fibrin and Heart-Failure

Topics: Animals; Blood Coagulation; Blood Platelets; Fibrin; Heart Failure; Heart-Assist Devices; Humans; Platelet Activation; Prosthesis Design; Regional Blood Flow; Risk Factors; Stress, Mechanical; Thrombosis; Ventricular Function, Left

Topics: Animals; Antifibrinolytic Agents; Autopsy; Blood Coagulation Factors; Dogs; Fibrin; Fibrinolysis; Fibrinolytic Agents; Heart Failure; Humans; Hypoxia; Kidney; Lung; Lymph; Plasminogen Activators; Plasminogen Inactivators; Prostaglandins; Pulmonary Embolism; Pulmonary Veins; Respiration; Respiratory Insufficiency; Syndrome; Thrombin; Wounds and Injuries

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: Animals; Antibodies; Arteries; Blood Platelets; Capillaries; Coronary Disease; Coronary Vessels; Cortisone; Dogs; Endocarditis; Fibrin; Graft Rejection; Heart Failure; Heart Transplantation; Hemorrhage; Humans; Immunosuppression Therapy; Immunosuppressive Agents; Infections; Kidney Transplantation; Male; Microscopy, Electron; Middle Aged; Myocarditis; Myocardium; Necrosis; Rabbits; Shwartzman Phenomenon; Time Factors; Transplantation Immunology; Transplantation, Homologous

Cardiovascular disease is the leading cause of death in the United States, which can result in blockage of a coronary artery, triggering a myocardial infarction (MI), scar tissue formation in the myocardium, and ultimately heart failure. Currently, the gold-standard solution for total heart failure is a heart transplantation. An alternative to total-organ transplantation is surgically remodeling the ventricle with the implantation of a cardiac patch. Acellular cardiac patches have previously been investigated using synthetic or decellularized native materials to improve cardiac function. However, a limitation of this strategy is that acellular cardiac patches only reshape the ventricle and do not increase cardiac contractile function. Toward the development of a cardiac patch, our laboratory previously developed a cell-populated composite fibrin scaffold and aligned microthreads to recapitulate the mechanical properties of native myocardium. In this study, we explore micropatterning the surfaces of fibrin gels to mimic anisotropic native tissue architecture and promote cellular alignment of human induced pluripotent stem cell cardiomyocytes (hiPS-CM), which is crucial for increasing scaffold contractile properties. hiPS-CMs seeded on micropatterned surfaces exhibit cellular elongation, distinct sarcomere alignment, and circumferential connexin-43 staining at 14 days of culture, which are necessary for mature contractile properties. Constructs were also subject to electrical stimulation during culture to promote increased contractile properties. After 7 days of stimulation, contractile strains of micropatterned constructs were significantly higher than unpatterned controls. These results suggest that the use of micropatterned topographic cues on fibrin scaffolds may be a promising strategy for creating engineered cardiac tissue.

Topics: Fibrin; Heart Failure; Humans; Induced Pluripotent Stem Cells; Myocardium; Myocytes, Cardiac; Tissue Engineering; Tissue Scaffolds

Mesenchymal stromal cell (MSC) transplantation has been investigated as an advanced treatment of heart failure; however, further improvement of the therapeutic efficacy and mechanistic understanding are needed. Our previous study has reported that epicardial placement of fibrin sealant films incorporating rat amniotic membrane-derived (AM)-MSCs (MSC-dressings) could address limitations of traditional transplantation methods. To progress this finding toward clinical translation, this current study aimed to examine the efficacy of MSC-dressings using human AM-MSCs (hAM-MSCs) and the underpinning mechanism for myocardial repair. Echocardiography demonstrated that cardiac function and structure were improved in a rat ischemic cardiomyopathy model after hAM-MSC-dressing therapy. hAM-MSCs survived well in the rat heart, enhanced myocardial expression of reparative genes, and attenuated adverse remodeling. Copy number analysis by qPCR revealed that upregulated reparative genes originated from endogenous rat cells rather than hAM-MSCs. These results suggest hAM-MSC-dressing therapy stimulates a secondary release of paracrine factors from endogenous cells improving myocardial repair ("secondary paracrine effect"), and cardiac M2-like macrophages were identified as a potential cell source of repair. We demonstrated hAM-MSCs increased M2-like macrophages through not only enhancing M2 polarization but also augmenting their proliferation and migration capabilities via PGE

Topics: Animals; Cell Polarity; Cell Proliferation; Cells, Cultured; Disease Models, Animal; Echocardiography; Female; Fibrin; Gene Expression Regulation; Heart Failure; Humans; Macrophages; Mesenchymal Stem Cell Transplantation; Mesenchymal Stem Cells; Mice; Rats

The objective of this study was to bioengineer 3D patches from cardiac myocytes that have been reprogrammed from human adipogenic mesenchymal stem cells (hADMSCs).. Human adipogenic mesenchymal stem cells (hADMSCs) were reprogrammed to form cardiac myocytes using transcription factors ETS2 and MESP1. Reprogrammed cardiac myocytes were cultured in a fibrin gel to bioengineer 3D patch patches. The effect of initial plating density (1-25 million cells per patch), time (28-day culture period) and treatment with 1 μM isoproterenol and 1 μM epinephrine were evaluated.. 3D patches were fabricated using cardiac myocytes that have been reprogrammed from hADMSCs. Based on optimization studies, it was determined that 10 million cells were needed to bioengineer a single patch, that measured 2 × 2 cm. Based on the results of this study, there is evidence to support the successful fabrication of a highly functional 3D patches with measurable electrical activity using cardiac myocytes reprogrammed from hADMSCs. 3D patches fabricated using optimal conductions described in this study can be used to improve the functional properties of failing hearts. Predominantly, in case of the infarcted hearts with partial loss of electrical activity, the electrical properties of the 3D patches may restore the electrical activity of the heart.

Topics: Adipogenesis; Adrenergic Agonists; Cells, Cultured; Cellular Reprogramming; Cellular Reprogramming Techniques; Electric Conductivity; Epinephrine; Fibrin; Gene Expression Regulation; Heart Failure; Humans; Isoproterenol; Membrane Potentials; Mesenchymal Stem Cell Transplantation; Mesenchymal Stem Cells; Myocytes, Cardiac; Time Factors; Tissue Engineering

The clinical benefit of second-generation drug-eluting stents (2nd DES) has been established, compared to first-generation drug-eluting stents (1st DES). However, pathological response after 2nd DES implantation remains unclear, particularly in the Japanese population.. Using specimens obtained by autopsy, we compared the histology between 2nd DES (41 sections) and 1st DES (38 sections) lesions within 1 year after stent implantation to evaluate early tissue reaction in Japanese patients. Stent segments were fixed with 10% buffered formalin and embedded in plastic, followed by hematoxylin-eosin and Masson's trichrome staining. Ratio of covered stent struts was calculated, and the area of fibrin deposition was morphometrically evaluated. The degree of inflammation around struts was examined semi-quantitatively (score 0-3).. The ratio of covered struts and mean fibrin area of 2nd DES were 0.69±0.05 and 658.0±173.4μm. Histopathological analysis showed advanced healing process in 2nd DES compared with 1st DES lesions. These results are consistent with clinical beneficial outcome of 2nd DES implantation.

Topics: Aged; Aneurysm, Ruptured; Colitis, Ischemic; Coronary Vessels; Drug-Eluting Stents; Everolimus; Female; Fibrin; Heart Failure; Humans; Inflammation; Japan; Male; Middle Aged; Neointima; Pancreatitis; Pneumonia; Renal Insufficiency; Risk Factors; Sepsis; Sirolimus; Treatment Outcome

Cardiac-committed cells and biomimetic scaffolds independently improve the therapeutic efficacy of stem cells. In this study we tested the long-term effects of their combination.. Eighty immune-deficient rats underwent permanent coronary artery ligation. Five to 7 weeks later, those with an echocardiographically measured ejection fraction (EF) ≤55% were re-operated on and randomly allocated to receive a cell-free fibrin patch (n = 25), a fibrin patch loaded with 700,000 human embryonic stem cells (ESC) pre-treated to promote early cardiac differentiation (SSEA-1(+) progenitors [n = 30]), or to serve as sham-operated animals (n = 25). Left ventricular function was assessed by echocardiography at baseline and every month thereafter until 4 months. Hearts were then processed for assessment of fibrosis and angiogenesis and a 5-component heart failure score was constructed by integrating the absolute change in left ventricular end-systolic volume (LVESV) between 4 months and baseline, and the quantitative polymerase chain reaction (qPCR)-based expression of natriuretic peptides A and B, myosin heavy chain 7 and periostin. All data were recorded and analyzed in a blinded manner.. The cell-treated group consistently yielded better functional outcomes than the sham-operated group (p = 0.002 for EF; p = 0.01 for LVESV). Angiogenesis in the border zone was also significantly greater in the cell-fibrin group (p = 0.006), which yielded the lowest heart failure score (p = 0.04 vs sham). Engrafted progenitors were only detected shortly after transplantation; no grafted cells were identified after 4 months. There was no teratoma identified.. A fibrin scaffold loaded with ESC-derived cardiac progenitors resulted in sustained improvement in contractility and attenuation of remodeling without sustained donor cell engraftment. A paracrine effect, possibly on innate reparative responses, is a possible mechanism for this enduring effect.

Topics: Angiogenesis Inducing Agents; Animals; Cell Adhesion Molecules; Coronary Vessels; Echocardiography; Embryonic Stem Cells; Female; Fibrin; Heart Failure; Humans; Immunohistochemistry; Ligation; Mice, Nude; Myocardium; Myosin Heavy Chains; Natriuretic Peptides; Polymerase Chain Reaction; Rats; Stem Cells; Stroke Volume; Tissue Scaffolds; Ventricular Function, Left

To determine whether dogs with ascites secondary to right-sided congestive heart failure (CHF) have bleeding disorders associated with hypofibrinogenemia and discordant plasma fibrin-fibrinogen degradation products (FDPs) and D-dimer assay results (ie, a circulating concentration of FDPs higher than the reference range and a circulating concentration of D-dimer within the reference range).. Retrospective case-control study.. 80 client-owned dogs.. Dogs with ascites secondary to right-sided CHF (group 1; n = 20), unhealthy dogs without cardiac disease (group 2; 40), and dogs with left-sided CHF (group 3; 20) were included in the study. Urine bile acids-to-creatinine concentration ratios were calculated as a marker of liver function. Differences among groups regarding coagulation profile analysis results and prevalence of discordant FDPs and D-dimer assay results were determined.. No significant differences were detected among the 3 groups regarding urine bile acids-to-creatinine concentration ratios. Plasma fibrinogen concentration was significantly lower for group 1 versus groups 2 or 3. Prevalence of discordant FDPs and D-dimer assay results was significantly higher for group 1 versus groups 2 or 3. Eighteen group 1 dogs had discordant FDPs and D-dimer assay results. Ten of these dogs had concurrent hypofibrinogenemia, 2 of which had clinical signs of bleeding. Only 10 dogs in groups 2 or 3 had discordant FDPs and D-dimer assay results; none of these dogs had hypofibrinogenemia or clinical signs of bleeding.. Dogs with right-sided CHF and ascites may be at increased risk for primary hyperfibrinogenolysis (ie, hypofibrinogenemia and discordant FDPs and D-dimer assay results).

Topics: Animals; Ascites; Biomarkers; Blood Coagulation Disorders; Cardiovascular Agents; Case-Control Studies; Dog Diseases; Dogs; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Heart Failure; Male; Partial Thromboplastin Time; Prothrombin Time; Retrospective Studies

Thromboembolic complications occur more frequently in patients with chronic heart failure (CHF) than in the general population. Formation of a compact fibrin clot resistant to lysis has been shown in arterial and venous thrombosis.. To investigate fibrin clot properties in patients with CHF.. Plasma clot permeability, compaction, turbidity and fibrinolysis were assessed in 36 consecutive patients with stable CHF (30M, 6F; aged 64+/-10 years, left ventricular ejection fraction (LVEF) 34.9+/-6.7%) and 36 controls matched for age, sex, cardiovascular risk factors and medication. Exclusion criteria were LVEF >40%, anticoagulant therapy, previous thromboembolic events, atrial fibrillation.. Clots obtained from plasma of patients with CHF had 23% lower clot permeability (p<0.0001), 13% less clot compaction (p<0.001), 15% faster fibrin polymerisation (p<0.0001) and tended to have prolonged fibrinolysis time (p=0.1) compared with controls. C-reactive protein and fibrinogen were associated inversely with clot permeability (R(2)=0.84, p<0.0001 and R(2)=0.79, p<0.0001, respectively) and positively with fibrinolysis time (R(2)=0.88, p<0.0001 and R(2)=0.80, p<0.0001, respectively) in patients with CHF. Plasma thrombin-antithrombin complex concentrations were inversely correlated with clot permeability (R(2)=0.88, p<0.0001) and positively with fibrinolysis time (R(2)=0.91, p<0.0001). Left atrium diameter, but not LVEF, correlated with fibrinolysis time (R(2)=0.61, p=0.027).. Patients with CHF with sinus rhythm are characterised by faster formation of compact plasma fibrin clots, which might predispose to thromboembolic complications.

Topics: Aged; Aged, 80 and over; Blood Coagulation; Blood Coagulation Tests; Case-Control Studies; Female; Fibrin; Fibrinolysis; Heart Failure; Heart Rate; Hemorheology; Humans; Male; Middle Aged; Thromboembolism; Ultrasonography

A warfarin treated patient unexpectedly presented with an elevated international normalized ratio (INR). Repeat testing in two laboratories gave conflicting results. The chromogenic assay of factor X was used to determine the correct INR result. The patient had laboratory results consistent with a dysfibrinogenemia, which prevented detection of the endpoint with a photo-optical detection system. The chromogenic assay of factor X is recommended for monitoring patients on warfarin when the INR cannot be accurately determined due to interference with the fibrin endpoint in the INR.

Topics: Aged; Anticoagulants; Blood Coagulation; Chromogenic Compounds; Factor X; Female; Fibrin; Fibrinogen; Heart Failure; Humans; International Normalized Ratio; Lung Neoplasms; Prothrombin Time; Time Factors; Warfarin

Prosthetic heart valve obstruction is a severe and potentially fatal complication. We present a patient with a Bjork-Shiley prosthetic mitral and aortic valve implantation and recurrent pulmonary edema. Echocardiogram showed a rate-dependent "obstruction alternans" of the prosthetic mitral valve due to pannus formation.

Topics: Aged; Aortic Valve; Echocardiography, Doppler; Electrocardiography; Female; Fibrin; Heart Failure; Heart Rate; Heart Valve Prosthesis; Humans; Mitral Valve; Postoperative Complications; Prosthesis Design; Prosthesis Failure; Pulmonary Edema; Reoperation; Thrombosis

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.

Topics: Adult; Anticoagulants; Fibrin; Heart Failure; Heart Transplantation; Heart-Assist Devices; Humans; Male; Monitoring, Physiologic; Thrombelastography; Thrombophilia

Repeated thoracenteses is indicated in patients with refractory, symptomatic transudative effusions. However, their effect on cytokines and fibrinolytic activity in pleural transudates remains unclear.. Twenty-one patients with symptomatic, large amount of free-flowing transudative effusions caused by heart failure were studied. Thoracentesis with drainage of 500 mL of pleural fluid per day was done for 3 consecutive days (days 1 to 3). Pleural fluid characteristics, tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-8, vascular endothelial growth factor (VEGF), tissue-type plasminogen activator (tPA), and plasminogen activator inhibitor type 1 (PAI-1) were measured during each tap. Chest ultrasonography was done on day 6 to detect the fibrin strands in pleural effusion and the outcome of effusion was evaluated within 7 days after repeated thoracenteses.. Effusion levels of lactate dehydrogenase, neutrophils, TNF-alpha, IL-1 beta, IL-8, VEGF, and PAI-1 increased significantly during repeated thoracenteses. Furthermore, the values of PAI-1 and PAI-1/tPA obtained on days 2 and 3 were highly correlated with those of TNF-alpha, IL-1 beta, IL-8, and VEGF. On day 6, pleural fibrins were observed on chest ultrasonography in 6 patients (29%, fibrinous group) but were absent in the remaining 15 patients (nonfibrinous group). Compared with the nonfibrinous group, the effusion levels of TNF-alpha, IL-1 beta, VEGF, and PAI-1 on day 2 and day 3, and recurrence of symptomatic effusion after repeated thoracenteses were significantly higher in fibrinous group.. Repeated thoracenteses may induce local release of proinflammatory cytokines, VEGF and PAI-1, which may result in fibrin deposition and impair resolution of pleural transudates.

Topics: Aged; Aged, 80 and over; Cell Count; Cytokines; Erythrocytes; Female; Fibrin; Fibrinolysis; Glucose; Heart Failure; Humans; Hydrogen-Ion Concentration; Interleukin-1beta; L-Lactate Dehydrogenase; Leukocytes; Lung; Male; Paracentesis; Plasminogen Activator Inhibitor 1; Pleural Effusion; Retreatment; Tissue Plasminogen Activator; Tumor Necrosis Factor-alpha; Vascular Endothelial Growth Factor A

To investigate whether there are any basic abnormalities of coagulation and fibrinolysis in muscular dystrophy, we measured serum levels of the MM isozyme of creatine kinase (CK-MM), fibrin and fibrinogen degradation products (FDP), plasma levels of fibrinogen, antithrombin (AT), and D-dimer in 36 patients with Duchenne muscular dystrophy (DMD), 11 with Becker muscular dystrophy (BMD), 5 with Fukuyama congenital muscular dystrophy (FCMD), 5 with myotonic dystrophy (MyD), and 5 with spinal muscular atrophy (SMA) type 2. FDP levels were elevated in the patients with DMD, BMD, and FCMD (1.0 to 84.9 microg/ml), but not in the patients with MyD and SMA type 2. In DMD, BMD, and FCMD, FDP levels significantly correlated with CK-MM, but not with age, fibrinogen, AT, D-dimer, and type of dystrophy (multiple regression analysis; r(2) = 0.814, P < 0.0001). These findings suggested that enhanced coagulation and fibrinolysis are associated with muscle degeneration in patients with DMD, BMD, and FCMD.

Topics: Adolescent; Adult; Blood Coagulation Disorders; Child; Creatine Kinase; Creatine Kinase, MM Form; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Heart Failure; Humans; Isoenzymes; Male; Muscular Dystrophy, Duchenne; Regression Analysis; Spinal Muscular Atrophies of Childhood

Topics: Cardiomyopathy, Dilated; Fibrin; Heart Failure; Humans; Kidney; Male; Middle Aged; Radionuclide Imaging; Radiopharmaceuticals; Technetium Tc 99m Aggregated Albumin

Intrapleural fibrin deposition commonly accompanies pleural injury and may contribute to the organization of exudative pleural effusions, which leads to lung entrapment. Previous investigators have observed an increase in procoagulant proteins in pleural effusions but very little thrombin formation. FVa is the protein cofactor in the prothrombinase complex that dramatically enhances the generation of thrombin from prothrombin by the serine protease fXa. The presence of fVa within the pleural space could influence fibrin formation and pleural scarification. We examined pleural fluids obtained from patients who had lung cancer, CHF, and empyema for the presence of fV/fVa. The fV antigen was increased in exudative pleural fluids, in comparison with transudates. However, the specific activity of fV antigen present in exudates was significantly less than that observed for the lower concentration of antigen present in transudate and could not be activated to the same degree by thrombin. Immunoblots of fV antigen in exudates indicated that fV was partially cleaved and inactivated by unidentified proteases. We conclude that although fV is present in pleural fluid, it may be present in a degraded form, which may partially account for a lack of thrombin-generating capacity in these pleural fluids. The presence of fV does not necessarily correlate with pleural loculation.

Topics: Blood Coagulation Factors; Empyema; Factor V; Fibrin; Fibrinolysin; Glucose; Heart Failure; Humans; Immunoblotting; L-Lactate Dehydrogenase; Lung Neoplasms; Molecular Weight; Pleural Effusion; Thrombin

Two-dimensional transesophageal echocardiographic findings are reported in 13 patients with structurally and functionally normal St. Jude Medical bileaflet mitral valve prostheses. Multiple mobile linear echogenic densities attached to the pivot of the prosthesis were present in 9 of 13 patients. These densities may represent fibrin strands. These mobile strands alternatively resolve and reform over a period of 5 to 14 months after mitral valve replacement. No adverse clinical events were attributable to these prosthetic mitral valve strands. We conclude that mobile stands are frequently attached to the structurally and functionally normal St. Jude Medical mitral valve prosthesis. The clinical significance of these prosthetic mitral valve strands requires clarification.

Topics: Adult; Aged; Aged, 80 and over; Chi-Square Distribution; Echocardiography; Female; Fibrin; Heart Failure; Heart Valve Prosthesis; Humans; Male; Middle Aged; Mitral Valve

The potential importance of pleural fibrin deposition in the pathogenesis of pleural injury is supported by both clinical and experimental observations. We hypothesized that the local equilibrium between procoagulant and fibrinolytic activities is disrupted to favor fibrin deposition in exudative pleuritis. To test this hypothesis, we characterized procoagulant and fibrinolytic activities in pleural exudates from patients with pneumonia, lung cancer, or empyema and transudates from patients with congestive heart failure. Procoagulant activity was generally increased in exudative processes and was due mainly to tissue factor. All effusions contained antithrombin III and inhibited factor Xa and thrombin, but endogenous prothrombinase or thrombin activities were variably detected. Pleural fluid fibrinolytic activity was increased in congestive heart failure and was due to both tissue plasminogen activator and urokinase. Depressed fibrinolytic activity was found in pleural exudates despite increased concentrations of plasminogen, mainly glu-1-plasminogen, and was due to inhibition of plasminogen activation by plasminogen activator inhibitors 1 and 2 and of plasmin, in part by alpha 2-antiplasmin. Concentrations of PAI-1 in exudative pleural fluids were increased up to 913-fold, compared with normal pooled plasma. Exudative pleural effusions are characterized by increased procoagulant and depressed fibrinolytic activity, favoring fibrin deposition in the pleural space. The balance of these activities is reversed and favors fibrin clearance in congestive heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Blood Coagulation; Blood Coagulation Factors; Empyema; Fibrin; Fibrinolysis; Heart Failure; Humans; Pleura; Pleural Effusion; Pleural Effusion, Malignant; Pneumonia

Patients with the hypereosinophilic syndrome (HES) are at increased risk of thrombosis and have signs of fibrin deposition in the myocardial cavity; the pathogenesis of these complications is still unknown. We have studied a 51-year-old man affected by HES with heart, lung, skin, and gastrointestinal involvement. Routine laboratory parameters of the hemostatic system were normal with the exception of blood fibrinolytic activity. The latter was evaluated by both diluted blood clot lysis time and euglobulin lytic activity on fibrin plates before and after 10 min venous occlusion. The fibrinolytic activity measured on four occasions during a 3-month period, was impaired both in basal conditions and following venous occlusion. Platelet studies on two different occasions before and during therapy showed spontaneous platelet aggregation, lowered threshold concentrations of various aggregating agents, reduced platelet regeneration time and increased plasma beta-thromboglobulin concentration. The patient's polymorphonuclear cells (more than 75% eosinophils) were devoid of any procoagulant activity (PCA). Instead, patient's mononuclear cells studied before therapy generated significantly higher PCA on stimulation by endotoxin than cells from control subjects. The procoagulant response to endotoxin decreased markedly during therapy. The observed abnormalities could, at least partially, contribute to fibrin deposition in HES.

Topics: beta-Thromboglobulin; Blood Coagulation Factors; Blood Coagulation Tests; Eosinophilia; Fibrin; Fibrinolysis; Heart Failure; Humans; Male; Middle Aged; Platelet Aggregation; Syndrome

During a period of 18 months, between July 1978 and January 1980, 4 adult horses were referred to the New York State College of Veterinary Medicine with evidence of congestive heart failure. Characteristic clinical abnormalities included marked muffling of heart sounds, tachycardia, jugular vein distention, and peripheral edema. Treatment with antibiotics, diuretics, and anti-inflammatory drugs was unsuccessful, and all four died or were euthanatized and necropsied. At necropsy, there was marked distention of the pericardial sac with fluid, and thick layers of fibrin were deposited uniformly over the epicardium. In 3 cases, attempts to isolate bacteria and viruses from pericardial fluid were unsuccessful; in the 4th case, Actinobacillus equuli was isolated on culture of the pericardial fluid.

Topics: Actinobacillus; Animals; Electrocardiography; Female; Fibrin; Heart Failure; Horse Diseases; Horses; Lung; Pericarditis; Radiography

A 31-year-old man presented with rapid onset of intractable congestive heart failure during the course of chemotherapy for eosinophilic leukemia. Patients with a hypereosinophilic syndrome usually die from complications of eosinophilic infiltration and fibrosis in target organs. The resulting cardiac lesions are a cause of death among these patients. Surgical intervention enabled our patient to survive the immediate medical crisis and has prolonged his life.

Topics: Adult; Endocardium; Eosinophils; Fibrin; Heart Failure; Humans; Leukemia; Male

Patients with ischaemic heart disease of severe forms with congested insufficiency of the circulation have chronic latent disseminated intravascular blood coagulation, which is confirmed by the increased level of soluble fibrin, products of breakdown of fibrinogen-fibrin, decreased activity of antithrombin III, marked sludging of erythrocytes at the microcirculatory level. A high degree of the correlation between the content of soluble fibrin and the marked sludge-phenomenon was found. Thromboembolic complications arising in this group of patients were accompanied by marked progress of the disorders found, which permitted one to isolate a limited as the the number of parameters coagulogram for the diagnosis of acute intravascular thrombosis in the patients with ischaemic heart diseases with congested insufficiency of the circulation. The important role of a preserved plasmin system for the prognosis in patients with congested insufficiency of the circulation with thromboembolic complications is shown.

Topics: Aged; Antithrombin III; Coronary Disease; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Heart Failure; Humans; Male; Middle Aged; Syndrome; Thromboembolism

Topics: Aged; Arthritis, Rheumatoid; Blood Cell Count; Blood Platelets; Carbon Radioisotopes; Collagen Diseases; Factor XIII; Female; Fibrin; Fibrinolysis; Heart Failure; Humans; Hypertension, Malignant; Infections; Leukemia; Liver Diseases; Neoplasms; Pulmonary Embolism; Sepsis; Streptokinase

Topics: Acenocoumarol; Aged; Fibrin; Fibrinogen; Half-Life; Heart Failure; Heparin; Humans; Injections, Intravenous; Iodine Radioisotopes; Leg; Middle Aged; Radionuclide Imaging; Thrombophlebitis

Topics: Adult; Aged; Alpha-Globulins; Arm; Constriction; Female; Fibrin; Fibrinogen; Fibrinolysis; Heart Defects, Congenital; Heart Diseases; Heart Failure; Humans; Macroglobulins; Male; Middle Aged; Plasminogen; Serum Globulins; Trypsin Inhibitors; Veins

Topics: Aged; Angiography; Antigens; Female; Femoral Neck Fractures; Fibrin; Fibrinogen; Fibrinolysis; Heart Failure; Humans; Iodine Radioisotopes; Male; Neoplasm Metastasis; Postoperative Complications; Pulmonary Embolism; Radionuclide Imaging; Sepsis; Thrombophlebitis

Topics: Arrhythmias, Cardiac; Burns; Diabetic Coma; Fibrin; Fibrinogen; Heart Failure; Humans; Intensive Care Units; Lung Diseases, Obstructive; Myocardial Infarction; Poisoning; Shock, Cardiogenic; Tetanus

Topics: Adult; Echocardiography; Female; Fibrin; Heart Auscultation; Heart Failure; Heart Valve Prosthesis; Humans; Male; Middle Aged; Mitral Valve; Phonocardiography; Thrombosis

Topics: Accidents, Traffic; Adolescent; Adult; Aged; Asphyxia Neonatorum; Brain Abscess; Capillaries; Child; Child, Preschool; Fibrin; Heart Arrest; Heart Failure; Humans; Infant; Infant, Newborn; Lung; Macrophages; Meningitis; Microcirculation; Middle Aged; Myocardial Infarction; Pancreatic Diseases; Postoperative Complications; Proteins; Pulmonary Alveoli; Pulmonary Atelectasis; Pulmonary Circulation; Pulmonary Edema; Respiration, Artificial; Respiratory Insufficiency; Shock, Traumatic; Suicide; Tetanus

Topics: Animals; Blood Coagulation; Blood Platelets; Fatty Acids; Fibrin; Heart; Heart Failure; In Vitro Techniques; Injections, Intravenous; Rabbits; Thromboembolism; Thrombosis

Topics: Edetic Acid; Fibrin; Heart Failure; Humans; Polymerization