Transient deep and giant negative T waves in dogs with myocardial injury

Bertaglia²,

Bertaglia³

et al. 2021

Animals

Self Cite

A six-year-old Cavalier King Charles spaniel was referred with a two-month history of severe exercise intolerance and syncope. Clinical signs had developed during a local wave of coronavirus disease (COVID-19) two weeks after its family members had manifested symptoms of this viral disease and their positivity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was confirmed. Cardiologic assessment documented myocardial injury complicated by systolic dysfunction. An extensive diagnostic work-up allowed us to rule out common causes of myocardial compromise, both infective and not. Accordingly, serological and molecular tests aimed at diagnosing SARS-CoV-2 infection were subsequently performed, especially in light of the dog’s peculiar history. Results of such tests, interpreted in the light of previous findings and current knowledge from human medicine, supported a presumptive diagnosis of COVID-19-associated myocardial injury, a clinical entity hitherto poorly described in this species.

Section: Materials Methods and Resultsmentioning

confidence: 99%

“…In dogs, the term MI is conventionally used for subjects in which at least one cardiac troponin concentration, especially cTnI, is above the upper reference limit [ 26 , 27 ]. Both infectious and non-infectious diseases can cause MI in this species [ 25 , 26 , 32 , 33 , 34 ].…”

Section: Discussionmentioning

confidence: 99%

Myocardial Injury Complicated by Systolic Dysfunction in a COVID-19-Positive Dog

Bertaglia²,

Bertaglia³

et al. 2021

Animals

Self Cite

“…Blood work showed increased alanine aminotransferase (189 U/l; hospital reference interval [HRI] 20–72), urea (139 mg/dl; HRI 30–65), creatine kinase (CK; 1427 IU/l; HRI 91–326), serum amyloid A (10 µg/ml; HRI 0–5) and cTnI (5.1 ng/ml; HRI 0–0.2). In the light of the ongoing MI and the history of hunting mice, 3 , 4 further blood samples were subsequently obtained and sent for toxoplasmosis indirect fluorescence antibody titres (IgM and IgG) and Bartonella PCR. The cat tested positive exclusively for T gondii (IgM and IgG titres 1/80 and 1/1280, respectively) 22 and was started on clindamycin (9.5 mg/kg PO q12h).…”

Section: Case Series Descriptionmentioning

confidence: 99%

“…In cats, transient myocardial thickening (TMT) represents a recently described clinical entity characterised by reversible left ventricular myocardial thickening (LVMT) mimicking primary hypertrophic cardiomyopathy. 1 , 2 Transient left atrial (LA) dilation and dysfunction leading to congestive heart failure (CHF) and increased cardiac troponin I (cTnI), indicating ongoing myocardial injury (MI), 3 , 4 represent additional common features of feline TMT. 1 , 2 Although the mechanism of this condition is still a subject of debate in veterinary medicine, 1 , 2 interstitial oedema due to myocarditis represents the main explanation of reverse remodelling of human TMT.…”

Section: Introductionmentioning

confidence: 99%

Transient myocardial thickening associated with acute myocardial injury and congestive heart failure in two Toxoplasma gondii-positive cats

Journal of Feline Medicine and Surgery Open Reports

Fracassi

Cipone

2022

Self Cite

Case series summary In this report, we provide detailed clinical, laboratory, electrocardiographic and echocardiographic descriptions of two Toxoplasma gondii-positive cats diagnosed with transient myocardial thickening (TMT) and acute myocardial injury (MI). In both cases, aetiological diagnosis was based on the antibody screening test (all cats had IgM titres ⩾1:64) and MI was demonstrated by a concomitant severe increase of the serum concentration of cardiac troponin I (5.1–23.6 ng/ml; upper hospital limit <0.2 ng/ml). In both cats, TMT and MI were aggravated by left atrial dilation and dysfunction, as well as congestive heart failure. In one cat, atrial standstill was also documented, while the other cat showed an intracardiac thrombus. Both cats underwent an extensive diagnostic work-up aimed at excluding additional comorbidities that could contribute to able to contribute to TMT and MI, and received appropriate antiprotozoal (ie, clindamycin) and cardiovascular therapy (eg, furosemide, pimobendan and clopidogrel). This was followed by a simultaneous decline in T gondii serology titres, normalisation of troponin level and the resolution of clinical, electrocardiographic, radiographic and echocardiographic abnormalities. In the light of these results, therapies were interrupted and subsequent controls ruled out any disease relapse. Relevance and novel information Although T gondii represents an often-cited cause of myocarditis in feline medicine, the existing literature on the demonstration of T gondii-associated cardiac compromise in cats is extremely limited. Accordingly, this report provides a useful contribution to pertinent scientific literature since it describes TMT and acute MI in two T gondii-positive cats.

“…Further diagnostic steps aimed at excluding systemic diseases able to impair systolic function and cause ventricular arrhythmias (complete blood count, biochemistry, urinalysis and abdominal ultrasound) were unremarkable. The serum concentration of cTnI was also measured (IMMULITE 2000, Siemens, Erlangen, Germany) (9.6 ng/ml, hospital reference interval [HRI] <0.15 ng/ml) revealing myocardial injury (MI) [15,24]. Additionally, a Holter monitoring was performed employing a commercially available software program designed for humans (Cube Holter software, Cardioline S.p.A., Milan, Italy) and validated for use in dogs [25,26] and using a non-corrected orthogonal 3-lead system [21].…”

mentioning

confidence: 99%

Reversible myocardial injury aggravated by complex arrhythmias in three <i>Toxoplasma gondii</i>-positive dogs

The Journal of Veterinary Medical Science

Venturelli²,

Tintorri³

et al. 2022

Although Toxoplasma gondii represents an oft-cited cause of myocarditis in veterinary medicine, the existing literature on the pre-mortem demonstration of T. gondiiassociated myocardial injury (MI) in dogs is scant. In this case series, we provide detailed clinical, laboratory, echocardiographic and electrocardiographic description of three T. gondii-positive dogs diagnosed with MI. In all cases, etiological diagnosis was based on the antibody screening test (all dogs had IgM titres ≥1:64) and MI was demonstrated by a concomitant increase of the serum concentration of cardiac troponin I (0.25-9.6 ng/ml, upper hospital limit <0.15 ng/ml). In all dogs, MI was aggravated by complex arrhythmias (ventricular in two dogs, and either ventricular and supraventricular in the remaining dog). In one case, left ventricular systolic dysfunction was also present. All dogs underwent an extensive diagnostic work-up aimed at excluding additional comorbidities, either cardiac and extra-cardiac, possibly able to contribute to MI, arrhythmias and systolic dysfunction. All dogs received appropriate antiprotozoal (i.e., clindamycin) and antiarrhythmic (i.e., amiodarone, sotalol) therapy. This was systematically followed by a simultaneous decline in T. gondii serology titres, normalisation of troponin level and left ventricular systolic function, and the resolution of clinical and electrocardiographic abnormalities. In light of this result, therapies were interrupted and subsequent controls ruled out any disease relapse. In these cases, the clinical and instrumental findings obtained at admission and rechecks strongly supported the clinical suspicion of toxoplasmic myocarditis.