होम Journal of Medical Primatology The normal and abnormal owl monkey (Aotus sp.) heart: looking at cardiomyopathy changes with...

The normal and abnormal owl monkey (Aotus sp.) heart: looking at cardiomyopathy changes with echocardiography and electrocardiography

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खंड:
39
साल:
2010
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DOI:
10.1111/j.1600-0684.2010.00403.x
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J Med Primatol doi:10.1111/j.1600-0684.2010.00403.x

ORIGINAL ARTICLE

The normal and abnormal owl monkey (Aotus sp.) heart:
looking at cardiomyopathy changes with
echocardiography and electrocardiography
Rashmi S. Rajendra1, Alan G. Brady2, Virginia L. Parks2, Clara V. Massey3, Susan V. Gibson1 &
Christian R. Abee2
1 Center for Neotropical Primate Research and Resources, University of South Alabama (USA), Mobile, AL, USA
2 Department Veterinary Sciences, Michale Keeling Center, UT MD Anderson Cancer Center, Bastrop, TX, USA
3 Division of Cardiology, Department of Medicine, USA College of Medicine, Mobile, AL, USA

Keywords
Aotus sp. – cardiology – cardiomyopathy –
echocardiography – electrocardiography –
heart
Correspondence
Dr Alan Brady, Michale Keeling Ctr., UT MD
Anderson Cancer Center, 650 Cool Water
Dr., Bastrop, TX 78602, USA.
Tel.: 512/332 7360;
fax: 512/332 7366 or 5208;
e-mail: agbrady@mdanderson.org
Accepted January 6, 2010.

Abstract
Background Cardiovascular disease, especially cardiomyopathy, was the
major cause of death among owl monkeys (Aotus sp.) at a major colony
and threatened colony sustainability. For this study, echocardiography
(echo) and electrocardiography (ECG) normal values were established, and
cardiomyopathy animals identified.
Methods Forty-eight owl monkeys were studied, 30 older than 10 years of
age (‘aged’) and 8 of age 5 years (‘young’). Eight aged owl monkeys had
cardiomyopathy.
Results and Conclusions Aged Aotus had increased left ventricular posterior
wall thickness over young animals. Left ventricular diameter and ejection
fraction appeared to be the best identifying measurements for cardiomyopathy. There were no differences in the ECG.

Introduction
Cardiovascular disease is the major cause of death
among owl monkeys at the University of South
Alabama Center for Neotropical Primate Research
and Resources (CNPRR). In addition, cardiovascular
disease has been identified as the most important
problem in maintaining a self-sustaining breeding
colony (Akkoc CC, Personal;  Communication, 2005).
Owl monkeys are the only nocturnal primates. They
are a tree dwelling genus and are found in the Amazon
Basin of South America and in Central America. They
reach a maximum size of 1.5–2.0 kg. Owl monkeys
become sexually mature at 3 years of age and are full
grown at 5 years [1].
At the Batelle Primate Facility in Richland,
Washington, a 1994-report stated that forty percent of
owl monkeys that died showed some evidence of
J Med Primatol 39 (2010) 143–150
ª 2010 John Wiley & Sons A/S

cardiovascular disease, such as a large globose heart
caused by ventricular dilation or concentric left ventricular hypertrophy [2]. At the CNPRR colony, we
have also observed left ventricular hypertrophy in
some owl monkeys (Brady AG and Abee CR, Unpublished data, 2003). Spontaneous death of owl monkeys
may occur during periods of high stress or physical
activity [2]. Many monkeys may display no clinical
signs of heart disease before death. Other animals may
die suddenly during or after routine manipulations
such as weighing or cage changes.
Although observations at the CNPRR have shown
that many owl monkeys do not show clinical signs of
cardiovascular disease before death, some monkeys
may develop clinical signs that can be associated with
heart failure. Those signs include ascites, dyspnea,
mouth breathing, reduced exercise tolerance, subcutaneous edema [2], and hepatomegaly. Some owl
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Heart disease, echo, ECG in owl monkeys

monkeys also have partial or complete paralysis caused
by secondary thromboembolic disease [3]. Microscopic
lesions, such as arteriolosclerosis in the small vessels of
the kidney, heart, and small intestine, and microthrombi or emboli in multiple sites have also been
identified in owl monkeys post-mortem. Interestingly,
these lesions have also been found in humans with
chronic severe hypertension [17].
Cardiomyopathy causes the weakening of the heart
muscle [2]. Echocardiography (Echo) is effective for
diagnosing cardiomyopathy when combined with other
diagnostic modalities, such as physical examination,
laboratory analysis, radiology, and electrocardiography
(ECG) and provides information about other cardiovascular diseases as well. It allows for the study of cardiac function and provides measurements of wall
thickness, chamber size, and ejection fraction (EF) by
using measurements of left ventricular diameter at
diastole and systole, interventricular septum at diastole, and left ventricular posterior wall at diastole [5].
This technique is non-invasive and allows the studies
to be carried out rapidly, which is important in small,
medically compromised animals. An electrocardiogram
(ECG) can also be taken, while the animal is anesthetized. Parameters that are measured in the ECG
included PR, P, and QRS duration, QT interval, and
atrial and ventricular rate.
A study that used both echo and ECG has been performed at the Center for Neotropical Research and
Resources on squirrel monkeys. This study established
normal echo and ECG values and compared ECG values of squirrel monkeys and human infants [6]. The
2003-study also identified monkeys that had cardiomyopathy [5]. In 2005, Rishniw and colleagues published
echocardiographic data and evaluation for owl monkeys with cardiomyopathy in captivity. They found
that the echo parameters for left ventricular end-systolic cross-sectional area and left ventricular fractional
area change were the two echo parameters that showed
the greatest difference between healthy monkeys and
cardiomyopathy monkeys [7]
The objectives of the present study were to establish
a set of normal parameters for both echocardiography
and ECG for healthy owl monkeys at our center and
to identify animals with the evidence of cardiomyopathy before the onset of disease. This study also compares the echocardiographic and electrocardiographic
trends of cardiomyopathy in owl monkeys to those
found in the previous studies on squirrel monkeys and
humans. Specifically, we wished to:
l Determine normal parameters of both echocardiography and ECG for healthy owl monkeys (Based on echo,
absence of clinical signs and physical examination).
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Rajendra et al.

Parameters for echocardiography included EF, left ventricular diameter at end-diastole (LVDd) and end-systole (LVDs), interventricular septal thickness at enddiastole (IVSd), and left ventricular posterior wall thickness at end-diastole (LVPWd). Parameters for ECG
included P wave amplitude, P, PR, and QRS duration,
QT interval, and atrial and ventricular rate.
l Identify owl monkeys with the evidence of cardiomyopathy using the above parameters before the onset of
the disease, and study the disease progression of two
representative cases.
Materials and methods
The University of South Alabama Institutional Animal
Care and Use Committee approved this study. All animals were housed at the CNPRR at the University of
South Alabama at the time of the study. The Owl
Monkey Breeding and Research Resource at the
CNPRR consists of approximately 300 animals.
Species in the colony include Aotus nancymai, Aotus
vociferans, Aotus azarae, and a small number of hybrid
animals. Approximately 20% of animals were feralsource. Animals are socially housed whenever possible
(either in male–female or same-sex pairs) in stainless
steel cages measuring 83 cm · 83 cm · 71 cm. Diet
consisted of a nutritionally balanced monkey biscuit
(Purina 5049 Fiber Plus, Purina LabDiet, St. Louis,
MO, USA) and a canned diet (Zupreem Primate
Diet, Zupreem, Shawnee, KS, USA). Diet was also
supplemented with a variety of fresh fruits and vegetables. Thirty animals, age 10 years or older, were the
aged animal group in this study. Animals that were
feral-source had to be documented as being in captivity longer than 10 years. Ten owl monkeys at age
5 years were selected as a control group. ECGs and
echos were recorded using the animal anesthetized with
ketamine or isoflurane. The animals were given 30 mg
ketamine by intramuscular injection. Medically, fragile
animals were anesthetized using isoflurane. Anesthesia
was induced with a mixture of oxygen and 4–5%
isoflurane and maintained with 1–3% isoflurane. Both
the echo and ECG were performed only once for each
animal, unless the animal showed signs of cardiomyopathy, such as ascites, dyspnea, mouth breathing
exercise intolerance, subcutaneous edema, and hepatomegaly. Nephropathy and severe anemia are also seen
in owl monkeys, and may show similar clinical signs
but are ruled out by hematology and serum chemistry
testing. If signs were seen, the frequency of the echo
and ECG examinations was increased based on the
progression of the disease. If an owl monkey was identified as healthy initially, and during the course of the
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Rajendra et al.

study showed signs of cardiomyopathy, then that animal was excluded from the study for healthy animals
and identified as having cardiomyopathy. Many of the
research techniques that were used are similar to published squirrel monkey studies [5, 6]. Diagnosis of cardiomyopathy was based on the presence of clinical
signs described above and confirmation by ultrasound.
Other testing was performed as described above to rule
out renal disease and severe anemia.
ECG study
The ECG was recorded after anesthesia induction, but
before echo was performed to allow time for muscle
relaxation. ECGs were recorded using a Welch Allyn
AT-1 electrocardiograph (Welch Allyn Inc., San
Diego, CA, USA), and skin contact was made by the
application of Welch Allyn disposable ECG Electrodes, which are adhesive gel pads. Lead placement
was standard as performed in humans (Leads 1, 2, 3
AVR, AVL, AVF) [6]. All ECGs were recorded at a
chart speed of 50-mm sec, and the gain was adjusted
to 1-cm deflection per millivolt [6]. A 5 mm · 5 mm
patch of fur was clipped from the medial surface of
the forearms and ankle for lead placement. The ECG
was recorded using the animal positioned in right lateral recumbency. The intervals recorded include PR, P,
and QRS duration, QT interval, and the atrial and
ventricular rate. These were defined in accordance with
standard clinical usage [8, 9].
Echocardiography study
Echo was performed using a Siemens Accuson Aspen
Ultrasound Machine with a V7 transducer (Siemens
Accuvue, Mountain View, CA, USA). Chest fur was
removed with clippers.
The transducer was placed in parasternal, apical, or
subcostal areas of the chest and set to a penetration
depth of 30–40 mm and a frequency of 7.0 MHz. The
animals were positioned in dorsal recumbency, and a
foam wedge was used as a positioning aid in most
cases. The views that were recorded included parasternal long axis, parasternal short axis, apical four chamber, apical five chamber, and M-modes of the mitral
valve, left ventricle, aortic valve, and left atrium. Placement of the transducer initially began to the right of
the sternum and was then moved ventrolaterally to the
right pectoralis major muscle. The transducer was then
moved deep to the lateral edge of the pectoralis major
muscle. The transducer reference mark was oriented
craniad. This position allowed for an unobstructed
path to and from the free wall of the heart by directing
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Heart disease, echo, ECG in owl monkeys

the beam around, instead of through the sternum. This
positioning also allowed for the parasternal long-axis
view. The short-axis view was obtained by keeping the
transducer in the same position as the long-axis view,
but it was rotated until the view had been obtained.
To view all four heart chambers, the transducer was
positioned subcostally on the left side. These techniques have been used previously in neotropical primates [5]. The parameters recorded include wall
thickness, EF, LVDd and systole, interventricular
septal thickness at end-diastole.
Statistical analysis
Echocardiography and ECG parameters were analyzed
using one-way analysis of variance. The groups of
monkeys analyzed included healthy owl monkeys, age
10 years and older, cardiomyopathy owl monkeys, age
10 and over, and the control group, age 5 years. Comparisons were made between the healthy monkeys (age
10 and over) and the control group to establish normal
parameters. These were then compared to the values
found for those owl monkeys found to have cardiomyopathy. Echocardiography provides excellent visualization of the left ventricle and readily distinguishes the
three major forms of cardiomyopathy. Dilated cardiomyopathy is characterized by dilated chambers, most
prominently the left ventricle, and reduced EF [10]. All
colony animals are necropsied. Necropsy cardiac examination findings are compared with those obtained ante
mortem by echocardiographic examination with excellent agreement. For this reason, we consider echocardiographic results to be diagnostic for cardiomyopathy.
The groups compared for statistical analysis are the
control vs. aged, healthy monkeys, control vs. cardiomyopathy monkeys (age 10 and over), and healthy
(age 10 and over) vs. cardiomyopathy monkeys (age 10
and over). In addition, data were analyzed from aged,
healthy owl monkeys in comparison with one of the
owl monkeys that had cardiomyopathy. A separate
one-way analysis of variance (ANOVA) was conducted
for each parameter measured, with each One-Way
ANOVA comparing the three groups. A P value of
<0.05 was considered to be significant. Post-hoc tests
were conducted to determine which groups were different. Post-hoc testing was used to check for statistical
differences in the ECG and echo between the control
group and the healthy group.
In addition, comparisons between the parameters
that define cardiomyopathy in owl monkeys were compared with parameters of squirrel monkeys and
humans [5]. A statistical analysis software package,
Sigma Stat, was used to analyze the data, and graphs
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Rajendra et al.

were made using Sigma Plot (Systat Software, Point
Richmond, CA, USA).
Results
A total of 48 owl monkeys were studied. There were
10 owl monkeys in the control group (age five) and 38
monkeys age 10 and over. Thirty were classified as
healthy, and eight were diagnosed as having cardiomyopathy. The control group had six males and four
females. The healthy group had 25 males and five
females. The cardiomyopathy group had four males
and four females.
Diagnosis of cardiomyopathy was based on physical
examination, supplemented by imaging (ultrasound,
radiology) and laboratory analysis (serum chemistry,
hematology), to rule out other diseases with similar
presentations, such as renal and pulmonary disease.
Disease other than cardiomyopathy was ruled out for
all animals in this study.
The comparison groups had no significant differences in the ECG parameters. Normal parameters for
ECG were established for healthy owl monkeys age 10
and over (Table 1). In the comparison of healthy aged
owl monkeys with the control group, there were no
significant differences in EF, left ventricular diameter
at diastole and systole, interventricular septal thickness
at end-diastole, and data for each parameter are not
included. The LVPWd for healthy owl monkeys was
23% higher than the control group (Fig. 1). Normal
parameters for ECG and Echo were established for
healthy owl monkeys age 10 and over (Tables 1 and 2).
Two cases illustrate the range of clinical progression
with owl monkey cardiomyopathy and suggest the
potential usefulness of prognostic indicators for the
disease:
Case one
Eleven-year-old domestically born male was identified
on a research echo as having left ventricular hypertrophy and aortic root dilation. Echo was repeated at 6,
9, and 34 weeks post-presentation. There was no
progression of any of the abnormal measurements

Fig. 1 The LVPWd for healthy owl monkeys had a 23% increase
when compared to the control group (P < 0.05). In addition, there
was a 22% increase in cardiomyopathy monkeys when compared
to the control group (P < 0.05). The a above the graph represents
that both healthy and cardiomyopathy were greater than control.

during this time. The animal remains alive and asymptomatic at the time of this report.
Case two
Twelve-year-old domestically bred male presented for
ascites on September 10, 2001. The animal was treated
with 12 mg furosemide PO twice daily until March 20,
2006, when an echocardiogram showed poor contractility, pericardial effusion, an aortic aneurysm, and
an EF of 25% (Fig. 5, see Fig. 4 for comparison).
Two milligrams enalopril (Enacard, Merial Ltd,
Duluth, GA, USA) and 25 mg spironolactone (both
twice daily, Aldactone, Pharmacia, Chicago, IL,
USA) were added to treatment. The animal’s condition
stabilized until April 3, 2006, when deterioration was
again noted, and another echo was performed that
revealed worsening pericardial effusion and an EF of
16%. The animal was euthanatized. Necropsy confirmed pericardial effusion, aortic aneurysm, hepatomegaly and revealed pulmonary edema, cardiomegaly,
and glomerulonephritis.

Table 1 Electrocardiography mean values with standard error for control, healthy, and cardiomyopathy owl monkeys

Control
Healthy 10+
CM

146

Atrial rate
(/minutes)

Ventricular
rate (/minutes)

P-Wave
amp (mm)

P-Wave
duration (s)

PR interval
(s)

QRS
interval (s)

QT
interval (s)

237 ± 16.6
225 ± 6.3
218 ± 17.3

237 ± 16.6
225 ± 6.3
218 ± 17.3

2.3 ± 0.3
2.7 ± 0.2
2.9 ± 0.4

0.03 ± 0.0
0.03 ± 0.0
0.04 ± 0.0

0.1 ± 0.0
0.1 ± 0.0
0.1 ± 0.0

0.04 ± 0.0
0.04 ± 0.0
0.1 ± 0.0

0.1 ± 0.0
0.2 ± 0.0
0.1 ± 0.0

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Rajendra et al.

Echocardiography data is shown in Table 1. When
comparing cardiomyopathy owl monkeys with the
healthy old and young groups, significant differences
were seen in the parameters EF, LVDd and end-systole,
and left ventricular posterior wall thickness at end-diastole. The interventricular septal thickness at end-diastole had no differences between any of the comparison
groups. The EF was 40% lower when compared to
both the healthy (P < 0.017) and control (P < 0.025)
groups (Fig. 2). Cardiomyopathy monkeys had a 19%
increase when compared to healthy (P < 0.017) and a
14% increase when compared to the control group
(P < 0.025) for the LVDd (Fig. 3). The left ventricular
diameter at end-systole (LVDs) had a 36% increase in
cardiomyopathy monkeys, when compared to healthy
monkeys (P < 0.017), and a 25% increase when compared to the control group (P < 0.025). The left ventricular posterior wall thickness at end-diastole had a
22% increase in cardiomyopathy monkeys when compared to the control group (P < 0.05) (Fig. 1).
The owl monkey in case one was compared with the
healthy owl monkeys age 10 and over. This monkey
had cardiomyopathy based on his echo. Both IVSd
and IVSs were 38% thicker when compared to the
healthy group. LVPWd was 28% thicker when compared to the healthy group.
Discussion
Our study examined the echocardiographic and electrocardiographic parameters to establish normal values

Fig. 2 The ejection fraction (EF), which is a measure of pump function, was decreased by 40% in cardiomyopathy owl monkeys when
compared to both the healthy owl monkeys (P < 0.017) and control
owl monkeys (P < 0.025). The * above the graph represents that
both control and healthy owl monkeys have a greater EF than cardiomyopathy owl monkeys.
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Heart disease, echo, ECG in owl monkeys

Fig. 3 The left ventricular diameter at end-diastole (LVDd) for cardiomyopathy owl monkeys increased by 19% when compared to
the healthy owl monkeys (P < 0.017) and increased by 14% when
compared to the control owl monkeys (P < 0.025). The * above the
graph represents that both control and healthy owl monkeys have a
decreased LVDd than cardiomyopathy monkeys.

for healthy owl monkeys, age 10 and over, and to
identify owl monkeys that had cardiomyopathy. We
found significant changes in parameters for those owl
monkeys that were identified as having cardiomyopathy compared with healthy owl monkeys age 10 and
over and the 5-year-old control group. There was also
a change in parameters for healthy owl monkeys age
10 and over when compared to the control group.
To determine whether there was a change in any of
the echo parameters based on increasing age, a comparison was made between healthy owl monkeys, age
10 and over, and the control group (age 5 years). The
left ventricular posterior wall thickness at end-diastole
was increased in the older healthy group when compared to the control group. In human adults, thickening of the posterior wall is attributed to cardiovascular
diseases such as hypertension and coronary disease
[11]. We speculate that an increase in left ventricular
posterior wall thickness in owl monkeys may also be
attributed to hypertension. From these results, we conclude that aging owl monkeys are more likely to have
an increase in LVPWd than younger owl monkeys.
Increase in myocardial wall dimensions is associated
with aging in humans. Other risk factors for hypertrophy include hypertension, obesity, and valvular heart
disease [4]. In our experience, valvular heart disease
and obesity are rare in owl monkeys.
Decrease in EF indicates decreased pumping capacity and is usually associated with systolic heart failure
in humans [12]. Cardiomyopathy owl monkeys had an
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Rajendra et al.

Table 2 Echo mean values with standard error for control, healthy, and cardiomyopathy owl monkeys

Control
Healthy 10+
CM

Ejection
fraction (%)

Left
ventricular
diameter at
end-diastole
(cm)

Left
ventricular
diameter at
end-systole
(cm)

Interventricular
septal
thickness
at end-diastole
(cm)

Left
ventricular
posterior wall
thickness at
end-diastole (cm)

68.1 ± 3.0
68.2 ± 2.1
41.3 ± 5.9

1.3 ± 0.0
1.2 ± 0.0
1.5 ± 0.0

1.0 ± 0.0
0.9 ± 0.0
1.2 ± 0.1

0.3 ± 0.0
0.3 ± 0.0
0.3 ± 0.0

0.3 ± 0.0
0.4 ± 0.0
0.3 ± 0.0

increase in LVPWd. LVPWd was increased in all older
owl monkeys, regardless of whether they were diagnosed with cardiomyopathy or not. This increase is
indicative of left ventricular hypertrophy [11]. These
kinds of changes are also seen with advanced age in
humans [4]. Although the squirrel monkey study [5]
found that LVDd was not identified as clinically
important, we believe that it may be clinically important in owl monkeys. A previous owl monkey study
documented an increase in LVDd and LVDs, which
are possibly associated with systolic heart failure [7].
We conclude that cardiomyopathy owl monkeys may
show differences in EF, LVDd and end-systole.
The first published echocardiographic values for
both normal and cardiomyopathy owl monkeys [7]
contain both similarities and differences when compared to our study. The first study found that the most
reliable parameters that distinguished between normal
and cardiomyopathy owl monkeys were the left ventricular end-systolic cross-sectional area and left ventricular fractional area change. They found that
monkeys that developed cardiomyopathy had an
increase in left ventricular diameter at systole. Our
study did not include these as parameters of study,

because cross-sectional area is no longer commonly
used in primate species because of improvements in
echocardiographic imaging. We used instead EF as a
measure of pump function. The EF is derived from the
fractional shortening (end-diastolic diameter minus
end-systolic diameter divided by end-diastolic diameter, times 1.7) [13]. In our study, LVDd and EF appear
to be the most important identifying factors of cardiomyopathy in owl monkeys.
Approximately five million patients in the United
States have heart failure [12]. Owl monkeys may be
useful as a model for heart failure in humans. In our
study, three monkeys exhibited the four stages in evolution of heart failure, which was published by the
American College of Cardiology and American Heart
Association. This classification scheme is inclusive of
all types of cardiovascular diseases and not just cardiomyopathy. Stage A identifies a patient that is at risk of
heart failure but does not have a structural disorder of
the heart. In this study, stage A would be represented
by healthy aged owl monkeys, because cardiomyopathy is the most common cause of death in this colony.
Stage B identifies patients that have a structural disorder of the heart but show no symptoms of heart

Fig. 4 Normal parasternal long-axis view for a healthy owl monkey.
MV = mitral valve; LV = left ventricle; LVPW = left ventricular posterior wall; S = interventricular septum; LA = left atrium; AV = aortic valve; RV = right ventricle.

Fig. 5 Parasternal long-axis view of the owl monkey in case one,
where the arrow indicates thickening of left ventricular posterior
wall, and the asterisk indicates thickening of the septum.

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Rajendra et al.

failure. In our study, stage B is represented by healthy
owl monkeys that had an increase in wall thickness,
demonstrated by an increase in left ventricular posterior wall thickness at end-diastole. In humans, this
increase is associated with hypertension or infiltrative
disease [11]. The third stage, stage C, represents
patients that not only have structural heart disease,
but also have had past or current symptoms. Owl
monkey one exhibited an increase in interventricular
septum thickness at end-diastole, which is associated
with left ventricular hypertension in humans. The
increase in left ventricular posterior wall thickness at
end-diastole and subjective 2D assessment in the parasternal long-axis view demonstrated left ventricular
hypertrophy in this animal (Fig. 5). Left ventricular
hypertrophy may also be seen in humans at stage C.
In stage D, patients have clinical signs that are refractory to treatment [12]. Owl monkey two exhibited this
type of end-stage heart failure. Not only did this monkey exhibit poor contractility and both left and right
ventricular hypertrophy, but it also had pericardial
effusion. Additional findings at necropsy included dilatation of the ascending aorta and a dissecting aortic
aneurysm that extended into the renal arteries. In addition, this owl monkey exhibited nephropathy. Most
owl monkeys with cardiomyopathy also have nephropathy [14].
An unexpected finding in this study was the large
number of animals that were identified with cardiomyopathy. This strengthened our comparison studies for
the control, healthy, and cardiomyopathy monkeys.
Studies using non-human primates may have
increased variability, because some animals may be of
feral origin or their genetic backgrounds may not be
well characterized. Most animals in this study were
domestically bred and have known pedigrees. This
reduces some of this variability. Subject animals were
not directly related. The echo imaging may also have
variability from one animal to another. This underscores the need to examine echo findings in the broader
context of findings from physical examination, laboratory results, echo, and husbandry observations. The
variability in imaging technique was reduced by using
the same sonographer and using the same methodology
previously developed and tested in squirrel monkeys.
Anesthesia may also be a source of variability. In
studies with children with congenital heart disease, the
use of isoflurane as an anesthetic increased heart rate
and lowered vascular resistance but maintained systemic cardiac output, with little change in contractility
[15]. Thus, the use of isoflurane vs. other halogenated
anesthetics, such as halothane, is favored during echo
examinations of medically fragile animals. Although
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Heart disease, echo, ECG in owl monkeys

the evidence is subjective, we have not observed differences between echocardiograms of owl monkeys anesthetized by the two different methods.
There were no ECG changes observed that were
associated with age. This differs from findings in squirrel monkeys, where longer P and QRS durations were
found [5] in older animals. A squirrel monkey diagnosed with cardiomyopathy in that report had
increased heart rate over its own healthy ECG and
age-matched controls. This change was not seen in owl
monkeys with cardiomyopathy. The possibility that a
larger study might unmask subtle differences cannot be
ruled out.
Studies are ongoing to investigate the role of hypertension as a possible cause of cardiomyopathy in owl
monkeys. Cardiomyopathy has a decreased prevalence
in owl monkeys that have not been in captivity for an
extended period of time [14]. A previous study indicated that owl monkeys react to laboratory disturbances with significant, prolonged elevations in blood
pressure [16]. The study of cardiomyopathy in owl
monkeys is not only important in maintaining a selfsustaining breeding colony, but it may be a useful
model for human cardiomyopathy.
Acknowledgments
The assistance of Leah Carmichael, George Tustin,
Jenne Westberry, and Craig Youngman with this study
is gratefully acknowledged. Supported in part by grant
5R24RR020052-03 from the National Center for
Research Resources (NCRR). Contents are solely the
responsibility of the authors and do not necessarily
represent the official views of NCRR. Supported in
part by grant 5R24RR020052-03 from the National
Center for Research Resources (NCRR), a component
of the National Institutes of Health (NIH). Its contents are solely the responsibility of the authors and
do not necessarily represent the official views of
NCRR or NIH.
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J Med Primatol 39 (2010) 143–150
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