Human atrial fibrogenesis is enhanced with increasing duration of AF: a longer AF duration is associated with elevated atrial interstitial MMP activity, but decreased PAI and TIMP expression.

Feline hippocampal and piriform lobe necrosis (FHN) has been reported from several countries worldwide and is considered an important aetiology for feline epileptic seizures. The aetiology of FHN remains unclear, however it is suspected that FHN might occur secondary to intense epileptic activity as described in humans and dogs although this has not yet been documented in cats. The purpose of our report is to describe the first cases of FHN in Finland diagnosed by magnetic resonance imaging (MRI) and histopathology. The two cases we describe had a well documented history of pre-existing seizures with normal brain MRI at the onset of cluster seizures but MRI done when the cats exhibited clinical deterioration secondary to severe seizure activity, revealed lesions in the hippocampus and piriform lobes typical of FHN. Our report confirms that feline hippocampus and piriform lobe necrosis does occur in the Finnish cat population and should therefore be considered as a differential diagnosis in cats with seizures. In addition, the presentation, clinical findings, results of MRI and/or histopathology shows that cats may develop FHN secondary to severe seizure activity.

Background There is a successful outcome after surgical management of spinal arachnoid diverticula (SAD) in up to 82% of cases. Hypothesis/Objectives We hypothesized that Pugs have favorable short‐term and poor long‐term prognosis after surgical treatment of thoracolumbar SAD. The aim of the present investigation was to describe clinical findings, short‐ and long‐term outcomes, and follow‐up magnetic resonance imaging (MRI) findings in Pugs with thoracolumbar SAD. Animals Twenty‐five client owned Pugs with 12‐month follow‐up information after surgical treatment of thoracolumbar SAD. Methods Multicenter retrospective case series. All medical records were searched for Pugs diagnosed with SAD. Data regarding signalment, history, surgical procedure, outcome, histopathology, and follow‐up MRI results were extracted. Results Mean age at presentation was 7.32 (range 2‐11) years, 80% were males. Short‐term outcome was available in 25 dogs, and improvement was confirmed in 80% of dogs. Long‐term outcome was available in 21 dogs, and deterioration was confirmed in 86% of cases, with late‐onset recurrence of clinical signs after initial postsurgical improvement affecting 85% of Pugs. A moderate correlation (r = 0.50) was found between duration of clinical signs and outcome. In 8 dogs with deteriorating clinical signs, follow‐up MRI revealed regrowth of the SAD in 2 cases, new SAD formation in 2 cases, and intramedullary T2W hyperintensity/syringomyelia in 6 cases. Conclusions and Clinical Importance This study suggests that Pugs with thoracolumbar SAD do not have a favorable long‐term prognosis after surgical treatment for reasons yet to be determined.

Peritoneal lavage with chlorhexidine gluconate 0.05% solution in the treatment of experimental peritonitis results in increased adhesion formation.

A six-year-old Ragdoll cat underwent examination due to a six-month history of slowly progressive gait abnormalities. The cat presented with an ambulatory tetraparesis with a neurological examination indicating a C1-T2 myelopathy. Radiographs of the spine showed a radiopaque irregular line ventrally in the vertebral canal dorsal to vertebral bodies C3-C5. In this area, magnetic resonance imaging revealed an intradural extramedullary/extradural lesion compressing the spinal cord. The spinal cord was surgically decompressed. The cause of the spinal cord compression was dural ossification, a diagnosis confirmed by histopathological examination of the surgically dissected sample of dura mater. The cat gradually improved after the procedure and was ambulating better than prior to the surgery. The cat’s locomotion later worsened again due to ossified plaques in the dura causing spinal cord compression on the same cervical area as before. Oral prednisolone treatment provided temporary remission. Ten months after surgery, the cat was euthanized due to severe worsening of gait abnormalities, non-ambulatory tetraparesis. Necropsy confirmed spinal cord compression and secondary degenerative changes in the spinal cord on cervical and lumbar areas caused by dural ossification. To our knowledge, this is the first report of spinal dural ossification in a cat. The reported cat showed neurological signs associated with these dural changes. Dural ossification should be considered in the differential diagnosis of compressive spinal cord disorders in cats.