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      Establishment of a Model of Spontaneously-Running-Tokushima-Shikoku Rats with Left Atrial Thrombosis

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          Abstract

          Studies that investigate the underlying mechanisms of disease and treatment options typically require the use of a suitable animal model. Few suitable animal models exist for left atrial thrombosis. Here, we demonstrated that the Spontaneously-Running-Tokushima-Shikoku (SPORTS) rat — a Wistar strain known for its running ability—is predisposed to the development of thrombi in the left atrium. We investigated the incidence of left atrial thrombosis in male (n = 16) and female (n = 17) SPORTS rats and observed organized atrial thrombosis in 57% and 38% of males and female rats, respectively. In the male rats, systolic blood pressures and heart rates were significantly higher in SPORTS rats than in control Wistar rats. We could not find any evidence of arrhythmias, such as atrial fibrillation, during electrocardiographic examination of SPORTS rats. We believe that the SPORTS rat could serve as a new research model for left atrial thrombosis; further, it may be suitable for research investigating the development of new antithrombotic approaches for the control of atrial thrombosis or familial thrombophilia in humans.

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          Most cited references 25

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          Development of a strain of spontaneously hypertensive rats.

           K. Okamoto,  K. Aoki (1963)
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            Mutation in the gene coding for coagulation factor V and the risk of myocardial infarction, stroke, and venous thrombosis in apparently healthy men.

            A specific point mutation in the gene coding for coagulation factor V is associated with resistance to degradation by activated protein C, a recently described abnormality of coagulation that may be associated with an increased risk of venous thrombosis. Whether this mutation also predisposes patients to arterial thrombosis is unknown, as is the value of screening for the mutation in order to define the risk of venous thrombosis among unselected healthy people. Among 14,916 apparently healthy men in the Physicians' Health Study who provided base-line blood samples, 374 had myocardial infarctions, 209 had strokes, and 121 had deep venous thrombosis, pulmonary embolism, or both, during a mean follow-up of 8.6 years. We determined whether a mutation at nucleotide position 1691 of the factor V gene was present or absent in these 704 men and in an equal number of matched participants who remained free of vascular disease. The prevalence of heterozygosity for the mutation among men who had myocardial infarctions (6.1 percent, P = 0.9) or strokes (4.3 percent, P = 0.4) was similar to that among men who remained free of vascular disease (6.0 percent). However, the prevalence of the mutation was significantly higher among men who had venous thrombosis, pulmonary embolism, or both (11.6 percent, P = 0.02). In adjusted analyses, the relative risk of venous thrombosis among men with the mutation was 2.7 (95 percent confidence interval, 1.3 to 5.6; P = 0.008). This increased risk was seen with primary venous thrombosis (relative risk, 3.5; 95 percent confidence interval, 1.5 to 8.4; P = 0.004) but not with secondary venous thrombosis (relative risk, 1.7; 95 percent confidence interval, 0.6 to 5.3; P = 0.3), and it was most apparent among older men. Specifically, the prevalence of the mutation among men over the age of 60 in whom primary venous thrombosis developed was 25.8 percent (relative risk, 7.0; 95 percent confidence interval, 2.6 to 19.1; P < 0.001). In a large cohort of apparently healthy men, the presence of a specific point mutation in the factor V gene was associated with an increased risk of venous thrombosis, particularly primary venous thrombosis. The presence of the mutation was not associated with an increased risk of myocardial infarction or stroke. This mutation appears to be the most common inherited factor thus far recognized that predisposes patients to venous thrombosis.
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              Structural remodeling of the left atrial appendage in patients with chronic non-valvular atrial fibrillation: Implications for thrombus formation, systemic embolism, and assessment by transesophageal echocardiography.

              Left atrial appendage (LAA) is frequently the site of thrombus formation in patients with chronic atrial fibrillation (AF). Transesophageal echocardiography and hematologic studies have identified blood flow stasis (spontaneous echogenic contrast) and abnormal coagulation (increased serum fibrinogen) as important predisposing factors to formation of LAA thrombi. However, the third component of the Virchow's triad, i.e., endothelial abnormalities, has not been adequately studied. Accordingly, we studied, at necropsy, the LAA morphology in 46 hearts of patients with (n = 22) and without (n = 24) chronic AF. Compared to patients without AF, those with AF had significantly larger LAA volumes (1.7% 1.1 vs. 5. 4% 3.7 mL, p = 0.0002), and larger luminal surface area of the bisected LAA (4.4% 1.8 vs. 7.1% 4.5 cm(2), p = 0.01). However, both the absolute and relative surface area of the transected pectinate muscles were reduced in patients with AF (2.6% 1.1 vs. 1.8% 1.0 cm(2), p = 0.02 and 38% 15 vs. 21% 14%, p = 0.0003). In addition, in most patients (73%) with chronic AF, the LAA showed significant endocardial thickening with fibrous and elastic tissue (endocardial fibroelastosis) compared to those without AF (13%, p < 0.0001). Endocardial fibroelastosis resulted in a smooth LAA luminal surface and encased the pectinate muscles. These findings suggest that LAA remodeling (dilation, stretching, and reduction in pectinate muscle volume, as well as endocardial fibroelastosis) occurs frequently in chronic AF and may contribute to the increased risk of thrombus formation and systemic embolism. Additionally, the information may have relevance in interpreting transesophageal echocardiographic images of the LAA in patients with chronic AF.
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                Author and article information

                Journal
                J Toxicol Pathol
                J Toxicol Pathol
                TOX
                Journal of Toxicologic Pathology
                Japanese Society of Toxicologic Pathology
                0914-9198
                1881-915X
                30 April 2014
                April 2014
                : 27
                : 1
                : 51-56
                Affiliations
                [1 ] Department of Nutrition Management, Faculty of Health Science, Hyogo University, 2301 Shinzaike, Hiraoka-cho, Kakogawa, Hyogo 675-0195, Japan
                [2 ] Department of Molecular and Environmental Pathology, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto-cho, Tokushima, Tokushima 770-8503, Japan
                [3 ] Faculty of Human Life Science, Shikoku University, 23-1 Ebisuno Furukawa, Oujinn-cho, Tokushima, Tokushima 771-1192, Japan
                [4 ] Department of Nutrition, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto-cho, Tokushima, Tokushima 770-8503, Japan
                [5 ] Department of Laboratory of Clinical Nutrition Management, School of Food and Nutritional Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku, 422-8526 Shizuoka, Japan
                Author notes
                *Corresponding author: T Ohnishi (e-mail : tohnishi@ 123456hyogo-dai.ac.jp )
                Article
                2012-0032
                10.1293/tox.2012-0032
                4000073
                24791067
                ©2014 The Japanese Society of Toxicologic Pathology

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License.

                Categories
                Original Article

                Pathology

                rat, atrial thrombosis, heart

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