Transient Myocardial Thickening in Cats Associated with Heart Failure.

BACKGROUND: Cats with hypertrophic cardiomyopathy (HCM) and congestive heart failure (CHF) can have resolution of both left ventricular hypertrophy and CHF. OBJECTIVES: To describe the clinical characteristics of cats with transient myocardial thickening (TMT) and CHF compared with a control population of cats without resolution of HCM. ANIMALS: A total of 21 cats with TMT, 21 cats with HCM. METHODS: Retrospective study. Clinical records at 4 veterinary centers were searched for TMT cases and a control group of cats with HCM and CHF. TMT was defined as initial maximal left ventricular wall thickness (LVWT) ≥6 mm with left-sided CHF, with subsequent resolution of CHF, reduction in left atrium/aorta (LA/Ao), and LVWT<5.5 mm. HCM was defined as persistent LVWT ≥6 mm. RESULTS: Cats with TMT were younger (2 [0.4-11.4] years) than cats with HCM (8 [1.6-14] years) (P < 0.0001), and antecedent events were more common (15/21 versus 6/21, respectively) (P = 0.01). In cats with TMT, LVWT normalized from 6.8 [6.0-9.7] mm to 4.8 [2.8-5.3] mm and LA/Ao decreased from 1.8 [1.6-2.3] to 1.45 [1.2-1.7] after a mean interval of 3.3 (95% CI: 1.8-4.7) months. CHF recurred in 1 of 21 TMT and 15 of 21 cats with HCM. Cardiac treatment was discontinued in 20 of 21 cats with TMT and 0 of 21 HCM cats. All cats with TMT survived, whereas 8 of 19 cats with HCM died during the study period. CONCLUSIONS AND CLINICAL IMPORTANCE: TMT occurs in younger cats, and antecedent events are common. The prognosis is better in cats with CHF associated with TMT than HCM.

Pulmonary artery thrombosis in experimental Angiostrongylus vasorum infection does not result in pulmonary hypertension and echocardiographic right ventricular changes.

BACKGROUND: Dogs experimentally inoculated with Angiostrongylus vasorum develop severe pulmonary parenchymal lesions and arterial thrombosis at the time of patency. HYPOTHESIS: A. vasorum-induced thrombosis results in arterial hypoxemia, pulmonary hypertension (PH), and altered cardiac morphology and function. ANIMALS: Six healthy Beagles experimentally inoculated with A. vasorum. METHODS: Thoracic radiographs and arterial blood gas analyses were performed 8 and 13 weeks postinoculation (wpi) and 9 weeks posttherapy (wpt). Echocardiography was done before and 2, 5, 8, 13 wpi and 9 wpt. Invasive pulmonary artery pressure (PAP) measurements were obtained 8 wpi. Two untreated dogs were necropsied 13 wpi and 4 treated dogs 9 wpt. RESULTS: All dogs had patent infections at 7 wpi and clinical respiratory signs at 8 wpi. Moderate hypoxemia (median PaO2 of 73 and 74 mmHg) present at 8 and 13 wpi had resolved by 9 wpt. Echocardiographically, no evidence of PH and no abnormalities in cardiac size and function were discernible at any time point. PAP invasively measured at 8 wpi was not different from that of control dogs. Severe radiographic pulmonary parenchymal and suspected thrombotic lesions at 13 wpi were corroborated by necropsy. Most histopathologic changes had resolved at 9 wpt, but focal inflammatory, thrombotic, and fibrotic changes still were present in all dogs. CONCLUSION: In experimentally infected Beagles, pulmonary and vascular changes induced by A. vasorum are reflected by marked radiographic changes and arterial hypoxemia. These did not result in PH and echocardiographic changes in cardiac size and function.

Pancreatitis associated with clomipramine administration in a dog.

A three-year-old, male, entire, Yorkshire terrier was presented with peracute onset of abdominal pain and vomitus. Clinicopathological abnormalities included severely increased serum lipase activity, immeasurably high serum trypsin-like immunoreactivity and mild hypocalcaemia. Canine pancreatic lipase immunoreactivity (cPLI) was intended to be measured, however, the sample got lost. Ultrasonography revealed a hypoechoic pancreas with small amounts of peripancreatic fluid and hyperechogenic mesentery. Acute pancreatitis (AP) was diagnosed and the dog recovered with appropriate therapy within 48 hours. Clomipramine, a selective serotonin reuptake inhibitor (SSRI) for alleviating signs of separation anxiety had been given for seven weeks. Two similar, albeit less severe, episodes associated with previous courses of clomipramine had occurred eight months earlier that responded to discontinuing clomipramine and supportive care. As SSRIs are associated with AP in human beings and no other trigger could be identified, we conclude that clomipramine should be considered as a potential cause when investigating causes for AP in susceptible breeds or other dogs presenting with compatible clinical signs.

Recent advances in the discovery of tissue factor/factor VIIa inhibitors and dual inhibitors of factor VIIa/factor Xa.

The search for an ideal anticoagulant has spanned decades and has taken several approaches to the identification of novel target molecules for preventing and treating thrombosis. In the group of anticoagulants acting through direct inhibition of coagulation factors, most research has focused on thrombin and factor Xa inhibitors. Attention has been drawn most recently to factor VIIa as a promising anticoagulation target, because of its role in complex with tissue factor, in initiating the coagulation cascade following blood vessel damage. Several reports suggest that inhibitors of the tissue factor/factor VIIa complex prevent thrombosis with a lower bleeding risk than other types of inhibitors. Accordingly, there is increasing interest in the generation of potent and selective small-molecule factor VIIa inhibitors that can be safely administered once or twice daily in an oral formulation with no need for routine coagulation monitoring. The emphasis of this review will be placed on recent advances in the development of the small-molecule inhibitors of factor VIIa complexed with tissue factor. The role of factor VIIa and tissue factor as initiators of the coagulation cascade following blood vessel damage is described, along with the structure of the active site of factor VIIa.

Dual inhibitors of the blood coagulation enzymes.

The search for an ideal anticoagulant has spanned decades and has resulted in several approaches and the identification of novel target molecules for preventing and treating thrombosis. The first group of new anticoagulant agents acting through direct inhibition of coagulation factors were inhibitors of thrombin, but factor Xa inhibitors and, most recently, factor VIIa inhibitors have become attractive candidates. The structures of thrombin, factor Xa and factor VIIa show similarities in their active sites and, for this reason, attempts have been made to develop synthetic agents containing in a single molecule inhibitory activity against two of the enzymes of the blood coagulation cascade. Such dual inhibitors are now in preclinical studies and are, potentially, new anticoagulant drugs with improved properties. The emphasis of this review will be placed on dual inhibitors of thrombin/factor Xa and factor Xa/factor VIIa. Comparison of the active sites of these enzymes is included for better understanding of the structural demands to be met in designing effective dual inhibitors.