%0 Journal Article
%T Hemostatic Markers in Congestive Heart Failure Dogs with Mitral Valve Disease
%A Kreangsak Prihirunkit
%A Amornrate Sastravaha
%A Chalermpol Lekcharoensuk
%A Phongsak Chanloinapha
%J Journal of Veterinary Medicine
%D 2014
%R 10.1155/2014/589873
%X Prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen, D-dimer, antithrombin III (AT III), protein C (PC), factor VII (F.VII), and factor VIII (F.VIII), as well as hematocrit (HCT), platelets number (PLT), total plasma protein (TP), and albumin (ALB), were studied on fifty-eight congestive heart failure (CHF) dogs with mitral valve disease (MVD) and fifty control dogs. All of variables of MVD group, except APTT, were significantly different from control group. The variables were also compared among functional classes of CHF dogs and control dogs. It was determined that the higher the functional class of CHF dogs was, the greater the levels of fibrinogen and D-dimer were, whereas the lesser the activities of AT III and PC were presented. Additionally, TP had linear correlation with fibrinogen, D-dimer, HCT, and PLT (, 0.30, 0.43, and 0.38, resp., ). These findings suggested that fibrinogen and D-dimer were the factors predisposing hypercoagulability through an increase in blood viscosity. The hemorheological abnormalities would shift an overall hemostatic balance toward a more thrombotic state in CHF dogs with MVD. 1. Introduction Degenerative valve disease is one of the most common forms of canine heart disease and is also known as endocardiosis [1]. The most commonly affected valve in the dog is the mitral valve [2]. It is a well-compensated disease with a long evolution [3]. A genetic tendency to develop the disease has been proved in Cavalier King Charles Spaniel and Dachshunds [4]. Grossly, mitral valve disease (MVD) is a markedly thickened valve with the swollen free edge. As the disease progresses, the regurgitation of blood from the ventricle into the atrium causes volume overload and possibly leads to congestive heart failure (CHF) [5]. CHF has been associated with the profound clinical effects of hemostasis. The high plasma markers of thrombin activity, fibrinolytic activity, and platelet activation have been reported [6, 7]. Even though heart failure in human is associated with thromboembolic stroke risk, the prevalence of overt clinical thromboembolism in dogs with CHF is rarely reported [8]. Thromboembolic complications have been attributed to an imbalance between procoagulant and anticoagulant factors, including thrombocytosis, hemoconcentration, hyperviscosity, and immobilization [9]. Protein C (PC) and antithrombin III (AT III) are major natural anticoagulants. They play an important role in preventing excessive coagulation, whereas fibrinogen and D-dimer indicate the thromboembolic tendency [10]. The diagnosis
%U http://www.hindawi.com/journals/jvm/2014/589873/