Topics in Medicine and Surgery

Clinical Approach to Avian Cardiac Disease

Martine de Wit, DVM,
Nico J. Schoemaker, DVM, PhD, Dipl. ABVP-Avian, Dipl. ECAMS

Abstract
Cardiovascular diseases are common among avian species but also have been
known for their difficulty to diagnose. Knowledge on these disorders has
increased considerably over the past few years, and cardiology has become an
important and challenging field in avian medicine. This article reviews clinical
aspects of avian cardiovascular disease. Clinical presentation, diagnostic pro-
cedures, and general management of heart disease in birds are discussed. An
overview of common avian cardiovascular diseases is included. Copyright 2005
Elsevier Inc. All rights reserved.

Key words: Avian; cardiovascular; heart disease; cardiology; bird

The Cardiovascular Examination

T
he avian cardiovascular system is de-
signed to match the high metabolic de-
mand of birds, comprising a large heart,
high heart rate, high cardiac output, and high
blood pressure.1 These unique high-perfor-
mance features of the avian heart enable birds
to fly, run, or dive. However, pet birds often are
compromised in their cardiovascular capabili-
ties by restricted exercise, poor diet, and abnor-
mal climate. These factors may predispose for
cardiovascular disease in captive birds. Patho-
logical studies have demonstrated the presence
of heart abnormalities in 9.7%2 and 36%3 of
surveyed birds. In the past, heart disease was an
under-recognized problem in the avian clinic.
Most cases were associated with sudden death
and diagnosed at necropsy. In modern avian
medicine, diagnostic techniques such as radiog-
raphy, ultrasonography, and electrocardio-
graphy have become routine procedures, which
lead the way to a clinical diagnosis of heart
disease in birds. Despite increasing knowledge
on the presentation and diagnosis of avian car-
diac disease, information on treatment is still
limited, and most therapeutic protocols are ex-
trapolated from other species.
History and Clinical Signs
A thorough history is the first step in the diagnosis
of avian cardiac disease. This includes the descrip-
tion of the bird; species and age may predispose
for cardiovascular disease. For example, gray par-
rots (Psittacus erithacus) and Amazon parrots (Am-
azona sp.) over 15 years of age are more suscep-
tible to atherosclerosis3-5 Clinical signs that can
indicate heart disease include dyspnea, periodic
weakness, syncope, coughing, exercise intoler-
ance, coelomic swelling, or lethargy.1 Any use of
drugs, potential exposure to toxins, or concurrent
disease should be evaluated. Diet factors can play
From the White Oak Conservation Center, 581705 White
Oak Road, Yulee, FL; and Department of Clinical Sciences of
Companion Animals, Division of Avian and Exotic Animal
Medicine, Faculty of Veterinary Medicine, Utrecht University,
Yalelaan 8, 3584 CM Utrecht, the Netherlands.
Address correspondence to: Martine de Wit, White Oak
Conservation Center, 581705 White Oak Road, Yulee, FL
32097. E-mail: MartineD@wogilman.com
© 2005 Elsevier Inc. All rights reserved.
1055-937X/05/1401-00083$30.00
doi:10.1053/j.saep.2005.12.004

6 Seminars in Avian and Exotic Pet Medicine, Vol 14, No 1 ( January), 2005: pp 6 –13
Avian Cardiac Disease 7

a role in the development of heart disease in pet

birds, and should therefore be discussed. High-fat
foods such as sunflower seeds can contribute to
obesity and subsequent cardiovascular disease.5,6

Physical Examination
Before the avian patient is manipulated for the phys-
ical examination, it is important to assess the bird’s
condition at rest. In cases with severe dyspnea, place-
ment into an oxygen cage may be indicated before
continuation of the examination.
Assessment of the peripheral circulatory system
is limited in the avian patient. Cyanosis is difficult
to detect because mucus membranes are pig-
mented in most avian species. Palpation of a pe-
ripheral pulse (eg, medial of the wing at the ulnar
artery) may assist in assessment of peripheral per-
fusion. Extremities can be checked for the pres-
ence of edema, although this is a rare occurrence
in birds with cardiovascular disease. The capillary
refill time (CRT) may be measured by applying
some light pressure on the bone-colored rham-
photheca or toenail. The hydration status of the
bird may be assessed by tenting of the skin over
the feet or the upper eyelid. The mucous mem-
branes should be moist and pink.
Auscultation of the avian heart has been re-
ported to be difficult due to the rapid heart rate Figure 1. Abdominocentesis in a love bird. A 26-gauge needle
of birds.1 Brief placement under isoflurane anes- with a length of 1.2 cm is inserted just next to the midline just
thesia has been suggested to decrease the heart caudal to the sternum in a slightly cranial direction.
rate and facilitate the evaluation of the ausculta-
tion procedure. In the author’s experience, how-
ever, abnormalities such as murmurs and arrhyth- The authors treated a hill mynah bird (Gracula reli-
mias can be detected in conscious birds with rapid giosa), weighing 280 g with severe ascites due to
heart rates. Auscultation of the heart can best be hemachromatosis. Treatment with furosemide was
performed at the base of the sternum on the left not successful in alleviating the ascites, and there-
and right ventral side. fore, the owner opted for aspiration of the fluid on
Coelomic distention may be found in birds with a regular basis. A total of 60 to 80 mL of fluid was
cardiovascular disease and may be related to ascites removed from this bird twice a week for almost half
or organomegaly due to congestion. Ascites can a year without seeing any apparent complications.
occur with right-sided and generalized heart failure. The bird eventually died of hemorrhage associated
In cases with severe ascites, abdominocentesis may with a coagulopathy caused by severe liver cirrhosis.
be indicated before other diagnostic procedures are
performed (Fig 1). The aspect of the aspirated fluid, Diagnostic Tests
followed by measurement of specific gravity, cytol-
ogy, and culture, can aid in the diagnosis of the Blood Examination. A complete blood count,
disease. The volume of aspirated fluid should be plasma biochemistry, and protein electrophoresis
sufficient to alleviate clinical symptoms caused by may help determine the origin of the heart dis-
the pressure of the fluid on the air sacs and the ease. Changes in complete blood count and pro-
heart; however, removal of larger volumes should be tein electrophoresis may indicate infectious
avoided since this may result in hypoproteinemia causes of heart disease (eg, leukocytosis in bacte-
and hypovolemia.7 Nevertheless, in some cases with rial endocarditis).8 A packed cell volume (PCV)
ascites, aspiration of large volumes of coelomic fluid over 55% has been noted in older Amazon par-
can be an important palliation if other therapy fails. rots with right heart failure associated with
8 de Wit and Schoemaker

chronic pulmonary interstitial fibrosis.9 Plasma

biochemistry panels can give information on un-
derlying causes for cardiac failure and on the
general condition of the bird. For example, liver
enzymes and bile acids might be elevated if heart
failure has caused liver congestion. Changes in
electrolyte levels are associated with cardiac ar-
rhythmias and therefore should be measured.
When measuring potassium, one should realize
that storage of blood after collection has great
influence on the concentration of that particular
electrolyte. Cooled storage will decrease concen-
tration by more than 10%, whereas storage at
room temperature will increase concentrations by
up to 20%. These changes are not seen when
plasma and cells are separated immediately after
collection.10 Plasma cholesterol may aid in the
diagnosis of atherosclerosis.5 Blood culture is in-
dicated if bacterial endocarditis is suspected.11

Radiography. Ventrodorsal and lateral radio-

graphs allow assessment of size and shape of the
avian heart (Fig 2).12 In the VD view of a normal
Amazon parrot, the cardiac silhouette as measured
across the heart base at the level of the atria is about
50% of the width of the coelomic cavity measured at
the fifth thoracic vertebra.13 Attention also should
be paid to size of the liver, presence of coelomic
density due to ascites, and great vessels.

Electrocardiography. The electrocardiogram

(ECG) is an important tool in the diagnosis of
avian cardiac disease.1 Direct indications for elec-
trocardiography are the auscultation of a murmur
or an arrhythmia and the presence of an enlarged
heart silhouette on radiography. Electrocardiog-
raphy also is useful in monitoring changes in
electrolyte concentrations and determining dif-
ferential disease diagnosis in any bird with signs of
weakness, lethargy, or seizures. For the evaluation Figure 2. Ventro-dorsal (VD) and lateral (LL) radiographs of a
of an avian ECG, a paper speed of at least 100 27-year-old blue and gold macaw (Ara ararauna) of unknown sex
mm/s (preferably 200 mm/s) and a setting of 1 that was presented with lethargy. The radiographs show an
cm ⫽ 1 mV is required.1 Isoflurane anesthesia is enlarged cardiac and hepatic silhouette.
recommended for recording ECGs in psittacines;
however, manual restraint can be used to perform complex, ST-segment, T-wave, and QT-interval
the ECG on very calm, lethargic, or moribund are measured.
birds. ECG measurements commonly are made
on the lead II rhythm strip. One unique aspect of Ultrasonography. Ultrasound (U/S) examina-
the avian ECG is the negative mean electrical axis tion of the avian heart can be very useful in the
with negative deflection of the rS-complex in diagnostic workup of cardiomegaly, heart mur-
leads II, III, and aVF. The evaluation method of murs, and presence of coelomic effusion. The
the avian ECG is similar to that in mammals. most common approach when viewing the avian
Heart rate, rhythm, axis, P-wave, P-R-interval, rS- heart is placing the transducer just caudal to the
Avian Cardiac Disease
sternum. This technique allows a view on the
heart through the liver. In most birds, U/S can be
performed under manual restraint. With the aid
of color flow Doppler enhanced ultrasonography
evaluation for the presence of pericardial fluid,
ventricular wall thickness and contractility, cham-
ber size, and valvular function is possible.12,14
Other Diagnostic Tests. Angiocardiography
and computed tomography (CT) can be useful in
the diagnosis of heart disease; however, informa-
tion on the application in avian medicine is lim-
ited and indications are rare.12,15
Management of Congestive
Heart Failure
Heart failure occurs when the heart either is un-
able to adequately deliver blood for the bird’s
metabolic demands or when it can do so only with
elevated filling pressures. Heart failure is not a
specific disease diagnosis, but a syndrome caused
by one or more underlying processes. The clinical
syndrome of congestive heart failure results from
a chronic activation of several neurohormonal
compensatory mechanisms that over-react to hy-
potension and hypovolemia.1 In response to low
blood volume, renin is released from the renal
juxtaglomerular apparatus. Renin facilitates con-
version of angiotensinogen to angiotensinogen I,
which is converted to the active angiotensinogen
II by angiotensin-converting enzyme (ACE). An-
giotensinogen II promotes aldosterone release
and vasoconstriction; aldosterone facilitates so-
dium and fluid retention. As failure worsens, neu-
rohormonal “compensation” increases. Ulti-
mately, the increased vascular volume and tone
result in edema and effusion, and prolonged va-
soconstriction further increases the workload on
the heart.
Major underlying abnormalities in dogs and
cats include myocardial failure, pressure over-
load, volume overload, and impaired filling.16
Similar etiologies can be expected in birds. Myo-
cardial failure is characterized by poor ventricular
contraction and can be caused by myocarditis,
myocardial infarction, or dilated cardiomyopathy.
Pressure overload results when the ventricle must
generate higher than normal systolic pressure to
eject blood. In birds, pulmonary hypertension de-
velops quickly due to the rigidity of pulmonary
vasculature and the relatively low colloid osmotic
pressure.17 Diseases that cause a volume overload
to the heart include defects in the valves, ventric-
9
ular septum, or large vessels. Pulmonary intersti-
tial fibrosis also may lead to a cardiac overload.9
Diseases that restrict ventricular filling may dimin-
ish cardiac output and are mainly related to con-
strictive pericardial disease.
Treatment strategies for chronic heart failure
are aimed at blocking excessive neurohormonal
activation, improving cardiac output, supporting
myocardial function, and controlling signs of con-
gestion.1 Diuretic therapy is indicated for control-
ling cardiogenic pulmonary edema and effusions.
Diuresis can be achieved with furosemide (0.15-2
mg/kg PO, SC, IM) administered every 12 to 24
hours.18 Overdosing diuretics can promote exces-
sive volume contraction and activate the renin-
angiotensin-aldosterone cascade. Therefore, the
lowest effective dose should be used.
ACE inhibitors have become the cornerstone
of therapy for dogs and cats with chronic heart
failure16 and may be useful in the treatment of
avian heart disease as well. By blocking the forma-
tion of angiotensin II, ACE inhibitors reduce the
effects of neurohormonal activation and promote
vasodilatation and diuresis. In birds, enalapril has
been dosed empirically at 0.5 mg/kg q12h PO.19
To avoid hypotension and reflex tachycardia,
therapy with ACE inhibitors is started at a low
dose including a recommendation to reduce the
concurrent diuretic dosage. Adverse effects of
ACE inhibitors include hypotension, GI upset,
renal function deterioration, and hyperkalemia.
Digoxin is indicated in heart failure caused
by myocardial dysfunction, chronic mitral insuf-
ficiency, and other chronic volume or pressure
overloads.1 It is not useful for pericardial dis-
eases and usually is contraindicated in hypertro-
phic cardiomyopathy, ventricular tachycardia,
and in birds diagnosed with sinus or atrioven-
tricular node disease. Digitalis glycosides are
positive inotropic, and their antiarrhythmic ef-
fects are mediated primarily via increased para-
sympathetic tone to the sinus and AV nodes and
the atria.16 This results in slowing of the sinus
rate, a reduced ventricular response rate to
atrial fibrillation and flutter, and suppression of
atrial premature depolarizations. Reported dos-
ages of digoxin in birds range from 0.0219,20 to
0.0519,21 mg/kg q24h PO. However, elimination
times vary strongly; to achieve therapeutic se-
rum concentrations, in a macaw with heart fail-
ure, the authors had to increase the digoxin
dosage to 0.1 mg/kg. Myocardial toxicity from
digitalis glycosides can cause almost any cardiac
rhythm disturbance, occurring before any other
10
clinical signs appear. To evaluate therapeutic
response in the avian patient being treated with
digoxin, one should monitor the ECG for a
prolonged PR-time, measure therapeutic serum
concentrations, and observe for clinical im-
provement. The therapeutic serum concentra-
tion range has been determined to range from
1 to 2.4 ng/mL. Measurement of serum concen-
tration is recommended at 7 to 10 days after
initiation of therapy, with samples being drawn
8 to 10 hours after the previous dose.16 If the
serum concentration is less than 0.8 ng/mL, the
digoxin dose can be increased by up to 30%. It
is important to remeasure the serum concentra-
tion the following week after the beginning of a
new dose regime. If toxicity is suspected, ther-
apy should be discontinued for 1 to 2 days and
then reinstituted at half the original dosage.
Cardiovascular Diseases
Endocardial Disease
The most common etiology of avian endocardial
disease is infection; other causes include degen-
erative and idiopathic disease. Bacterial valvular
endocarditis has been reported in a variety of
avian species8,22-25 and can result from chronic
infections such as salpingitis, hepatitis, and podo
dermatitis.1 Endocardial infections often are the
result of heart exposure to blood-borne bacteria.
After damage to the valves by alterations in the
blood flow through the heart, the endocardial
surface of the valve can be infected by the bacteria
found in the circulating blood. Lesions may ex-
tend from the endocardium to the myocardium.
Valve insufficiency commonly results in volume
overload, which ultimately may lead to congestive
heart failure. Other infectious etiologies for en-
docarditis include parasitic infections (eg, heart-
worm disease26 and trichomoniasis27) and nonin-
fectious causes of endocardial disease (eg, myxo-
matous degeneration,28 endocardial fibrosis,29
and idiopathic valve insufficiency20).
Auscultation of a murmur during the physical
examination may indicate endocardial disease.
Diagnosis of endocardial disease can be difficult
and is made on the basis of a positive blood
culture in addition to echocardiographic evi-
dence of valve lesions.11 Endocarditis is a possible
differential diagnosis even when blood culture
results are negative. Electrocardiographic find-
ings may be normal and radiography often is
unremarkable until the development of conges-
tive heart failure. Aggressive therapy with bacteri-
de Wit and Schoemaker
cidal antibiotics (eg, enrofloxacin or amoxicillin/
clavulanate) is indicated for birds with infective
endocarditis. Antibiotic drug choice is ideally
guided by blood culture and sensitivity results
with supportive care including treatment for con-
gestive heart failure.
Myocardial Disease
Myocardial diseases can result in poor myocardial
contractility, cardiac chamber enlargement, and
arrhythmias. Myocardial disorders that are associ-
ated with impaired contractile function include
primary idiopathic cardiomyopathy and second-
ary mycocardial diseases caused by inflammation,
ischemia, neoplasia, toxicity, and metabolic ab-
normalities.1 Infectious causes are varied and
include agents such as E. Coli, Pasteurella spp.,
polyoma virus,1 sarcocystis,30 and toxoplasma.31
Myocarditis also has been described as a compo-
nent of proventricular dilation disease.32,33
In cases with myocardial disease, radiography
may reveal cardiomegaly. ECG findings may in-
clude cardiac arrhythmias, a right heart axis devi-
ation from negative to positive, an increase in the
amplitude of the P-wave and a negative T-wave in
leads I, II, and III.34 Echocardiography is the best
diagnostic tool in birds with cardiomyopathy,12,14
assessing dilation of cardiac chambers, thickness
of the ventricular muscle, and myocardial func-
tion. Therapy is aimed at controlling the signs of
congestive heart failure, optimizing cardiac out-
put, managing arrhythmias, and treatment of the
underlying cause.1 Inotropic support such as
digoxin is prescribed to increase cardiac output,
arterial pressure, and stroke volume. ACE inhibi-
tors can improve cardiac output and have been
reported to have a positive effect on survival in
humans and dogs with myocardial failure. Di-
uretic therapy with furosemide is indicated when
volume overload is a problem in cases with pul-
monary edema or ascites.
Pericardial Disease
Pericardial effusion is the most common pericar-
dial disorder. The accumulated fluid may be ex-
udate, transudate, or hemorrhage. Exudates are
often the result of bacterial, viral, or mycotic in-
fections.1,35 Transudative effusions may be related
to congestive heart failure or hypoalbuminemia.1
Pericardial effusion may, just as in dogs, be of
idiopathic origin. Hemopericardium may be
caused by trauma, neoplasia, or rupture of the left
atrium.1 Accumulation of pericardial fluid causes
external compression on the heart muscle, which
Avian Cardiac Disease
progressively limits filling and decreases cardiac
output. Fibrinous pericarditis is a disease condi-
tion where adhesions of the pericardium may lead
to constrictive heart failure.1 In cases with pericar-
dial effusion, radiography may demonstrate en-
largement of the cardiac silhouette. Ultrasonog-
raphy is used to differentiate pericardial effusion
from cardiomegaly when the cardiac silhouette is
enlarged. Electrocardiography, another diagnos-
tic parameter, may demonstrate a low-voltage
ECG in these patients. Treatment should be
aimed at management of the initiating etiology.
Furosemide use is considered contraindicated
due to the severe hypertension seen in pericardial
disease patients. If the pericardial effusion devel-
ops into cardiac tamponade, pericardiocentesis is
the therapy of choice. Endoscopic fenestration of
the pericardium is recommended for collection
of pericardial fluid and may prevent refilling of
the pericardium. The collected fluid should be
cultured and submitted for a cytological evalua-
tion. The endoscopic approach to the heart
should be through the ventral hepatic peritoneal
cavities to prevent drainage of fluids into the air
sacs. Because the entire pericardium cannot be
removed, it is possible that the surgical opening of
the pericardium will close. This closure often will
result in a recurrence of the pericardial effusion.
Cardiac Arrhythmias
Although cardiac arrhythmias often are diag-
nosed, there are relatively few cases in which the
arrhythmias are determined to be of clinical con-
sequence.36 When selecting an appropriate ther-
apy, it is important to correlate an accurate ECG
diagnosis with the bird’s clinical appearance. The
origin of an arrhythmia can be localized in the
sinoatrial (SA) node, atria, junctional area, atrio-
ventricular (AV) node, or ventricles.1
Electrocardiography is essential when specifi-
cally diagnosing cardiac arrhythmias. Sinus ar-
rhythmias are usually bradycardias caused by a
lack of atrial activation during the expected sinus
rhythm and result in a pause recorded on the
electrocardiogram (ECG). The ECG demon-
strates unequal P-P intervals and associated S-S
intervals. Physiologic sinus arrhythmia can be re-
lated to vagal stimulation in association with the
respiratory cycle.37,38 Pathologic conditions that
may induce sinus arrhythmia include hyperkale-
mia,39 hypothermia, or diseases that increase vagal
tone.1 When the arrhythmia is caused by patho-
logic conditions of the atrium, the ECG usually
reveals tachycardia characterized by abnormal P
11
waves with normal rS complexes. An example of
atrial arrhythmia is atrial fibrillation, character-
ized by a permanent diastole of the atrium, with
baseline undulations instead of P waves on the
ECG. Junctional tachycardias can be diagnosed by
the presence of negative P waves in lead II. AV
blocks lead to bradycardia with a delay of impulse
conduction through the AV node or complete
interruption of impulses from the atria to the
ventricles. In first-degree AV block, P-R intervals
are prolonged, but all P waves are followed by rS
complexes. In second-degree AV block, there is
failure of some atrial impulses to reach the ven-
tricles. Mobitz type I second-degree AV block is
characterized by progressive lengthening of the
P-R interval until a ventricular beat is dropped.
Mobitz type II second-degree AV block shows a
fixed P-R interval with occasional missing of the rS
complexes. Third-degree AV block represents to-
tal disruption of atrioventricular conduction.
Atria and ventricles beat independently of one
another, whereby the ventricular rate usually is
slower than the atrial rate. AV conduction distur-
bances may result from certain drugs (eg,
digoxin), high vagal tone, bacterial endocarditis,
cardiomyopathy, or myocarditis. Ventricular ar-
rhythmia causes tachycardia with ventricular pre-
mature contractions (VPCs), which are character-
ized by the occurrence of rS complexes that are
unrelated to P waves. VPCs are associated with
hypokalemia, cardiomyopathy, myocarditis, viral
infection, hypoxia, or digoxin toxicity.1
In addition to the ECG, diagnostic tests such as
CBC, plasma biochemistry and protein electro-
phoresis, blood culture, radiography, and echo-
cardiography should provide information on the
possible underlying etiology for the arrhythmia.
If arrhythmias cause hemodynamic instability
in the bird, treatment is necessary. Treatment of
arrhythmias is directed at the underlying cause
and possibly antiarrhythmic drugs or therapeutic
agents for cardiovascular support may be used.
Because there are no references on the clinical
use of antiarrhythmic drugs in avian medicine,
most treatment protocols are extrapolated from
antiarrhythmic therapy in the dog and cat. In
cases with supraventricular tachycardia (eg, atrial
fibrillation), treatment is directed at slowing AV
conduction, allowing more time for ventricular
filling, which reduces the relative importance of
atrial contraction. The initial drug of choice in
cases of supraventricular tachycardia is digoxin,36
but a beta-blocker can be added to further de-
crease AV conduction and ventricular rate. Beta-
12
blockers reported in birds include propanolol 0.2
mg/kg IM and oxprenolol 2 mg/kg PO q24 h in
turkeys.18,40 Because digoxin can predispose to the
development of ventricular arrhythmias, it is not
the first-choice drug in the treatment of ventricu-
lar tachyarrhythmias. Beta-blockers can be useful
in the treatment of these arrhythmias. In the
treatment of bradycardias and AV blocks, pharma-
cological therapy is usually of limited value. How-
ever, anticholinergic or sympathomimetic agents
are sometimes administered to try and increase
the ventricular response rate and reduce signs
associated with severe bradyarrhythmias. Admin-
istration of atropine usually corrects bradycardia
and AV blocks that are related to high vagal tone.
The sympathomimetic drug epinephrine (0.1
mg/kg IV, IT, IO, IC) has been described for
treating cardiac arrest in birds.18 The authors
treated a gray parrot (Psittacus erithacus) with bra-
dycardia and second-degree AV block with the
sympathomimetic drug ephedrine (0.5 mg/kg PO
q8 h) without any adverse reactions for more than
1 year.
Congenital Cardiac Disease
Several congenital heart defects have been re-
ported in birds, which include ventricular septal
defect,41,42 persistent truncus arteriosus, and aor-
tic hypoplasia.42 Most cases result in death at an
early age because the abnormal heart anatomy
prevents the organ from functioning at a life-
sustaining level as the bird grows.43
Atherosclerosis
Atherosclerosis is characterized by degenerative
changes in the internal and medial tunics of the
wall of muscular and elastic arteries. The degen-
erative lesions can include proliferation of
smooth muscle cells, deposition of collagen and
proteoglycans, and deposition of cholesterol or
calcium.1 Atherosclerosis has been reported in
many avian orders and is a common disease
among parrots. Amazon3,4 and gray parrots5 seem
to be specifically prone to atherosclerosis. Athero-
sclerotic lesions are located primarily in the be-
ginning of the aorta and the brachiocephalic
trunk. Atherosclerosis is a disease of older birds,4,5
and is seen in both males and females.3,5 Sug-
gested risk factors include a high-fat diet with a
low concentration of polyunsaturated fatty acids,44
obesity, and an elevated plasma cholesterol
level.1,5 Unfortunately, most cases of atherosclero-
sis are diagnosed after death because clinical signs
are subtle and may be attributed to decreased
de Wit and Schoemaker
blood flow to tissues. Radiographs may demon-
strate increased density and size of affected ves-
sels, and ultrasonography may detect atheroscle-
rotic processes close to the heart. Angiography
was used to detect an aneurysm of the right cor-
onary artery in a cockatoo,15 and cardiac dilation
with a reduction in blood flow through the aorta
and brachiocephalic arteries in a macaw,45 both of
which were confirmed to be related to athero-
sclerosis at necropsy. Treatment is based on clin-
ical signs; however, information on therapies is
limited. Study models on the development of ath-
erosclerotic plaques in poultry demonstrated a
preventative effect of beta-blockers40,46 and a re-
gressive effect of calcium channel-blockers.47 It
also has been speculated that a high dietary intake
of alpha linolenic acid may protect against the
development of atherosclerosis in parrots.5
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