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Transient Myocardial Thickening in Cats Associated

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J Vet Intern Med 2017

Transient Myocardial Thickening in Cats Associated with Heart


Failure
J. Novo Matos , N. Pereira, T. Glaus, L. Wilkie, K. Borgeat, J. Loureiro, J. Silva, V. Law, A. Kranjc,
D.J. Connolly, and V. Luis Fuentes
Background: Cats with hypertrophic cardiomyopathy (HCM) and congestive heart failure (CHF) can have resolution of
both left ventricular hypertrophy and CHF.
Objectives: To describe the clinical characteristics of cats with transient myocardial thickening (TMT) and CHF com-
pared with a control population of cats without resolution of HCM.
Animals: A total of 21 cats with TMT, 21 cats with HCM.
Methods: Retrospective study. Clinical records at 4 veterinary centers were searched for TMT cases and a control group
of cats with HCM and CHF. TMT was defined as initial maximal left ventricular wall thickness (LVWT) ≥6 mm with left-
sided CHF, with subsequent resolution of CHF, reduction in left atrium/aorta (LA/Ao), and LVWT<5.5 mm. HCM was
defined as persistent LVWT ≥6 mm.
Results: Cats with TMT were younger (2 [0.4–11.4] years) than cats with HCM (8 [1.6–14] years) (P < 0.0001), and ante-
cedent events were more common (15/21 versus 6/21, respectively) (P = 0.01). In cats with TMT, LVWT normalized from 6.8
[6.0–9.7] mm to 4.8 [2.8–5.3] mm and LA/Ao decreased from 1.8 [1.6–2.3] to 1.45 [1.2–1.7] after a mean interval of 3.3 (95%
CI: 1.8–4.7) months. CHF recurred in 1 of 21 TMT and 15 of 21 cats with HCM. Cardiac treatment was discontinued in 20
of 21 cats with TMT and 0 of 21 HCM cats. All cats with TMT survived, whereas 8 of 19 cats with HCM died during the
study period.
Conclusions and Clinical Importance: TMT occurs in younger cats, and antecedent events are common. The prognosis is
better in cats with CHF associated with TMT than HCM.
Key words: HCM phenocopy; Hypertrophic cardiomyopathy; Myocarditis; Takotsubo cardiomyopathy.

hypertrophic cardiomyopathy (HCM) phenotype


A is characterized by increased left ventricular wall
thickness (LVWT) in the absence of abnormal loading
Abbreviations:
95% CI 95% confidence intervals
conditions capable of producing a similar degree of ven- CHF congestive heart failure
tricular thickening.1,2 Myocardial wall thickness depends CMR cardiac magnetic resonance
on 3 elements: the number of myocytes, myocyte size, cTnI cardiac troponin I
and the volume of the interstitial space.3,4 In HCM, the HCM hypertrophic cardiomyopathy
increased LVWT is mediated by an increase in mass of LA/Ao left atrium to aorta ratio
individual myocytes and interstitial fibrous connective LAFS% left atrial fractional shortening
tissue,5 with the former being the most important LVFS% left ventricle fractional shortening
LVIDd left ventricular internal dimension in diastole
LVWT left ventricular wall thickness
From the Royal Veterinary College, University of London, RPLA right parasternal long-axis view
Hatfield, UK (Novo Matos, Wilkie, Law, Connolly, Luis Fuentes); RPSA right parasternal short-axis view
Vetsuisse Faculty, University of Zurich, Zurich, Switzerland (Novo SAM systolic cranial motion of the mitral valve
Matos, Pereira, Glaus, Kranjc); Highcroft Veterinary Referrals, TMT transient myocardial thickening
Bristol, (Borgeat); North Downs Specialists Referrals, Surrey, UK
(Loureiro, Silva);
Present address: Borgeat, Langford Veterinary Services, University
of Bristol, Bristol, UK (Borgeat). component.3,4,6 Other diseases can mimic HCM by caus-
This study was not supported by any grant. ing an increase in LVWT that is not due to myocyte
This work was done at the Royal Veterinary College, Vetsuisse hypertrophy or hyperplasia, such as intracellular accu-
Faculty, Highcroft Veterinary Referrals and North Downs Specialist mulation of metabolic products (storage diseases) or
Referrals. interstitial infiltration of proteins, cells or fluid, such as
The results of this study were presented as an abstract at the 26th in amyloidosis or myocarditis.2,7 These conditions repre-
ECVIM-CA Annual Congress 2016, Gothenburg, Sweden.
Corresponding author: J. Novo Matos, Royal Veterinary College,
sent up to 10% of all adult human cases with an HCM
Hawkshead Lane, North Mymms, Hatfield, Hertfordshire AL9 phenotype.2 In cats, an HCM phenotype has been
7TA, UK; e-mail: jnovomatos@rvc.ac.uk described with endocrine disorders, such as hyperthy-
Submitted June 3, 2017; Revised October 25, 2017; Accepted roidism or acromegaly, dehydration (pseudohypertro-
November 7, 2017. phy), and infiltrative disease (cardiac lymphoma).8–11 It
Copyright © 2017 The Authors. Journal of Veterinary Internal is not known whether metabolic diseases or inflammatory
Medicine published by Wiley Periodicals, Inc. on behalf of the Ameri- disease are responsible for the abnormal phenotype seen
can College of Veterinary Internal Medicine.
This is an open access article under the terms of the Creative
in some cats diagnosed with HCM.
Commons Attribution-NonCommercial License, which permits use, Cats with HCM and congestive heart failure (CHF)
distribution and reproduction in any medium, provided the original are generally reported to have a poor prognosis.12,13 We
work is properly cited and is not used for commercial purposes. were aware of anecdotal reports of cats presenting with
DOI: 10.1111/jvim.14897
2 Novo Matos et al.

HCM and CHF that appeared to have a good progno- by 1 observer (JNM) for quality control and to ensure the inclu-
sis, and a longitudinal echocardiographic study con- sion criteria were met. Left ventricular free wall and interventricu-
ducted by one of the authors (LW) confirmed that in lar septal thicknesses were measured by a leading edge to leading
some cats, apparent left ventricular hypertrophy had edge technique from a two-dimensional (2D) right parasternal
long-axis 4- or 5-chambered view (RPLA) and a short-axis view at
resolved by subsequent echocardiographic examinations
the papillary muscle level (RPSA), as the average of the thickest
(unpublished data). Furthermore, it has been suggested end-diastolic segment on 3 different cardiac cycles in each view
that cats with this clinical course are often young and (RPLA and RPSA). End-diastolic frames were defined as the first
have a history of an antecedent event, such as general frame after mitral valve closure in RPLA and as the time point in
anesthesia for neutering within days of presentation the cardiac cycle of greatest left ventricular internal diameter in
with CHF.14 As reverse remodeling with normalization RPSA.32 The maximal averaged end-diastolic wall thickness from
of cardiac structure and function is not an expected both the interventricular septum and left ventricular free wall on
outcome in HCM,15,16 these clinical observations these 2 views was recorded, and the highest value was used for
describe a transient form of myocardial thickening asso- final data analysis, defined as LVWT. All 2D measurements of
ciated with CHF in cats. Transient myocardial thicken- cardiac chambers were made by an inner edge to inner edge tech-
nique on the interface between the blood pool and myocardial
ing (TMT) mimicking HCM has been described in
wall.33 Left ventricular internal diameter in diastole (LVIDd) was
some forms of acute/fulminant myocarditis in measured in 2D from a RPLA and RPSA view at the level of the
humans7,17–19 and in atypical cases of stress-induced chordae tendineae, in an end-diastolic frame, on 3 different cardiac
(Takotsubo) cardiomyopathy.20–23 In both situations, cycles in each view. The ratio of the left atrium to aorta (LA/Ao)
the increased LVWT is associated with myocardial was measured in 2D from a short-axis view at the heart base, in
edema.7,20,22–27 the frame after aortic valve closure (end-ventricular systole).30 Left
The aims of this study were to identify case details of atrial (LAFS%) and left ventricular (LVFS%) fractional shorten-
cats with TMT and CHF from multiple veterinary car- ing were measured by M-Mode from a right parasternal short-axis
diologists and describe their clinical and echocardio- at the heart base30 and right parasternal short-axis at the papillary
muscle, respectively. The presence of systolic cranial motion of the
graphic characteristics. Additionally, the clinical and
mitral valve (SAM) was assessed on 2D and color Doppler from a
echocardiographic features of cats with TMT were com-
right parasternal long-axis 5-chambered view, as a systolic motion
pared with a control population of cats with HCM and of the tip of the cranial mitral valve leaflet toward the interventric-
CHF, to identify characteristics at presentation that ular septum producing turbulent flow in the left ventricular out-
might distinguish cats with TMT from HCM. flow tract and mitral regurgitation.34 The presence of spontaneous
echocardiographic contrast (SEC) or a thrombus was assessed
from a RPLA and short-axis views at the heart base.
Materials and Methods Exclusion criteria included normal left atrial size (LA/Ao < 1.6)
This study was approved by the Clinical Research Ethical and the presence of systemic diseases known to affect the cardio-
Review Board of the Royal Veterinary College (URN 2015–1397). vascular system, such as hyperthyroidism (all cats >8 years of age
The medical records and echocardiographic database of 4 refer- had T4 measured), systemic hypertension (systolic blood pressure
ral centers (Royal Veterinary College, Vetsuisse Faculty, Highcroft ≥160 mmHg),35 diabetes mellitus, and chronic kidney disease
Veterinary Referrals, and North Downs Specialists Referrals) were (IRIS Stage >II).
searched for cats diagnosed as HCM associated with CHF that
showed normalization of LVWT over time. TMT cases were Clinical Data
defined as cats with at least 2 echocardiographic examinations that
had increased LVWT (LVWTd ≥ 6 mm)28,29 and left atrial dilata- Additional data collected from the medical and echocardio-
tion (left atrium to aorta ratio [LA/Ao] ≥1.6)30 with left-sided graphic records included age at diagnosis, sex, breed, presenting
CHF at presentation but showed subsequent normalization of clinical signs, heart rate, respiratory rate, temperature, presence of
LVWT (LVWTd < 5.5 mm) and left atrial size.31 Additionally, a murmur, gallop or arrhythmia (and ECG diagnosis when avail-
cats with left ventricular fractional shortening <40% or with evi- able), and systolic blood pressure at presentation. In addition, tho-
dence of focal left ventricular wall thinning with hypokinetic or racic radiographic findings (ie pulmonary edema, pleural effusion,
dyskinetic myocardial segments at their final echocardiographic or both), number of echocardiographic examinations performed,
examination were excluded from the TMT group.15,16 A control treatment, and any clinical pathology results available at presenta-
group of cats with HCM was selected from the medical records tion, such as cardiac biomarkers, complete blood count, serum
and echocardiographic database at each center involved in the chemistry, or serology for Toxoplasma gondii, Bartonella henselae,
study. Cats with at least 2 echocardiographic examinations at least or FIV/FeLV, were recorded. The medical history of each cat was
5 months apart with left atrial dilatation (LA/Ao ≥ 1.6) and left- carefully evaluated for the presence of antecedent events, defined
sided CHF on presentation and persistently increased LVWT as any new medication, general anesthesia, and/or traumatic inci-
(LVWTd ≥ 6 mm) were selected as control HCM cats. All cats dent occurring within 14 days of presentation with CHF.
had CHF documented on thoracic radiographs or echocardiogra-
phy (pleural effusion).
Outcome Data
Echocardiographic Data Medical records were additionally reviewed for relapses of
CHF, aortic thromboembolism, and cardiac death (death or eutha-
All echocardiographic examinations were reviewed and remea- nasia because of signs of CHF and/or aortic thromboembolism, or
sured at each center by an ECVIM (3 centers) or ACVIM (1 cen- sudden death). In cases where treatment was discontinued, the
ter) board-certified veterinary cardiologist. Echocardiographic duration of treatment was determined from the discharge date
video loops from all cats with TMT submitted to the study (before from hospital until all cardiac treatment was stopped. At the time
and after ventricular thickening resolution) were further reviewed of data collection (September 2015 to September 2016), owners of
Transient Myocardial Thickening in Cats 3

cats identified with TMT were contacted and invited for follow-up foreign body, tooth extraction, and draining abscess (1
echocardiographic examinations. All echocardiographic parameters cat each). Other antecedent events included vaccination,
in cats with TMT at the time of normalization of LVWT (“normal bite wound, pneumonia, fever of unknown origin, fever
echo”) were compared with the last available echo (“final echo”). with thoracolumbar pain, and abdominal pain with
vomiting (1 cat each). A range of drug combinations
Statistical Analysis were administered during these events, including antibi-
otics (n = 12), NSAIDs (n = 7), opioids (n = 5), fluids
Data were tested for normality graphically and by Shapiro-Wilk
IV (n = 4), corticosteroids (n = 3), bronchodilators
test and for homogeneity of variances by Levene’s test. Between-
group (TMT versus HCM) comparisons were carried out by Fish- (n = 2), and antacids (n = 1). In the HCM group, ante-
er’s exact for categorical variables and a Mann-Whitney U-test for cedent events included general anesthesia, eye prolapse,
continuous variables. A Wilcoxon signed-rank test was used for vaccination, abscess, and anorexia (1 cat each). Medica-
within-group comparisons of continuous variables. Data are tions administered to the HCM group included antibi-
reported as median [range], mean (95% confidence interval, 95% otics (n = 4), corticosteroids (n = 2), antiemetics (n = 2),
CI), frequency, and percentage. P values <0.05 were considered and bronchodilators (n = 1). There were no differences
statistically significant. Statistical analysis was performed by com- between groups in the other clinical examination vari-
mercially available software.a ables evaluated (Table 1).

Results Echocardiographic Data


Twenty-one TMT cases were identified in the 4 cen- A total of 174 echocardiographic scans were evaluated
ters, and 21 HCM cases were selected as control group. from the 42 cats enrolled in the study. Cats with TMT
The frequency of TMT cases seen at the 4 centers ran- had a median of 3 [2–7] scans and cats with HCM 4 [2–
ged between 1 and 4 cases every 2 years. Cats with TMT 9] scans performed during the study period. The time
were younger (2 [0.4–11.4] years) than cats with HCM (8 elapsed between the first and last echo was 8 [1.0–57]
[1.6–14] years), P < 0.0001. Males were over-represented months for the whole population and 6 [1–57] months
in the HCM group (18 of 21 cats were male versus 10 of for cats with TMT and 10 [5–48] months for cats with
21 males in the TMT group, P = 0.02). Cats with HCM HCM. At presentation, cats with TMT had thinner left
were also heavier than cats with TMT (P = 0.04) Several ventricular walls than cats with HCM (P = 0.001)
breeds were represented in both groups with equal distri- (Table 2, Fig 1). Similarly, at presentation, cats with
bution. Domestic shorthair (DSH) was the most com- TMT had smaller left atria than cats with HCM
mon breed (10 DSH with TMT and 14 DSH with (P < 0.0001) (Table 2, Fig 1). In cats with TMT, after a
HCM). The TMT population also included 4 British median period of 3.3 (95% CI: 1.8–4.7) months, the
shorthair, 2 Ragdoll, and 2 Domestic Long Hair. The LVWT normalized (Fig 2). Left atrial size decreased
HCM population also included 2 British Shorthair and over time in the TMT group, while it remained severely
2 Maine Coon. Other breeds included 1 Birman, 1 Rus- dilated in the HCM group (Table 3, Fig 1). Left atrial
sian Blue and 1 Sphynx in the TMT group and 1 fractional shortening was reduced in both groups at pre-
Domestic Long Hair and 1 Exotic Shorthair in the sentation but improved significantly in the TMT group
HCM group. Antecedent events were identified in 71% over time (P = 0.001), while it remained markedly
of cats with TMT (15/21) and 29% of cats with HCM reduced in the HCM group (P = 0.67) (Table 3, Fig 3).
(6/21, P = 0.01). In the TMT group, the most frequent Cardiac troponin I (cTnI) was available in 13 of 21
antecedent event was general anesthesia (7 cats) followed cats with TMT and 6 of 21 cats with HCM at presenta-
by road traffic accident (2 cats). Anesthesia was per- tion. Median cTnI was 2.1 [0.05–63.8] ng/mL in cats
formed for ovariohysterectomy (3 cats), and placement with TMT and 1.2 [0.3–6.4] ng/mL in HCM (P = 0.2).
of indwelling urinary catheter, extraction of intestinal In 7 of 13 cats with TMT, cTnI was repeated at the

Table 1. Summary of additional clinical characteristics and laboratory parameters at initial presentation in cats
with TMT and HCM
TMT HCM P Value
Body weight (kg) 4.1 (1.9–6.2) 4.8 (2.7–7.2) 0.04
Heart rate (bpm) 180 (90–250) 190 (155–220) 0.8
Respiratory rate (breaths per minute) 64 (40–104) 58 (40–130) 0.8
Murmur (% yes) 7/21 (33%) 9/15 (60%) 0.18
Arrhythmia (% yes) 2/21 (10%) (VPCs, transient 3AVB) 3/17 (18%) (1 AF, 1 FAT, 1 VPCs) 0.64
Pulmonary edema/pleural effusion/both 6/2/13 11/1/9 0.28
Hematocrit (%) 33% (15–54) 35% (24–51) 1.0
Urea (mmol/L) 12.8 (3.9–34) 11.4 (6.6–20.5) 0.27
Furosemide dose at discharge (mg/kg/d) 2.1 (0.9–5.4) 2.0 (1.4–4.0) 0.99

AF, atrial fibrillation; 3AVB, third-degree atrioventricular block; FAT, focal atrial tachycardia; HCM, hypertrophic cardiomyopathy;
TMT, transient myocardial thickening; VPCs, ventricular premature complexes.
4 Novo Matos et al.

Table 2. Echocardiographic variables at initial presen- reference <1:20), although only 1 of 3 cats was treated
tation in cats with TMT and HCM for Bartonella.
Cats from both groups received various combinations
TMT HCM P Value of cardiac medications at the time of CHF diagnosis.
LVWT (mm) 6.8 (6.0–9.7) 8.1 (6.0–12.3) 0.001 All cats received furosemide but a greater proportion of
LA/Ao 1.8 (1.6–2.3) 2.4 (1.6–3.4) <0.0001 cats with HCM (19/21) than cats with TMT (12/21)
Papillary muscle 13/21 (62%) 14/21 (67%) .75 received medications in addition to furosemide (eg dilti-
hypertrophy (% yes) azem, atenolol, spironolactone, pimobendan, and ACE
Symmetric wall 20/21 (95%) 16/21 (76%) .18
inhibitors, P = 0.03). Additional characteristics of the
thickening (%yes)
SAM (% yes) 6/21 (29%) 6/21 (29%) 1.0
study population are presented in Table 1.
Pericardial 9/21 (43%) 8/21 (38%) 0.5
effusion (% yes) Long-term Follow-up in Cats with TMT
SEC (% yes) 4/21 (19%) 8/21 (38%) 0.3
After normalization of LVWT to <5.5 mm, 15 of 21
LVWT, left ventricular wall thickness; LA/Ao, left atrium to cats with TMT had a further follow-up scan up to 5 [1–
aorta ratio; SAM, systolic cranial motion; SEC, spontaneous 57] months later. In all cases, there was a further
echocardiographic contrast. decrease in LVWT from a median LVWT of 5.1 [3.8–
5.4] mm to 4.8 [2.8–5.3] mm (P = 0.02, Fig 4), while left
ventricular systolic function and left atrial size remained
normal.

Outcome Data
Congestive heart failure recurred in 1 of 21 cats with
TMT shortly after discharge, and all cats were alive at
the time of writing. CHF recurred in 15 of 21 cats with
HCM; 2 of 21 had an aortic thromboembolus; and 8 of
19 died during the study period (2 cats were lost to fol-
low-up). In 20 of 21 cats with TMT, all cardiac drugs
were discontinued at 4.6 (95% CI: 2.3–6.9) months after
discharge, as the heart was morphologically normal on
repeated echocardiographic examinations (ie normal
LVWT and LA size), and none of the cats showed clini-
cal signs thereafter. Conversely, all cats with HCM (21/
21) received medications for heart disease during the
duration of the study or until death. In 1 cat with
TMT, administration of clopidogrel and aspirin were
not stopped, even though the heart was normal on the
last echocardiographic examination, as the cat had a
previous suspicion of a thrombus on the mitral valve.
The cat was lost to follow-up.

Fig 1. Left ventricular wall thickness (LVWT) (A) and left atrial
size (LA/Ao) (B) in cats with TMT and HCM at presentation and
Discussion
final echocardiographic examination. At presentation, left ventricu- In this study, we describe a transient form of myocar-
lar walls were thicker in cats with HCM. The left atrium was lar-
dial disease in cats that mimics HCM and is associated
ger in cats with HCM at presentation and remained dilated over
time, while it decreased over time in the TMT population. By defi-
with CHF but has an excellent long-term prognosis.
nition, the LVWT and LA/Ao decreased between the initial and TMT is a relatively uncommon condition that seems to
the final echo in the TMT population, and so those two datasets affect young cats, often with a history of an antecedent
were not subjected to statistical analysis. Echo, echocardiogram; event.
TMT, transient myocardial thickening; HCM, hypertrophic The underlying pathophysiology causing the transient
cardiomyopathy. ventricular wall thickening is unknown, but in view of
the fast reverse remodeling seen in our cases, myocar-
time of LVWT normalization. Median cTnI was ele- dial edema and/or transient cellular infiltration might
vated at presentation and normalized once myocardial be responsible. Acute myocarditis in humans can cause
thickening resolved (2.1 [0.05–63.8] ng/mL versus 0.01 TMT that resembles HCM at initial presentation.2,7,17–
[0.0–0.3] ng/mL, P = .018) (reference <0.16 ng/mL).36 19,25,26,37–40
In these cases, the increased ventricular wall
IgM and IgG antibodies for T. gondii and B. henselae thickness was shown to be associated with severe
were measured in 4 cats with TMT. Toxoplasma was myocardial interstitial edema.7,24–26 Myocardial edema
negative in 4 of 4 and Bartonella was positive in 3 of 4 is one of the main features of the inflammatory
cats (IgM 1:160–640, reference <1:20; IgG 80–640, response in acute myocarditis in humans.41 Myocarditis
Transient Myocardial Thickening in Cats 5

A B

C D

E F

G H

Fig 2. Right parasternal long-axis (A, B, E, F) and short-axis views (C, D, G, H) at end-diastolic frame from 2 TMT cases at initial pre-
sentation (A, C and E, G) and 7 months later (B, D and F, H). The initial severely increased left ventricular wall thickness (A, C, E, G)
and mild pericardial effusion (E, G) resolved completely, with a morphologically normal heart 7 months later.

Table 3. Selective echocardiographic variables at presentation and final echocardiographic examination in cats with
TMT and HCM
TMT HCM

Initial Echo Final Echo Initial Echo Final Echo


LVWT (mm) 6.8 (6.0–9.7) 4.8 (2.8–5.3) 8.1 (6.0–12.3) 7.9 (5.5–11)
LA/Ao 1.8 (1.6–2.3) 1.45 (1.2–1.7) 2.4 (1.6–3.4) 2.6 (2.0–5.3)
LAFS% 17 (4.3–21) 27 (15–49.6) 8.6 (0.9–17) 9 (1.7–16)

Cats with TMT showed a marked and clinically significant decrease in LVWT and LA size over time. LA/Ao, left atrium to aorta ratio;
LVWT, left ventricular wall thickness; LAFS%, left atrial fractional shortening; LVWT, left ventricular wall thickness.

is poorly described in small animals but increased the patient survives the acute CHF episode, as
LVWT can occur with toxoplasma myocarditis, described in a cat with toxoplasma myocarditis.42
myocarditis caused by FIV, and in eosinophilic Cats with TMT were younger than cats with HCM
myocarditis.42–44 The increased LVWT can normalize if (median age 1.7 versus 8 years). In people, acute
6 Novo Matos et al.

were more common in cats with TMT than HCM (71%


of TMT versus 29% of HCM cases). Stalis et al50de-
scribed very similar antecedent stressful events to those
observed in our TMT population in 75% of young cats
with endomyocarditis. Many cats received drugs before
presenting with TMT, and hypersensitivity drug reac-
tions are a known cause of myocarditis in humans.45,49
Alternatively, the myocardial changes observed could
potentially be a consequence of a catecholamine surge
caused by emotional or physical triggers. In humans,
catecholamines may cause toxic myocarditis in cases of
phaeocromocytoma45,51 or stress-induced (Takotsubo)
cardiomyopathy due to an exaggerated sympathetic
stimulation.52 Takotsubo cardiomyopathy is a transient
left ventricular dysfunction most frequently character-
ized by an apical “ballooning” phenotype in
people,27,52,53 but myocardial edema mimicking HCM
has also been described in Takotsubo cases, and differ-
entiation from true HCM requires advanced cross-sec-
tional imaging.20–23,27,54 TMT could then potentially be
caused by an emotional or physical stress associated
with the reported antecedent events.
Fig 3. Left atrial fractional shortening (LA%FS) in cats with Cardiac troponin I was markedly elevated in most
TMT (A) and HCM (B) at presentation and final echocardio- cats with TMT where it was assessed. Blood concentra-
graphic examination. LA%FS was reduced in both groups at pre- tion of cardiac troponins is highly sensitive and specific
sentation but improved in the TMT group over time. Echo, for cardiac myocyte injury, and highly suggestive of
echocardiogram. acute myocarditis when other causes of severe myocar-
dial injury have been excluded.45,55,56 However, serum
concentration of cardiac troponins is elevated in Takot-
subo patients,53 and the differentiation between these 2
entities might require cardiac magnetic resonance
(CMR) imaging.57 cTnI might potentially be useful to
differentiate TMT from HCM cases, although there is
likely to be overlap between groups. Cats with HCM
can also have substantially elevated serum cTnI concen-
trations, and some cats with TMT have normal to
mildly increased cTnI.
At presentation, cats with TMT had thinner left ven-
tricular walls than cats with HCM. If myocardial edema
Fig 4. Long-term follow-up in 15 cats with TMT. Normal left is indeed the mechanism behind increased wall thickness
ventricular wall thickness was defined as <5.5 mm (normal echo), in TMT, it makes sense that the degree of wall thicken-
but all cats with serial echos showed a further decreased in wall ing is limited and potentially not as extreme as seen
thickness over time. Echo, echocardiogram. with left ventricular hypertrophy in HCM cases. There
was marked overlap in LVWT between the 2 groups,
and this feature cannot be used to differentiate cats with
myocarditis is most common in young individuals,45 TMT from HCM.
with an average age of 10 years reported in 43 patients The cats with TMT had mild increases in left atrial
from 9 different publications (95% CI: 0.45–19.6).7,17– size and decreased atrial fractional shortening that nor-
19,38–40,46,47
It is possible that TMT is a form of malized over time. These findings suggest an acute
myocarditis as described in people. In our study, very myocardial insult without time for the left atrium to
few cats had serological testing for Bartonella and Tox- adapt to the increased filling pressures (ie dilate), which
oplasma done which hinders any meaningful conclusion, caused acute increase in left atrial and pulmonary capil-
especially considering the high prevalence of Bartonella lary pressure resulting in acute pulmonary edema.
seropositivity in healthy cats.48 In humans, a cause for Cats with an HCM phenotype and CHF following
myocarditis is not identified in the majority of cases, corticosteroid administration can show normalization of
although various infectious agents, drugs (eg hypersensi- the morphological cardiac changes over time and can
tivity reactions), and toxins have all been reported to have an excellent long-term prognosis.58 This has been
cause myocarditis. Viral infections are considered to be postulated to be a unique form of CHF induced by cor-
the most common underlying cause.7,40,45,49 ticosteroids. The clinical findings and clinical course of
The majority of cats with TMT in our study had cats with corticosteroid-associated CHF were very simi-
events preceding their presentation in CHF, and these lar to our population, although older (9.3 [5.6–12.4])
Transient Myocardial Thickening in Cats 7

than the cats in this study (2 [0.4–11.4] years).58 In our prognosis than expected for cats with HCM and CHF.
study, there was no difference in the proportion of cats TMT appears to preferentially affect young cats and
receiving corticosteroids between the TMT and HCM often follows an antecedent event but is difficult to dif-
populations. The cats with corticosteroid-associated ferentiate from HCM at presentation. The recognition
CHF received these drugs for a variety of medical rea- of TMT could have an important impact in daily clini-
sons, including events that would have been classified as cal cardiology, leading to clinicians and owners
antecedent stressful events in our study. attempting treatment in cases classically thought to
Based on our results, there were no clinical or have a poor prognosis, and potentially avoiding prema-
echocardiographic characteristics at presentation differ- ture euthanasia. Additionally, TMT might influence the
entiating TMT from HCM, besides the younger age of definition of HCM and design of studies of HCM in
cats with TMT and the presence of antecedent events. cats.
The different progression over time may be the only
way of differentiating TMT from HCM, where cats
with TMT show reverse remodeling with normalization
of LVWT and left atrial size, while cats with HCM Footnote
show a progressive deterioration of their cardiac func- a
SPSS 22.0.1, IBM Company, Chicago, IL
tion. CMR imaging and endomyocardial biopsy are
both used in humans to make the diagnosis of
myocarditis, with biopsy being the gold standard.45
Transient myocardial thickening should be considered
as a differential diagnosis in cats with an HCM pheno- Acknowledgment
type, especially in young cats with a history of an ante- JNM’s PhD was funded by Everts Luff Feline
cedent event. Additionally, the perception of a poor Endowment.
prognosis in symptomatic HCM (specifically with CHF) Conflict of Interest Declaration: Authors declare no
and the need for lifelong treatment may discourage clin- conflict of interest.
icians and owners from attempting treatment and might Off-label Antimicrobial Declaration: Authors declare
result in premature euthanasia. The identification and no off-label use of antimicrobials.
description of a transient form of heart failure in cats
associated with an excellent prognosis may have an
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