Clinical and diagnostic imaging findings in dogs with atrial appendage aneurysm: 7 cases (2014-2020).

INTRODUCTION/OBJECTIVE: Atrial appendage aneurysm in dogs is a rare condition and has not been well described. The aim of this study is to describe clinical and diagnostic imaging findings, especially computed tomography (CT), of atrial appendage aneurysms in dogs. ANIMALS: Seven client-owned dogs with a presumptive diagnosis of left or right atrial appendage aneurysm. MATERIALS AND METHODS: Retrospective study. Medical records were searched to identify dogs with a presumptive diagnosis of left (LAAA) or right atrial appendage aneurysm (RAAA). Signalment, history, examination findings, diagnostic test results, and imaging procedures were reviewed. Archived diagnostic images were retrieved and evaluated by two board-certified radiologists and a board-certified cardiologist. Data analysis was descriptive. RESULTS: Six cases were diagnosed with RAAA and one with LAAA with a median age of 8 years. Five affected dogs were small to medium-breed male dogs. All dogs underwent a thoracic CT examination for various reasons and all cases of RAAA were incidental findings. CT was useful to identify and assess the atrial appendage aneurysm, as well as neighboring structures, although possible pericardial defects could not be visualized. Five dogs had a concurrent echocardiographic examination, which successfully identified the LAAA and two RAAA. CONCLUSIONS: This case series described the clinical and CT findings in seven dogs with atrial appendage aneurysm, as well as echocardiographic findings in five of these cases. Right atrial appendage aneurysms appear to be mainly incidental findings. CT seems to be more sensitive than echocardiography in the detection of atrial appendage aneurysm.

[Delay in the effect of antidepressive agents: pharmacologic approach]. / Le délai d'action des antidépresseurs: l'approche pharmacologique.

A paradox which is not resolved in the use of antidepressants (ATD) is that in pharmacological studies of animal models of depression and in neurochemical studies, the onset of activity of all drugs is extremely rapid, whereas in human clinical practice the onset is delayed (15 days). An attempt is made to explain this in 3 ways, involving the synapse, transduction mechanisms, and cognition. Analysis of the impact of all ATDs shows that we are confronted with slow adaptive processes which are correlated with the delay observed in clinical practice. The interest of such considerations is that they may give rise to alternative therapies which are able not only to accelerate response, but also to increase it.