Abdominal aortic thromboembolism and subsequent pelvic limb myositis secondary to colitis and septicaemia in a 5-day-old Oldenburg colt

This case report describes the clinical progression of a 5-day-old Oldenburg colt presented for acute severe right hindlimb lameness. The foal had diarrhoea at presentation, and over the next 24 h became tachycardic and febrile with cold extremities in the hindlimbs and began to bear weight on the dorsum of both hind fetlocks. Diagnostic work-up included physical examination, radiography, ultrasonography and clinicopathological testing. Treatment consisted of antibiotics, anti-inflammatories, gastroprotectants, oral di-tri-octahedral smectite, hyperimmune plasma and isotonic crystalloid fluids for diarrhoea. Bandages and splints were applied to the hindlimbs to assist ambulation and prevent weightbearing on the dorsum of the fetlocks. The foal developed oedema of both hindlimbs, and ultrasonographic evaluation revealed gas pockets within the subcutaneous tissues. An ultrasound-guided aspirate of the right hindlimb oedema was submitted for cytology, which revealed presumed Clostridial spores, and culture, which yielded heavy growth of Escherichia coli. Surgical fenestration of the hindlimbs was performed due to suspected Clostridial myositis. The foal continued to decline clinically and was humanely subjected to euthanasia. Post-mortem evaluation revealed septicaemia and thromboembolism of the terminal abdominal aorta resulting in partial obstruction of blood flow to the pelvic limbs with resultant bacterial myositis (Clostridium [suspected] and Escherichia coli [confirmed]). In summary, thrombosis is a potential sequela to coagulopathy seen in septicaemia and should be considered a differential diagnosis in neonatal foals presenting for lameness.     

The utility of plasma D-dimer to identify thromboembolic disease in dogs

This prospective study was designed to investigate D-dimer concentrations in clinically healthy dogs, clinically ill dogs without thromboembolic disease (TE), and dogs with TE. The goals of this study were to determine whether the coagulation cascade is activated in nonembolic metabolic and inflammatory conditions and whether differentiation from TE is possible. Group 1 consisted of 30 clinically healthy dogs presented for routine care. Group 2 consisted of 67 clinically ill dogs without TE. This group was subdivided into the following categories: postoperative surgical procedures, congestive heart failure, renal failure, hepatic disease, and neoplastic disease. Group 3 consisted of 20 dogs diagnosed with TE. A CBC and a measurement of prothrombin time (PT), activated partial thromboplastin time (PTT), fibrinogen degradation product (FDP) concentration, and plasma D-dimer concentration was performed on dogs in all groups. D-dimer concentrations were highest in dogs with TE; next highest was the hepatic disease group. Only these 2 groups had median D-dimer concentrations markedly different from clinically healthy dogs. The frequency of platelet abnormalities was markedly greater for the TE and neoplastic disease groups. The sensitivity of D-dimer concentrations >500 ng/mL for predicting TE was 100%; however, the specificity of D-dimer for TE at that concentration was 70%. The specificity of D-dimer concentrations >1,000 ng/mL to predict TE was 94% (sensitivity, 80%), and the specificity of D-dimer concentrations >2,000 ng/mL was 98.5% (sensitivity, 36%). FDPs were not high in any TE patient; thus, they may be an insensitive indicator of thromboembolism, with or without overt disseminated intravascular coagulation (DIC).     

Multimodality imaging of an azygous continuation of the caudal vena cava in a dog with pulmonary thromboembolic disease

A 5‐year‐old spayed female English Bulldog was evaluated for acute anorexia, lethargy, respiratory distress, and syncope. Contrast‐enhanced computed tomography revealed the vascular malformation of azygous continuation of the caudal vena cava with extensive thrombus formation and pulmonary arterial thromboembolic disease. The patient was hospitalized for supportive treatment and was prescribed long‐term clopidogrel therapy. The patient survived to discharge and at last follow‐up remained clinically stable. While this vascular malformation has been reported in canines, to the authors’ knowledge, this is the first reported case of pulmonary thromboembolic disease in a canine concurrent with this condition.     

Aberrant migration and surgical removal of a heartworm (Dirofilaria immitis) from the femoral artery of a cat

A cat was evaluated for an acute‐onset of right pelvic limb paresis. Thoracic radiographs revealed normal cardiac size and tortuous pulmonary arteries. Abdominal ultrasound identified a heartworm (HW) extending from the caudal abdominal aorta into the right external iliac artery and right femoral artery. The cat was HW‐antigen positive. Echocardiography revealed a HW within the right branch of the main pulmonary artery and evidence of pulmonary hypertension. An agitated‐saline contrast echocardiogram revealed a small right to left intracardiac shunt at the level of the atria. Surgical removal of the HW was performed with no substantial postoperative complications. There was return of blood flow and improved motor function to the limb. The cat remains mildly paretic on the affected limb with no other clinical signs.     

Aortopulmonary fistula in a Warmblood mare associated with an aortic aneurysm and supravalvular aortic stenosis

This case report describes the clinical presentation, the necropsy findings, and genetic results of a 13-year-old Warmblood mare presented with colic and a bilaterally loud, holosystolic murmur. Echocardiographic examination revealed the presence of a thoracic aortic aneurysm, an aortic pseudoaneurysm, a periaortic hematoma (circumferential cuffing by perivascular hemorrhage), and aortopulmonary fistulation. A supravalvular aortic stenosis (SVAS) was visible during echocardiography. Necropsy confirmed that the thoracic aortic aneurysm had ruptured and connected to the pseudoaneurysm, which fistulated into the pulmonary artery. Histologically, the aneurysm wall revealed chronic lesions such as fibrosis, mucin depositions, mineralizations, and elastin fragmentation. The mid abdominal aorta showed lesions suggestive of a systemic elastin arteriopathy. Molecular analysis, however, could not attribute this disease to a variant in the elastin gene, the most common causative gene for SVAS. To the authors' knowledge, this case report describes a case of aortopulmonary fistulation in a Warmblood horse associated with the presence of SVAS and an aortic aneurysm.     

Effect of curcumin on ox-LDL-induced HAEC injury

AIM: To investigate the effect of curcumin on oxidized low-density lipoprotein (ox-LDL)-induced injury of human aortic endothelial cells (HAECs). METHODS: HAECs were pre-treated with curcumin at different concentrations and then treated with ox-LDL. The cell viability was assessed by MTT assay. The cell proliferation ability was analyzed by EdU assay. ELISA was used to determine the concentrations of interleukin-6 (IL-6), transforming growth factor β1 (TGFβ1), high mobility group box-1 protein (HMGB1) and secretory receptor for advanced glycation end products (sRAGE) in the HAEC culture medium. The binding activity of peroxisome proliferator-activated receptor γ (PPARγ) was evaluated by electrophoretic mobility shift assay. The protein levels of HO-1, HMGB1, RAGE,IL-6,TGFβ1 and phosphorylated PPARγ in the HAECs were determined by Western blot. RESULTS: The viability and the proliferation ability decreased significantly in the HAECs treated with ox-LDL. The PPARγ/HO-1 signaling pathway was inhibited while its down-stream HMGB1/RAGE signaling pathway was activated by ox-LDL. The levels of IL-6, TGFβ1, HMGB1 and sRAGE were increased. Pre-treatment with curcumin activated PPARγ/HO-1 signaling pathway and inhibited HMGB1/RAGE signaling pathway in ox-LDL treated HAECs in a concentration-dependent manner. The levels of IL-6, TGFβ1, HMGB1 and sRAGE were also decreased dramatically by pre-treatment of curcumin in a concentration-dependent manner. CONCLUSION: ox-LDL induces HAEC damage by inhibiting PPARγ/HO-1 to activate HMGB1/RAGE inflammatory signaling. Curcumin exerts protective effect on ox-LDL treated HAECs via activating PPARγ/HO-1 signaling pathway.     

Effects of clopidogrel therapy on whole blood platelet aggregation,the Plateletworks® assay and coagulation parameters in cats with asymptomatic hypertrophic cardiomyopathy: a pilot study

Background: Although scientific evidence is limited, clopidogrel is frequently used as prophylaxis for arterial thromboembolism in cats with hypertrophic cardiomyopathy (HCM).

Objectives: Evaluating effects of clopidogrel therapy in asymptomatic cats with HCM on (1) conventional whole blood aggregation (WBA), (2) alternative platelet aggregation assessed with tubes of the Plateletworks® assay and (3) standard coagulation parameters.

Animals and methods: Prospective, randomized, double-blind, placebo-controlled pilot study. Fourteen asymptomatic HCM cats were randomly allocated to receive placebo (n = 5) or clopidogrel (18.75 mg/cat q24h, n = 9) as part of a larger study. Aggregation responses (to 20 µM adenosine diphosphate (ADP) and 10 µg/ml collagen) in WBA and the Plateletworks® assay and standard coagulation parameters were evaluated at baseline and after seven days of therapy.

Results: Clopidogrel therapy significantly reduced aggregation responses to ADP and collagen in the Plateletworks® agonists tubes (ADP and collagen: P < 0.001), but did not significantly reduce aggregation responses to ADP and collagen in the WBA technique (ADP: P = 0.07, collagen: P = 0.30). Clopidogrel therapy did not show a significant effect on prothrombin time, activated partial thromboplastin time, antithrombin, D-dimers and fibrinogen concentrations.

Conclusion and clinical importance: Clopidogrel therapy at a dose of 18.75 mg/cat q24h for seven days causes a significant decrease in in vitro platelet aggregation evaluated with the Plateletworks® assay, without affecting standard coagulation parameters in cats with asymptomatic HCM.     

拳参-413对大鼠离体胸主动脉环的舒张作用机制研究

[目的]研究拳参-413对大鼠离体胸主动脉血管的舒张作用机制。[方法]采用离体血管环灌流方法观察拳参-413在含Ca+或无Ca+的Krebs液孵育条件下对去甲肾上腺素(NA)引起的血管平滑肌收缩的影响,考察拳参-413舒张血管作用的时间依赖性,并观察拳参-413对浓度40和80 mmol/L的KCl引起的血管平滑肌收缩的影响。[结果]拳参-413能舒张NA引起的血管收缩,且呈浓度依赖性;拳参-413(100μmol/L)在30 min达到最大舒张效应;无Ca+组拳参-413抑制NA所致血管平滑肌收缩效应大于含Ca+组;拳参-413对浓度40和80 mmol/L的KCl引起的血管平滑肌收缩均有抑制作用,且两者量效曲线明显上移。[结论]拳参-413可舒张血管平滑肌,其作用机制可能与该药促进NO合成释放,开放钙激活的钾通道以及抑制血管平滑肌细胞外钙内流和内钙释放有关。     

Retrospective Study of Streptokinase Administration in 46 Cats with Arterial Thromboembolism

A retrospective evaluation was performed on 46 cats with arterial thromboembolism (ATE) that were treated with streptokinase (SK). Significant heart disease was diagnosed in 45/46 cats, and 21/46 cats had congestive heart failure. Variable dosing schemes of streptokinase were administered within 1–20 hours following the onset of clinical signs (median = 5.5 hours). There was no difference between survivors (S) and non-survivors (NS), based on time of administration of SK after onset of clinical signs. Twenty-five (54%) of the cats had return of pulses within 2–24 hours of treatment. Fourteen (30%) of the cats had return of motor function between 9 hours and 6 days. Fifteen of the cats (33%) were discharged from the hospital, 18 (39%) died in the hospital, and 13 (28%) cats were euthanized due to complications or poor response to treatment. Four of 5 cats (80%) with single limb dysfunction survived to hospital discharge. Life threatening hyperkalemia was diagnosed in 16 cats (35%) after SK administration. Hyperkalemia was more likely to occur with the longer duration of SK infusion. Eleven cats (24%) developed clinical signs of bleeding following SK administration and 3 of these cats required a blood transfusion. Laboratory testing documented coagulopathy following SK administration in 11 out of 17 cats tested. Hypothermia and azotemia prior to SK administration and the development of hyperkalemia were negatively associated with survival.