Transient myocardial thickening (TMT) is a hypertrophic cardiomyopathy (HCM) phenotype characterized by subsequent normalization of cardiac structure and function in cats (12,15). It has been noted that feline cases of TMT tend to occur at a young age and often followed an antecedent event (15). The most frequent antecedent event was general anesthesia, while others included traffic accidents, vaccination, bite wounds, and pain (16). Sharpe et al. (19) also discovered that a high prevalence of cats (18/51) with thermal burns from wildfires in California experienced myocardial thickening. Herein, we present the first case in South Korea of a 4-year-old cat with suspected TMT following a history of stressful antecedent events.

A 4-year-old neutered female domestic shorthair cat weighing 5.1 kg was referred to Jeju National University Hospital with acute onset respiratory distress, weakness, and anorexia. The cat lived with multiple cats, one of which had caused distress to the patient, resulting in ongoing stress. Physical examination have detected abnormalities including tachypnea (respiratory rate, 72 breaths/min), hypotension (systolic blood pressure, 70 mmHg), and mild hypothermia (37.3°C). However, there was no evidence of dehydration such as delayed skin turgor or dry gums. In addition, cardiac auscultation revealed normal heart rate (150/min) without murmur. Complete blood count and serum chemistry profiles were within reference ranges. Blood abnormalities included elevated serum amyloid A ([SAA] 40.3 μg/mL; reference interval, 0-5 μg/mL) and feline pro-BNP (773.8 pmol/L; reference interval, 0-100 pmol/L). The SNAP Feline Triple Test, which tests for feline immunodeficiency virus antibody, feline leukemia virus antigen, and feline heartworm antigen, was negative. Also, T4 concentration was also measured and was within the reference range (2.3 μg/dL; reference interval, 0.8-4.7 μg/dL). Thoracic radiographs (50 kVp, 8 mAs) revealed an unclear cardiac silhouette and a moderate interstitial lung pattern in all lung lobes, with a partial alveolar pattern (Fig. 1A). Interlobar fissure lines were also observed (Fig. 1A). Echocardiography showed moderate left atrium (LA) enlargement (LA 17.8 mm, LA/Ao 2.28; Fig. 2A) and a thickening of the left ventricular and interventricular septum wall (7.1 mm, 6.8 mm at end-diastole; Fig. 2B, Supplementary Video 1). Furthermore, pericardial effusion was observed (Fig. 1B). Based on the clinical signs and imaging results, the patient was diagnosed with HCM phenotype stage C based on the American College of Veterinary Internal Medicine classification system with pulmonary edema, pleural effusion, and pericardial effusion at the same time. Furthermore, no systemic diseases known to induce HCM phenotype, such as systemic hypertension, hyperthyroidism, or dehydration, were identified.

Figure 1. (A, B) Thoracic images of the cat at day 0. (A) Dorsoventral and right lateral views of thoracic radiographs show cardiomegaly, alveolar patterns in overall lung lobes, and interlobar fissure lines. (B) Anehcoic space surrounding the heart, indicating the presence of pericardial effusion is identified by echocardiography. (C, D) Thoracic radiographs showing ventrodorsal views (C) at day 0 (discharge), and (D) at day 8. Marked resolution of alveolar patterns and fissure lines are detected at day 8.

Figure 2. (A, B) Echocardiographic images of the cat at Day 0. (A) Right parasternal short axis view (aortic valve) shows moderate left atrium enlargement. (B) Right parasternal short axis view (papillary muscle) shows thickening of the left ventricular wall at end-diastole. (C, D) Echocardiographic images of the cat at Day 30. (C) Right parasternal short-axis view (aortic valve) showing a normal left atrial size. (D) Right parasternal short-axis view (papillary muscle) showing the normal left ventricular wall.

The patient was hospitalized and treated with furosemide (2 mg/kg IV q 1-2 h, total 7 mg/kg) with continuous respiratory rate monitoring. Pimobendan (0.25 mg/kg PO q 12 h) and rivaroxaban (1 mg/kg PO q 12 h; to lower the thromboembolic risk) were also administered. Despite furosemide therapy, the patient’s respiratory rate and blood pressure did not improve completely. Pericardiocentesis was performed because cardiac tamponade was suspected, and 100 mL of pericardial fluid was removed. Even after pericardiocentesis, persistent thickening of the left ventricular wall (over than 6 mm) at end-diastole was detected. The cat became clinically stable. Thoracic radiographs showed slight radiolucency of the cranial lung lobes with a clearer cardiac silhouette, and the Valentine shape of the cardiac silhouette was present (Fig. 1C). The patient was discharged with oral furosemide (2 mg/kg PO q 12 h), pimobendan, and rivaroxaban (unchanged dosages).

After 8 days, the cat was living separately from the cohabiting cats and was clinically normal, with a normalized systolic blood pressure of 90 mmHg and thoracic radiography showing resolution of the pulmonary edema and pleural effusion (Fig. 1D). Therefore, the furosemide dose was reduced to 1.5 mg/kg PO q 12 h.

The patient remained stable at home and was re-evaluated after 30 days. Thoracic radiography revealed a normal cardiac shape (Fig. 3). An echocardiogram revealed normalized cardiac measurements (LA 11.5 mm, LA/Ao 1.37; Fig. 2C, end-diastolic left ventricular free wall 5.4 mm; Fig. 2D). Both SAA (< 5 μg/mL) and pro-BNP (< 50 pmol/L) levels were normal as well. The patient was tentatively diagnosed with TMT and all medications were discontinued. The cat continued to do well without any clinical signs or left ventricular wall thickening 12 months after the initial hospitalization.

Figure 3. Thoracic radiographic Images of the cat on day 30. Ventrodorsal and right lateral thoracic radiographs showing a normal cardiac shape.

The pathophysiology of TMT is unknown, but catecholamines may potentially cause myocardial changes (15). In humans, catecholamine-induced cardiomyopathy, known as Takotsubo cardiomyopathy, stress cardiomyopathy, or transient left apical ballooning syndrome, occurs when excessive catecholamine released due to stress is presented directly to the adrenoreceptors of the myocardium, leading to transient myocardial toxicity and myocardial contraction band necrosis (1,10,13). It is associated with emotional or physical stress and presents with acute reversible heart failure syndrome, which shares similarities with our case.

Similar cases have also been reported in veterinary medicine. Pheochromocytoma-associated cardiomyopathy, which is another type of catecholamine-induced cardiomyopathy, has been reported in dogs. Among 62 patients with pheochromocytoma, histological examination revealed cardiomyocyte necrosis with a contraction band in 6 patients, and ventricular hypertrophy was observed on echocardiography in 3 patients (4). In the red-necked wallaby, left ventricular concentric hypertrophy and elevated serum cardiac troponin levels were observed following anesthesia, with histological findings resembling those seen in Takotsubo cardiomyopathy (21). Therefore, TMT may be a consequence of a catecholamine surge caused by emotional or physical stress as seen with catecholamine-induced cardiomyopathy.

In humans, severe myocardial interstitial edema due to acute myocarditis can result in reversible ventricular wall thickening (7,8,14). In veterinary medicine, myocarditis caused by toxoplasma, bartonella, feline immunodeficiency virus, feline infectious peritonitis, feline leukemia virus infection, toxins, or eosinophilic myocarditis can lead to an increase in ventricular wall thickness (5,11,16,22). However, myocarditis has been rarely identified in cats and is poorly described in small animals, as it requires histological diagnosis which typically involves post-mortem examination or endomyocardial biopsy (20). Several case reports have described TMT in cats secondary to Toxoplasma gondii infection (17) and Bartonella henselae infection (9,14). As we did not conduct tests for infections other than feline immunodeficiency virus and feline leukemia virus in our case, the possibility of acute myocarditis cannot be completely ruled out, especially considering the observed elevation in SAA.

Pulmonary edema, pleural effusion, and pericardial effusion can occur in cats with HCM phenotype that develop congestive heart failure (CHF). In two prior studies, among cats with HCM phenotype with CHF, pulmonary edema occurred most frequently (119/181 cases, 66% and 14/61 cases, 23%), while pleural effusion was observed less frequently in 6/181 cases (34%) and 4/61 cases (6.6%) (6,18). Furthermore, among 769 patients with HCM phenotype, pericardial effusion was present in 17 patients (3). However, the severity of cardiac tamponade was not measured in these cases (3). In a comparative study between TMT and HCM, pulmonary edema occurred in 11/21 cases of cats with HCM, pleural effusion occurred in 1 case, both pulmonary edema and pleural effusion in 9 cases, and pericardial effusion in 8 cases. In cats with TMT, 6/21 cases had pulmonary edema, 2 had pleural effusion, both pulmonary edema and pleural effusion in 13 cases, and pericardial effusion in 9 cases (15).

There are some limitations in this case report. The first limitation was the inability to conduct histopathological examination of myocardium to discern the cause of myocardial changes. Also, the echocardiogram at first emergency visit was not conducted under ECG guidance due to the patient’s critical condition and the need to minimize stress. In addition, we could not rule out heartworm infection by antibody test. Although SNAP feline triple kit shows relatively high sensitivity and specificity (90.2%, 100%, respectively) (11), running both an antibody and antigen test improves sensitivity compared with running either test alone (20). Also, methods for recognition, evaluation, and physiological measurement of chronic stress in the cat are lacking. Quantitative stress measures in cats historically have been based on serum cortisol concentration and more recently salivary, urinary, and fecal cortisol concentrations (2). Lastly, the absence of fluid analysis of the pericardial effusion hindered the accurate determination of its cause.

Despite of those limitations, our case is noteworthy as it involves a rare instance in which pulmonary edema, pleural effusion, and pericardial effusion, which induced cardiac tamponade, occurred simultaneously in TMT-related CHF.

To the best of our knowledge, this is the first report describing feline TMT in Korea involving a rare case of pulmonary edema, pleural effusion, and pericardial effusion that simultaneously induced cardiac tamponade due to TMT-related CHF. Moreover, this significant case demonstrates the impact of stress during TMT, as rapid normalization of left ventricular hypertrophy was observed when the stress factors were alleviated.

This study was supported by the research grant of Jeju National University in 2023.

No conflicts of interest have been declared.