Perioperative Arrhythmia of Unknown Etiology in a Cat: Infection Involvement?

Perioperative arrhythmias may be life-threatening if left untreated, and diverse etiologies should be considered. We encountered an arrhythmia of unknown etiology in a cat with a chronic urinary tract infection (UTI). A domestic short-hair (DSH) castrated male cat of unknown age sustained a torn urethra due to a traffic accident and underwent urethral-vesical fistula formation. Subsequently, the cat repeatedly experienced urinary retention and a lower streptococcal UTI was detected; therefore, urethral reconstruction and a button-type fistula were performed. The cat’s electrocardiogram (ECG) initially showed no abnormalities; however, five months later, the UTI worsened.

Following the removal of the bladder catheter under general anesthesia, an increase in the ST segment of the ECG was observed. Ultrasonography revealed mild thickening of the ventricular muscle, and a 6-lead ECG showed alternating pulse and ST elevation. After six days of antimicrobial treatment, the left ventricular wall thickening improved, but ST elevation persisted. The catheter was then removed under general anesthesia. At the months follow-up, the arrhythmia completely resolved.

In humans, bacterial infections and inflammation can cause myocarditis that may lead to arrhythmia. In this case, although a direct causal relationship could not be definitively established chronic UTI-associated inflammation was considered a possible contributing factor affecting myocardial conduction. Therefore, the risk of arrhythmia in the perioperative period should be considered not only for acute or severe infections such as sepsis, but also for chronic infections and inflammatory diseases.

Introduction

In veterinary practice, arrhythmia is frequently observed during the perioperative period. If left untreated, arrhythmia can progress to life-threatening conditions, such as ventricular fibrillation, underscoring the importance of identifying the underlying etiology and providing appropriate treatment. However, determining the cause of arrhythmia is often challenging, and in some cases, careful anesthetic management is required to prevent progression.

Here, we encountered an unexplained arrhythmia in a male cat of unknown age during and after surgery, with chronic urinary tract infection a possible contributing factor. While myocarditis associated with infections is generally linked to viral pathogens such as parvoviruses and enteroviruses, bacterial myocarditis is relatively rare [1]. Although cases of myocarditis secondary to bacterial urinary tract infections have been reported in humans [1], [2], and a few cases have been reported in cats [3], [4], there are, to our knowledge, no previous reports suggesting a potential association between urinary tract infection and arrhythmia in cats.

Case Presentation

The timeline of the patient’s clinical course is summarized in Table I.

Table I. Timeline of Clinical Events and Diagnostic Findings

Hospital day	Event	Findings/Notes
Day 1	Admission to the veterinary teaching hospital	History of pelvic fracture, urethral tear, cystostomy, and repeated fistula issues
Day 11	CT scan	Urethral stones and strictures identified
Day 37	Button-type anastomosis performed	Streptococcus faecalis isolated from urine (lower UTI confirmed)
Day 183	Pre-anesthetic ECG for catheter removal, Echocardiography, and ECG	ST elevation observed; procedure cancelled due to suspected cardiac abnormality LV/IVS wall thickening, FS 51.08%, E/e′ = 12.8, electrical alternans, ST elevation
Day 183–185	Empirical antibiotic therapy initiated	Ceftriaxone (25 mg/kg IV BID for 2 days)
Day 185	Antibiotic adjusted based on culture and sensitivity	Switched to piperacillin/tazobactam (50 mg/kg IV BID)
Day 189	Surgical removal of a urinary catheter	Procedure completed with buprenorphine analgesia
Day 413	Follow-up echocardiography and ECG	ST elevation and alternans resolved; wall thickness and E/e′ improved
Ongoing	Periodic monitoring	No recurrence of arrhythmia; stable clinical condition maintained

Summary of diagnostic imaging, laboratory data, and treatments during the clinical course.

Clinical History

A neutered male domestic shorthair cat (weight: 4.56 kg, age unknown) was referred to a university-affiliated veterinary teaching hospital for chronic lower urinary tract issues. The cat had a history of trauma from a vehicular accident, resulting in pelvic fracture and urethral tear. Initial management included creation of a ventral wall urethral fistula. However, subsequent anastomotic obstruction necessitated cystostomy the following year. The cat experienced recurrent episodes of fistula obstruction, leading to multiple interventions prior to referral. All day numbers mentioned in this report refer to the number of days since the cat’s admission to our hospital.

Diagnostics

On hospital day 11, computed tomography (CT) revealed urethral calculi and strictures. On day 37, a button-type urethral anastomosis was performed. Streptococcus faecalis was isolated from a urine sample, confirming the presence of a lower urinary tract infection (UTI). Electrocardiography (ECG) at this time showed no abnormalities (Fig. 1A).

Fig. 1. Electrocardiograms (ECGs) at different time points: (A) ECG recorded during computed tomography (CT) and urethral-vesical fistula formation, showing no abnormalities, (B) ECG on day 183, showing ST-segment elevation (red arrows), (C) ECG on day 189, following 6 days of antibiotic treatment; ST-segment elevation persists (red arrows). Abbreviation: ECG: electrocardiogram, CT: computed tomography.

Perioperative Event

On hospital day 183, worsening lower UTI was observed. During anesthesia induction for urinary catheter removal, ECG revealed ST-segment elevation (Fig. 1B), leading to cancellation of the procedure due to suspected cardiac abnormalities. The cat remained normothermic (36°C–37°C), and blood work showed no leukocytosis or electrolyte imbalances relevant to the ECG findings (Table II).

Table II. Complete Blood Count and Serum Biochemistry During the Clinical Course

Days post	183	189	413		Days post	183	189	413
WBC (K/μL)	15.86	19.85	13.76		TP (g/dL)	9.3	7.6	–
RBC (M/μL)	10.43	8.46	7.73		ALB (g/dL)	3.8	3.3	–
Hct (%)	43.4	36	32.7		IP (mg/dL)	5.7	5.8	–
Hb (g/dl)	15.2	12.3	11.3		Ca (mg/dL)	10.1	9.6	–
BUN (mg/dL)	24.4	34.5	–		Na (mEq/L)	135.2	156.4	–
Cre (mg/dL)	1.4	1.58	–		K (mEq/L)	4.15	4.15	–
					Cl (mEq/L)	98.3	117.6	–

Electrolytes and calcium remained within normal limits throughout.

Echocardiography revealed left ventricular (LV) wall thickening (6.3 mm), interventricular septal (IVS) thickening (5.3 mm), and increased fractional shortening (FS) of 51.08% (Table III; Fig. 2A).

Table III. Echocardiographic Measurements over Time

Days post	183	189	413
End-diastolic interventricular septal thickness (IVSd) (mm)	2.6	3	4.8
Left ventricular posterior wall thickness at end-diastole (LVPWd) (mm)	3.5	2.9	3.9
Left ventricular internal diameter at end-diastole (LVIDd) (mm)	14.9	17.7	15.4
Left ventricular internal diameter at end-systole (LVIDs) (mm)	7.3	8.8	5.3
Basal interventricular septal wall thickness (mm)	5.3	3.8	5
Left ventricular wall thickness (mm)	6.3	5.7	4.8
Left atrial/aortic diameter ratio (LA/Ao)		1.45	1.26
Left ventricular fractional shortening (FS)	51.08	50.28	65.32
Maximum aortic flow velocity (Avmax) (m/s)	2.00	1.14	0.82

Fig. 2. Right parasternal long-axis echocardiographic images: (A) Day 183: increased myocardial wall thickness observed at the time of ECG abnormalities, (B) Day 189: partial improvement in wall thickness after antibiotic therapy, (C) Day 413: normalization of wall thickness at follow-up. Abbreviation: ECG, electrocardiogram.

Includes interventricular septal thickness (IVS), left ventricular posterior wall (LVPW), left atrial-to-aortic ratio (LA/Ao), and fractional shortening (FS).

Color Doppler imaging showed aortic jet flow with a peak velocity of 2.0 m/s (Figs. 3 and 4), and tissue Doppler imaging (TDI) showed an E/e′ ratio of 12.8, indicating impaired LV diastolic function (Table IV).

Fig. 3. Color Doppler imaging of the aortic outflow tract on day 183: (A) Mosaic flow pattern within the aortic outflow tract suggests turbulence, (B) Areas of elevated flow velocity identified, consistent with dynamic obstruction.

Fig. 4. Pulsed-wave Doppler of aortic flow (apical five-chamber view): (A) Day 183: elevated aortic velocity with sharp jet contours, (B) Day 189: flow velocity decreases after antibiotic treatment, (C) Day 413: normalization of flow with no detectable jet.

Table IV. Tissue Doppler Imaging (TDI) of the Mitral Valve

Days post	183	189	413
E	4.65	6.83	6.17
S	11.06	14.77	12.49
A	6.9	9.37	8.7
E/e′	12.8	10.6	10.3

Serial E/e′ ratios are shown to evaluate changes in diastolic function.

Six-lead ECG showed ST-segment elevation in leads II, III, and aVF, corresponding to the inferior LV wall, along with electrical alternans in all leads (Fig. 5A).

Fig. 5. Six-lead electrocardiograms (ECGs): (A) on day 183, Electrical alternans observed in all leads (blue arrows); ST-segment elevation in leads II, III, and aVF (red arrows), (B) Electrical alternans and ST-segment elevation resolved by day 413. Abbreviation: ECG, electrocardiogram.

Urinalysis confirmed the presence of Escherichia coli, Enterococcus faecalis, and Pseudomonas aeruginosa, indicating a chronic lower UTI.

Treatment and Clinical Course

Empirical broad-spectrum antibiotic therapy was initiated on days 183–185 with ceftriaxone (25 mg/kg IV, twice daily). Based on antimicrobial susceptibility testing of the urine, therapy was switched to piperacillin/tazobactam (50 mg/kg IV, twice daily).

Cardiac Response to Treatment

Follow-up echocardiography revealed improvement: LV wall thickness decreased to 5.7 mm and IVS thickness to 3.8 mm (Fig. 2B). FS decreased slightly to 50.28% (Table III), aortic flow velocity improved to 1.14 m/s (Fig. 4), and the E/e′ ratio improved to 10.6 (Table IV). However, ST-segment elevation on ECG persisted (Fig. 1B).

Surgical Management

On day 189, surgical removal of the urinary catheter was performed under buprenorphine (BUP) based analgesia to reduce arrhythmia risk. The procedure was completed successfully without complications.

Follow-Up and Outcome

On day 413, follow-up evaluations revealed complete resolution of ST-segment elevation and electrical alternans (Fig. 5B). LV wall thickness further decreased to 4.8 mm (Fig. 2C), and the LA/Ao ratio improved from 1.45 to 1.26 (Table III). The E/e′ ratio also improved to 10.3 (Table IV), suggesting sustained improvement in diastolic function.

The cat remains stable and is undergoing regular monitoring every few months, including urinalysis, echocardiography, and ECG. No recurrence of arrhythmia has been observed to date.

A detailed timeline is provided in Table I.

All echocardiographic and electrocardiographic examinations were performed by a veterinarian with advanced training in cardiology and several years of experience in small animal cardiac imaging.

Discussion

Although the precise age of the cat in this case was unknown, it was estimated to be in the middle-to-older age range, and hypertrophic cardiomyopathy (HCM) was initially suspected. Following the detection of abnormal ECG findings on day 183, a transthoracic echocardiogram revealed moderate thickening of the left ventricular wall measuring 6.3 mm. Histologically, HCM is associated with disorganized myocardial fibers, interstitial infiltration, and fibrosis [5], rendering the condition irreversible. It is highly unlikely that HCM can be completely reversed with medication. However, in this case, after a short 6-day course of antibiotic therapy, the left ventricular wall thickness improved from 6.3 to 5.7 mm, and the interventricular septal thickness decreased from 5.3 to 3.8 mm, suggesting that HCM was unlikely.

On day 183, color Doppler imaging of the right parasternal long-axis view identified turbulent flow within the aortic outflow tract, with an aortic velocity of 2.0 m/s, raising the suspicion of left ventricular outflow tract obstruction secondary to basal septal thickening. Additionally, M-mode echocardiography demonstrated an elevated fractional shortening (FS) of 51.08%. On day 189, the left atrium-to-aortic root (LA/Ao) ratio was 1.45, indicating moderate left atrial enlargement. Tissue Doppler imaging (TDI) showed an elevated E/e′ ratio of 12.8, suggesting impaired left ventricular diastolic function. Between days 189 and 413, the aortic velocity decreased, and turbulent flow was no longer observed. Concurrently, the LA/Ao ratio decreased from 1.45 to 1.26, and the E/e′ ratio on the TDI improved from 12.8 to 10.3, indicating enhanced cardiac function. The FS decreased slightly from 51.08% to 50.28%, likely owing to the effects of fluid therapy during the treatment period. Conversely, a slight increase in the FS on day 413 was attributed to dehydration.

An ECG performed on day 183 revealed electrical alternans in all leads, a phenomenon commonly associated with cardiac tamponade. However, as no pericardial effusion was detected on echocardiography, it was hypothesized that this finding could be explained in terms of heterogeneous myocardial conduction due to myocardial thickening. ST-segment elevation was observed in leads II, III, and aVF, corresponding to the inferior wall of the left ventricle [6]. As this region is primarily supplied by the right coronary artery, ischemia or embolism of the right coronary artery is considered a potential cause.

Potential etiologies of arrhythmia include primary cardiac disease, electrolyte imbalances, metabolic or endocrine disorders, infections, inflammation, external factors, and drug-related effects. In this case, the electrolyte and calcium levels were within normal limits, no endocrinopathies or drug-induced arrhythmias were identified, and thoracic CT findings indicated no evidence of neoplasia.

The cat’s body temperature consistently ranged from 36.8°C to 37.9°C, with no fever. On day 183, the WBC count was elevated at 15.86 K/μL but remained within the reference range. However, by day 189, the WBC count further increased to 19.85 K/μL, confirming a significant inflammatory response only after the detection of ECG abnormalities. It has been reported that a significant rise in body temperature is not typically observed in feline infectious endocarditis [7]. Similarly, fever may not occur in cats with cardiac diseases. Therefore, we could not exclude the possibility that the inflammatory response in this case was not reflected in body temperature. In this case, the serum amyloid A (SAA) and troponin I levels were not measured. However, they may be useful biomarkers for myocardial inflammation.

Bacterial infections rarely affect the myocardium; however, cases of myocarditis resulting from Escherichia coli [1], [2] and Pseudomonas aeruginosa [8], both of which were detected in the urine in this case, have been previously reported. Similarly, Enterococcus identified in the urine of this cat has also been reported to be a causative agent of endocarditis in chickens [9], [10]. In human medicine, bacterial UTIs have been reported to cause myocarditis, which can lead to arrhythmias [1], [2]. Given the chronic nature of the lower UTI in this cat, it was hypothesized that inflammation associated with prolonged catheterization may have contributed to myocardial conduction abnormalities.

A definitive diagnosis of myocarditis typically requires a myocardial biopsy or postmortem histopathological examination. However, myocardial biopsy is highly invasive and rarely performed in veterinary medicine, and the diagnosis is often made postmortem [11]. In this case, as the cat survived, neither a postmortem examination nor myocardial biopsy was performed, precluding a definitive diagnosis of myocarditis. Additionally, ruling out feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV) is recommended when diagnosing myocarditis or endocarditis [11], [12]. However, this was not performed in this case. Consequently, a direct causal relationship between UTI and myocarditis cannot be conclusively established. Although a causal relationship between chronic UTI and myocardial changes cannot be definitively confirmed without histopathology, the temporal association and resolution following antibiotic therapy support a likely contributory role.

However, as no ECG abnormalities were observed at the time of initial CT imaging or during the first surgery, and arrhythmia developed approximately 5 months later, it is highly likely that factors contributing to myocardial conduction abnormalities emerged during that period. Furthermore, considering that cardiac function and ECG abnormalities improved following short-term antibiotic therapy, a bacterial UTI was strongly suspected to be a contributing factor.

There are some studies about myocarditis in cats, such as infection with feline infectious peritonitis virus, which may be correlated with electrocardiogram changes including ST-segment elevations and arrhythmias, abnormalities of left ventricular wall thickening, and increased fractional shortening; these changes improved with administration of GS-441524 [13]. These findings support the clinical course observed in this cat and reinforce our hypothesis that UTI was involved in myocarditis. Additionally, Joung et al. described a case of transient myocardial thickening (TMT) in a cat [14], where thoracic radiography and echocardiography mimicked stage C HCM and showed evidence of congestive changes, including pulmonary edema, pleural effusion, and pericardial effusion. These changes resolved with symptomatic treatment. TMT is a reversible cardiac condition characterized by temporary thickening of the ventricular walls, often mimicking HCM on echocardiography. While the exact pathogenesis is not fully understood, acute physical or emotional stress is considered a possible trigger; Joung et al. attributed TMT in their case to emotional stress related to the adoption of a new cat. In our case, TMT may explain the clinical course, as the echocardiogram resembled HCM but improved following treatment of the “physical stress” caused by the UTI.

We usually opted for fentanyl as an analgesic agent for abdominal surgery because of its strong analgesic effect. However, in this case, arrhythmia could not be completely eliminated preoperatively, and we were obliged to manage the risk of worsening arrhythmia throughout the perioperative period. Therefore, buprenorphine (BUP) was selected as the analgesic during surgery instead of fentanyl. BUP is a partial agonist of the μ-opioid receptor and is used to treat mild-to-severe pain in cats. As the risk of inducing arrhythmia is lower than that with fentanyl [15], we considered that BUP could be used for pain management in this cat during the surgical procedure. It has been suggested that BUP may not provide sufficient analgesia in all cats. Assessing the efficacy of BUP and determining whether additional analgesic treatment is needed depends on pain assessment [16]. However, in this case, no symptoms required rescue analgesic medication throughout the perioperative period, indicating that the analgesic effect of BUP was sufficient. A limitation of this case report is that testing for feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV) was not performed. Although these viral infections can cause myocarditis and cardiac abnormalities in cats, the marked improvement of cardiac symptoms and arrhythmias following antibiotic treatment makes a primary viral etiology less likely in this case. Nevertheless, screening for FIV and FeLV is recommended in future cases to definitively exclude their involvement.

Conclusion

Perioperative arrhythmias are commonly considered in the context of acute or severe infections such as sepsis. However, in cats, urinary tract inflammation is frequently encountered owing to a variety of causes. This case highlights the possibility that chronic inflammatory conditions such as UTIs may be associated with cardiac changes, including arrhythmias. Therefore, even in cases of chronic inflammatory conditions, particularly tract infections, careful electrocardiographic monitoring should be considered during the perioperative period. Nevertheless, a direct causal relationship between chronic urinary tract infection and arrhythmias could not be definitively established in this case. Further studies are needed to clarify whether chronic inflammation can directly contribute to cardiac conduction abnormalities in cats.