The medical records of 100 cats with distal aortic thromboembolism were reviewed. The average age was 7.7 years, with the neutered male being the most common signalment (63%). Evidence of preexisting cardiac disease was noted in 11% of the cases. A murmur or arrhythmia was noted in 57% of the cases on presentation. Frequent laboratory abnormalities included elevations in blood glucose, alanine aminotransferase, aspartate aminotransferase, blood urea nitrogen, and creatinine. Radiographic and electrocardiographic abnormalities were common (89% and 85%, respectively). The most frequent, underlying disease was hypertrophic feline cardiomyopathy (58%), with the left atrial size (as measured by M-mode) significantly increased in the majority of cases (mean left atrial-to-aortic ratio, 2.08). The average, long-term survival in the 37% of cases which survived the initial thromboembolic episode was 11.5 months. The remaining cases either died (28%) or were euthanized (35%).
M-mode echocardiography was completed and plasma taurine concentrations were determined in 79 healthy cats and 77 cats with dilated cardiomyopathy (DCM). In healthy cats, a relationship was not observed between plasma taurine concentrations and any M-mode echocardiographic measurement. End-systolic and end-diastolic cardiac chamber dimensions were larger; wall thickness measures were smaller; and calculations of fractional shortening were less in cats with DCM than in healthy cats. Plasma taurine concentrations < 30 nmol/mL were detected in 7/79 healthy cats and in 52/77 cats with DCM. Of the 52 cats with D C M and an initial plasma taurine concentration < 30 nmol/mL, 23 died or were euthanized during the first post-treatment week, 7 were lost to further study, and 22 improved after taurine supplementation. Of the 25 cats with D C M and an initial plasma taurine concentration 2 30 nmol/mL, 9 died or were euthanatized during the first post-treatment week, and 9 were lost to further study. Two cats did not improve, of which one died and one was euthanatized 4 to 8 weeks after initiation of taurine supplementation. Five cats with a plasma taurine concentration 2 30 nmol/mL improved after taurine supplementation. Myocardial function subsequently deteriorated in three of these cats. Two of the three cats had signs of congestive heart failure redevelop. (Journal of Veterinary Internal Medicine 199 1; 5~232-238) HAYES et al.' reported in 1975 that retinal degeneration could be induced in cats by feeding a taurine-deficient diet. Subsequent investigations confirmed this finding
Results indicated that heart murmurs are detectable in a large proportion of overtly healthy cats and that many murmurs appear to be caused by structural heart disease that is in a clinically latent state.
A retrospective study evaluated cases of feline esophageal dysfunction. Cats identified had contrast esophagrams performed during a six-year period. Of 56 cases undergoing esophagography, 51 had complete records available for review. Forty-four cases were felt to be abnormal and were included in the study. Cases were analyzed for signalment, presenting complaints, and identifiable causes of abnormal esophageal motility. Response to treatment and case outcome were also reviewed. The signalment of the cases varied widely, especially in age. The occurrence of esophageal motility dysfunction was low, comprising only 0.05% of all feline cases seen in a six-year period. Forty-three percent of cases were considered idiopathic, and 57% were congenital or diagnosed with conditions known to cause esophageal motility dysfunction. The causative disease states included myasthenia gravis, mediastinal masses, vascular ring anomalies, dysautonomia, and esophageal stricture. Seventy-eight percent of those treated with medical therapy (i.e., combinations of sucralfate, H2 receptor antagonists, and either metoclopramide or cisapride) showed clinical improvement.
Results suggest that AF occurs primarily in older adult male cats with structural heart disease severe enough to lead to atrial enlargement. Atrial fibrillation in these cats was most commonly first detected when signs of decompensated cardiac disease were evident, but also was commonly identified as an incidental finding.
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