Transmural Myocardial Infarction Caused by Thromboembolism Associated with Mitral Insufficiency in a Dog.

Seki, Yoshihisa; Motomura, Noboru; Arimura, Takuro; Kiryu, Keiji; Kondoh, Masahiro

doi:10.1292/jvms.60.741

Cited by 8 publications

(3 citation statements)

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“…Another common histologic finding in dogs affected with chronic valvular heart disease is microscopic intramural myocardial infarction (MIMI), also known as small-vessel coronary artery arteriosclerosis. [2][3][4] To the author's knowledge, the role that inflammation plays in the degeneration of the valves is unknown.…”

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confidence: 99%

C‐Reactive Protein Concentration in Dogs with Chronic Valvular Disease

Lee

Freeman

Brewer

2006

Veterinary Internal Medicne

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The purpose of the study reported here was to determine whether dogs with chronic valvular disease have increased plasma Creactive protein concentration, compared with that in clinically normal dogs. Blood was collected from 47 dogs with physical and echocardiographic evidence of chronic valvular disease and from 20 healthy controls. C-reactive protein concentration was determined with a commercial canine C-reactive protein enzyme immunoassay. Compared with controls, dogs with chronic valvular disease had higher plasma concentration of C-reactive protein (median 2.17 mg/mL [range, 0.86-33.8 mg/mL]) versus 1.43 mg/mL [range, 0.84-4.99 mg/mL]; P , .001). C-reactive protein concentration was not related to the presence of congestive heart failure or murmur grade. The results of this study suggest that increased concentration of C-reactive protein is found in dogs with chronic valvular disease.

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confidence: 99%

C‐Reactive Protein Concentration in Dogs with Chronic Valvular Disease

Lee

Freeman

Brewer

2006

Veterinary Internal Medicne

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“…On the other hand, atherosclerosis is not a condition commonly recognized in dogs. 41 Humans and dogs differ greatly in this regard, making comparison of MR in dogs with that in humans difficult. Moreover, some differences in pathologic findings in the heart between humans and dogs with MR have been reported.…”

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confidence: 99%

Changes in Platelet Life Span in Dogs with Mitral Valve Regurgitation

et al. 2002

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Platelet life span was measured in dogs with experimentally-induced mitral regurgitation (MR) by using an in vitro whole-blood biotinylation technique to evaluate the effects of shear stress induced by MR. Mitral regurgitation was created in healthy dogs by ablation of the mitral valve chordae tendineae. Mitral regurgitation was identified by auscultation and postoperative color Doppler echocardiography. Platelets were biotinylated, and derivatized blood was reinfused into the dogs. Biotinylated platelet disappearance was measured over time to determine platelet life span. Pre-and postablation platelet life span was compared in each dog. Platelet life span was shorter in dogs with experimentally induced MR. Shear stress from MR was postulated to shorten platelet life span. Alternations in platelet function and life span may contribute to the progression of cardiovascular disease in dogs with MR. Further studies are required to determine if platelet dysfunction is related to disease progression in these patients.

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“…In dog, CATE was found in the subsinuosal interventricular branch of the coronary artery composed of mostly platelets and fibrin with the same histology characteristics as those of the mural thrombi of the leftatrial endocardium. Dislodgement of part of the mural thrombus (i) might have caused TE of the subsinuosal interventricular branch (Seki et al 1998). …”

Section: Coronary Artery Thrombo-embolism (Cate)mentioning

confidence: 99%

Thromboembolic Conditions, Aetiology Diagnosis and Treatment in Dogs and Cats

Konecny¹

2010

Acta Vet. Brno

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In veterinary medicine, thrombo-embolism (TE) is an under-appreciated medical condition that requires immediate recognition. Since TE is multifactorial and its mode of presentation may vary, veterinarians face great difficulties in making a definitive diagnosis in a timely manner. In addition, most of the underlying conditions that give rise to TE are life-threatening and an aggressive diagnostic and therapeutic approach is required. Not only does the diagnosis and treatment of this condition require the collaboration of many specialties, the costs of therapy can be excessive with a high risk of recurrence. As such, owners have to be thoroughly informed before the therapy commences. While TE has been well-characterized in humans and is associated with significant morbidity and mortality, little information of similar quality is available in veterinary medicine. In addition, TE in animals is distinct from its human counterpart and we cannot simply adapt what is known from human clinical trials. With the promise of improvements in imaging modalities that improve our diagnostic capabilities, the window of opportunity to treat TE increases. This article focuses on aetiology, clinical presentation, diagnosis, and treatment of dogs and cats affected by TE. Prothrombotic conditions, non-pulsatile blood flow, endothelial damage, hypercoagulability, clinical presentationThrombo-embolism (TE) in animal patients (canine and feline) can occur at various anatomical locations, including pulmonary vessels, portal vein, vena cava, aortic trifurcation, heart, renal and cerebral arteries, intestinal and mesenteric vessels, spleen, iliac, femoral, coronary and brachial arteries, femoral vein, and vessels of the microcirculation (Butler 1971;Liu et al. 1986; Klein et al. 1989;LaRue and Murtaugh 1990;Laste et al. 1992;Van Winkle and Bruce 1993;Rawlings et al. 1993;Sottiaux and Franck 1998;Palmer et al. 1998;Driehuys et al. 1998;Sottiaux and Franck 1999; Diaz Espineira 1999;Bateman et al. 1999;Norris et al. 1999;Boswood et al. 2000; Tsujino et al. 2005; Gonçalves et al. 2008). The clinical effects of thrombo-embolism depend mainly on the size and site of the final destination of the thrombus/embolus.It is commonly accepted that arterial thrombi are composed predominantly of platelets as compared to fibrin. This is in contrast to vein thrombi, where platelets are scarce and there are larger amounts of cross-linked fibrin. Arterial clots are also generally firmly attached to the underlying vessel wall. In this setting, clot dislodgement will sometimes occur, causing re-canalization of the vessel with relief of the obstruction, but the threat of embolism distally remains. In contrast, venous thrombi are mainly associated with lower limb deep vein thrombosis (DVT) in humans. DVT, however, is not common in veterinary patients. This is thought to be due to the differences in the epigenetics, platelet structure, vascular anatomy and physiological non-bipedal circulation. In fact, venous thrombi tend to be occlusive with resulting ...

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Transmural Myocardial Infarction Caused by Thromboembolism Associated with Mitral Insufficiency in a Dog.

Cited by 8 publications

References 1 publication

C‐Reactive Protein Concentration in Dogs with Chronic Valvular Disease

C‐Reactive Protein Concentration in Dogs with Chronic Valvular Disease

Changes in Platelet Life Span in Dogs with Mitral Valve Regurgitation

Thromboembolic Conditions, Aetiology Diagnosis and Treatment in Dogs and Cats

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