Acetaminophen-induced transient myocardial thickening in a British Shorthair cat with hypertrophic cardiomyopathy

Acetaminophen-induced transient myocardial thickening in a British Shorthair cat with hypertrophic cardiomyopathy | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Acetaminophen-induced transient myocardial thickening in a British Shorthair cat with hypertrophic cardiomyopathy Sin-Wook Park, Keon Kim, Yoon-Jung Do, Jong-Won Lee, Woong-Bin Ro, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6234030/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 9 You are reading this latest preprint version Abstract Background Transient myocardial thickening (TMT) is a cause of hypertrophic cardiomyopathy (HCM) that is characterized by reversible left ventricular wall thickening. Case presentation A 6-year-old castrated male British Shorthair with a history of a heart murmur detected on its annual examination was presented for echocardiography. Based on physical examination, blood analysis, and echocardiography (maximum left ventricular wall thickness (LVWT): 7.5 mm), the cat was diagnosed with HCM. Three days after the first presentation, the cat presented with a history of acetaminophen ingestion. Three days after hospitalization, the cat developed tachypnea, and radiography showed a pleural effusion and generalized interstitial lung pattern. Echocardiography showed a remarkably increased LVWT (11.4 mm) and an enlarged left atrial diameter (LAD). The cat was treated with diuretics, and its condition clinically normalized. Six months after the first presentation, echocardiography revealed a decreased LVWT (6.9 mm) and LAD. Conclusions This is the first case report to demonstrate that TMT can occur in cats with HCM, and acetaminophen may induce TMT in cats. The possibility of comorbid HCM and TMT should always be considered. In such cases, even though a cat with HCM may develop congestive pulmonary edema, life-long cardiac medication may not be needed. Echocardiography Feline Heart disease Left ventricular wall thickness Myocardial disease Figures Figure 1 Figure 2 Background The hypertrophic cardiomyopathy (HCM) phenotype is the most common form of feline cardiomyopathy; affected animals are primarily asymptomatic, and HCM can affect approximately 15% of the domestic cat population ( 1 ). The diagnosis of HCM is made when the left ventricular (LV) diastolic wall thickness (≥ 6 mm) is confirmed on echocardiography and other disorders that can cause mild to moderate LV wall thickening (e.g., hyperthyroidism, systemic hypertension, acromegaly, dehydration) are ruled out ( 1 , 2 ). Transient myocardial thickening (TMT) is one cause of the HCM phenotype ( 3 , 4 ). TMT is characterized by reversible LV wall thickness and may be associated with concurrent transient left atrial (LA) dilation and dysfunction, and congestive heart failure (CHF); however, the exact etiology of TMT is unknown ( 3 , 5 ). The most frequent antecedent event associated with TMT is surgical/anesthetic procedures, but others include traffic accidents and diseases that cause pain, and one study revealed that thermal burns may cause myocardial thickening ( 3 , 5 , 6 ). To the author’s knowledge, TMT is well demonstrated in cats, but there are no reports that describe acute myocardial thickening in cats with HCM induced by acetaminophen toxicosis and provide echocardiography measurements pre- and post-TMT. This report describes significant thickening of the myocardium, a dilated LA, and the development of CHF in a cat with asymptomatic HCM within a week after acetaminophen toxicosis and demonstrates a subsequent decrease in the LV wall thickness (LVWT) and LA diameter (LAD). Case presentation A 6-year-old castrated male British Shorthair weighing 5.5 kg was referred to Re-born Animal Medical Center for echocardiography with a history of a heart murmur detected at the local animal hospital 2 weeks prior to presentation. On physical examination, a grade 3/6 systolic heart murmur (point of maximum intensity: mitral valve) with a regular heart rate (200 beats/min) was detected, and the cat’s systolic blood pressure was normal (120 mmHg). Thoracic radiography in ventral and right lateral recumbency revealed no remarkable findings. The cat’s serum NT-proBNP level (reference range < 100 pmol/L) was elevated at 266 pmol/L, and the total thyroxine concentration was within the reference range (1.8 µg/dL; reference range: 0.8–4.7 µg/dL). Echocardiographic measurements were performed by one veterinary radiologist and analyzed retrospectively by a board-certified internist (Table 1 ). Symmetrical hypertrophy of the LV wall (LVWT maximum: 7.5 mm) and systolic anterior motion (SAM) with a normal LAD were observed (Fig. 1 , Table 1 ). The cat was diagnosed with HCM. Twice daily atenolol (6.25 mg/cat, PO) was prescribed to relieve the effects of SAM. Table 1 Selective two-dimensional echocardiographic variables at presentation (day 0) and on follow-up echocardiographic examinations. Variable Unit Day 0 Day 6 Day 180 Day 450 Heart rate beat/min 200 120 175 180 Blood pressure mmHg 130 80 130 140 LAD max mm 10.6 16.3 10.4 11.6 LA/Ao 1.07 1.79 1.33 1.15 LVIDd mm 13 8 13.3 12.6 LV FS % 57.4 62 64.7 58 LVWT Max mm 7.5 11.4 6.9 7 IVSd MAX (RPLax) mm 7.5 9.5 6.9 6.7 LVFWd MAX(RPLax) mm 6.4 11.4 6.3 6.8 IVSd MAX (RPSax) mm 7.1 9.4 6.9 7 LVFWd MAX(RPSax) mm 6.7 9.2 6.1 6.4 AV Vmax cm/s 141 233 110 104 PV V max cm/s 81 56 64 77 SAM Yes Yes No No LVOTO No Yes No No LAD Max: Maximal left atrial diameter; LA/Ao: Left atrium to aortic root ratio; LVIDd: Left ventricular internal diameter in end-diastole; LV FS: Left ventricular fractional shortening; LVWT Max: Maximal left ventricular wall thickness; IVSd Max: Maximal interventricular septal thickness in end-diastole; LVFWd Max: Maximal left ventricular free wall thickness in end-diastole; AV Vmax: Peak velocity across the aortic valve; PV Vmax: Peak velocity across the pulmonary valve; RPLax4C: Right parasternal long-axis four-chamber view, RPLax5C: Right parasternal long-axis five-chamber view, RPSax: Right parasternal short-axis view; LVOTO: Left ventricular outflow tract; SAM: systolic anterior motion.Echocardiographic measurements were performed by one radiologist and analyzed retrospectively by a single author. No sedation was used for each echocardiogram. Three days after the first presentation, the cat presented with signs of vomiting, anorexia, and lethargy and had a history of acetaminophen ingestion (the cat was administered one 500 mg tablet by the owner) one day before prior to presentation. The cat’s vital signs were within the normal range (rectal temperature: 38.7°C, resting respiratory rate: 30 breaths/min, pulse: 150 beats/min, systolic blood pressure: 110 mmHg). The cat was hospitalized (day 0), and blood (which was brown in color) was collected. A complete blood count (CBC), plasma biochemical analysis, and electrolyte analysis were performed prior to the initiation of any therapy. The cat’s hematocrit (38.9%; reference range: 30.3–52.3%) and liver enzymes were normal, and a low plasma creatinine (0.7 mg/dL; reference range: 0.8–2.4 mg/dL), hypophosphatemia (3 mg/dL; reference range: 3.1–7.7 mg/dL), and hypokalemia (3.4 mmol/L; reference range: 3.5–5.5 mmol/L) were also identified. Significant Heinz bodies were found on a blood smear with new methylene blue stain. Therapy was initiated with intravenous fluids (Hartmann solution, 3 ml/kg/h on day 0 and continued at 1 ml/kg/h on days 1–2), N-acetylcysteine (140 mg/kg IV once and continued at 70 mg/kg IV q6h), glutathione (100 mg/cat IV q12h), and vitamin C (30 mg/kg IV q6h), S-adenosylmethionine (50 mg/cat PO q12h), and silymarin (10 mg/kg PO q12h). On day 3, the cat’s hematocrit decreased to 27.3%, and the plasma alanine transaminase levels were above the normal range (193 U/L; reference range: 12–130 U/L). In addition, the cat’s resting respiratory rate increased to 72 breaths/min, and the systolic blood pressure decreased to 80 mmHg. Thoracic radiography in ventral and right lateral recumbency showed an increased cardiothoracic ratio, a pleural effusion, and a generalized interstitial lung pattern (Fig. 2 ). Echocardiography revealed a mild pericardial effusion, a pleural effusion, an increased LVWT (LVWT maximum: 11.4 mm) with heterogenous echogenicity of ventricular myocardium, an enlarged LAD (16.3 mm), and a left ventricular outflow tract obstruction (LVOTO) ( 7 ). Based on the rapid changes in the cardiovascular imaging results, the cat was diagnosed with CHF, intravenous fluid therapy was discontinued, and oxygen therapy was initiated. Furosemide (2 mg/kg IV once and continued at 2 mg/kg PO q12h) and clopidogrel (18.75 mg/cat PO q24h) were also administered. The cat’s resting respiratory rate decreased to 30 breath/min on day 5, and radiography showed a reduced pleural effusion and interstitial lung pattern. On day 7, the cat’s hematocrit increased to 36.5%, and the plasma alanine transaminase levels normalized. The cat was subsequently discharged with furosemide (2 mg/kg PO q12h), silymarin (10 mg/kg PO q12h), clopidogrel (18.75 mg/cat PO q24h), and atenolol (6.25 mg/cat PO q12h) for 14 days. Follow-up medical treatment was recommended at the local animal hospital. Six months after the first presentation, the cat was presented for repeat echocardiography. Echocardiography revealed a reduced LVWT (LVWT maximum: 6.9 mm) and LAD (10.4 mm), and SAM and LVOTO were not detected. The cat was diagnosed with TMT on HCM, and a tapering regimen of furosemide was prescribed (1 mg/kg PO q12h), clopidogrel was maintained, and atenolol was discontinued. Fifteen months after the first presentation, the cat presented for echocardiography again and was not receiving cardiac medications. Echocardiography revealed a similar LVWT (LVWT maximum: 7 mm) and LAD (11.6 mm), and SAM and LVOTO were not detected. The owner reported that the cat was doing clinically well. Discussion This report describes a 6-year-old British Shorthair with HCM that developed TMT following acetaminophen ingestion. In the present case, myocardial thickening developed, and the LAD was increased within 6 days, and an associated pleural effusion and pulmonary edema had developed. In addition, a reduced LVWT and LAD were confirmed 6 and 15 months later. The cat was doing clinically well without signs of CHF even after stopping the cardiac medications. To the author’s best knowledge, recent studies have defined TMT by confirming an initially increased LVWT (≥ 6 mm) and a reduced LVWT (< 5.5 mm) on follow-up echocardiography ( 3 , 5 , 8 , 9 ). Strict criteria were required for prior experimental groups because echocardiography was not performed just before LV wall thickening in previous studies. According to these criteria, this cat may not have been diagnosed with TMT. However, the decreased ratio of the left ventricular free wall was 45% in this case, which significantly higher than previous results (24–31%) ( 3 , 5 , 8 – 10 ). In addition, the echocardiographic measurements made before and after the development of TMT demonstrate that there was reversible myocardial hypertrophy in this cat with primary HCM, as in humans in very few reported cases ( 11 ). Therefore, the author suggests that the term TMT may be used in cats with primary HCM. In addition, the LVWT may decrease due to fibrosis of the myocardial wall at the end of HCM, which is characterized by a significant decrease in LV function and an increase in the LAD ( 14 ). Therefore, when diagnosing TMT, considering both the LV function and LAD is essential in cats with HCM ( 15 ). The pathophysiology causing the acute ventricular wall thickening in cats remains unknown, but a catecholamine surge may result in myocardial thickening due to a form of myocardial edema ( 6 , 8 , 10 ). Furthermore, there are reports of TMT that may be associated with recent events such as anesthesia/surgery and road traffic accidents and several diseases or conditions including thermal burn injuries, infectious diseases including toxoplasmosis, bartonellosis, and sepsis ( 3 , 5 , 8 – 10 ). However, several reported cases of TMT in cats did not have an antecedent event or identifiable underlying disease ( 3 , 5 ). In this case, the cat showed acetaminophen toxicosis, and no concurrent disease other than HCM was identified. Specific diseases (e.g. toxoplasmosis) were not ruled out, but this cat was strictly indoor, which made such an infection less likely ( 8 ). Takotsubo cardiomyopathy (TTC), also known as stress cardiomyopathy in humans, is characterized by transient systolic, diastolic left ventricular dysfunction, and myocardial edema may develop ( 16 – 18 ). The exact etiology of TTC is still unknown, but excessive catecholamine levels play a major role in the pathology of this disorder, and stress can also trigger this condition ( 19 ). TTC may result in LVOTO, and a combination of TTC with obstructive HCM can lead to low cardiac output and acute heart failure; administration of beta blockers is the main management option ( 13 , 20 ). Similarly, this cat showed LVOTO, CHF, and decreased systolic blood pressure. Although the prescription of atenolol in this case did not prevent these cardiovascular changes, administration of atenolol was maintained because it was considered the best treatment option and was associated with a good prognosis. Therefore, beta blockers may be used in cats with TMT with LVOTO. Acetaminophen exposure may lead to cellular injury and death of hepatocytes, and ingestion of even small amounts can be a substantial risk for the cat ( 21 , 22 ). The common clinical signs are anorexia, dullness, facial and paw edema, muddy mucous membranes, respiratory distress, and hematuria ( 23 ). In addition, oxidative damage may develop with the formation of methemoglobin that causes anemia ( 24 ). Moreover, myocardial infarctions, CHF, cardiac arrhythmias, pericarditis, and myocarditis due to acetaminophen toxicity have been reported in humans ( 25 , 26 ). Potential causes of cardiotoxicities are oxidative stress and decreased sulfhydryl groups that may lead to cardiac cell death ( 25 ). In addition, one report demonstrated that TTC developed with acetaminophen toxicity, and the echocardiographic findings of this patient were decreased LV systolic function and ventricular wall thickness ( 27 ). There is no report of such cardiotoxicity in cats, and one study reported that pulmonary edema developed in a cat with acetaminophen exposure, but echocardiography was not performed ( 28 ). In this case, it is difficult to determine whether TMT occurred due to direct cardiac toxicity from acetaminophen or if it was secondary to catecholamine surges caused by liver dysfunction, oxidative stress, or other triggering factors. However, unlike the echocardiography features of other cases of feline TMT, this cat showed significant heterogeneous echogenicity of the ventricular wall that might be the result of inflammation and edematous changes induced by myocardial toxicity from acetaminophen ( 5 , 8 – 10 , 29 ). Since the exact mechanisms of TMT are unknown, this case suggests the possibility of acetaminophen myocardial toxicity that may cause TMT. The main limitation of this report is that cardiac biomarkers, inflammatory biomarkers, and stress biomarkers were not analyzed. The second limitation is that fluid analysis of the pleural effusion was not performed, and underlying infectious diseases were not ruled out. In addition, an electrocardiogram was not conducted in this case. Finally, the follow-up interval was relatively long, and the process of normalization of the myocardial wall was not confirmed. Despite these limitations, this case is meaningful as there was reversible myocardial hypertrophy after acetaminophen ingestion in this cat with asymptomatic HCM. Conclusion To the best of the author’s knowledge, this is the first report to describe echocardiography findings before and after the development of TMT. In addition, this report described reversible myocardial thickening in a cat with HCM. This case suggests the possibility that acetaminophen toxicity may cause TMT in cats. Considering that the prevalence of HCM in cats is significantly high, the possibility of comorbid HCM and TMT should always be considered. In such cases, even though a cat with HCM may develop congestive pulmonary edema, life-long cardiac medication may not be needed. Therefore, follow-up echocardiography is essential in cats with the HCM phenotype due to the characteristic of dynamic changes in the LVWT. Abbreviations Congestive heart failure (CHF) Hypertrophic cardiomyopathy (HCM) Left atrium (LA) Left atrial diameter (LAD) Left ventricular outflow tract obstruction (LVOTO) Left ventricular wall thickness (LVWT) Systolic anterior motion (SAM) Transient myocardial thickening (TMT) Takotsubo cardiomyopathy (TTC) Declarations Ethics approval and consent to participate Since this is a case report, ethical review and approval were not required. Written informed consent was obtained from the owners for the participation of their animals in this study. Consent for publication Not applicable Availability of data and materials Not applicable Competing interests The authors declare that they have no competing interests Funding This work was supported financially by Rural Development Administration (RDA) under grant number RS-2023-00232301. Authors’ contributions S-WP and KK were involved in case analysis and were responsible for writing the manuscript. Y-JD, J-W were involved in the draft preparation and case analysis. W-BR and C-ML were involved in the coordination of the case and were responsible for interpretation of results. All authors contributed to the article and approved the submitted version. Acknowledgements Not applicable References Kittleson MD, Côté E. The feline cardiomyopathies: 2. Hypertrophic cardiomyopathy. J Feline Med Surg. 2021;23(11):1028–51. Visser L, Sloan C, Stern J. Echocardiographic assessment of right ventricular size and function in cats with hypertrophic cardiomyopathy. 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Acetaminophen toxicity in a cat and its treatment. Indian J Veterinary Med. 2021;41(1):75–7. Webb C, Twedt D, Fettman M, Mason G. S-adenosylmethionine (SAMe) in a feline acetaminophen model of oxidative injury. J Feline Med Surg. 2003;5(2):69–75. KhabazianZadeh F, Kazemi T, Nakhaee S, Ng PC, Mehrpour O. Acetaminophen poisoning-induced heart injury: a case-based review. DARU J Pharm Sci. 2019;27:839–51. Lip GY, Vale JA. Does acetaminophen damage the heart? J Toxicology: Clin Toxicol. 1996;34(2):145–7. Jophlin LL, Koch DG. Takotsubo cardiomyopathy following acute liver failure. Hepatology. 2015;61(4):1430–1. Anvik J. Acetaminophen toxicosis in a cat. Can Veterinary J. 1984;25(12):445. Joseph J, Oxford E, Santilli R. Transient myocardial thickening in a Bartonella henselae–positive cat. J veterinary Cardiol. 2018;20(3):198–203. Additional Declarations No competing interests reported. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-6234030","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":432260751,"identity":"1c750310-b5cd-40af-b872-0cdf6c99d102","order_by":0,"name":"Sin-Wook Park","email":"","orcid":"","institution":"Chonnam National University","correspondingAuthor":false,"prefix":"","firstName":"Sin-Wook","middleName":"","lastName":"Park","suffix":""},{"id":432260752,"identity":"d8ed8be8-d595-4226-9a82-ace5db46e341","order_by":1,"name":"Keon Kim","email":"","orcid":"","institution":"Chonnam National University","correspondingAuthor":false,"prefix":"","firstName":"Keon","middleName":"","lastName":"Kim","suffix":""},{"id":432260753,"identity":"99924218-49e9-472e-96e5-2743157d79c0","order_by":2,"name":"Yoon-Jung Do","email":"","orcid":"","institution":"National Institute of Animal Science, Rural Development Administration","correspondingAuthor":false,"prefix":"","firstName":"Yoon-Jung","middleName":"","lastName":"Do","suffix":""},{"id":432260754,"identity":"7cfca1c8-a5f7-43a8-ad5f-2162958c2535","order_by":3,"name":"Jong-Won Lee","email":"","orcid":"","institution":"Re-born Animal Medical Center","correspondingAuthor":false,"prefix":"","firstName":"Jong-Won","middleName":"","lastName":"Lee","suffix":""},{"id":432260755,"identity":"d608f2dd-485d-4bed-a88c-5ebdf2184396","order_by":4,"name":"Woong-Bin Ro","email":"","orcid":"","institution":"Chonnam National University","correspondingAuthor":false,"prefix":"","firstName":"Woong-Bin","middleName":"","lastName":"Ro","suffix":""},{"id":432260759,"identity":"a8c40b6f-c103-482d-822f-e6a4a753e111","order_by":5,"name":"Chang-Min Lee","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA+UlEQVRIiWNgGAWjYFAC5gYGBgMJOX72BjYk0QP4tDACtRRYGEv2HCBJy4eKxA03EojUwj/tYOODDwYSjA03Hz978HHHHXndBuaHHxjO3MOpReJ2YrPhDAMJZsbZaeaGM888M9x2gM1YguFGMU4tBtKJbdI8BhJszNI5bNK8bYcZtx1gMAM6NQGflvbffwwkeNgkz4C12G87wP6NkJY2ZmAgS/AAdYG0JG47wAO05QZuLSC/SPYYSADtSTOTnNl2OHnbYZ5iiYQzuLXwz04++OHHn7r6/ccPP5P42HbYdtvx9o0fPhzDrQULYAZikjSMglEwCkbBKMAAAGGoVcYFHax2AAAAAElFTkSuQmCC","orcid":"","institution":"Chonnam National University","correspondingAuthor":true,"prefix":"","firstName":"Chang-Min","middleName":"","lastName":"Lee","suffix":""}],"badges":[],"createdAt":"2025-03-15 16:53:07","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-6234030/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6234030/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":79574137,"identity":"c8dcaf2a-3f70-481d-83aa-a3f9750b066b","added_by":"auto","created_at":"2025-03-31 11:08:47","extension":"jpg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":965235,"visible":true,"origin":"","legend":"\u003cp\u003eTwo-dimensional echocardiographic images of right parasternal views at three timepoints. From the left, a right parasternal long-axis four-chamber view, right parasternal short-axis view at the papillary muscle level, and a right parasternal short-axis view at the aortic valve level are shown. The LVWT was measured from the thickest segment using two- dimensional imaging of the right parasternal long-axis four- and five-chamber views and the short-axis view at the papillary muscle level. Note the drastic increase in left atrial enlargement and left ventricular thickening with heterogenous myocardial wall echogenicity (white arrow) and pleural effusion (white arrowhead) on day 6.\u003c/p\u003e","description":"","filename":"OriginalImageforFig1.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6234030/v1/890653f870f2e3d8b039a6fd.jpg"},{"id":79574154,"identity":"642f5195-5942-4bac-8bd8-ccb89a758f0f","added_by":"auto","created_at":"2025-03-31 11:08:48","extension":"jpg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":477785,"visible":true,"origin":"","legend":"\u003cp\u003eRight lateral (A, C) and ventrodorsal thoracic radiographs (B, D). Remarkable cardiomegaly, pleural effusion, and an interstitial pattern suggest that congestive heart failure had developed within 6 days (C, D).\u003c/p\u003e","description":"","filename":"OriginalImageforFig2.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6234030/v1/8cf0302fd238b7658b622117.jpg"},{"id":79575675,"identity":"e9af6186-08c2-4cf5-9484-9faa85720475","added_by":"auto","created_at":"2025-03-31 11:16:52","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1930682,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6234030/v1/50b7c8f4-a505-4768-803f-1a8c78bf4c04.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Acetaminophen-induced transient myocardial thickening in a British Shorthair cat with hypertrophic cardiomyopathy","fulltext":[{"header":"Background","content":"\u003cp\u003eThe hypertrophic cardiomyopathy (HCM) phenotype is the most common form of feline cardiomyopathy; affected animals are primarily asymptomatic, and HCM can affect approximately 15% of the domestic cat population (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). The diagnosis of HCM is made when the left ventricular (LV) diastolic wall thickness (\u0026ge;\u0026thinsp;6 mm) is confirmed on echocardiography and other disorders that can cause mild to moderate LV wall thickening (e.g., hyperthyroidism, systemic hypertension, acromegaly, dehydration) are ruled out (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eTransient myocardial thickening (TMT) is one cause of the HCM phenotype (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e). TMT is characterized by reversible LV wall thickness and may be associated with concurrent transient left atrial (LA) dilation and dysfunction, and congestive heart failure (CHF); however, the exact etiology of TMT is unknown (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e). The most frequent antecedent event associated with TMT is surgical/anesthetic procedures, but others include traffic accidents and diseases that cause pain, and one study revealed that thermal burns may cause myocardial thickening (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eTo the author\u0026rsquo;s knowledge, TMT is well demonstrated in cats, but there are no reports that describe acute myocardial thickening in cats with HCM induced by acetaminophen toxicosis and provide echocardiography measurements pre- and post-TMT. This report describes significant thickening of the myocardium, a dilated LA, and the development of CHF in a cat with asymptomatic HCM within a week after acetaminophen toxicosis and demonstrates a subsequent decrease in the LV wall thickness (LVWT) and LA diameter (LAD).\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cp\u003eA 6-year-old castrated male British Shorthair weighing 5.5 kg was referred to Re-born Animal Medical Center for echocardiography with a history of a heart murmur detected at the local animal hospital 2 weeks prior to presentation. On physical examination, a grade 3/6 systolic heart murmur (point of maximum intensity: mitral valve) with a regular heart rate (200 beats/min) was detected, and the cat\u0026rsquo;s systolic blood pressure was normal (120 mmHg). Thoracic radiography in ventral and right lateral recumbency revealed no remarkable findings. The cat\u0026rsquo;s serum NT-proBNP level (reference range\u0026thinsp;\u0026lt;\u0026thinsp;100 pmol/L) was elevated at 266 pmol/L, and the total thyroxine concentration was within the reference range (1.8 \u0026micro;g/dL; reference range: 0.8\u0026ndash;4.7 \u0026micro;g/dL). Echocardiographic measurements were performed by one veterinary radiologist and analyzed retrospectively by a board-certified internist (Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). Symmetrical hypertrophy of the LV wall (LVWT maximum: 7.5 mm) and systolic anterior motion (SAM) with a normal LAD were observed (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e, Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). The cat was diagnosed with HCM. Twice daily atenolol (6.25 mg/cat, PO) was prescribed to relieve the effects of SAM.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eSelective two-dimensional echocardiographic variables at presentation (day 0) and on follow-up echocardiographic examinations.\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"6\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eVariable\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eUnit\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eDay 0\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eDay 6\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eDay 180\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e \u003cp\u003eDay 450\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHeart rate\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003ebeat/min\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e200\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e120\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e175\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e180\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eBlood pressure\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003emmHg\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e130\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e80\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e130\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e140\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLAD max\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003emm\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e10.6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e16.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e10.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e11.6\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLA/Ao\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e1.07\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e1.79\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e1.33\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e1.15\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLVIDd\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003emm\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e13\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e13.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e12.6\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLV FS\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e57.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e62\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e64.7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e58\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLVWT Max\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003emm\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e7.5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e11.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e6.9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIVSd MAX (RPLax)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003emm\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e7.5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e9.5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e6.9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e6.7\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLVFWd MAX(RPLax)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003emm\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e6.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e11.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e6.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e6.8\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIVSd MAX (RPSax)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003emm\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e7.1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e9.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e6.9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e7\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLVFWd MAX(RPSax)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003emm\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e6.7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e9.2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e6.1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e6.4\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAV Vmax\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003ecm/s\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e141\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e233\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e110\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e104\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePV V max\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003ecm/s\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e81\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e56\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e64\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e77\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSAM\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eYes\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eYes\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eNo\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eNo\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLVOTO\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eNo\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eYes\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eNo\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eNo\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003ctfoot\u003e \u003ctr\u003e\u003ctd colspan=\"6\"\u003eLAD Max: Maximal left atrial diameter; LA/Ao: Left atrium to aortic root ratio; LVIDd: Left ventricular internal diameter in end-diastole; LV FS: Left ventricular fractional shortening; LVWT Max: Maximal left ventricular wall thickness; IVSd Max: Maximal interventricular septal thickness in end-diastole; LVFWd Max: Maximal left ventricular free wall thickness in end-diastole; AV Vmax: Peak velocity across the aortic valve; PV Vmax: Peak velocity across the pulmonary valve; RPLax4C: Right parasternal long-axis four-chamber view, RPLax5C: Right parasternal long-axis five-chamber view, RPSax: Right parasternal short-axis view; LVOTO: Left ventricular outflow tract; SAM: systolic anterior motion.Echocardiographic measurements were performed by one radiologist and analyzed retrospectively by a single author. No sedation was used for each echocardiogram.\u003c/td\u003e\u003c/tr\u003e \u003c/tfoot\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eThree days after the first presentation, the cat presented with signs of vomiting, anorexia, and lethargy and had a history of acetaminophen ingestion (the cat was administered one 500 mg tablet by the owner) one day before prior to presentation. The cat\u0026rsquo;s vital signs were within the normal range (rectal temperature: 38.7\u0026deg;C, resting respiratory rate: 30 breaths/min, pulse: 150 beats/min, systolic blood pressure: 110 mmHg). The cat was hospitalized (day 0), and blood (which was brown in color) was collected. A complete blood count (CBC), plasma biochemical analysis, and electrolyte analysis were performed prior to the initiation of any therapy. The cat\u0026rsquo;s hematocrit (38.9%; reference range: 30.3\u0026ndash;52.3%) and liver enzymes were normal, and a low plasma creatinine (0.7 mg/dL; reference range: 0.8\u0026ndash;2.4 mg/dL), hypophosphatemia (3 mg/dL; reference range: 3.1\u0026ndash;7.7 mg/dL), and hypokalemia (3.4 mmol/L; reference range: 3.5\u0026ndash;5.5 mmol/L) were also identified. Significant Heinz bodies were found on a blood smear with new methylene blue stain. Therapy was initiated with intravenous fluids (Hartmann solution, 3 ml/kg/h on day 0 and continued at 1 ml/kg/h on days 1\u0026ndash;2), N-acetylcysteine (140 mg/kg IV once and continued at 70 mg/kg IV q6h), glutathione (100 mg/cat IV q12h), and vitamin C (30 mg/kg IV q6h), S-adenosylmethionine (50 mg/cat PO q12h), and silymarin (10 mg/kg PO q12h).\u003c/p\u003e \u003cp\u003eOn day 3, the cat\u0026rsquo;s hematocrit decreased to 27.3%, and the plasma alanine transaminase levels were above the normal range (193 U/L; reference range: 12\u0026ndash;130 U/L). In addition, the cat\u0026rsquo;s resting respiratory rate increased to 72 breaths/min, and the systolic blood pressure decreased to 80 mmHg. Thoracic radiography in ventral and right lateral recumbency showed an increased cardiothoracic ratio, a pleural effusion, and a generalized interstitial lung pattern (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). Echocardiography revealed a mild pericardial effusion, a pleural effusion, an increased LVWT (LVWT maximum: 11.4 mm) with heterogenous echogenicity of ventricular myocardium, an enlarged LAD (16.3 mm), and a left ventricular outflow tract obstruction (LVOTO) (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). Based on the rapid changes in the cardiovascular imaging results, the cat was diagnosed with CHF, intravenous fluid therapy was discontinued, and oxygen therapy was initiated. Furosemide (2 mg/kg IV once and continued at 2 mg/kg PO q12h) and clopidogrel (18.75 mg/cat PO q24h) were also administered.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eThe cat\u0026rsquo;s resting respiratory rate decreased to 30 breath/min on day 5, and radiography showed a reduced pleural effusion and interstitial lung pattern. On day 7, the cat\u0026rsquo;s hematocrit increased to 36.5%, and the plasma alanine transaminase levels normalized. The cat was subsequently discharged with furosemide (2 mg/kg PO q12h), silymarin (10 mg/kg PO q12h), clopidogrel (18.75 mg/cat PO q24h), and atenolol (6.25 mg/cat PO q12h) for 14 days. Follow-up medical treatment was recommended at the local animal hospital.\u003c/p\u003e \u003cp\u003eSix months after the first presentation, the cat was presented for repeat echocardiography. Echocardiography revealed a reduced LVWT (LVWT maximum: 6.9 mm) and LAD (10.4 mm), and SAM and LVOTO were not detected. The cat was diagnosed with TMT on HCM, and a tapering regimen of furosemide was prescribed (1 mg/kg PO q12h), clopidogrel was maintained, and atenolol was discontinued. Fifteen months after the first presentation, the cat presented for echocardiography again and was not receiving cardiac medications. Echocardiography revealed a similar LVWT (LVWT maximum: 7 mm) and LAD (11.6 mm), and SAM and LVOTO were not detected. The owner reported that the cat was doing clinically well.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThis report describes a 6-year-old British Shorthair with HCM that developed TMT following acetaminophen ingestion. In the present case, myocardial thickening developed, and the LAD was increased within 6 days, and an associated pleural effusion and pulmonary edema had developed. In addition, a reduced LVWT and LAD were confirmed 6 and 15 months later. The cat was doing clinically well without signs of CHF even after stopping the cardiac medications.\u003c/p\u003e \u003cp\u003eTo the author\u0026rsquo;s best knowledge, recent studies have defined TMT by confirming an initially increased LVWT (\u0026ge;\u0026thinsp;6 mm) and a reduced LVWT (\u0026lt;\u0026thinsp;5.5 mm) on follow-up echocardiography (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e). Strict criteria were required for prior experimental groups because echocardiography was not performed just before LV wall thickening in previous studies. According to these criteria, this cat may not have been diagnosed with TMT. However, the decreased ratio of the left ventricular free wall was 45% in this case, which significantly higher than previous results (24\u0026ndash;31%) (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan additionalcitationids=\"CR9\" citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). In addition, the echocardiographic measurements made before and after the development of TMT demonstrate that there was reversible myocardial hypertrophy in this cat with primary HCM, as in humans in very few reported cases (\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e). Therefore, the author suggests that the term TMT may be used in cats with primary HCM. In addition, the LVWT may decrease due to fibrosis of the myocardial wall at the end of HCM, which is characterized by a significant decrease in LV function and an increase in the LAD (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e). Therefore, when diagnosing TMT, considering both the LV function and LAD is essential in cats with HCM (\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eThe pathophysiology causing the acute ventricular wall thickening in cats remains unknown, but a catecholamine surge may result in myocardial thickening due to a form of myocardial edema (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). Furthermore, there are reports of TMT that may be associated with recent events such as anesthesia/surgery and road traffic accidents and several diseases or conditions including thermal burn injuries, infectious diseases including toxoplasmosis, bartonellosis, and sepsis (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan additionalcitationids=\"CR9\" citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). However, several reported cases of TMT in cats did not have an antecedent event or identifiable underlying disease (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e). In this case, the cat showed acetaminophen toxicosis, and no concurrent disease other than HCM was identified. Specific diseases (e.g. toxoplasmosis) were not ruled out, but this cat was strictly indoor, which made such an infection less likely (\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eTakotsubo cardiomyopathy (TTC), also known as stress cardiomyopathy in humans, is characterized by transient systolic, diastolic left ventricular dysfunction, and myocardial edema may develop (\u003cspan additionalcitationids=\"CR17\" citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e). The exact etiology of TTC is still unknown, but excessive catecholamine levels play a major role in the pathology of this disorder, and stress can also trigger this condition (\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e). TTC may result in LVOTO, and a combination of TTC with obstructive HCM can lead to low cardiac output and acute heart failure; administration of beta blockers is the main management option (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e, \u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e). Similarly, this cat showed LVOTO, CHF, and decreased systolic blood pressure. Although the prescription of atenolol in this case did not prevent these cardiovascular changes, administration of atenolol was maintained because it was considered the best treatment option and was associated with a good prognosis. Therefore, beta blockers may be used in cats with TMT with LVOTO.\u003c/p\u003e \u003cp\u003eAcetaminophen exposure may lead to cellular injury and death of hepatocytes, and ingestion of even small amounts can be a substantial risk for the cat (\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e, \u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e). The common clinical signs are anorexia, dullness, facial and paw edema, muddy mucous membranes, respiratory distress, and hematuria (\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e). In addition, oxidative damage may develop with the formation of methemoglobin that causes anemia (\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e). Moreover, myocardial infarctions, CHF, cardiac arrhythmias, pericarditis, and myocarditis due to acetaminophen toxicity have been reported in humans (\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e, \u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e). Potential causes of cardiotoxicities are oxidative stress and decreased sulfhydryl groups that may lead to cardiac cell death (\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e). In addition, one report demonstrated that TTC developed with acetaminophen toxicity, and the echocardiographic findings of this patient were decreased LV systolic function and ventricular wall thickness (\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e). There is no report of such cardiotoxicity in cats, and one study reported that pulmonary edema developed in a cat with acetaminophen exposure, but echocardiography was not performed (\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e). In this case, it is difficult to determine whether TMT occurred due to direct cardiac toxicity from acetaminophen or if it was secondary to catecholamine surges caused by liver dysfunction, oxidative stress, or other triggering factors. However, unlike the echocardiography features of other cases of feline TMT, this cat showed significant heterogeneous echogenicity of the ventricular wall that might be the result of inflammation and edematous changes induced by myocardial toxicity from acetaminophen (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan additionalcitationids=\"CR9\" citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e). Since the exact mechanisms of TMT are unknown, this case suggests the possibility of acetaminophen myocardial toxicity that may cause TMT.\u003c/p\u003e \u003cp\u003eThe main limitation of this report is that cardiac biomarkers, inflammatory biomarkers, and stress biomarkers were not analyzed. The second limitation is that fluid analysis of the pleural effusion was not performed, and underlying infectious diseases were not ruled out. In addition, an electrocardiogram was not conducted in this case. Finally, the follow-up interval was relatively long, and the process of normalization of the myocardial wall was not confirmed. Despite these limitations, this case is meaningful as there was reversible myocardial hypertrophy after acetaminophen ingestion in this cat with asymptomatic HCM.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eTo the best of the author\u0026rsquo;s knowledge, this is the first report to describe echocardiography findings before and after the development of TMT. In addition, this report described reversible myocardial thickening in a cat with HCM. This case suggests the possibility that acetaminophen toxicity may cause TMT in cats. Considering that the prevalence of HCM in cats is significantly high, the possibility of comorbid HCM and TMT should always be considered. In such cases, even though a cat with HCM may develop congestive pulmonary edema, life-long cardiac medication may not be needed. Therefore, follow-up echocardiography is essential in cats with the HCM phenotype due to the characteristic of dynamic changes in the LVWT.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eCongestive heart failure (CHF)\u003c/p\u003e\n\u003cp\u003eHypertrophic cardiomyopathy (HCM)\u003c/p\u003e\n\u003cp\u003eLeft atrium (LA)\u003c/p\u003e\n\u003cp\u003eLeft atrial diameter (LAD)\u003c/p\u003e\n\u003cp\u003eLeft ventricular outflow tract obstruction (LVOTO)\u003c/p\u003e\n\u003cp\u003eLeft ventricular wall thickness (LVWT)\u003c/p\u003e\n\u003cp\u003eSystolic anterior motion (SAM)\u003c/p\u003e\n\u003cp\u003eTransient myocardial thickening (TMT)\u003c/p\u003e\n\u003cp\u003eTakotsubo cardiomyopathy (TTC)\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eSince this is a case report, ethical review and approval were not required. Written informed consent was obtained from the owners for the participation of their animals in this study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis work was supported financially by Rural Development Administration (RDA) under grant number RS-2023-00232301.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors’ contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eS-WP and KK were involved in case analysis and were responsible for writing the manuscript. Y-JD, J-W were involved in the draft preparation and case analysis. W-BR and C-ML were involved in the coordination of the case and were responsible for interpretation of results. All authors contributed to the article and approved the submitted version.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eKittleson MD, C\u0026ocirc;t\u0026eacute; E. The feline cardiomyopathies: 2. Hypertrophic cardiomyopathy. J Feline Med Surg. 2021;23(11):1028\u0026ndash;51.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eVisser L, Sloan C, Stern J. Echocardiographic assessment of right ventricular size and function in cats with hypertrophic cardiomyopathy. J Vet Intern Med. 2017;31(3):668\u0026ndash;77.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNovo Matos J, Pereira N, Glaus T, Wilkie L, Borgeat K, Loureiro J, et al. Transient myocardial thickening in cats associated with heart failure. J Vet Intern Med. 2018;32(1):48\u0026ndash;56.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLuis Fuentes V, Abbott J, Chetboul V, C\u0026ocirc;t\u0026eacute; E, Fox PR, H\u0026auml;ggstr\u0026ouml;m J, et al. ACVIM consensus statement guidelines for the classification, diagnosis, and management of cardiomyopathies in cats. J Vet Intern Med. 2020;34(3):1062\u0026ndash;77.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eRomito G, Elmi A, Guglielmini C, Poser H, Valente C, Castagna P, et al. Transient myocardial thickening: a retrospective analysis on etiological, clinical, laboratory, therapeutic, and outcome findings in 27 cats. J Veterinary Cardiol. 2023;50:51\u0026ndash;62.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSharpe AN, Gunther-Harrington CT, Epstein SE, Li RH, Stern JA. Cats with thermal burn injuries from California wildfires show echocardiographic evidence of myocardial thickening and intracardiac thrombi. Sci Rep. 2020;10(1):2648.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTrehiou-Sechi E, Tissier R, Gouni V, Misbach C, Petit A, Balouka D, et al. Comparative echocardiographic and clinical features of hypertrophic cardiomyopathy in 5 breeds of cats: a retrospective analysis of 344 cases (2001\u0026ndash;2011). J Vet Intern Med. 2012;26(3):532\u0026ndash;41.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWang Y, Seo J. Transient myocardial thickening after routine ovariohysterectomy in a 15-month‐old Ragdoll cat. J Small Anim Pract. 2024.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eRomito G, Fracassi F, Cipone M. Transient myocardial thickening associated with acute myocardial injury and congestive heart failure in two Toxoplasma gondii-positive cats. J Feline Med Surg Open Rep. 2022;8(2):20551169221131266.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJoung Y, Ahn H, Choi J, Yun Y, Song W-J. Transient Myocardial Thickening in a 4-year-old Korean Domestic Shorthair Cat. J veterinary Clin. 2024;41(2):106\u0026ndash;11.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNalluri N, Asti D, Anugu VR, Ibrahim U, Lafferty JC, Olkovsky Y. Cardiogenic shock secondary to takotsubo cardiomyopathy in a patient with preexisting hypertrophic obstructive cardiomyopathy. CASE. 2018;2(3):78\u0026ndash;81.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMaron BJ, Desai MY, Nishimura RA, Spirito P, Rakowski H, Towbin JA, et al. Diagnosis and evaluation of hypertrophic cardiomyopathy: JACC state-of-the-art review. J Am Coll Cardiol. 2022;79(4):372\u0026ndash;89.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDaralammori Y, El Garhy M, Gayed M, Farah A, Lauer B, Secknus M. Hypertrophic Obstructive Cardiomyopathy Masked by Tako-Tsubo Syndrome: A Case Report. Case Rep Cardiol. 2012;2012(1):486427.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWhite AJ. End-stage hypertrophic cardiomyopathy in a cat. Can veterinary J. 2015;56(5):509.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWess G, Sarkar R, Hartmann K. Assessment of left ventricular systolic function by strain imaging echocardiography in various stages of feline hypertrophic cardiomyopathy. J Vet Intern Med. 2010;24(6):1375\u0026ndash;82.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTemplin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, et al. Clinical features and outcomes of takotsubo (stress) cardiomyopathy. N Engl J Med. 2015;373(10):929\u0026ndash;38.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKato K, Daimon M, Sano M, Matsuno K, Sakai Y, Ishibashi I, et al. Dynamic trend of myocardial edema in takotsubo syndrome: A serial cardiac magnetic resonance study. J Clin Med. 2022;11(4):987.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMigliore F, Zorzi A, Marra MP, Iliceto S, Corrado D. Myocardial edema as a substrate of electrocardiographic abnormalities and life-threatening arrhythmias in reversible ventricular dysfunction of takotsubo cardiomyopathy: Imaging evidence, presumed mechanisms, and implications for therapy. Heart Rhythm. 2015;12(8):1867\u0026ndash;77.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNef HM, M\u0026ouml;llmann H, Akashi YJ, Hamm CW. Mechanisms of stress (Takotsubo) cardiomyopathy. Nat Reviews Cardiol. 2010;7(4):187\u0026ndash;93.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eParato VM, Gizzi G, D'Agostino S. 675 A rare case of tako-tsubo syndrome in a patient with hypertrophic cardiomyopathy. Eur Heart J Supplements. 2021;23(SupplementG):suab142.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDorigon O. Almeida AdVd, Costa Fd. Acetaminophen toxicity in cats. 2013.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGrave TW, Boag AK. Feline toxicological emergencies: when to suspect and what to do. J Feline Med Surg. 2010;12(11):849\u0026ndash;60.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSidhu S, Randhir S, Neetu S. Acetaminophen toxicity in a cat and its treatment. Indian J Veterinary Med. 2021;41(1):75\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWebb C, Twedt D, Fettman M, Mason G. S-adenosylmethionine (SAMe) in a feline acetaminophen model of oxidative injury. J Feline Med Surg. 2003;5(2):69\u0026ndash;75.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKhabazianZadeh F, Kazemi T, Nakhaee S, Ng PC, Mehrpour O. Acetaminophen poisoning-induced heart injury: a case-based review. DARU J Pharm Sci. 2019;27:839\u0026ndash;51.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLip GY, Vale JA. Does acetaminophen damage the heart? J Toxicology: Clin Toxicol. 1996;34(2):145\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJophlin LL, Koch DG. Takotsubo cardiomyopathy following acute liver failure. Hepatology. 2015;61(4):1430\u0026ndash;1.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAnvik J. Acetaminophen toxicosis in a cat. Can Veterinary J. 1984;25(12):445.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJoseph J, Oxford E, Santilli R. Transient myocardial thickening in a Bartonella henselae\u0026ndash;positive cat. J veterinary Cardiol. 2018;20(3):198\u0026ndash;203.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"irish-veterinary-journal","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"","sideBox":"Learn more about [Irish Veterinary Journal](https://irishvetjournal.biomedcentral.com/)","snPcode":"13620","submissionUrl":"https://submission.springernature.com/new-submission/13620/3?","title":"Irish Veterinary Journal","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"BMC/SO AJ","inReviewEnabled":true,"inReviewRevisionsEnabled":false},"keywords":"Echocardiography, Feline, Heart disease, Left ventricular wall thickness, Myocardial disease","lastPublishedDoi":"10.21203/rs.3.rs-6234030/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6234030/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eTransient myocardial thickening (TMT) is a cause of hypertrophic cardiomyopathy (HCM) that is characterized by reversible left ventricular wall thickening.\u003c/p\u003e\u003ch2\u003eCase presentation\u003c/h2\u003e \u003cp\u003eA 6-year-old castrated male British Shorthair with a history of a heart murmur detected on its annual examination was presented for echocardiography. Based on physical examination, blood analysis, and echocardiography (maximum left ventricular wall thickness (LVWT): 7.5 mm), the cat was diagnosed with HCM. Three days after the first presentation, the cat presented with a history of acetaminophen ingestion. Three days after hospitalization, the cat developed tachypnea, and radiography showed a pleural effusion and generalized interstitial lung pattern. Echocardiography showed a remarkably increased LVWT (11.4 mm) and an enlarged left atrial diameter (LAD). The cat was treated with diuretics, and its condition clinically normalized. Six months after the first presentation, echocardiography revealed a decreased LVWT (6.9 mm) and LAD.\u003c/p\u003e\u003ch2\u003eConclusions\u003c/h2\u003e \u003cp\u003eThis is the first case report to demonstrate that TMT can occur in cats with HCM, and acetaminophen may induce TMT in cats. The possibility of comorbid HCM and TMT should always be considered. In such cases, even though a cat with HCM may develop congestive pulmonary edema, life-long cardiac medication may not be needed.\u003c/p\u003e","manuscriptTitle":"Acetaminophen-induced transient myocardial thickening in a British Shorthair cat with hypertrophic cardiomyopathy","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-03-31 11:08:42","doi":"10.21203/rs.3.rs-6234030/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2025-07-21T16:09:05+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-07-10T20:01:09+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"269928297271701574702966548853010189120","date":"2025-06-13T07:04:57+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-04-07T08:00:30+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"127291321749733132387089278054481780222","date":"2025-03-21T19:16:20+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-03-19T15:08:42+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-03-18T09:27:40+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-03-18T06:42:07+00:00","index":"","fulltext":""},{"type":"submitted","content":"Irish Veterinary Journal","date":"2025-03-15T16:43:21+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"irish-veterinary-journal","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"","sideBox":"Learn more about [Irish Veterinary Journal](https://irishvetjournal.biomedcentral.com/)","snPcode":"13620","submissionUrl":"https://submission.springernature.com/new-submission/13620/3?","title":"Irish Veterinary Journal","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"BMC/SO AJ","inReviewEnabled":true,"inReviewRevisionsEnabled":false}}],"origin":"","ownerIdentity":"475bed4f-6ef0-4222-ad59-ec5eb9f48428","owner":[],"postedDate":"March 31st, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-05-12T22:53:47+00:00","versionOfRecord":[],"versionCreatedAt":"2025-03-31 11:08:42","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-6234030","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6234030","identity":"rs-6234030","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}