Quantitative Assessment of Platelet Function and Clot Structure in Patients With Severe Coronary Artery Disease

Greilich, Philip E.; Carr, Marcus E.; Zekert, Sheryl L.; Dent, Rosa M.

doi:10.1097/00000441-199401000-00003

Cited by 49 publications

(29 citation statements)

References 36 publications

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“…Despite aspirin therapy, patients with severe CAD had more rigid clot structures and an elevated fiber mass-length ratio. 10 In a further report, the fibrin gel structure of patients with type 1 diabetes was found to be less porous than that of nondiabetic controls, but this was not related to fibrinogen levels, and there was no difference in fiber mass-length ratio. 11 Fatah et al 12,13 identified both reduced permeability and fiber masslength ratio in the fibrin gels from young patients after myocardial infarction.…”

Section: Discussionmentioning

confidence: 89%

Altered Fibrin Clot Structure in the Healthy Relatives of Patients With Premature Coronary Artery Disease

et al. 2002

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Background-A family history of premature coronary artery disease (CAD) is an independent cardiovascular risk factor.Fibrin clots composed of dense fiber networks are found in young CAD patients and may occur in the relatives of such individuals. Methods and Results-The ex vivo fibrin structure of 100 healthy male relatives of patients with premature CAD and 100 age-matched control subjects was assessed by measurement of permeability (K s ), fiber mass-length ratio (), and turbidity (lag phase and maximum absorbency [max ⌬Abs]). Scanning electron microscopy was performed on selected samples. Relatives and controls shared similar levels of conventional cardiovascular risk factors. K s was lower in relatives than in controls, 12.2 (11.1 to 13.3) versus 15.2 (14.0 to 16.5) ϫ10 Ϫ9 cm 2 ( PϽ0.001), associated with a smaller decrease in , 8.5 (7.7 to 9.2) versus 9.7 (8.9 to 10.5) ϫ1013 Da/cm (PϽ0.05), respectively. Lag phase was shorter in relatives than in controls, 39 (37 to 41) versus 47 (44 to 50) seconds (PϽ0.001), and max ⌬Abs was higher in relatives, 0.78 (0.74 to 0.82) versus 0.71 (0.67 to 0.74) in controls (Pϭ0.02), which indicates the presence of thicker fibers in relatives. After adjustment for fibrinogen levels, lag phase and K s remained significantly different between relatives and control subjects. Scanning electron microscopy images confirmed increased fiber diameter in relatives, possibly of reduced density. Factor XIII Val34Leu and fibrinogen A␣ Thr312Ala and B␤ -455 G/A showed no association with clot structure. Conclusions-The male relatives of patients with premature CAD form fibrin clots that begin polymerization more quickly, have thicker fibers, and are less permeable than those of control subjects.

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Section: Discussionmentioning

confidence: 89%

Altered Fibrin Clot Structure in the Healthy Relatives of Patients With Premature Coronary Artery Disease

et al. 2002

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“…As a consequence, none of the studies could draw definite conclusions regarding the complex relationships between premature CAD, abnormal fibrin properties, and hypofibrinolysis. For example, Greilich et al found patients with severe CAD to have more rigid clot structures and an elevated fiber mass/ length ratio, 15 but neither morphological properties of fibrin nor lysis experiments were performed. Fatah et al identified reduced permeability and reduced fiber mass/length ratio in the fibrin gels from young patients after MI.…”

Section: Discussionmentioning

confidence: 99%

Altered Fibrin Architecture Is Associated With Hypofibrinolysis and Premature Coronary Atherothrombosis

Collet

Allali

Lesty

et al. 2006

ATVB

310

262

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Objective-Hypofibrinolysis promotes atherosclerosis progression and recurrent ischemic events in premature coronary artery disease. We investigated the role of fibrin physical properties in this particular setting. Methods and Results-Biomarkers of recurrent thrombosis and premature coronary artery disease (CAD) were measured in 33 young post-myocardial infarction patients with angiographic-proven CAD and in 33 healthy volunteers matched for age and sex. Ex vivo plasma fibrin physical properties were assessed by measuring fibrin rigidity and fibrin morphological properties using a torsion pendulum and optical confocal microscopy. The fibrinolysis rate was derived from continuous monitoring of the viscoelastic properties after addition of lytic enzymes. Young CAD patients had a significant increase in plasma concentration of fibrinogen, von Willebrand factor, plasminogen activator inhibitor type 1, and lipoprotein(a) as compared with controls (PϽ0.05). Fibrin of young CAD patients was stiffer (Pϭ0.002), made of numerous (Pϭ0.002) and shorter fibers (Pϭ0.04), and lysed at a slower rate than that of controls (Pϭ0.03). Fibrin stiffness was an independent predictor for both premature CAD and hypofibrinolysis. Conclusions-This first detailed study of clot properties in such a group of patients demonstrated that abnormal plasma fibrin architecture is an important feature of both premature CAD and fibrinolysis rate. Key Words: acute coronary syndromes Ⅲ coagulation Ⅲ fibrinolysis Ⅲ pathophysiology Ⅲ fibrinogen Ⅲ thrombophilia T he mechanical properties of clots and their major constituent fibrin are normally finely tuned to optimize bleeding control while also minimizing their effect on atherothrombosis. 1,2 A decreased rate of fibrinolysis and increased thrombosis are generally associated with stiff clots, although such relationships are complex. 3,4 Many factors that affect clot structure have a great impact on the mechanical properties fibrin and fibrinolysis through modifications of various steps in the fibrin polymerization process and clot stabilization. 1,4,5 See page 2419Premature coronary artery disease (CAD) is associated with increased plasma levels of prothrombotic and proinflammatory biomarkers, including fibrinogen and plasminogen activator inhibitor (PAI) type 1, which are known to favor hypofibrinolysis 6 and to be independent predictors of CAD. 7,8 Epidemiological studies have also revealed a relationship between myocardial infarction (MI) and reduced permeability and increased stiffness of fibrin, especially in young post-MI patients. 9 These aspects of altered fibrin clot network architecture were not found to be attributable to classic risk factors including fibrinogen concentrations or common polymorphisms. 2 However, the relationships among premature CAD, abnormal fibrin physical properties, and hypofibrinolysis remain little explored. The lack of appropriately designed studies of the physical properties of fibrin, including simultaneous determination of viscoelastic and morphological properties o...

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“…16,[32][33][34] Fatah et al 34 report that patients who experience first myocardial infarction (MI) before the age of 45 years form clots with tighter and less permeable fibrin networks than control subjects. This type of clot structure is more resistant to fibrinolysis, 35 possibly because the small pores within the clot restrict the access of fibrinolytic enzymes.…”

Section: Discussionmentioning

confidence: 99%

Genetics of fibrin clot structure: a twin study

Dunn

Ariëns

Lange

et al. 2004

Blood

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Quantitative Assessment of Platelet Function and Clot Structure in Patients With Severe Coronary Artery Disease

Cited by 49 publications

References 36 publications

Altered Fibrin Clot Structure in the Healthy Relatives of Patients With Premature Coronary Artery Disease

Altered Fibrin Clot Structure in the Healthy Relatives of Patients With Premature Coronary Artery Disease

Altered Fibrin Architecture Is Associated With Hypofibrinolysis and Premature Coronary Atherothrombosis

Genetics of fibrin clot structure: a twin study

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