fibrin and Rupture--Spontaneous

Although mortality rates from coronary heart disease in the western countries have declined in the last few decades, morbidity caused by this disease is increasing and a substantial number of patients still suffer acute coronary syndrome (ACS) and sudden cardiac death. Acute coronary syndrome occurs as a result of myocardial ischaemia and its manifestations include acute myocardial infarction and unstable angina. Culprit plaque morphology in these patients varies from thrombosis with or without coronary occlusion to sudden narrowing of the lumen from intraplaque haemorrhage. The coronary artery plaque morphologies primarily responsible for thrombosis are plaque rupture, and plaque erosion, with plaque rupture being the most common cause of acute myocardial infarction, especially in men. Autopsy data demonstrate that women <50 years of age more frequently have erosion, whereas in older women, the frequency of rupture increases with each decade. Ruptured plaques are associated with positive (expansive) remodelling and characterized by a large necrotic core and a thin fibrous cap that is disrupted and infiltrated by foamy macrophages. Plaque erosion lesions are often negatively remodelled with the plaque itself being rich in smooth muscle cells and proteoglycans with minimal to absence of inflammation. Plaque haemorrhage may expand the plaque rapidly, leading to the development of unstable angina. Plaque haemorrhage may occur from plaque rupture (fissure) or from neovascularization (angiogenesis). Atherosclerosis is now recognized as an inflammatory disease with macrophages and T-lymphocytes playing a dominant role. Recently at least two subtypes of macrophages have been identified. M1 is a pro-inflammatory macrophage while M2 seems to play a role in dampening inflammation and promoting tissue repair. A third type of macrophage, termed by us as haemoglobin associated macrophage or M(Hb) which is observed at site of haemorrhage also can be demonstrated in human atherosclerosis. In order to further our understanding of the specific biological events which trigger plaque instability and as well as to monitor the effects of novel anti-atherosclerotic therapies newer imaging modalities in vivo are needed.

Topics: Acute Coronary Syndrome; Cardiac Imaging Techniques; Chronic Disease; Coronary Artery Disease; Coronary Thrombosis; Female; Fibrin; Hemorrhage; Humans; Macrophages; Male; Necrosis; Plaque, Atherosclerotic; Platelet Aggregation; Risk Factors; Rupture, Spontaneous; Vascular Calcification

Inhibition of thrombosis is proving to be an important treatment goal in many clinical situations, including coronary thrombolysis, angioplasty, and unstable angina. Heparin is a potent inhibitor of thrombin and thrombin generation, but its ability to accelerate thrombolysis, prevent acute reocclusion after vascular injury in angioplasty, and prevent myocardial infarction in unstable angina is relatively limited, possibly because clot-bound thrombin plays an important role in these clinical situations. Thus, when thrombin binds to fibrin, it remains enzymatically active and relatively impervious to inactivation by heparin or other fluid-phase inhibitors. However, direct thrombin inhibitors--such as D-Phe-L-Pro-L-Arg-CH2Cl (PPACK), hirudin, hirugen, and hirulog--inhibit free and clot-bound thrombin with equal efficacy, presumably because their sites of interaction are not masked when thrombin binds to fibrin. Advanced clinical trials suggest that the direct thrombin inhibitors and 7E3, an inhibitor of platelet glycoprotein IIb/IIIa, will soon be incorporated into the armamentarium against arterial thrombosis.

Topics: Angioplasty, Balloon, Coronary; Animals; Arteriosclerosis; Blood Coagulation; Fibrin; Heparin; Humans; Rupture, Spontaneous; Thrombin; Thrombolytic Therapy

Liver pathology is one of the main features of HELLP syndrome and develops on the basis of a generalised activation of intravascular coagulation. Fibrin deposits and haemorrhagic necrosis predominantly develop in the periportal areas and may eventually lead to subcapsular haematomas or even rupture of the liver. While the compensated form of activation of intravascular coagulation, which is diagnosed by a decrease in antithrombin III and an increase in thrombin-antithrombin III complex (TAT) and the appearance of fibrin, monomers and D-dimers, is found in almost all cases of HELLP syndrome, the decompensated form of intravascular coagulation with prolonged bleeding time (PT, PTT) and drop in fibrinogen is found only in the most severe forms. The development of a decompensation of coagulation correlates with the appearance of severe complications such as liver haematoma, abruptio placentae, renal failure and pulmonary oedema. The best prophylaxis against the development of life-threatening complications is early diagnosis and termination of pregnancy after stabilisation of the maternal condition, consisting of magnesium sulphate infusion, antihypertensive treatment with dihydralazine or calcium antagonists, steroids etc. Severe complications of HELLP syndrome have occasionally been observed in the postpartum period. As prophylaxis against postpartal worsening of HELLP syndrome, curettage of the uterus and continuation of the treatment with calcium antagonists and dexamethasone have been recommended.

Topics: Biopsy; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Female; Fibrin; HELLP Syndrome; Hemorrhage; Humans; Infant, Newborn; Liver; Necrosis; Pregnancy; Rupture, Spontaneous

Fibrin and fibrinogen degradation products in the cerebrospinal fluid (CSF-FDP) were first studied in a group of 29 patients observed during the first and the second week after subarachnoid hemorrhage (SAH), then in a second group of 26 patients for a total of 55 patients. In the latter group only the first FDP value obtained as soon as possible after SAH was taken in consideration. In the whole series of 55 patients several noteworthy factors were found: 1) FDP determination should be performed as soon as possible after SAH; 2) CSF-FDP at or above 40, 80 micrograms/ml was found both in the patients with severe neurological deficits and in those with cerebral ischemia (statistically significant); 3) the significance of CSF-FDP in patients who rebled was also evaluated. In conclusion CSF-FDP could be considered useful in predicting cerebral ischemia.

Topics: Aneurysm, Ruptured; Biomarkers; Brain Ischemia; Cerebrospinal Fluid Proteins; Consciousness Disorders; Convalescence; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinolysis; Humans; Intracranial Aneurysm; Ischemic Attack, Transient; Recurrence; Rupture, Spontaneous; Severity of Illness Index; Subarachnoid Hemorrhage

Topics: Acrylic Resins; Alkenes; Animals; Arteries; Biocompatible Materials; Blood Coagulation; Blood Flow Velocity; Blood Vessel Prosthesis; Blood Vessels; Connective Tissue; Dilatation; Evaluation Studies as Topic; Fascia; Fibrin; Humans; Polyethylene Terephthalates; Polymers; Rupture, Spontaneous; Surface Properties; Suture Techniques; Thrombosis; Transplantation, Autologous; Veins

Topics: Animals; Antibodies, Bacterial; Bacteria; Blood Platelets; Coronary Disease; Endocarditis; Endocarditis, Bacterial; Endocarditis, Subacute Bacterial; Fibrin; Heart Failure; Heart Valves; Humans; Platelet Aggregation; Prognosis; Rupture, Spontaneous; Sepsis; Thrombosis

Topics: Abdomen, Acute; Blood Platelets; Endoscopy, Gastrointestinal; Esophageal and Gastric Varices; Fibrin; Hematemesis; Humans; Hypertension, Portal; Ligation; Liver Cirrhosis; Male; Middle Aged; Pressure; Rupture, Spontaneous; Treatment Outcome; Varicose Veins

Coagulation factor XI is proposed as therapeutic target for anticoagulation. However, it is still unclear whether the antithrombotic properties of factor XI inhibitors influence atherosclerotic disease and atherothrombosis. Our aim is to investigate whether factor XI antisense oligonucleotides could prevent thrombus formation on acutely ruptured atherosclerotic plaques.. Atherosclerotic plaques in the carotid arteries of Apoe(-/-) mice were acutely ruptured using ultrasound. The subsequent thrombus formation was visualized and quantified by intravital microscopy and immunohistochemistry. Mice were pretreated with either factor XI antisense or nonsense oligonucleotides (50 mg/kg) to lower factor XI plasma levels. A tail bleeding assay was used to determine the safety. On plaque rupture, initial platelet adhesion and platelet plug formation were not impaired in animals treated with factor XI antisense oligonucleotides. However, the ensuing thrombus formation and fibrin deposition were significantly lower after 5 to 10 minutes (P<0.05) in factor XI antisense oligonucleotide-treated animals without inducing a bleeding tendency. Furthermore, thrombi from antisense-treated animals were less stable than thrombi from placebo-treated animals. Moreover, macrophage infiltration and collagen deposition were lower in the carotid arteries of factor XI antisense-treated animals. No neutrophils were present.. Factor XI antisense oligonucleotides safely prevent thrombus formation on acutely ruptured atherosclerotic plaques in mice. Furthermore, perturbed carotid arteries from factor XI antisense-treated animals show a less severe inflammatory response.

Topics: Animals; Apolipoproteins E; Atherosclerosis; Blood Coagulation; Blood Platelets; Carotid Arteries; Carotid Artery Diseases; Cholesterol, Dietary; Collagen; Disease Models, Animal; Factor XI; Fibrin; Inflammation; Macrophages; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Oligonucleotides, Antisense; Plaque, Atherosclerotic; Platelet Adhesiveness; Platelet Aggregation; Rupture, Spontaneous; Thrombosis; Time Factors

Topics: Cellulitis; Fibrin; Hernia, Inguinal; Humans; Male; Middle Aged; Peritonitis; Postoperative Complications; Rupture, Spontaneous

Eighteen percent of heart specimens with isolated ventricular septal defect also had a floppy mitral valve. There was no statistical difference in the incidence of floppy mitral valve in the three age groups considered (less than 1 year, 1 to 16 years and 17 to 91 years). In no patient was a floppy mitral valve considered to be the cause of death. Complications of floppy mitral valve (ruptured chordae tendineae, bacterial endocarditis, mitral regurgitation and fibrin deposits at the mitral valve-left atrial angle) occurred at approximately the same frequency as that reported in autopsy studies of isolated floppy mitral valve. In the specimens with floppy mitral valve and ventricular septal defect, 63% also had floppiness of the tricuspid valve, 16% of the pulmonary valve and 5% of the aortic valve. The anatomic basis for floppy mitral valve was considered to be spongiosal invasion and disruption of the fibrosa of the valve leaflet. In this study, spongiosal invasion of the fibrosa was fully developed by 3 months of age and there was no evidence that the incidence or severity of spongiosal invasion increased between the ages of 3 months and 88 years. These data suggest that the floppy mitral valve is a congenital lesion that reaches full anatomic expression in infancy. No evidence was found that ventricular septal defect and floppy mitral valve share a common etiology.

Topics: Adolescent; Adult; Age Factors; Aged; Child; Child, Preschool; Chordae Tendineae; Endocarditis, Bacterial; Female; Fibrin; Heart Diseases; Heart Septal Defects, Ventricular; Humans; Infant; Male; Middle Aged; Mitral Valve; Mitral Valve Insufficiency; Mitral Valve Prolapse; Rupture, Spontaneous

A consumption coagulopathy was demonstrated in each of four patients with either ruptured aneurysm of the aorta or a dissecting aortic aneurysm. The most prominent features of this disorder were (1) a prolonged prothrombine time due to a decrease of one or more clotting factors, and (2) formation of fibrin and fibrinogen degradation products. Recognition of this coagulation disorder could be a valuable diagnostic tool to differentiate a ruptured or dissecting aortic aneurysm from other conditions with a similar acute onset. The coagulation disorder could be due to liberation of coagulant material from the aortic wall into the circulation or to an accumulation of clotting factors at the site of the lesion, secondary to the local exposition of tissue factors from the torn arterial wall. The probability of the latter mechanism is suggested by the local increase of radioactivity after the injection of 125I-fibrinogen.

Topics: Aged; Aortic Aneurysm; Blood Coagulation Tests; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Humans; Male; Middle Aged; Rupture, Spontaneous

Topics: Animals; Cattle; Cattle Diseases; Fibrin; Rupture; Rupture, Spontaneous; Urinary Bladder; Urinary Bladder Diseases

Topics: Adult; Antibodies; Antilymphocyte Serum; Azathioprine; Fibrin; Fluorescent Antibody Technique; Graft Rejection; Heparin; Humans; Hydrocortisone; Immunoglobulin G; Immunosuppression Therapy; Kidney; Kidney Transplantation; Male; Methylprednisolone; Nephrectomy; Postoperative Complications; Rupture, Spontaneous; Transplantation, Homologous

Topics: Aged; Aorta, Abdominal; Aortic Aneurysm; Autopsy; Blood Vessel Prosthesis; Fibrin; Fibrinogen; Fluorescent Antibody Technique; Humans; Immunoglobulin G; Kidney; Kidney Diseases; Kidney Glomerulus; Middle Aged; Polytetrafluoroethylene; Postoperative Complications; Rupture, Spontaneous

Topics: Adult; Aortic Valve; Capillaries; Epithelial Cells; Erythrocytes; Ethylene Oxide; Fibrin; Fibroblasts; Heart Valve Diseases; Heart Valves; Humans; Lactones; Leukocytes; Lymphocytes; Macrophages; Microscopy, Electron; Middle Aged; Plasma Cells; Rupture, Spontaneous; Sterilization; Transplantation, Homologous

Topics: Birth Weight; Blood Vessels; Female; Fibrin; Gestational Age; Glycosaminoglycans; Hematoma; Humans; Myofibrils; Placenta; Placenta Diseases; Pregnancy; Pregnancy Complications; Rupture, Spontaneous; Thromboembolism; Thrombosis; Umbilical Arteries

Topics: Aged; Anuria; Cystitis; Diverticulum; Duodenal Ulcer; Female; Fibrin; Hernia, Inguinal; Humans; Ileum; Laparotomy; Male; Necrosis; Peritonitis; Rupture, Spontaneous; Tuberculosis, Urogenital; Urinary Bladder Calculi; Urinary Bladder Diseases; Urinary Bladder Neoplasms; Urination Disorders; Urography