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Background Platelets play a central role in the development of cardiovascular diseases and changes in their proteins are involved in the pathophysiology of heart diseases in humans. There is lack of knowledge about the possible role of platelets in congestive heart failure (CHF) in dogs. Thus, this study aimed to investigate the changes in global platelet proteomes in dogs with CHF, to clarify the possible role of platelets in the physiopathology of this disease. Healthy-dogs (n = 10) and dogs with acute CHF due to myxomatous mitral valve disease (MMVD, n = 10) were used. Acute CHF was defined based on the clinical (increased respiratory rate or difficulty breathing) and radiographic findings of pulmonary edema. Dogs Blood samples were collected into tubes with acid-citrate-dextrose, and platelet-pellets were obtained by centrifuge and washing steps. Platelet-proteomes were identified using LC-MS based label-free differential proteome expression analysis method and matched according to protein database for Canis lupus familiaris. Results Totally 104 different proteins were identified in the platelets of the dogs being 4 out of them were significantly up-regulated and 6 down-regulated in acute CHF dogs. Guanine-nucleotide-binding protein, apolipoproteins (A-II and C-III) and clusterin levels increased, but CXC-motif-chemokine-10, cytochrome-C-oxidase-subunit-2, cathepsin-D, serine/threonine-protein-phosphatase-PP1-gamma-catalytic-subunit, creatine-kinase-B-type and myotrophin levels decreased in acute CHF dogs. These proteins are associated with several molecular functions, biological processes, signaling systems and immune-inflammatory responses. Conclusion This study describes by first time the changes in the protein composition in platelets of dogs with acute CHF due to MMVD. Our findings provide a resource for increase the knowledge about the proteome of canine platelets and their roles in CHF caused by MMVD and could be a tool for further investigations about the prevention and treatment of this disease.

MMVD, the most common cause of CHF in dogs, is a chronic disease with variable clinical signs, with some patients remaining asymptomatic while others develop CHF. Here, we aimed to evaluate serum proteins by proteomic analysis in dogs at different stages of CHF due to MMVD, and proteome behaviors after conventional treatment. A total of 32 dogs were divided equally into four groups—stage A (healthy/controls), stage B2 (asymptomatic), stage C and stage D (symptomatic)—according to the ACVIM consensus. Serum proteomes were evaluated using LC/MS-based label-free differential proteome analysis. The study revealed 157 different proteins; 11 were up- and 21 down-regulated in dogs with CHF compared to controls. In stage B2 dogs, angiotensinogen (AGT) was up-regulated, but immunoglobulin iota chain-like, lipopolysaccharide-binding protein, and carboxypeptidase (CPN) were down-regulated. In stage C dogs, complement C3 (C3) and inter-alpha-trypsin inhibitor heavy chain were up-regulated, but hemopexin, and actin-cytoplasmic-1 (ACT-1) were down-regulated. In stage D dogs, AGT was up-regulated, whereas tetranectin, paraoxonase-1, adiponectin and ACT-1 were down-regulated. A decrease in CPN, C3 and AGT and an increase in ACT-1 were observed after treatment of dogs in stage C. This pilot study identified that dogs at different stages of CHF show different serum protein composition which has potential to be biomarker for diagnose and treatment monitorization.

This study aimed to evaluate the hemostatic function by thromboelastography (TEG) and determine if there was an association between the changes in hemostatic parameters and serum cardiac troponin I (cTnI) in dogs with dilated cardiomyopathy (DCM). DCM was diagnosed by echocardiography in 19 dogs. Ten healthy dogs were selected as controls. Myocardial injury was confirmed by increased serum cTnI levels. Coagulation was assessed by TEG evaluating clot kinetics (reaction time [R] and kinetic time [K]), clot strengthening (alpha [α] angle and G value), platelet function (maximum amplitude [MA] and coagulation-index [CI]), clot stability (LY30, the percentage of lysis 30 min after MA), and global clotting times (activated partial thromboplastin time [aPTT] and prothrombin time [PT]). Dogs with DCM had higher R and K times but lower MA, α-angle, G, and CI compared to controls (P < 0.05). LY30 and PT did not statistically differ between groups, but the aPTT in dogs with DCM was higher than that of the controls. Serum cTnI (median [range], ng/mL) was higher in dogs with ) than in healthy dogs (0.03 [0.01-0.06]). There was no statistical relation between cTnI and coagulation parameters. This study showed that alterations of the coagulation status in dogs with DCM could develop independently of serum cTnI elevations.

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