ArticleCase reports in veterinary medicine2026
Transient Myocardial Thickening in an 11-Year-Old Cat Infected With Feline Infectious Peritonitis and Treated With GS-441524.
Article in Case reports in veterinary medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Transient Myocardial Thickening in an 11-Year-Old Cat Infected With Feline Infectious Peritonitis and Treated With GS-441524.Case reports in veterinary medicine · 2026Article
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Abstract
This case report provides a thorough description of the clinical assessment and management of an extremely rare case of transient myocardial thickening associated with feline infectious peritonitis (FIP) and highlights the overlap of clinical signs secondary to FIP or congestive heart failure. An 11-year-old male Norwegian cat was presented with a 3-week history of weakness, dysorexia, tachypnea, dyspnea, and weight loss. Thoracic point-of-care ultrasound (POCUS) revealed severe bilateral pleural effusion without cardiac chamber enlargement. Blood work including serum protein electrophoresis (demonstrating polyclonal gammopathy) was suggestive of FIP. Analyses of pleural effusion consisted of real-time PCR being positive for FCoV nucleic acids with a high viral load and slightly equivocal increased NT-proBNP. Together with the noncardiogenic nature of the effusion, these findings were consistent with a diagnosis of FIP. Three days after the presentation, the cat exhibited progressive dyspnea secondary to newly collected pleural effusion with markedly increased NT-proBNP. At that time, echocardiography revealed left ventricular wall thickening and left atrial enlargement, thus suggesting hypertrophic cardiomyopathy or myocarditis with left-sided congestive heart failure. Cardiac troponin I concentration was increased. Nine days after admission, the patient was discharged on cardiac therapy and nucleoside analog GS-441524. Fifteen days after initiation of GS treatment, echocardiography showed a decrease in left ventricular wall thickness. No long-term complications or recurrences of FIP or myocardial hypertrophy were observed at the 1.5-, 4-, and 18-month follow-ups, with normalization of cardiac troponin I concentration and echocardiographic variables, thus supporting the hypothesis of FIP-related transient myocardial thickening. To the authors' knowledge, this is one of the rare reports of transient myocardial thickening in the FIP setting, following GS-441524 treatment. Cardiac POCUS and NT-proBNP dosage in pleural effusion should systematically be performed in order to unmask congestive heart failure.
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