Veterinary Internal Medicne - 2020 - Luis Fuentes - ACVIM Consensus Statement Guidelines For The Classification Diagnosis

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Received: 8 January 2020 Accepted: 14 February 2020
DOI: 10.1111/jvim.15745
CONSENSUS STATEMENT
Consensus Statements of the American College of Veterinary Internal Medicine (ACVIM) provide the veterinary community with up-to-date infor-
mation on the pathophysiology, diagnosis, and treatment of clinically important animal diseases. The ACVIM Board of Regents oversees selection
of relevant topics, identification of panel members with the expertise to draft the statements, and other aspects of assuring the integrity of the
process. The statements are derived from evidence-based medicine whenever possible and the panel offers interpretive comments when such
evidence is inadequate or contradictory. A draft is prepared by the panel, followed by solicitation of input by the ACVIM membership that may be
incorporated into the statement. It is then submitted to the Journal of Veterinary Internal Medicine, where it is edited before publication. The
authors are solely responsible for the content of the statements.
ACVIM consensus statement guidelines for the classification,

diagnosis, and management of cardiomyopathies in cats
Virginia Luis Fuentes1 | Jonathan Abbott2 | Valérie Chetboul3 |

4 5 6
Etienne Côté | Philip R. Fox | Jens Häggström | Mark D. Kittleson7 |
8 7
Karsten Schober | Joshua A. Stern
1
Department of Clinical Science and Services, Royal Veterinary College, Hatfield, United Kingdom
2
Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee
3
Alfort Cardiology Unit (UCA), Université Paris-Est, École Nationale Vétérinaire d'Alfort, Centre Hospitalier Universitaire Vétérinaire d'Alfort (CHUVA), Maisons-Alfort
cedex, France
4
Department of Companion Animals, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
5
Animal Medical Center, New York, New York
6
Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, Sweden
7
Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California Davis, Davis, California
8
Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio
Correspondence
Virginia Luis Fuentes, Department of Clinical Abstract
Science and Services, Royal Veterinary Cardiomyopathies are a heterogeneous group of myocardial disorders of mostly
College, Hatfield AL9 7TA, United Kingdom.
Email: [email protected] unknown etiology, and they occur commonly in cats. In some cats, they are well-
tolerated and are associated with normal life expectancy, but in other cats they
can result in congestive heart failure, arterial thromboembolism or sudden death.
Cardiomyopathy classification in cats can be challenging, and in this consensus
statement we outline a classification system based on cardiac structure and func-
tion (phenotype). We also introduce a staging system for cardiomyopathy that
includes subdivision of cats with subclinical cardiomyopathy into those at low risk
Abbreviations: ACE, angiotensin converting enzyme; ACVIM, American College of Veterinary Internal Medicine; AHA, American Heart Association; ARVC, arrhythmogenic right ventricular
cardiomyopathy; ATE, arterial thromboembolism; CHF, congestive heart failure; cTnI, cardiac troponin-I; DCM, dilated cardiomyopathy; DLVOTO, dynamic left ventricular outflow tract
obstruction; ESC, European Society of Cardiology; HCM, hypertrophic cardiomyopathy; LA, left atrial; LMWH, low-molecular-weight heparin; LOE, level of evidence; LV, left ventricle; NT-
proBNP, N-terminal pro-brain natriuretic peptide; RCM, restrictive cardiomyopathy; SAM, systolic anterior motion; SEC, spontaneous echocardiographic contrast; UCM, unclassified
cardiomyopathy.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium,
provided the original work is properly cited.
© 2020 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.
1062 wileyonlinelibrary.com/journal/jvim J Vet Intern Med. 2020;34:1062–1077.

19391676, 2020, 3, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/jvim.15745 by Cochrane Colombia, Wiley Online Library on [16/01/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
LUIS FUENTES ET AL. 1063
of life-threatening complications and those at higher risk. Based on the available

literature, we offer recommendations for the approach to diagnosis and staging of
cardiomyopathies, as well as for management at each stage.
KEYWORDS
arrhythmogenic, cardiovascular, congestive heart failure, consensus statement,

echocardiography, feline, heart, hypertrophic cardiomyopathy, restrictive cardiomyopathy,
review, treatment
1 | I N T RO DU CT I O N competing classification systems are used in humans, highlighting

the difficulties inherent in cardiomyopathy classification.4-7 The
Cardiomyopathies are a heterogeneous group of myocardial diseases aim of disease classification is to categorize conditions according to
with variable phenotype and prognosis. Cardiomyopathies are com- logical principles, such as by organ involvement, pathophysiology,
mon in cats, and cardiovascular disease is among the 10 most com- phenotype, or underlying cause. An ideal classification system
mon causes of death in cats.1-3 The following report by the American would standardize terminology and facilitate clinical management,
College of Veterinary Internal Medicine consensus statement panel but all classification systems have limitations, and this is particularly
on cardiomyopathy in cats proposes an updated classification of car- true when the underlying causes of disease are unknown. In
diomyopathies based on echocardiographic phenotype, and provides humans, the cause of cardiomyopathy often can be determined, but
recommendations for the diagnostic approach and management of this is rarely true in cats. We propose an adaptation of the
cats with myocardial disease. European Society of Cardiology (ESC) classification4 for use in cats,
because this scheme is based on phenotypic features without
assumptions regarding underlying cause, and it focuses on a clinical,
2 | CONSENSUS METHODS rather than genetic, approach to these disorders (Figure 1, Table 3).
A modified Delphi method was applied to a series of statements

produced by members of the committee that summarized the most TABLE 1 Levels of evidence
important issues related to cardiomyopathy in cats. A combination Levels of evidence
of online anonymous voting with free text comments, face-to-face
High Randomized controlled trials in cats
meetings and video-conferences was used to modify the state-
Prospective, nonrandomized controlled
ments. Consensus was defined as ≧6 of the 9 committee members trials in cats, with adequate sample size
agreeing with a statement. A PubMed search using the MeSH terms and lacking major methodological flaws
“feline” and “cardiomyopathies” yielded 475 references, and further Medium Experimental laboratory trials in cats
references were identified using other databases and other search Retrospective clinical studies with
terms. References documenting peer-reviewed published studies intervention & control groups
containing original data were reviewed by the panel and graded. For Low Case series in cats without control groups
each statement for which consensus was reached, a level of evidence Studies in other species
(low/medium/high), was determined based on review of the literature Expert opinion
(Table 1), and a class (strength) of recommendation was assigned
(is recommended/should be considered/may be considered/is not rec-
ommended) according to the results of voting (Table 2). TABLE 2 Class of recommendations
Class of recommendations
Evidence/agreement that intervention “is recommended/indicated”
3 | DEFINITIONS AND CLASSIFICATION is beneficial/useful/effective (Class I)
OF CARDIOMYOPATHIES IN CATS
Evidence/opinion in favor of “should be considered”
usefulness/efficacy (Class IIa)
Cardiomyopathy is defined as a myocardial disorder in which the Evidence/opinion less “may be considered”
heart muscle is structurally and functionally abnormal in the well established (Class IIb)
absence of any other cardiovascular disease sufficient to cause the Evidence/agreement that “is not recommended”
observed myocardial abnormality.4 Classification of cardiomyopa- intervention is not useful/effective
thies in cats previously has been based on schemes that were and in some instances may
be harmful (Class III)
applied to cardiomyopathy in humans, but currently several
1064 LUIS FUENTES ET AL.
F I G U R E 1 Classification of cardiomyopathy phenotypes. (adapted with permission from Clinical Small Animal Internal Medicine, Ed David
Bruyette, John Wiley & Son). ARVC, arrhythmogenic right ventricular cardiomyopathy; DCM, dilated cardiomyopathy; End-stage HCM, HCM
with systolic dysfunction; HCM, hypertrophic cardiomyopathy; RCM, restrictive cardiomyopathy; TMT, transient myocardial thickening
T A B L E 3 Definitions of cardiomyopathy phenotypes. Cardiomyopathy is defined as a myocardial disorder in which the heart muscle is
structurally and functionally abnormal in the absence of any other disease sufficient to cause the observed myocardial abnormality
Phenotype Definition
Hypertrophic cardiomyopathy (HCM) Diffuse or regional increased LV wall thickness with a nondilated LV chamber.
Restrictive cardiomyopathy (RCM)
Endomyocardial form Characterized macroscopically by prominent endocardial scar that usually bridges the
interventricular septum and LV free wall, and may cause fixed, mid-LV obstruction and
often apical LV thinning or aneurysm; LA or biatrial enlargement is generally present.
Myocardial form Normal LV dimensions (including wall thickness) with LA or biatrial enlargement
Dilated cardiomyopathy (DCM) LV systolic dysfunction characterized by progressive increase in ventricular dimensions,
normal or reduced LV wall thickness, and atrial dilatation.
Arrhythmogenic cardiomyopathy (AC), also known as Severe RA and RV dilatation and often, RV systolic dysfunction and RV wall thinning. The
arrhythmogenic right ventricular cardiomyopathy left heart may also be affected. Arrhythmias and right-sided congestive heart failure are
(ARVC) or dysplasia (ARVD) common.
Nonspecific phenotype A cardiomyopathic phenotype that is not adequately described by the other categories;
the cardiac morphology and function should be described in detail
The ESC classification is based on the traditional phenotypic cate- cat is said to have a “hypertrophic cardiomyopathy phenotype” or a “dilated
gories of hypertrophic cardiomyopathy (HCM), restrictive cardio- cardiomyopathy phenotype” (according to the cardiac morphology and
myopathy (RCM), dilated cardiomyopathy (DCM), unclassified function). If no underlying cause is found, a cat is said to have “hypertrophic
cardiomyopathy (UCM), and arrhythmogenic right ventricular car- cardiomyopathy (HCM)” or “dilated cardiomyopathy (DCM),” as appropri-
diomyopathy (ARVC), and we recommend retaining these catego- ate. The proposed classification therefore does not define specific disease
ries (with the exception of UCM) as a basic framework, while entities, but phenotypic categories instead. The description in any individ-
acknowledging their limitations. For example, in some cats, the car- ual cat can be further refined by details of cause when known. Thus, a cat
diac phenotype changes over time, because of disease progression, with left ventricular (LV) hypertrophy and hyperthyroidism is said to have
comorbidities or unknown factors. an HCM phenotype in conjunction with hyperthyroidism.
We propose a classification of cardiomyopathies in cats based on Some cats have myocardial disease that does not fit well into any
structural and functional characteristics, or phenotype. The phenotypic cat- category. Rather than describe these cases as having “unclassified
egories include cats with cardiomyopathy of both known causes (eg, hyper- cardiomyopathy,” according to the proposed classification these cats
thyroidism, sarcomeric gene mutation) and unknown causes (most cats should be described as having cardiomyopathy with a “nonspecific phe-
with a cardiomyopathy phenotype). Until an underlying cause is sought, a notype.” This term always should be accompanied by a description of
the morphologic and functional features to characterize the phenotype disease, with a 5-year cumulative incidence of cardiac mortality of
in more detail. approximately 23%, independent of age at diagnosis.17 Congestive
heart failure (CHF) is the most common cause of clinical signs in
cats with HCM, followed by arterial thromboembolism (ATE).17 A
3.1 | Staging cardiomyopathies in cats minority of cats die suddenly without prior clinical signs.11,17,18 The
prevalence of other cardiomyopathy phenotypes in the general cat
For describing the clinical impact of cardiomyopathy in affected population is not known, but a hypertrophic phenotype appears to
cats, we propose a staging system adapted from the American predominate in cats with subclinical cardiomyopathy.15
Heart Association (AHA) and American College of Veterinary Compared with normal cats, cats with HCM are more likely to be
Internal Medicine (ACVIM) heart disease staging systems8-10 older, male, and have a loud systolic murmur, although HCM still can
(Figure 2), with the aim of providing a framework for prognostica- be seen in young cats, females, and in cats without a murmur.15,19-22
tion and therapeutic decision-making. Stage A includes cats that Most cats with HCM are nonpedigree, but some pedigree breeds are
are predisposed to cardiomyopathy but have no evidence of myo- believed to be at increased risk, including Maine Coon, Ragdoll, British
cardial disease. Stage B describes cats with cardiomyopathy but Shorthair, Persian, Bengal, Sphynx, Norwegian Forest cat, and Birman
without clinical signs. Stage B is further divided into stage B1: breeds.20,23-27 However, comprehensive prevalence data are lacking
cats at low risk of imminent congestive heart failure (CHF) or for pedigree cats. Sarcomeric gene mutations are common in people
arterial thromboembolism (ATE), and stage B2: cats at higher risk with HCM, but only 2 mutations have been identified in cats, both in
of imminent CHF or ATE. Atrial size is an important prognostic the myosin binding protein C (MyBPC3) gene.23,28 The estimated
marker, and it can be used as a means of subdividing cats with prevalence of the MyBPC3-A31P mutation in Maine Coon cats is
subclinical cardiomyopathy into low risk (B1) and higher risk approximately 35% to 42%,29,30 which is substantially higher than the
(B2) cats. The more severe the left atrial (LA) enlargement, the prevalence of the HCM phenotype in this breed.30 Maine Coon cats
higher the risk of CHF and ATE.11 Other factors also should be that are homozygous for this mutation, Ragdolls homozygous for the
taken into consideration when staging cats with subclinical car- MyBPC3-R820W mutation, and first-degree relatives of affected cats
diomyopathy, such as LA and LV systolic function, and extreme are at higher risk of developing HCM.30-33 The role of nongenetic and
LV hypertrophy, among others (see Figure 2). Cats that have epigenetic factors in HCM in cats is unknown, although such factors
developed signs of CHF or ATE are classified as stage C, even if might be important in humans with HCM.34
clinical signs resolve with treatment. Cats with signs of CHF
refractory to treatment are classified as stage D.
4.1 | Prognosis
4 | PREVALENCE AND NATURAL HISTORY Some cats with an HCM phenotype remain subclinical, whereas others
develop CHF or ATE.13,17,19-21,32,35-37 Younger age22 and lack of clinical
The most common type of cardiomyopathic phenotype is HCM and signs19,20,22,35 have been associated with longer survival. Markers of
thus it is the major focus in these guidelines, but other phenotypes will increased risk of CHF or ATE include presence of a gallop sound or
be addressed separately where appropriate. Hypertrophic cardiomyopa- arrhythmia on physical examination, moderate to severe LA enlargement,
thy has an estimated prevalence of approximately 15% in the general decreased LA fractional shortening (LA FS%), extreme LV hypertrophy,
cat population.12-16 In older cats, the prevalence is much higher, with decreased LV systolic function, spontaneous echo-contrast or intracardiac
up to 29% reported affected, even when cats with hypertension and thrombus, regional wall thinning with hypokinesis, and a restrictive dia-
15
hyperthyroidism are excluded. Most cats with HCM have subclinical stolic filling pattern.11,22,38 Sudden cardiac death also occurs in cats with
F I G U R E 2 Stages of feline cardiomyopathy. Within stage B2, additional risk factors include a gallop sound, arrhythmia, decreased left atrial
function, extreme left ventricular hypertrophy, left ventricular systolic dysfunction, spontaneous echo-contrast/thrombus, regional wall motion
abnormalities. ATE, arterial thromboembolism; CHF, congestive heart failure
HCM.17,18,21 Less is known about risk factors for sudden cardiac death, of developing HCM (LOE medium). In Maine Coon cats it is primarily
but these might include a history of syncope, ventricular arrhythmias, LA individuals that are homozygous for the A31P mutation that develop
11
enlargement, and regional LV wall hypokinesis. Median survival times clinically relevant HCM.44 Maine Coon and Ragdoll cats that test neg-
are substantially shorter in cats with HCM that develop CHF or ATE com- ative for these MYBPC3 mutations have been reported with HCM
pared to those with subclinical cardiomyopathy.17,19-22,35 Cats that (LOE high),44,45 and thus regular echocardiographic screening should
develop CHF associated with stress, IV fluid therapy, general anesthesia, be considered even in Maine Coon and Ragdoll cats without these
or extended-release corticosteroid treatment might have longer survival mutations (LOE low). Genetic testing for the A31P and R820W
times compared with cats that develop CHF in the absence of these fac- MYBPC3 mutations in non-Maine Coon or non-Ragdoll cats is not
tors.3,17,39 Factors associated with longer survival times after treatment recommended, because these 2 mutations are almost completely spe-
for CHF include a greater decrease in NT-proBNP concentrations during cific to Maine Coon and Ragdoll cats (LOE high).29,30
40
hospitalization and resolution of CHF at reexamination.
In contrast to HCM in people, in whom dynamic left ventricular out-
flow tract obstruction (DLVOTO) has been associated with increased 5.2 | History
morbidity and mortality,41 DLVOTO does not appear to be a poor prog-
nostic factor in cats.17,21,22 This might be a true difference between The history is unremarkable in many cats with cardiomyopathy, partic-
HCM in humans and cats, but also could reflect differences in how ularly those with HCM. The most common presenting sign is labored
DLVOTO is defined between species, or the result of bias in retrospec- breathing,17 although some cats only show nonspecific signs such as
tive studies (cats with DLVOTO are more likely to be investigated for an hiding or inappetence. Congestive heart failure appears to be the
incidentally detected murmur than cats with nonobstructive HCM, which most common cause of respiratory distress in cats.46,47 Paresis or
often are not diagnosed until clinical signs develop). paralysis associated with ATE is also a common presenting sign,17
with syncope being less common.19 In some cats with cardiomyopa-
thy, sudden death may occur with no premonitory signs.18
5 | D I A G NO S I S
Establishing the diagnosis of cardiomyopathy in cats can be challeng- 5.3 | Physical examination
ing, particularly in general practice. Echocardiography performed by a
veterinary cardiology specialist is the diagnostic test of choice, but dif- 5.3.1 | Subclinical cardiomyopathy
ferentiation of the various phenotypic categories sometimes can be
challenging, even for specialists. Fortunately, with regard to therapeu- A parasternal systolic heart murmur has been reported in up to 80% of
tic decision-making, the requirement for diuretics in cats with CHF cats with subclinical HCM, compared with 30%-45% of healthy cats
and the approach to management of ATE are similar regardless of the without HCM.14-17 Third heart sounds such as gallop sounds have been
form of cardiomyopathy. A basic level of echocardiographic skill (eg, reported in 2.6%-19% of cats with subclinical HCM and are seldom pre-
ability to detect moderate to severe left atrial enlargement) can be sent in healthy cats.15 Arrhythmias also can be associated with cardiomy-
sufficient to identify the more advanced stages of cardiomyopa- opathies.48,49 Many affected cats have no auscultatory abnormality.15,42
42,43
thy. Other diagnostic tests may facilitate disease staging, identifi- Further investigations are recommended if a heart murmur is detected in
cation of important comorbidities and establishing prognosis. any cat (LOE medium).15,42 A loud systolic murmur (grade 3-4/6) is more
Importantly, tests are recommended to screen for a possible underly- common in cats with HCM than in normal cats, but an increase in heart
ing cause for the cardiomyopathy phenotype, such as serum thyroxine murmur intensity over time does not necessarily indicate the presence or
concentration for hyperthyroidism or blood pressure measurement worsening of disease. A palpable thrill (grade 5-6/6 murmur) seldom is
for systemic hypertension in cats with an HCM phenotype. associated with cardiomyopathy in cats and is more likely to be associ-
ated with a congenital malformation. Cats with more advanced disease
(or those with restrictive or dilated phenotypes) may not have an audible
5.1 | Genetic testing murmur.13,21,42,50 Auscultation of a gallop sound or an arrhythmia is more
likely to be associated with cardiomyopathy, although differentiation of a
Genetic testing for the MyBPC3-A31P mutation and the MyBPC3 gallop sound from other third heart sounds or a bigeminal rhythm can be
R820W mutation is recommended in Maine Coon and Ragdoll cats challenging.
(respectively) intended for breeding (level of evidence [LOE] high),
with the aim of decreasing the incidence of these mutations and HCM
in these breeds.29,30,44 It is recommended that cats homozygous for 5.3.2 | Cardiomyopathy associated with CHF
either mutation not be used for breeding, but heterozygous cats can
be bred to genotype-negative cats if they have other outstanding Tachypnea, labored breathing or both are the typical historical and
characteristics (LOE low). The same genetic tests can be considered in physical examination findings in cats with left heart failure. Compared
nonbreeding Maine Coon or Ragdoll cats to determine the relative risk with cats that have subclinical HCM, a gallop sound or an audible
arrhythmia are more common in cats with CHF, and murmurs are cats with suspected subclinical cardiomyopathy, but its principal value is
less common.13,21,43 In one study, cats presented to first opinion prac- in differentiating cats with severe subclinical cardiomyopathy from nor-
tices for evaluation of respiratory distress with respiratory rates mal cats or cats with only mild disease (LOE high).70,71

>80 breaths/min, gallop sounds, rectal temperatures <37.5 C or heart
rates >200 bpm were more likely to have CHF than other causes of
dyspnea.47 Pulmonary crackles can be heard when pulmonary edema 5.5.2 | Troponin-I
is present, and breath sounds are often diminished ventrally when
pleural effusion is present, together with paradoxical breathing.51 Measuring circulating cardiac troponin-I (cTnI) concentrations can help
discriminate between cardiac and noncardiac causes of respiratory
distress (LOE medium), but only when results can be obtained rap-
5.4 | Radiography idly.72-74 High-sensitivity assays for human cTnI might be considered
for differentiating between normal cats and cats with subclinical HCM
Cardiomyopathy might be suspected when severe cardiomegaly is pre- when cardiac disease is suspected (LOE medium).75,76 In addition, cTnI
sent radiographically, when a left auricular bulge is present on dorso- also might be considered for its prognostic value, because an
52,53
ventral/ventrodorsal radiographic views, or both. Thoracic increased circulating cTnI concentration is associated with increased
radiography is insensitive for identification of mild or moderate cardiac risk of cardiovascular death independent of LA size (LOE high).77
changes associated with cardiomyopathy, and in some cats the cardiac
silhouette may appear normal even when disease is severe enough to
cause CHF.54 Furthermore, it is difficult to identify the cardiomyopathy 5.6 | Electrocardiography
phenotype from the shape of the cardiac silhouette, and the classic “val-
entine-shaped” heart is not specific for HCM, as previously thought.55,56 The sensitivity of a 6-lead ECG for detecting LV hypertrophy or LA
Although radiography is considered the gold standard for confirming enlargement is low,13,78,79 and ECG is not recommended as a screening
the presence of cardiogenic pulmonary edema, if radiographs cannot be method for cardiomyopathies in cats (LOE medium), despite its use in
obtained safely consideration should be given to delaying thoracic radi- screening people for HCM.80 Nevertheless, a variety of arrhythmias can
ography (LOE low). In contrast to dogs, the radiographic pattern associ- occur in cats with cardiomyopathy,48,49,78,81-85 and can contribute to
ated with cardiogenic pulmonary edema in cats is highly variable.52,57 A clinical signs such as weakness, syncope, and hypoxic-anoxic sei-
combination of physical examination, point-of-care ultrasound examina- zures.86,87 Although ambulatory (Holter) ECG monitoring is tolerated less
tion and point-of-care NT-proBNP often can be helpful when deciding well by cats than dogs, it can identify arrhythmias that might otherwise
if CHF is the cause of respiratory distress (LOE high).58 go undetected.49,88 It is recommended that cats experiencing episodic
weakness and collapse (including seizure-like activity) should undergo a
cardiovascular evaluation that includes echocardiography, ECG, and tele-
5.5 | Cardiac biomarkers metric or Holter ECG monitoring if necessary. Implantable loop recorders
also should be considered for cats with intermittent clinical signs that
5.5.1 | NT-proBNP could be attributed to arrhythmias89,90 (LOE low). Other options for
recording cardiac rhythm in the cat's home environment include use of a
The quantitative feline-specific NT-proBNP assay using plasma or portable electrode plate (Kardia AliveCor) in conjunction with a
pleural fluid has good diagnostic accuracy for discriminating between smartphone to record an ECG that can be interpreted by a specialist.
cats with cardiac and noncardiac causes of respiratory distress (LOE
high),59-64 but it is not recommended for guiding therapeutic decision-
making in cats with respiratory distress because of the delay in receiv- 5.7 | Blood pressure
ing test results from an external laboratory. Instead, a point-of-care
NT-proBNP assay provides rapid results while maintaining reasonable Diffuse or segmental LV hypertrophy is common in cats with systemic
diagnostic accuracy in discriminating between cardiac and noncardiac hypertension and is observed in up to 85% of cases, although HCM
causes of respiratory distress, and should be considered when point- and systemic hypertension may exist concurrently. For many hyper-
of-care ultrasound examination is not available (LOE medium).58,65 tensive cats, LV hypertrophy is only mild to moderate.91-94 Blood
The point-of-care assay can be used on plasma or pleural fluid,64,66 pressure determination should be considered for all cats with
65
the latter diluted 1:1 with saline for greater specificity. increased LV wall thickness (LOE medium).
When investigating a cat suspected to have subclinical cardiomyopa-
thy there is less urgency for test results, and so the quantitative NT-
proBNP assay can be considered in situations where echocardiography is 5.8 | Thyroxine measurement
not available (LOE high). The quantitative NT-proBNP assay is not rec-
ommended for differentiating normal cats from cats with mild to moder- Hyperthyroidism is common in older cats, and is associated with auscul-
ate HCM (LOE high).67-69 The point-of-care assay can be considered in tatory abnormalities (murmur, gallop, arrhythmias), cardiac remodeling
(LV hypertrophy or increased cardiac chamber diameters), and in some mode is limited to focal sampling of the LV. Because of regional het-
cases, CHF or ATE.95-98 Hyperthyroid cats with severe LV hypertrophy erogeneity of LV hypertrophy in many cats with HCM, measurements
are sometimes seen, but this association is suspected to be the result of using M-mode echocardiography can miss focal wall thickening. Inad-
hyperthyroidism exacerbating preexisting mild to moderate HCM (LOE vertent measurement of papillary muscles also is possible as a result
low). It is recommended that serum thyroxine concentrations be mea- of translational motion of the heart. Two-dimensional echocardiogra-
sured in all cats ≧6 years of age with abnormal cardiac auscultation find- phy allows measurement of LV wall thickness in multiple locations.
ings with or without LV hypertrophy on an echocardiogram (LOE low). The frame rate should be sufficiently high (>40 Hz) to allow measure-
ment of the true end-diastolic wall thickness. Measurements of LV
wall thickness currently are made using 2D, M-mode or both, but the
5.9 | Echocardiography 2 techniques can yield different values for wall thickness and are not
interchangeable.16
Echocardiography is the gold standard test for diagnosis of cardiomyopa- If M-mode echocardiography is used, it is recommended that it be
thies in cats. Indications for echocardiography are listed in Table 4. Echo- guided by a 2D short-axis view (LOE low). With 2D echocardiography, it
cardiography ideally should be performed by trained operators99 in is recommended that end-diastolic LV wall thicknesses be measured in at
unsedated cats in quiet conditions, and cats should be handled with mini- least 2 right parasternal views (long axis and short axis), measuring the
mal restraint. When necessary, sedation of the cat may be considered thickest part of the septum and free wall in each view (LOE low). Using
for echocardiographic examination.100 Adequate echocardiographic 2D-guided M-mode, it is recommended that septal and free wall thick-
images can be obtained whether the cat is in lateral recumbency or nesses be measured using a leading edge-to-leading edge technique, so
99
standing. that for the septum, the LV endocardial layer is excluded, and for the free
Measurements of LV wall thickness traditionally have been made wall, the pericardium is excluded (LOE low).101 Using 2D echocardiogra-
from 2D-guided M-mode echocardiographic images, although this phy, a leading edge-to-trailing edge technique should be considered for
measuring the septum, and a leading edge-to-leading edge technique
(excluding the pericardium) for measuring the LV free wall (LOE low). In
TABLE 4 Main indications for cardiac evaluation regions in which marked endocardial thickening occurs, it is rec-
ommended that the endocardial layer be excluded from the measure-
History Syncope
Seizures (in the absence of other ments (LOE low). It is recommended that end-diastolic LV wall thickness
neurological abnormalities) be measured from at least 3 cardiac cycles and averaged (LOE low). End-
Diagnosis of cardiomyopathy in a diastolic and end-systolic LV diameters traditionally have been measured
close relative
using M-mode (using a leading edge-to-leading edge technique), but also
Weakness
Exercise intolerance/open-mouth can be measured from 2D images (using a trailing-to-leading edge tech-
breathing with exertion nique). Left ventricular fractional shortening is the most commonly used
Intolerance to parenteral fluid quantitative index of LV systolic function, and regional wall motion
administration
abnormalities usually are noted as a subjective finding. Papillary muscle
Pedigree cat intended for
breeding size and geometry are evaluated from right parasternal long and short
Maine coon or Ragdoll with a axis images and usually are described qualitatively, although they can be
MyBPC3 mutation quantitatively assessed.102
Any endocrinopathy Left atrial size can be measured in short axis and long axis views.
Heartworm positive status
Left atrial diameter can be measured in a right parasternal short-axis
Fever of unknown origin
view that includes the aortic valve cusps, and can be indexed to aortic
Physical exam Murmur
Gallop sound or systolic click diameter (LA/Ao) in the same frame. Measurements can be made
Muffled heart or lung sounds either at end-systole103 or end-diastole.104 Reference intervals will
Arrhythmia vary according to the timing within the cardiac cycle (LOE medium).
Tachypnea
The LA diameter also can be measured in a right parasternal long-axis
Pulmonary crackles
Jugular venous distention or 4-chamber view at end-systole, from the interatrial septum to the LA
pulsation free wall (LOE medium).105 Left atrial fractional shortening is an index
Ascites of LA function, and can be measured using 2D-guided M-mode from
Hypo- or hyperkinetic femoral
the same right parasternal short axis view as used for measurement of
arterial pulse pressure
Acute paresis/paralysis LA/Ao.103 The presence of spontaneous echo-contrast (SEC) is associ-
Absent femoral arterial pulses ated with decreased LA function and blood stasis, and it is rec-
Cats aged 9 years or older General anesthesia ommended that the LA appendage be evaluated in cats with LA
undergoing interventions Fluid treatment enlargement for the presence of SEC or thrombus106 and for evidence
that could precipitate CHF Extended-release of blood stasis using pulsed wave Doppler LA appendage flow veloci-
glucocorticosteroids
ties (LOE Low).
In addition to measuring cardiac chamber dimensions, it is rec- 5.9.1 | Echocardiographic protocol for
ommended that the presence or absence of dynamic left ventricular cardiomyopathy screening in pedigree breeding cats
outflow tract obstruction (DLVOTO) be evaluated. Assessment of
DLVOTO can be made using a combination of 2D, M-mode, and A standard-of-care scan should be undertaken at a minimum for
Doppler echocardiography. Careful imaging of the LVOT using 2D screening pedigree breeding cats. Such a scan consists of a quantita-
echocardiography should allow identification of systolic anterior tive assessment of left heart chamber dimensions, including LA size,
motion of the mitral valve (SAM), where the septal leaflet of the mitral LV wall thickness and LV diameter, as well as LA and LV fractional
valve is displaced towards the septum in systole, obstructing the shortening and a qualitative assessment of abnormal cardiac chamber
LVOT. Chordal anterior motion (CAM) also can be identified in the geometry and presence or absence of SAM of the mitral valve
same imaging view.107 Mitral valve SAM also can be imaged using M- (Table 5). No reference interval for maximal end-diastolic LV wall
mode echocardiography. Color Doppler can be used to identify the thickness is universally accepted, and it is overly simplistic to expect a
characteristic blood flow jets of LVOT obstruction and mitral regurgi- single cutoff value for wall thickness to differentiate a normal ventri-
tation, and spectral Doppler can be used to estimate the peak LVOT cle from a hypertrophied ventricle. Furthermore, wall thickness
gradient from left apical views (LOE Low). It is recommended that dia- increases with increasing body size,26,110,111 and is influenced by
stolic function be assessed and a class of diastolic dysfunction hydration112,113 and heart rate.114 For the majority of normally-sized
assigned using a combination of spectral Doppler and tissue Doppler cats, an end-diastolic LV wall thickness <5 mm is considered normal,
imaging (LOE medium).108,109 Table 5 summarizes recommended and ≧6 mm is indicative of hypertrophy. It is recommended that LV
echocardiographic protocols. wall thicknesses between 5 and 6 mm should be interpreted in the
TABLE 5 Echocardiographic protocols for a cat suspected of having cardiomyopathy according to level (basic to advanced)
Level of scan Measurements Qualitative assessment

Focused point-of-care Note presence of:
• Pleural, pericardial effusions
• Left atrial size & motion
• Pulmonary B-lines
• LV systolic function
Standard of care M-mode Note presence of:
• IVSd, LVFWd • Papillary muscle hypertrophy
• LVIDd, LVIDs, LV FS% • End-systolic LV cavity obliteration
• LA FS% • Papillary muscle/mitral leaflet abnormalities
2D • SAM or mid LV obstruction
• IVSd, LVFWd • Dynamic RVOTO
• LVIDd, LVIDs • Abnormal cardiac chamber geometry
• LA/Ao • Presence of spontaneous echo-contrast or thrombus
• LA diameter from RP long axis view • Regional wall motion abnormalities
Best practice M-mode and 2D as for standard Qualitative assessment as for standard of care
of care, with the following
additional measurements:
Spectral Doppler
• Mitral inflow velocities
• Isovolumic relaxation time
• LVOT velocities
• RVOT velocities
• PVF velocities
• LAA blood flow velocities
Tissue Doppler imaging
• Lateral and septal mitral annular
velocities (pulsed wave Doppler mode).
Note: “Focused point-of-care” scan: an abbreviated echocardiographic examination conducted because of patient instability, because the operator
has limited training in echocardiography, or both; “standard of care” scan: an echocardiographic examination that includes the content considered
to be standard by a trained, competent observer; “best practice” scan: an echocardiographic examination conducted by a cardiologist with
particular expertise in echocardiography. IVSd: end-diastolic interventricular septal thickness, LA: left atrial, LA FS%: left atrial fractional
shortening, LA/Ao: left atrial to aortic ratio at end-diastole and end-systole, or both, LAA: left atrial appendage, LV: left ventricular, LV FS%: left
ventricular fractional shortening, LVFWd: end-diastolic left ventricular free wall thickness, LVIDd: left ventricular internal dimension at end-
diastole, LVIDs: left ventricular internal dimension at end-systole, LVOT: left ventricular outflow tract, PVF: pulmonary venous flow, RP: right
parasternal, RVOT: right ventricular outflow tract, SAM: systolic anterior motion of the mitral valve.
context of body size, family history, qualitative assessment of LA and used to improve the accuracy of cardiomyopathy diagnosis by non-
LV morphology and function, presence of DLVOTO and tissue Dopp- specialist practitioners, particularly in cats with more advanced disease.42
ler imaging velocities. Where there is doubt, it is recommended that It is recommended that focused point-of-care echocardiography be
the cat be classified as equivocal for LV hypertrophy and reevaluated undertaken only after appropriate training and practice42,99 (LOE high)
at a later date. and a point-of-care examination should be followed at a later time point
with a standard echocardiographic examination to characterize the
phenotype.
5.9.2 | Echocardiographic protocol for a cat When echocardiography is unavailable, evaluation of NT-proBNP
suspected to have cardiomyopathy concentrations may be considered. Circulating NT-proBNP concentra-
tions increase with increasing clinical severity of cardiomyopathy in
Further investigations are recommended when history, physical groups of cats, but overlap precludes using NT-proBNP to categorize
examination findings, or both suggest that a cat might have cardiomy- individual cats into mild, moderate, and severe groups.69 The mea-
opathy (Table 4, LOE medium). Further investigations also should be surement of NT-proBNP can be considered as an initial screening test
considered in older cats when anesthesia or treatment with IV fluid for identifying advanced cardiomyopathy. Normal NT-pro-BNP results
therapy or extended-release corticosteroids is planned (LOE low). It is do not assure that a cat is free of cardiomyopathy, especially when
recommended that a standard of care examination include a qualitative mild heart disease is present, nor do they guarantee that a cat will
evaluation of SEC and regional wall motion abnormalities (Table 5). A remain free of cardiomyopathy later in life. They do however indicate
best practice examination includes the above evaluations and Doppler a low likelihood of cardiomyopathy that is immediately, clinically
blood flow velocities recorded in the LVOT, across the mitral valve, in harmful. Therefore, in a cat suspected of cardiomyopathy, follow-up
the pulmonary veins, and in the LA appendage. Mitral annulus veloci- echocardiography still should be considered, even if initial NT-proBNP
ties also should be recorded with tissue Doppler imaging. If a standard- results are within normal reference intervals (LOE low). It is rec-
of-care assessment is not possible, a focused point-of-care examination ommended that a positive NT-proBNP test always be followed by an
still can provide some information on the presence of disease and risk echocardiographic examination.
of CHF or ATE based on a qualitative assessment of LA size and cardiac In older cats with heart murmurs, gallop sounds or arrhythmias, it
chamber geometry. is recommended that serum T4 concentration and blood pressure be
measured (LOE high). Echocardiography also should be considered
(LOE low).
5.9.3 | Echocardiographic protocol for a cat
suspected to have congestive heart failure
5.11 | Approach to diagnosis in cats with
For clinically unstable cats or where specialist level echocardiography suspected CHF
is not available, a focused point-of-care examination can be used to
identify the presence of pleural or pericardial fluid or both, presence Physical examination findings of tachypnea, labored breathing,
of B lines in lungs, and to provide a subjective estimate of LA size and respiratory crackles, hypothermia, and a gallop sound are highly
58
LV systolic function (Table 5). It is recommended that this examina- suggestive of CHF,47 but in some cats tachypnea with labored
tion be followed by a best practice examination or at least a standard- breathing might be the only abnormality detected. Although tho-
of-care examination once the cat is more stable, using the protocol racic radiography traditionally has been considered the gold stan-
suggested for cats with suspected cardiomyopathy. dard test for detecting cardiogenic pulmonary edema, care should
be taken to minimize stress when taking radiographs of cats with
respiratory distress. Pulmonary infiltrates and cardiomegaly are the
5.10 | Approach to the diagnosis of subclinical key findings with CHF, but classic radiographic features of CHF
cardiomyopathy such as LA enlargement and distended pulmonary vessels are
inconsistently identified in affected cats.52,54
Cats with subclinical cardiomyopathy can be difficult to identify. Car- If radiographs cannot be obtained safely, point-of-care thoracic
diac evaluation should be considered for cats with a suspicious history ultrasound examination or a point-of-care NT-proBNP test should be
or physical examination findings that include a gallop sound, murmur, considered (LOE high). With point-of-care ultrasound examination,
or arrhythmia, and in cats judged to be at high risk of CHF if subjected the presence of effusions or B-lines in association with severe LA
to interventions such as anesthesia or IV fluid therapy (LOE low; enlargement is highly suggestive of CHF.58,115 A negative result on a
Table 4). Echocardiography is currently the most accurate clinical test point-of-care NT-proBNP test suggests that respiratory disease is
for diagnosis of cardiomyopathy in cats, and is also the best technique more likely to be the cause of respiratory distress than is cardiac dis-
99
for estimating prognosis, but is highly user-dependent. However, ease. Once a cat with CHF has been stabilized, a standard-of-care or
with appropriate training and experience, focused point-of-care echo- best practice echocardiographic examination should be considered
cardiography is feasible in first opinion (general) practice and can be (Table 5, LOE low).
6 | T R E A T M E NT had no effect on time to treatment failure compared to placebo in a

randomized placebo-controlled study that included cats with subclini-
6.1 | Stage B1 cardiomyopathy cal heart disease.127 No studies have been reported of pimobendan
use in cats with subclinical cardiomyopathy.
Treatment of cats with subclinical cardiomyopathy is controversial Ventricular ectopy is common in cats with HCM48,49and
because evidence is lacking. Although the majority of cats with stage ARVC48,128 and is associated with sudden death in people with these
B1 cardiomyopathy will not develop clinical signs, it is recommended cardiomyopathies.80,129,130 Treatment options in cats are limited, but
that stage B1 cats be monitored annually for development of moder- atenolol has been shown to decrease ventricular ectopy in cats with
ate to severe LA enlargement (progression to stage B2). Cats with HCM.117 It is recommended that cats with complex ventricular ectopy
stage B1 cardiomyopathy are considered at low risk of CHF or ATE, be treated with atenolol (6.25 mg/cat q12h PO) or sotalol (10-20 mg/
and in general treatment is not recommended (LOE low). cat q12h PO; LOE low). Markedly increased heart rate is observed in a
There is no evidence that DLVOTO is associated with increased minority of cats with atrial fibrillation (AF),83 but AF occurs most often
morbidity or mortality in cats, and atenolol has not been shown to in the setting of advanced cardiomyopathy where tachycardia is poorly
have any effect on the 5-year survival rate in cats with subclinical tolerated. Diltiazem, atenolol or sotalol may be considered in cats with
116
HCM. However, atenolol is expected to decrease DLVOTO gradi- AF and a rapid ventricular response rate (LOE Low).
ent and heart rate,117 and may be considered in cats with stage B1
cardiomyopathy and severe DLVOTO, provided it can be administered
consistently (LOE low). 6.3 | Stage C
6.3.1 | Acute decompensated heart failure

6.2 | Stage B2 cardiomyopathy
Cats with pulmonary edema or pleural effusion caused by CHF usually
Cats with stage B2 HCM have an increased risk of developing CHF or are presented with tachypnea and labored breathing. Empirical diuretic
ATE. Primary prevention of ATE in cats with subclinical cardiomyopa- treatment should be considered immediately when the index of suspicion
thy has not been studied, but thromboprophylaxis is recommended for CHF is high, for example, if hypothermia and a gallop sound are pre-
when known risk factors for ATE are present.11,106 Clopidogrel was sent, especially when echocardiography or thoracic radiography is
more effective than aspirin in cats that had survived a previous ATE unavailable or the risk of restraint for diagnostic evaluation appears to
episode,118 and no other randomized, controlled studies have been exceed the benefits (LOE low). Supplementary oxygen administration is
reported. Clopidogrel therefore is recommended in cats considered at recommended for any cat with respiratory distress, and sedation with an
risk of ATE (moderate to severe LA enlargement, low LA FS%, low LA anxiolytic (eg, butorphanol) also should be considered (LOE low). Stress
appendage velocities, SEC; LOE medium). Clopidogrel does not elimi- should be further minimized by gentle handling, a quiet environment, and
nate the risk of ATE, and thus other antithrombotic drugs can be con- provision of a hiding box.131
sidered in addition to clopidogrel in cats believed to be at very high Intravenous administration of furosemide, either as multiple boluses
risk of ATE (eg, clopidogrel plus aspirin, clopidogrel plus a PO factor of 1 to 2 mg/kg or a constant rate infusion, is recommended for CHF
Xa inhibitor, or clopidogrel plus aspirin plus a PO factor Xa inhibitor; and pulmonary edema in particular (LOE low). Thoracocentesis should be
LOE low). performed when respiratory distress results from pleural effusion (LOE
Cats with stage B2 cardiomyopathy should be monitored for pro- low). Intravenous fluid treatment is contraindicated in cats with clinically
gression of disease and development of clinical signs, but the effects evident congestion, edema or effusion, and can exacerbate signs of CHF
of stress caused by reexamination also should be taken into consider- even if diuretics are administered concurrently (LOE low). Ideally, mea-
ation. If a stage B2 cat is reexamined, attention to appropriate han- suring blood chemistries can be considered before treatment if samples
dling and minimizing stressful stimuli is important. If these measures can be obtained without compromising patient safety (LOE low), but
are (or are likely to be) insufficient, PO administration of appropriate diuretic treatment is recommended for acute heart failure regardless of
119,120 121-123
pharmaceuticals, synthetic feline pheromone application the presence of azotemia (LOE low).
or both can be considered (LOE medium). Once the LA is moderately In cats with signs of low cardiac output (eg, hypotension, hypo-
to severely enlarged and antithrombotic treatment is started, manage- thermia, bradycardia), PO treatment with pimobendan could be con-
ment is unlikely to change until clinical signs develop, but at a mini- sidered, provided DLVOTO is absent (LOE low). In cats with acute
mum, it is recommended that owners monitor the cat's resting or heart failure and low cardiac output signs that do not show clinical
sleeping respiratory rate124 (LOE medium). improvement after administration of pimobendan, a constant rate
In 2 randomized, placebo-controlled studies, neither an angioten- infusion of dobutamine could be considered (LOE low). Evidence of
sin converting enzyme (ACE) inhibitor (ramipril) nor spironolactone the efficacy of transdermal administration of nitroglycerin in cats is
had any effect on LV mass or diastolic function in cats with subclinical lacking or conflicting, and its use is not recommended (LOE medium).
HCM, but study populations were small and limited to cats of a single Angiotensin converting enzyme inhibition is not indicated during
breed that had heritable cardiomyopathy.125,126 Similarly, benazepril acute decompensation of cats with cardiomyopathy (LOE low).
Monitoring body temperature, respiratory rate, body weight, blood considered for management of chronic CHF.133 Adverse reactions (eg,
pressure, and estimated urine output is recommended (LOE high). ulcerative dermatitis) have been reported in Maine Coon cats treated
Once stabilized, it is recommended that cats be discharged to the with spironolactone at a dosage of 2 mg/kg q12h (LOE medium).126 In
care of their owners as soon as possible (LOE low). Reevaluation is cats with global LV systolic dysfunction, pimobendan is recommended
recommended 3-7 days after discharge to evaluate for resolution of (LOE low).134 Taurine supplementation at 250 mg PO q12h also is rec-
CHF and to evaluate renal function and serum electrolyte concentra- ommended for cats with global LV systolic dysfunction unless plasma
tions (LOE low). It is recommended that owners monitor the cat's rest- taurine concentrations are in the normal range (LOE low).135 Foods
ing or sleeping respiratory rate with the goal of maintaining the high in salt should be avoided (LOE low). As the number of medica-
respiratory rate <30 breaths/min (LOE medium). tions increases, owner compliance is likely to decrease, and unneces-
sary medications should be avoided (LOE low).
Cardiac cachexia, defined as loss of muscle or lean body mass
6.3.2 | Chronic heart failure associated with heart failure, may be present in cats with stage D car-
diomyopathy. Calorie intake should be prioritized over restriction of
Furosemide is the primary drug used for control of pulmonary edema sodium intake and body condition score should be recorded and an
and effusions in cats with CHF. Typically, treatment consists of furo- accurate body weight obtained at every clinic visit (LOE low). It is rec-
semide 0.5 to 2 mg/kg PO q8-12 h, depending on the severity of clini- ommended that serum potassium concentration be monitored and if
cal signs of CHF. A common starting dosage is 1 to 2 mg/kg PO q12h hypokalemia is identified, the diet should be supplemented with
(LOE low). Intravenous administration is preferred in cats with marked potassium from either natural or commercial sources (LOE low).
respiratory distress from pulmonary edema (see treatment of acute
decompensated heart failure, above). The maintenance dose of furose-
mide should be titrated to maintain a resting or sleeping respiratory rate at 6.5 | Management of ATE
home of <30 breaths/min (LOE low). Measurement of serum creatinine,
blood urea nitrogen, and electrolyte concentrations is recommended Most cats with ATE presented to first opinion practice are eutha-
3-7 days after initiating furosemide (LOE low). Angiotensin converting nized.136 This approach is justifiable In terms of the cat's welfare and
enzyme inhibition with benazepril did not delay the onset of treatment generally poor prognosis, but if analgesia is adequate and favorable
failure in a randomized, placebo-controlled study of cats with CHF127 prognostic factors are present (eg, normothermia, only 1 limb
(LOE high) although ACE inhibitors still are used by some cardiologists. affected, absence of CHF),136,137 an attempt at treatment can be con-
Prophylactic antithrombotic treatment with clopidogrel (18.75 mg/cat PO sidered provided the owner is fully informed of the risks and overall
q24h, with food) is recommended in any cat with a history of CHF and poor prognosis.
moderate to severe LA enlargement (LOE low). Some cats react to Analgesia is a priority for management of acute ATE in the first
clopidogrel with salivation and retching or vomiting, which can be mini- 24 hours, and treatment with a mu opioid agonist such as fentanyl,
mized by administering the medication in an empty gelatin capsule, hydromorphone, or methadone is recommended (LOE low). Anticoag-
followed by water. Pimobendan can be considered in cats without clini- ulant treatment is recommended using low-molecular-weight heparin
cally relevant LVOTO (LOE low).132 A commonly used dosage is 0.625 to (LMWH) or unfractionated heparin, or a PO factor Xa inhibitor, which
1.25 mg per cat q12h PO. should be started as soon as possible (LOE low). Thrombolytic treat-
It is recommended that cats with stage C cardiomyopathy be ment is not recommended for cats with ATE (LOE high).138-140 If CHF
reexamined at approximately 2-4 month intervals or as needed. Consid- is present with ATE, management with furosemide and oxygen is rec-
eration should be given to the effects of stress caused by reexamination ommended as necessary (LOE high), but it is important to note that
on an individual basis. Owner-recorded resting or sleeping respiratory pain also can cause tachypnea, and this should not be mistaken for
rate can provide useful information for adjusting medication over the the presence of CHF. It is recommended that clopidogrel be started as
phone without the need for clinic visits, although the presence of com- soon as the cat can tolerate PO medications, with an initial loading
orbidities and the risk of disease progression may necessitate periodic dose of 75 mg PO (LOE low) followed by 18.75 mg PO q24h (LOE
reexaminations. For cats with a DCM phenotype, enquiries about dietary high). Heparin can be replaced by a PO factor Xa inhibitor in combina-
history and measurement of plasma taurine concentrations are rec- tion with clopidogrel (LOE low).
ommended, with supplementation and dietary change as necessary.
6.5.1 | Post-ATE
6.4 | Stage D (refractory)
Reexamination is recommended 3-7 days after discharge from the
Torsemide may be considered in place of furosemide in cats with per- hospital, as well as 1-2 weeks after the ATE event. Evaluation should
sistent CHF despite high doses of furosemide (>6 mg/kg/day PO), at a include assessment of the distal limbs for evidence of necrosis, elec-
starting dose of 0.1 to 0.2 mg/kg PO q24h and uptitrating to effect trolyte status, appetite, and treatment compliance, as well as the
(LOE low). Spironolactone 1 to 2 mg/kg PO q12h to q24h also can be degree of improvement in neuromuscular function. Resolution of
lower motor neuron dysfunction can take weeks or months in some Philip R. Fox https://orcid.org/0000-0003-4089-0573
cats,141 and reexamination should be considered every 1-3 months, Jens Häggström https://orcid.org/0000-0003-3402-023X
considering the effects of stress in the individual cat. It is rec- Joshua A. Stern https://orcid.org/0000-0001-5611-5745
ommended that the owner continue to monitor resting or sleeping
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19391676, 2020, 3, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/jvim.15745 by Cochrane Colombia, Wiley Online Library on [16/01/2023].

ACVIM consensus statement guidelines for the classification,

Virginia Luis Fuentes1 | Jonathan Abbott2 | Valérie Chetboul3 |

1062 wileyonlinelibrary.com/journal/jvim J Vet Intern Med. 2020;34:1062–1077.

of life-threatening complications and those at higher risk. Based on the available

arrhythmogenic, cardiovascular, congestive heart failure, consensus statement,

1 | I N T RO DU CT I O N competing classification systems are used in humans, highlighting

A modified Delphi method was applied to a series of statements

Level of scan Measurements Qualitative assessment

6 | T R E A T M E NT had no effect on time to treatment failure compared to placebo in a

6.3.1 | Acute decompensated heart failure

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