fibrin and Ventricular-Dysfunction--Left

Formation of compact and poorly lysable fibrin clots have been demonstrated in patients following ischemic stroke. Recently, it has been shown that denser fibrin networks and impaired fibrinolysis occurs in subjects with permanent atrial fibrillation (AF). Fibrin clot phenotype in other types of AF remains to be established. We evaluated fibrin clot properties in paroxysmal (PAF) and persistent AF (PsAF).. We studied 88 non-anticoagulated patients with AF on sinus rhythm and free of stroke (41 with PAF, 47 with PsAF) versus 50 controls. Ex-vivo plasma fibrin clot permeability (Ks) and clot lysis time (CLT) were evaluated along with von Willebrand factor (vWF), peak thrombin generation (TG), platelet factor 4 (PF4) and fibrinolytic proteins.. Compared with control subjects, clots obtained from plasma of patients with PAF and PsAF had similarly lower Ks (-7.7%, P=0.01; -8.6%, P=0.005, respectively) and prolonged CLT (+10.8%, P=0.006; +7.8% P=0.04, respectively). No associations of Ks and CLT with CHA2DS2-VASc and HAS-BLED score were observed. Patients with AF had higher TG, vWF, PF4 and plasminogen activator inhibitor-1 (PAI-1) antigen compared with controls. Multiple linear regression adjusted for age, gender, body mass index and fibrinogen showed that TG (β=-0.41), vWF (β=-0.29) and PF4 (β=-0.28) are the independent predictors of Ks (R(2)=0.78), while CLT was independently predicted by TG (β=0.37), PAI-1 antigen (β=0.29) and vWF (β=0.26) in the AF group (R(2)=0.39).. Patients with PAF and PsAF while on sinus rhythm display unfavorably altered fibrin clot properties, which might contribute to thromboembolic complications.

Topics: Atrial Fibrillation; Blood Coagulation; Chronic Disease; Female; Fibrin; Fibrinolysis; Humans; Male; Middle Aged; Platelet Activation; Thrombin; Thromboembolism; Ventricular Dysfunction, Left

We report the early failure of two tissue valves within hours of surgery due to the accumulation of cellular debris in two different institutions in the United Kingdom. The valves were both found at explant to be covered in a cellular material - possibly fibrin. From clinical experience and careful review of the literature we have found no other reports of such early valve failure due to the build up of material on the structure of the valve. This rare occurrence needs to be reported in the literature to forewarn clinicians of an early complication that may not be recognized yet.

Topics: Aged; Aortic Valve Stenosis; Bioprosthesis; Device Removal; Fatal Outcome; Female; Fibrin; Heart Valve Prosthesis; Humans; Mitral Valve Insufficiency; Mitral Valve Prolapse; Postoperative Complications; Prosthesis Design; Prosthesis Failure; Reoperation; Thrombosis; Ventricular Dysfunction, Left

Disorders of hemostasis lead to vascular pathology. Endothelium-derived gene products play a critical role in the formation and degradation of fibrin. We sought to characterize the importance of these locally produced factors in the formation of fibrin in the cardiac macrovasculature and microvasculature. This study used mice with modifications of the thrombomodulin (TM) gene, the tissue-type plasminogen activator (tPA) gene, and the urokinase-type plasminogen activator (uPA) gene. The results revealed that tPA played the most important role in local regulation of fibrin deposition in the heart, with lesser contributions by TM and uPA (least significant). Moreover, a synergistic relationship in fibrin formation existed in mice with concomitant modifications of tPA and TM, resulting in myocardial necrosis and depressed cardiac function. The data were fit to a statistical model that may offer a foundation for examination of hemostasis-regulating gene interactions.

Topics: Animals; Cells, Cultured; Coronary Thrombosis; Disease Models, Animal; Endothelium, Vascular; Fibrin; Fibrosis; Genetic Predisposition to Disease; Genotype; Hemostasis; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Microcirculation; Myocardium; Thrombomodulin; Tissue Plasminogen Activator; Ultrasonography; Urokinase-Type Plasminogen Activator; Ventricular Dysfunction, Left

Transmyocardial laser revascularization is an investigational technique for revascularizing ischemic myocardium in patients with inoperable coronary arterial disease. This study tests the hypothesis that laser revascularization prevents left ventricular functional deterioration and aneurysm formation after acute anteroapical myocardial infarction.. An ultrasonic ascending aortic flow probe and snares around the distal left anterior descending and second diagonal coronary arteries were placed in 26 Dorsett hybrid sheep. Ten to 14 days later, snared arteries were occluded to produce an anteroapical infarction of 23% of left ventricular mass. Before infarction 14 animals had 34 +/- 4 transmyocardial perforations in the area of the anticipated infarction made with a carbon dioxide laser. Twelve animals served as controls. Hemodynamic measurements and transdiaphragmatic quantitative echocardiograms were obtained before, immediately after, and 2, 5, and 8 weeks after infarction. Eighteen sheep completed the protocol.. All animals had large anteroapical left ventricular aneurysms with massive ventricular enlargement. Immediately after infarction the anterior wall became thinner and dyskinetic in all sheep. At 8 weeks aneurysmal size and shape were indistinguishable between groups. Two days after infarction, laser holes were filled with fibrin. At 5 and 8 weeks the infarct consisted of dense collagen, fibroblasts, scattered calcifications, myocyte fragments, neutrophils, macrophages, and no laser holes. There were no significant differences at any time between groups for cardiac pressures or output, ventricular volumes, ejection fraction, stroke work, and the stroke work-left ventricular end-diastolic pressure index.. Transmyocardial laser perforations do not revascularize acute myocardial infarction in sheep.

Topics: Animals; Echocardiography; Fibrin; Heart Aneurysm; Heart Ventricles; Hemodynamics; Laser Therapy; Myocardial Infarction; Myocardial Revascularization; Myocardium; Sheep; Treatment Failure; Ventricular Dysfunction, Left