Download Severe aortic stenosis in a Persian kitten Estenose aórtica

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CIÊNCIAS VETERINÁRIAS
Severe aortic stenosis in a Persian kitten
Estenose aórtica severa em um gato Persa
Marlos G. Sousa1*, João Paulo da E. Pascon2, Alexandre M. de Brum3,
Priscila A. C. Santos2, Aparecido A. Camacho2
1
College of Veterinary Medicine and Animal Science, The Federal University of Tocantins (UFT),
Campus of Araguaína, Brazil
2
College of Agricultural and Veterinary Sciences, São Paulo State University (UNESP),
Campus of Jaboticabal, Brazil
3
College of Veterinary Medicine, University of Franca (UNIFRAN), Franca, Brazil
Summary: A case of severe aortic stenosis in a kitten is
reported. Although no obvious clinical signs were observed
initially, congestive left heart failure developed seven months
later. On presentation, severe pulmonary edema was diagnosed
and an incidental thrombus within the enlarged left atrium was
disclosed on echocardiographic examination. Clinical features
and diagnostic methods are discussed in this paper.
Keywords: congenital heart disease, echocardiography,
thromboembolism, concentric hypertrophy, pulmonary edema
Resumo: Relata-se um caso de estenose aórtica severa em
um gato Persa. Apesar da inexistência de sinais clínicos
inicialmente, desenvolveu-se insuficiência cardíaca congestiva
sete meses após o atendimento inicial, sendo diagnosticado
edema pulmonar e, ao exame ecocardiográfico, um trombo
incidental no interior do átrio esquerdo dilatado. Neste artigo,
são discutidas as características clínicas e os métodos diagnósticos empregados nesse caso de cardiopatia congênita.
Palavras-chave: doença cardíaca congênita, ecocardiografia,
tromboembolismo, hipertrofia concêntrica, edema pulmonar
Introduction
Aortic stenosis is a congenital narrowing of the left
ventricular outflow tract, aortic valve, or supravalvular
aorta (Bolton and Liu, 1977; Liu, 1977; Kienle, 1998).
Wherever it is located, obstruction to left ventricular
outflow increases left ventricular systolic pressure,
resulting in concentric hypertrophy of the left ventricle (Sisson et al., 2000).
Although reported as one of the most common
congenital heart disease in dogs, aortic stenosis has
only been described in a few cats (Liu, 1968; Stepien
* Correspondence: [email protected]
BR 153, Km 112, Campus EMVZ/UFT, Araguaína, TO, Brazil,
77804-970
Tel: +55 (63) 2112 2113; Fax: +55 (63) 2112 2136
and Bonagura, 1991; King, 1997). To date, Harpster
(1986) has documented this defect to count for only
6% of all congenital heart disease in domestic felines.
The increased left ventricular systolic pressure
propels blood at a higher velocity across the stenotic
area, thereby resulting in a turbulent flow that is
associated with a systolic ejection murmur (Bolton
and Liu, 1977; Stepien and Bonagura, 1991), which
may eventually be accompanied by a soft diastolic
murmur secondary to aortic valve insufficiency
(Sisson et al., 2000).
Clinical signs may be absent in many mildly-tomoderately affected patients, and most affected cats are
recognized when an ejection murmur is auscultated at
the time of initial vaccinations (Bonagura, 1994;
Kienle, 1998). In severely affected animals, exertional
fatigue, syncope, and even signs related to congestive
heart failure may be observed (Stepien and Bonagura,
1991; Kienle, 1998).
Definitive diagnosis of aortic stenosis requires
angiocardiography, or echocardiography (Bonagura,
1994). A fibrous obstructing lesion, left ventricular
concentric hypertrophy, and post-stenotic dilatation
may be observed on two-dimensional echocardiography (Belerenian, 2007; Ferraris, 2007). Doppler
echocardiography should reveal an increased peak
velocity of aortic flow. In dogs, Sisson et al. (2000)
documented that aortic velocity over 2.2 m/s is
regarded as indicative of aortic stenosis, whereas in
cats, Stepien and Bonagura (1991) reported that peak
aortic velocity greater than 2 m/s might suggest a
narrowed aortic tract.
As documented in literature, aortic stenosis is an
uncommon congenital heart defect in cats. Therefore,
the aim of this paper is to report a case of severe
aortic stenosis in an initially asymptomatic Persian
kitten, followed by the development of left atrial
thrombus and signs of congestive heart failure.
229
Sousa MG et al.
RPCV (2008) 103 (567-568) 229-232
Case description
A 5-month-old male Persian kitten weighing 2.5 kg
was brought to consultation for initial vaccination.
Except for a grade 3/6 systolic ejection murmur heard
best over the left basilar region and radiating both
cranially and dorsally, no obvious abnormalities were
found on physical examination.
The caretaker noted that the kitten had an adequate
appetite and was as active as its sibling. Although the
cat had demonstrated normal behavior and physical
activity with no overt medical conditions, ancillary
exams were requested to investigate the murmur.
Thoracic radiographs disclosed a normal cardiac
silhouette and no evidence of congestive heart failure.
Cardiac examination consisted in a 6-lead computerized electrocardiogram and echocardiography with
Doppler examination. Only sinus tachycardia was
documented on electrocardiography (200 bpm).
Echocardiography was performed from the right
parasternal and left apical locations. On two-dimensionally-guided M-mode echocardiography, a mildly
decreased left ventricular systolic diameter (0.55 cm),
decreased left ventricular diastolic diameter (1.26
cm), and increased fractional shortening (56%) were
consistent with mild left ventricular concentric hypertrophy. Left atrial diameter was within the reference
range. On the apical five-chamber view, a severely
increased peak aortic velocity (6.03 m/s) was identified using continuous-wave Doppler (Figure 1). Based
on the echocardiographic findings, the diagnosis of
aortic stenosis was established.
Four months later, the cat was brought to the
Veterinary Teaching Hospital for a follow-up consultation. On presentation, he weighed 4.7 kg, was very
active and his owner reported no abnormalities since
we last saw him. We auscultated a grade 4/6 systolic
ejection murmur, still radiating cranially and dorsally,
but the remainder of the physical examination findings were unremarkable. M-mode echocardiography
showed a moderate left atrial enlargement (1.74 cm,
with a left atrium-to-aorta ratio of 2.3), increased
interventricular septal thickness in systole (0.98 cm)
and diastole (0.89 cm), and decreased left ventricular
systolic (0.55 cm) and diastolic diameter (1.00 cm).
Color-flow and spectral Doppler demonstrated a highvelocity turbulent flow across the aorta.
Three months later, the cat was presented to the
Veterinary Teaching Hospital emergency service
with acute difficulty in breathing and tachypnea. On
physical examination, the patient had mildly cyanotic
mucous membranes, and was tachypneic, dyspneic,
and tachycardic. Peripheral pulse rate matched the
heart rate at 210 pulses/minute. Cardiac sounds were
inaudible over pulmonary crackles and wheezes.
Lateral radiographs showed severe pulmonary edema
and left atrial enlargement. Short-term emergency
therapy was immediately initiated and included
230
Figure 1 – Continuous-wave Doppler interrogation at initial
presentation showed a severely increased peak aortic velocity (6.03
m/s) and a turbulent flow across the aortic valve (arrow). (Ao: Aorta;
LA: left atrium; LV: left ventricle).
Figure 2 – Echocardiographic findings in a kitten with aortic stenosis:
Left atrial thrombus (between arrows) seen on the long-axis view. (LA:
left atrium; RA: right atrium; LV: left ventricle).
furosemide and a nitroglycerin transdermal patch
placed over a shaved area on lateral thorax. The patient
was continually supplemented with 100% oxygen
via a face mask, resulting in improvement in the color
of the mucous membranes. An ultrasonographic
examination of the heart disclosed a large thrombus
(approximately 0.94 x 0.52 cm) (Figure 2) inside the
severely enlarged left atrium (2.38 cm). Due to respiratory distress, the echocardiogram was not fully
performed. Therefore, no measures of left ventricular
chamber and aortic peak velocity were done at this
time.
Although every effort was made to treat pulmonary
edema, cardiopulmonary arrest occurred about three
hours after initial presentation.
Sousa MG et al.
Discussion
Congenital cardiac disease comprises about 10% of
cardiology cases in domestic mammals (Keirstead et
al., 2002). In cats, however, congenital heart diseases
are less common, counting for approximately 0.02%
to 0.1% of hospital admissions (Goodwin, 2001).
Although rare, some reports of congenital fixed aortic
stenosis in cats exist (Liu, 1968; Stepien and
Bonagura, 1991).
Although no clinical signs were observed at initial
presentation, a congenital heart disease was suspected
due to a loud systolic ejection murmur loudest over
the left basilar region. Cote et al. (2004) reported that
many murmurs detectable in overtly healthy cats
appear to be caused by a latent structural heart disease.
Because young animals can have physiologic or
innocent heart murmurs, it is important to consider
that, in general, loud heart murmurs are indicative of
cardiac disease (Kittleson, 1998). Therefore, ancillary
exams were requested to confirm the suspected heart
pathology.
Initial thoracic radiographs did not show any abnormalities. Left ventricular enlargement and widening of
the mediastinum (poststenotic dilatation) may be
detected by radiography in severely affected animals
(Liu, 1968; Bolton and Liu, 1977; Stepien and
Bonagura, 1991). In some cases, however, thoracic
radiographs may be normal (Sisson et al., 2000). Only
sinus tachycardia was observed on the electrocardiogram. Although the electrocardiogram is generally
normal in dogs with subaortic stenosis, severely
affected dogs may eventually have ventricular premature contractions (Kienle, 1998). Nevertheless, we did
not observe any abnormality in nearly three minutes of
ECG recording in this cat.
The suspected congenital heart anomaly was
confirmed by Doppler echocardiography. The highly
increased velocity across aortic valve is the definitive
diagnosis of aortic stenosis (Stepien and Bonagura,
1991; Ferraris, 2007), which has been recognized to
occur in subvalvular, valvular, and supravalvular
forms in cats (Kienle, 1998). Also, an incomplete
subaortic stenotic ring was detected at necropsy in one
cat (King et al., 1988). The obstruction was assumed
to be fixed rather than dynamic owing to the lack of a
delayed systolic peak in the continuous-wave Doppler
tracing of the left ventricular outflow tract (Thomas et
al., 1984; Kienle, 1998). Chronic pressure overload
associated to a normal or enhanced myocardial function resulted in secondary left ventricular concentric
hypertrophy, which is usually appreciated in moderately-to-severely affected animals (Kienle, 1998).
Interestingly, no poststenotic dilatation was recognized. In dogs, however, the dilatation may be slight
before 6 months of age (Kienle, 1998), which is likely to be similar in affected cats.
Due to questionable or unproven value, medical
RPCV (2008) 103 (567-568) 229-232
therapy was not initiated in this kitten (Fox, 1991;
Bonagura, 1994). Although the kitten was asymptomatic and had no electrocardiographic abnormalities,
the owner was informed of the possibility of starting a
beta-adrenergic receptor blocking drug and an
angiotensin-converting enzyme inhibitor empirically
(Kienle, 1998; Sisson et al., 2000; Belerenian, 2007),
since a severely increased gradient was measured
across aortic valve. By decreasing heart rate and
cardiac contractility, beta-blockers may reduce
myocardial oxygen demand and increase coronary
perfusion, thereby reducing the occurrence of
malignant arrhythmias (Kienle, 1998). However, this
option was declined and only restriction to vigorous
exercise was recommended.
Cats with cardiac disease are prone to develop
thromboembolism (Laste and Harpster, 1995; Smith
and Tobias, 2004). In general, the thrombus is formed
in the enlarged left atrium due to blood stasis,
endothelial damage, and altered coagulability (Pion
and Kittleson, 1989; Bonagura, 1994). In the case
reported herein, the abnormal diastolic filling pattern
as a consequence of concentric hypertrophy and
ventricular stiffness resulted in left atrial enlargement,
therefore predisposing for thrombogenesis (Bonagura,
1994; Kienle, 1998). On presentation, however, the
thrombus had not caused clinical abnormalities and
was an incidental finding. The thrombus within left
atrium was large enough to be easily observed on
standard long-axis four-chamber and short-axis views.
Although reports of intracardiac thrombi exist (Venco,
1997), we did not find any report of intracardiac
thrombus formation in a cat with aortic stenosis.
Conclusion
Although rare, aortic stenosis may occur in cats.
Loud heart murmurs auscultated in overtly healthy
kittens may indicate a congenital heart disease.
Therefore, clinicians are reminded to perform a
detailed physical examination prior to routine
vaccinations or exams. Also, cats with aortic stenosis
and enlarged left atrium should be considered at
risk for developing intracardiac thrombi and even
thromboembolism.
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