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Biomarkers can indicate physiological (such as
growth and aging), or pathophysiological processes
that occur with disease (e.g. cardiac damage and heart
failure). Among these biomarkers, cardiac biomarkers
can be helpful in the management of cardiac and
non-cardiac diseases (Jesty, 2012). In humans, cardiac
biomarkers aid in the early detection, diagnosis and
prognosis of cardiac diseases (Ginsburg and Haga,
2006).
Among cardiac biomarkers, cardiac troponin
I (cTnI), is a highly sensitive and specific marker
for myocardial injury in humans (Ladenson, 2007;
Reagan et al, 2013) and in veterinary medicine (Wells
and Sleeper, 2008; Fonfara et al, 2010; Tharwat,
2012; Tharwat et al, 2012; Tharwat et al, 2013a,b,c,d;
Tharwat and Al-Sobayil, 2014a,b,c; Tharwat et al,
2014a,b; Tharwat, 2015; Tharwat and Al-Sobayil,
2015). The serum concentration of cTnI elevates after
acute myocardial injury because of leakage from the
damaged myocardial cells (O’Brien et al, 2006). In
DOI : 10.5958/2277-8934.2020.00017.X Vol 27 No 1, p 121-128
THE CARDIAC BIOMARKERS TROPONIN I AND
CREATINE KINASE MYOCARDIAL BAND IN
CAMELS (Camelus dromedarius)– A REVIEW
Mohamed Tharwat1,2
1Department of Veterinary Medicine, College of Agriculture and Veterinary Medicine,
Qassim University, P.O. Box 6622, Buraidah, 51452, Saudi Arabia
2Department of Animal Medicine, Faculty of Veterinary Medicine, Zagazig University, Zagazig, Egypt
ABSTRACT
Cardiac biomarkers are helpful in the early detection, diagnosis and prognosis of cardiac and non-cardiac
diseases. Cardiac troponin I (cTnI), one of these biomarkers, is a highly sensitive and specic marker for myocardial
injury in humans and in veterinary medicine. cTnI elevates in serum after acute myocardial injury because of leakage
from the damaged myocardial cells. Creatine kinase myocardial band (CK-MB), another cardiac biomarker, has been
found high following exercise. With chest pain in humans, the level of CK-MB increases and subsequently declines
to normal range. In animals, however, a rise in CK-MB is not always indicative of acute myocardial infarction. cTnI
therefore is currently the preferred cardiac biomarker in human medicine for assessing myocardial damage, with
absolute specicity and higher sensitivity. The degree of increase in cTnI has been shown to correlate with the extent
of myocardial damage and with survival in humans and animals. In camels, the evaluation of cardiac disease can be
challenging; the patient history, clinical data and routine blood examination are often nonspecic. Therefore, blood-
based biomarkers that are capable of detecting and staging cardiac disease are a subject of considerable interest.
Myocardial damage, as demonstrated by elevated cTnI in blood, appears to be a common sequel to a wide variety
of both primarily cardiac disease and of other diseases that do not primarily involve the cardiovascular system. This
review was written to shed light on the commonly used cardiac biomarkers in camel medicine cTnI and CK-MB and
its clinical signicance.
Key words: Camels, cardiac biomarkers, cardiac troponin I, creatine kinase–myocardial band, heart diseases
veterinary medicine, cTnI has also a high sensitivity
and specicity in animals with diseases of cardiac
and noncardiac origin (O’Brien et al, 2006; Wells and
Sleeper, 2008). The degree of increase in cTnI has
been shown to correlate with the extent of myocardial
damage and with survival in humans (Stanton et al,
2005) and animals (Oyama and Sisson, 2004; Fonfara
et al, 2010).
Creatine kinase myocardial band (CK-MB) is
another cardiac biomarker that has been reported to
increase with exercise (Mamor et al, 1988; Rahnama
et al, 2011). With chest pain in humans, the level of
CK-MB reaches its peak at 10-24 hours subsequent
to the initial injury and declines to normal range
within 72-96 hours (Volz et al, 2012). Chronic
occlusion of the coronary artery signicantly increases
the serum levels of CK-MB (Sharkey et al, 1991).
However, a rise in CK-MB is not always indicative of
myocardial damage; it has been elevated in patients
with acute skeletal muscle trauma, dermatomyositis,
122 / April 2020 Journal of Camel Practice and Research
polymyositis, muscular dystrophy and renal failure
(Erlacher et al, 2001). Therefore, cTnI is nowadays
the superior biochemical parameter in humans
for assessing myocardial damage, with absolute
specicity and sensitivity than CK-MB (Alpert et al,
2000; Collinson et al, 2012).
In camels, heart diseases include pericarditis,
vegetative valvular endocarditis, hypertrophic
cardiomyopathy necrotic myocarditis, congenital
defects including septal defects, patent ductus
arteriosus, transposition of the aorta and pulmonary
artery, persistent aortic trunk, and persistent right
aortic arch and sarcocystosis (Fowler, 2010). These are
mostly diagnosed at slaughterhouses or incidentally
discovered during postmortem (Fowler, 2010). The
diagnosis of camel heart disease is a challenging
task especially when typical clinical signs of heart
failure are absent. Therefore, blood-based biomarkers
capable of detecting and staging diseases of cardiac
and non-cardiac origin are a subject of considerable
interest in camels.
This review was designed to shed light on the
commonly used cardiac biomarkers in camel medicine
cTnI and CK-MB as indicators of cardiac injury.
Cardiac troponins
Troponins are 3 distinct myobrillar proteins
(I, C, and T) that regulate the calcium-mediated
interaction between actin and myosin in both cardiac
and skeletal muscle (Babuin and Jaffe, 2005). Of
troponins, cTnI is the only one that is expressed in
the myocardium. The amino acid sequence for cTnI
is highly conserved among mammalian species so
human kits can be used; however, the references
and values can differently depend on the analyser
used since they can give different results (Apple
et al, 2008). Mildly elevated concentrations of cTnI
alone will unlikely lead to a denitive diagnosis, but
together with the clinical presentation and ndings
on ECG and echocardiography it can become an
important marker for myocardial disease. On the
other hand, marked elevations of cTnI alone could
be considered as a strong indication of myocardial
disease (Nostell and Haggstrom, 2008). However, A
constant elevation of cTnI indicates persistent damage
to the cardiomyocytes (O’Brien et al, 2006; Wells and
Sleeper, 2008), and the degree of elevation has been
shown to be correlated with the extent of myocardial
damage and with survival in humans (Stanton et al,
2005) and in animals (Fonfara et al, 2010; Tharwat,
2012; Tharwat and Al-Sobayil, 2014a).
Low to non-detectable cTnI levels have been
found in healthy mammals (Baker et al, 2011).
Elevated cTnI has been reported in calves (Peek et al,
2008), cattle (Varga et al, 2009; Mellanby et al, 2009),
horses (Kraus et al, 2010; Holbrook et al, 2011), foals
(Slack et al, 2005), dogs (Herndon et al, 2002; Spratt
et al, 2005) and lambs (Gunes et al, 2010) indicating
that elevations in the blood would serve as useful
biomarkers of myocardial injury.
Creatine kinase myocardial band
Creatine kinase is a dimeric enzyme found
primarily in brain and muscle tissue. Three isoforms
are known for creatine kinase: BB, MM, and MB. The
isoform BB is found in the brain. The second isoform
MM is found primarily in skeletal muscles. Cardiac
muscles also primarily contain the MM isoform, but
with higher amounts of MB, typically around 20% of
CK activity (Moss and Henderson, 1994). In humans,
serum from healthy individuals typically contains the
MM isoform and a small amount of the MB isoform.
CK-MB can be released into the bloodstream by a
number of actions, including skeletal muscular injury
and myocardial damage.
Cardiac biomarkers in camel medicine
In humans, nonprimary cardiac diseases
can induce myocyte damage leading to increased
serum troponin concentrations (Mahajan et al, 2006).
For example, study of 144 patients with increased
cTnI concentrations identied a wide range of
diseases that can be associated with increased cTnI
concentrations including sepsis, collagen vascular
disease, gastrointestinal bleeding, pulmonary
embolism, diabetic ketoacidosis, and chronic
obstructive pulmonary disease (Mahajan et al,
2006). Other studies in dogs with gastric dilatation
and volvulus and in dogs and cats with azotaemia
renal failure and in dogs with non-cardiac systemic
disease had increased cTnI concentrations indicating
cardiomyocyte degeneration and necrosis (Schober
et al, 2002; Porciello et al, 2008). Similar ndings have
been found in cattle with noncardiac and intrathoracic
diseases, even though no gross cardiac abnormalities
were detected at postmortem examination (Mellanby
et al, 2009). Most of these studies concluded that
the heart may be a non-target tissue bystander in
these processes that leads to elevations in cTnI, but
there is little strong data to denitively identify the
mechanism.
In recent years, our research group has
observed signicant elevations of cTnI in camel blood
Journal of Camel Practice and Research April 2020 / 123
following prolonged recumbency (Tharwat, 2012),
general anaesthesia (Tharwat et al, 2013a), long road
transportation (Tharwat et al, 2013b), racing (Tharwat
et al, 2013c), tick infestation (Tharwat and Al-Sobayil,
2014) and after stimulation by electroejaculation
(Tharwat et al, 2014a) and following parturition stress
(Tharwat, 2015). In humans, studies on the prognostic
signicance of cTnI concentrations in patients with
non-primary cardiac disorders have found that cTnI
can predict disease outcome. Recently, in cattle with
haemolytic anaemia, long-term follow-up of serum
cTnI concentrations was valuable in assessing the
relationship between anaemia and myocyte damage
(Fartashvand et al, 2012). In addition, an elevated
serum concentration of cTnI has been used as a
poor prognostic indicator in goats with pregnancy
toxaemia (Tharwat et al, 2012), in downer camels
(Tharwat, 2012) and in camels infested with ticks
(Tharwat and Al-Sobayil, 2014a).
In a study published recently in camels with
tick infestation (Tharwat and Al-Sobayil, 2014a),
14 recovered out of 15 camels (93.3%) had a serum
concentration of cTnI lower than 1.0 ng/ml, and
the remaining camel (6.7%) had a higher cTnI
concentration (1.65 ng/ml). In the same study, all 8
died camels had a serum concentration above 1.22
ng/ml, with a maximum value of 5.22 ng/ml (Fig
1). Therefore, it was assumed that the increased
serum concentration of cTnI above 1.0 ng/ml at
initial examination was a bad prognostic indicator
in the camels with tick infestation. Elevated serum
concentration of cTnI has been reported in cattle with
theileriosis (Fartashvand et al, 2013).
In camels infected with Trypanosoma
evansi (n=74), the values of cTnI and CK-MB
were signicantly higher in T. evansi infected
camel compared to controls (n=20) (El-Deeb and
Elmoslemany, 2015). Successfully treated camels
(n=43) had lower levels of cTnI and CK-MB
compared to camels with treatment failure. cTnI
showed better sensitivity and specicity than CK-
MB. Similar in cattle, serum concentration of cTnI
was significantly higher (P=0.003) in cattle with
theileriosis (mean: 0.028 ng/mL; range: 0.005–
0.21 ng/mL) compared to controls (mean: 0.011;
range: <0.005–0.09 ng/mL) (Fartashvand et al,
2013). Anaemia followed by hypoxia and increased
oxygen consumption by the myocardium during
a prolonged period of tachycardia will possibly
cause myocardial injury and subsequent increased
serum concentration of cTnI in animals with parasitic
infestation (Fartashvand et al, 2012; Tharwat and Al-
Sobayil, 2014a).
In a study carried out on 33 long-standing
recumbent camels (Tharwat, 2012), marked elevations
of cTnI in the downer camels was considered as a
strong indication of myocardial damage and was
used to predict treatment outcome and mortality
(Fig 2). In the same study (Tharwat, 2012), the serum
concentration of cTnI in the 11 cured camels was
0.05±0.02 ng/ml. In the remaining 22 camels that
did not recover, the serum concentration of cTnI
was 0.53±0.64 ng/ml. A recent study in dairy cows
with downer cow syndrome concluded that cTnI
concentrations could help to rapidly identify cows
that have poor chances of recovery and would benet
from a more aggressive treatment or euthanasia
(Labonte et al, 2018).
In 25 camels transported for a 5km round trip,
the mean cTnI concentration was 0.032±0.023 ng/mL
comparing to resting values of less than 0.08 ng/mL
Fig 1. Mean serum concentrations of serum cardiac troponin I
in camels with tick infestation. a,b,c,d Differ signicantly
(Tharwat and Al-Sobayil, 2014a).
Fig 2. Cardiac troponin I values in downer camels compared
to control healthy camels. a,b different letters indicate a
signicant difference (P=0.019). SD = standard deviation
(Tharwat, 2012).
124 / April 2020 Journal of Camel Practice and Research
(Tharwat et al, 2013b). The cTnI concentration was
signicantly higher (P<0.001) in all the 25 camels
compared to values before transportation. The CK-
MB concentration in the same camels was 0.19±0.05
ng/mL compared to resting values of less than 0.33
ng/mL. Only in 3 of the 25 camels (12%), the CK-
MB values were above values before transportation
and no statistical differences were recorded (Fig 3).
Transportation is a well-known stressor that has
adverse effects on livestock production and health
including muscular damages, generating concerns
of an economic as well as a welfare-related nature
(Tharwat et al, 2013b).
Following a 5 km race in 23 camels, 91.3% of the
camels had increases in serum cTnI concentrations,
while concentrations remained unchanged in 8.7%
(Tharwat et al, 2013c). The cTnI concentration
(median 0.06 ng/mL; range, 0.03–0.15 ng/mL) was
signicantly higher (P<0.001) than the pre-race values
(median 0.04 ng/mL; range, 0.01–0.07 ng/mL).
Twenty-four hours post-race, the cTnI concentrations
had returned very nearly to their pre-race values
(median 0.04 ng/mL; range, 0.00–0.09 ng/mL) and
were not signicantly different (P=0.35) from the
pre-race values (Fig 4). Following the 5 km race,
increases in CK-MB mass were seen in 17.4% of the
camels, with no changes in 4.3% and decreases in
78.3%. The CK-MB mass (median 0.41 ng/mL; range,
0.19–0.60 ng/mL) did not differ signicantly (P=0.84)
when compared to the pre-race values (median
0.42 ng/mL; range, 0.32–0.55 ng/mL). Twenty-four
hours post-race, the CK-MB mass concentrations
(median 0.41 ng/mL; range, 0.15–0.55 ng/mL) did not
differ signicantly (P>0.05) compared to pre-race or
immediate post-race values (Fig 4). Post-exercise cTnI
release and clearance were also reported in normal
Standardbred racehorses. All horses experienced an
increase in cTnI post-exercise, with peak occurring
2-6 h post-exercise (Rossi et al, 2019). In a study
carried out on 32 racing greyhounds following a
7 km race, 31/32 greyhounds showed increases in
cTnI concentrations which were signicantly higher
than the pre-race concentrations (P<0.0001). cTnI
concentrations dropped back 24h post-race to values
were not significantly different from the pre-race
concentrations. Only 5/32 greyhounds showed mild
increases in CK-MB concentrations but these were
Fig 3. Box and “whisker” plots of cTnI and CK-MB values in
camels before (T0), within 2h of transportation (T0) and
24h after transportation (T2). Values with different letters
differ signicantly (P<0.001) (Tharwat et al, 2013b).
Fig 4. Cardiac troponin I values in camels before (T0), 2h after
(T1) and 24h after (T2) a 5 km race. a,b different letters
indicate a signicant difference (P<0.05) (Tharwat et al,
2013c).
Journal of Camel Practice and Research April 2020 / 125
not signicantly different from the pre-race values
(Tharwat et al, 2013e).
After EEJ (electroejaculation) in 20 male camels,
the mean serum concentration of cTnI had increased
significantly in all camels following EEJ, but not
in controls (Fig 5) (Tharwat et al, 2014a). However,
at 24h post-EEJ, the serum concentration of cTnI
did not differ significantly compared to baseline
values. Because the serum concentration of cTnI
increased signicantly in the EEJ camels, it is therefore
recommended that the status of the cardiovascular
system of the camel be checked prior to applying
the EEJ technique. In another study, the
serum concentration of cTnI has been
increased significantly (P=0.0001) in 18
male camels with erectile dysfunction
compared to 10 healthy controls (Derar et
al, 2017). The rise of cTnI in the males with
erectile dysfunction is probably indicative
of myoctitic damage which support the
concept that failure to erect the penis or
maintain an erection is primarily related
to the inability to maintain a closed blood
circuit at the penile tissue (Barassi et al,
2015)
Cardiac injury had been reported
in camels with halothane and isourane
general anaesthesia (Tharwat et al, 2013a).
In this study, camels had mildly and
signicantly elevated cTnI with isourane
and halothane anaesthesia, respectively;
however, in the isourane group the upper
limit for the camel reference range was
not exceeded (Fig 6). The cause of the
cardiac cell compromise during halothane
anaesthesia was likely due to extreme
changes in heart rate and blood pressure,
and the increased arterial concentration of
PCO2. Based on the results of this study, it
was concluded that isourane is superior
to halothane as an inhalation anaesthetic in
camels especially in those with suspected
cardiac diseases. The inuence of general
anaesthesia on serum concentration cTnI
in healthy dogs has also been studied
(Verbiest et al, 2013). Fifty-ve percent of
the dogs had a post-anaesthetic increase
of cTnI concentration relative to their pre-
anesthetic cTnI concentration, whereas a
decrease was observed in eleven percent
of the dogs.
Conclusions
In camel medicine cardiac biomarkers are an
exciting and growing science. The most established
applications involve the use of cTnI to help detect
early myocardial injury following prolonged
recumbency, after general anaesthesia, secondary
to long road transportation, following racing, as an
influence of parasitic infestation and after semen
collection by electroejaculation. The cTnI assay helps
to rapidly determine the prognosis in camels and
thereafter deciding either continuing treatment or
euthanasia. CK-MB is a less sensitive biomarker
Fig 5. Effect of stimulation by electroejaculation (EEJ) on cardiac troponin
I in male dromedary camels (mean ± SD, n=20) compared to control
group (n=10). T0: just before EEJ; T1: directly after EEJ; T2: 24h after
EEJ. a,b Values differ signicantly (P=0.0001) (Tharwat et al, 2014a).
Fig 6. Pre-anesthetic, anesthetic and post-anesthetic serum concentration
of cardiac troponin I (means ± SEM) in camels (n = 6) undergoing
isoflurane and halothane anesthesia.T0, immediately before
anesthesia; T1, 20 min after xylazine administration; T2, 20 min after
ketamine administration; T3, 60 min during inhalation anesthesia; T4,
40 min of recovery; T5, 80 min of recovery; T6-T8, 24 h, 48 h and 72
h after anesthesia. bDiffers signicantly between the two anesthetic
agents at P<0.05 (Tharwat et al, 2013a).
126 / April 2020 Journal of Camel Practice and Research
for myocardial activity when compared with cTnI
in detecting myocardial injury. Finally, cardiac
biomarker tests are complementary to existing cardiac
diagnostic testing and should be interpreted in the
context of the overall clinical picture rather than being
used as a stand-alone test.
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