvasculature. It neutralizes the thrombotic potential of thrombin, mediating this anticoagulant effect through activation of protein C. Endothelial injury results in a localized loss of TM with a focal impairment of protein C activation and resultant thrombotic tendency. Mainly expressed on the endothelial cells, a small amount of TM is found in plasma with levels rising in certain pathological conditions. Although elevation in levels of TM can be due to endothelial TM proteolysis secondary to endothelial insult, ineffective clearance may account for this in renal and hepatic dysfunction. In P-EC not only is there ongoing endothelial injury, but renal function is also affected. To establish the cause of elevated TM level in P-EC, three groups of pregnant women were investigated. It appears that the elevation in plasma TM is not related to renal or hepatic dysfunction in P-EC. It is more likely that plasma TM is derived from placental or vascular endothelial cells subsequent to activation or damage, confirming the hypothesis that damage to vascular endothelial cells is the primary underlying cause of P-EC.


Subject(s)
Endothelium, Vascular/metabolism , Pre-Eclampsia/blood , Thrombomodulin/blood , Alanine Transaminase/blood , Aspartate Aminotransferases/blood , Creatinine/blood , Endothelium, Vascular/pathology , Female , Humans , Hypertension, Pregnancy-Induced/blood , Pregnancy , Protein C/metabolism , Urea/blood
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