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A CASE OF DILATED CARDIOMYOPATHY IN A

10 YEAR-OLD POODLE TERRIER BITCH

Rodel Jonathan S. Vitor II


Group 7

Veterinary Clinics 175


21 August 2008
I. Abstract

The four chambers of the heart comprise the pumping organ of the
cardiovascular system. It is important in maintaining proper circulation of the
blood. However, there are times wherein alteration happens and thus failure of
the heart occurs. One cause of this is dilated cardiomyopathy wherein the volume
capacity of the heart is increased with a decrease in myocardium size. It can be
diagnosed by using physical examination, radiography, echocardiography and
electrocardiography. Treatment and management of the disease is divided into
three phases namely stabilizing of the patient, maintenance therapy and the
treatment of arrhythmias. The outcome of the disease is dependent on the
management and therapy, however, it should be noted that treatment must go on
for life or the clinical signs will soon reappear.

The case is about a 10 year-old Poodle-Terrier bitch brought to the hospital


with the chief complaint of coughing. A complete hemogram with several other
ancillary diagnostic tools such as serum chemistry and diagnostic imaging tools
such as radiography and electrocardiography was employed to diagnose the said
condition.

II. Case Presentation

Mocha, a 10 year-old Poodle-Terrier, owned by Ms. Cindy Villadelgado was


brought to the hospital last August 2, 2008 with the chief complaint of progressive
coughing which started 1 ½ month ago. The owner describes the cough to be
asthmatic and usually starts at night. The dog has been previously diagnosed and
treated symptomatically for her coughing with carbocisteine which was given for 7
days then was asked to shift to Ascof® lagundi syrup. She was also diagnosed to
have amoebiasis and was given metronidazole given 3 times a day. The dog has no
record of vaccination and is fed with commercial dog food.

On physical examination, the dog weighs 10.9 kg with a temperature of 39.1 o C


and a body condition score of 6/9. On systematic examination, all other organs
seemed to be normal except for observed labored breathing, murmurs on thoracic
auscultation, pale mucous membrane and delayed capillary refill time of 4
seconds.

A complete hemogram, microfilaria test and serum creatinine levels were


assessed. Results of the laboratory examination are summarized in Table 1. It
should be noted that the dog is suffering from anemia, leukocytosis and
neutrophilia.
Table 1.Laboratory Examinations Last August 2, 2008.
Laboratory Test Laboratory Values Normal Values
Packed Cell Volume 27% clear 32-50%
Total WBC Count 20,950 cells/L 11,200-19,300 cells/L
N 15,713 N 608-12,300
Differential WBC Count
L 5,237 L 2,120-5,280
23 cells/OIO
Platelet Count 8-10 cells/OIO
(adequate)
Microfilaria Test Negative
Creatinine 0.520 mg/dL 0.5-1.6 mg/dL

The Simplify® antigen kit is used in adjunct with the microfilaria test because
there is a high chance that even if dirofilariasis is present, microfilaria will not be
exhibited in the blood smear. The result is negative which supports the results of
the laboratory microfilaria test.

Figure 1. Thoracic radiograph showing the enlarged cardiac silhouette.

On the thoracic radiograph, the trachea is normal and is patent due to the
presence of radioluscent area which may signify air. On the examination of the
cardiac silhouette however, deviations from the normal were observed. The
normal range for the cardiac silhouette in vertebral heart scale is 9.7 ± 0.5
(Buchanan and Bucherler, 1995). However, upon measuring the size of the
silhouette, the long axis is 6 vertebrae whereas the short axis measures 5
vertebrae. Also a classical sign of cardiomyopathy is the resting of the ventricles
within the sternum. However, this method is not as accurate as the vertebral
heart scale method.
Differential diagnosis of the case includes infectious tracheobronchitis,
tracheal collapse, upper airway obstruction, dirofilariasis and cardiomyopathy.
Infectious tracheobronchitis was ruled out because there is no thickening of the
tracheal lumen seen in the radiograph, tracheal collapse and upper airway
obstruction were also ruled out due to the presence of radioluscent area on the
radiograph on the area of the trachea suggesting patency. Dirofilariasis was ruled
by laboratory methods, however it should be noted that a negative result on wet
mount examination of blood for dirofilaria yields high negative, an antigen kit was
used to ultimately rule out the infection.

Using the clinical signs and radiograph as diagnostic tools, Mocha was
tentatively diagnosed to have cardiomyopathy. Furosemide, enalapril and
cefalexin were prescribed together with a Prescription Diet® h/d Canine dog food.
The dose, preparation and the amount to be given is summarized in Table 2.

Table 2. Drug, Dose, Preparation and Its Total Amount to be Administered.


Total
Amount/Frequency/
Drug Dose Preparation
Route of
Administration
Furosemide 4 mg/kg 40 mg 1 tab PO TID
Enalapril 0.5 mg/kg 10 mg ½ tab PO BID
Cephalexin 22 mg/kg 250 mg 1 cap PO TID
Prescription Diet®
1 to 1 1/3 can per
h/d Canine dog Can
day
food

Furosemide, a potent loop diuretic, is an effective drug in reducing preload and


pulmonary edema in patients with congestive heart failure. This may also be used
to promote diuresis in patients with oliguria. This promotes sodium and water
excretion by inhibiting chloride resorption at the ascending loop of Henle.
However, potassium is constantly excreted together with sodium and water.
Despite the symptomatic effect of diuretics, it should not be used alone in the
treatment and management of congestive heart failure because they further
activate the renin-angiotensin system (Bulmer and Sisson, 2005).

Enalapril, an ACE-inhibitor, is used for their vasodilatory effects in the


treatment of congestive heart failure, systemic hypertension, renal disease and
shock. Inhibiting the action of angiotension-converting enzyme would result to a
negative feedback on the release of aldosterone, ultimately resulting to Na + and
water excretion and K+ retention at the distal tubules of the kidney.

Cefalexin is a broad-spectrum, first generation cephalosporin that is usually


bactericidal to Gram-positive and several Gram-negative strains. They are used in
the treatment of several respiratory, skeletal, genitor-urinary, skin and soft-tissue
infections. This is used in junction with the observed neutrophilia signifying
secondary bacterial that may have resulted from the previous infection with
amoeba.

Prescription Diet® h/d Canine dog food is formulated to help manage dogs with
the symptoms of heart diseases and related fluid retention because sodium (0.03%)
is present at small amounts in the food with potassium at 0.23%.

The client was advised to restrict food intake with high sodium levels,
restriction of activity is not necessary and should allow the dog to choose its own
activity and giving adequate water because of the effects of furosemide and
enalapril which may in turn cause dehydration of the patient.

III. Follow-Up

On a follow-up call last August 7, 2008, the owner was enthusiastic to report
that coughing stopped even within 1 day of treatment and that diarrhea also
stopped. The dog was not also eating its prescribed food and “starving” itself at
day and scavenging the trashes at night. Since the client already went to another
clinica prior to admission at the hospital, the owner related that liver function
tests were high, however upon inquiry if the attending veterinarian gave a
prescription, he gave none. The client was asked to return on August 9, 2008.

On August 9, 2008, Mocha was apparently healthy, bright, alert and responsive.
Heart rate was 130 beats per minute and all other organ system seems to be
apparently normal. A series of laboratory examination were run to assess the
improvement of Mocha and to check for liver function and potassium levels due to
possible complications with diuretic treatment. Results of the laboratory
examination are summarized in Table 3.

Table 3. Laboratory Examinations Last August 9, 2008.


Laboratory Test Laboratory Values Normal Values
Packed Cell Volume 36% clear 32-50%
Total WBC Count 17,600 cells/L 11,200-19,300 cells/L
NSegmented 12,300 NSegmented 608-12,300
NBand 176 NBand 0-296
Differential WBC Count
L 4,752 L 2,120-5,280
E 528 E 480-2,660
SGPT 78.4 /L 39 /L
K+ 4.90 mmol/L 3.5-5.1 mmol/L
Figure 2. Electrocardiogram last August 9, 2008.

An electrocardiogram was made and significant findings include the sloping of


the S-wave, depression of the ST-segment and the widening of the QRS complexes.
The sloping of the S-wave and widening of the QRS complexes are suggestive of
left ventricular enlargement whereas a depression of the ST-segment may signify
myocardial ischemia, myocardial infarction, hyper or hypokalemia, digitalis
treatment and trauma to the heart (Tilley, 1979). Based on the electrocardiogram
and the previous results, Mocha was diagnosed to have dilated cardiomyopathy.

Liv 52, a liver tonic, was prescribed (I tablet s.i.d as supplement) together with
a home made recipe consisting of 125 g ground or lean beef, 2 cups cooked white
rice, one tablespoon of vegetable oil and pet vitamins. Calcium supplement may
also be added but was not since calcium levels have not yet been assessed.

On August 23, 2008, the client was asked to bring Mocha back to reevaluate her
condition and the drugs being used. A laboratory examination including potassium
and alanine transferase serum levels were reevaluated. Results of the laboratory
examination are summarized in Table 4.

Table 4. Laboratory Examinations Last August 23, 2008.


Laboratory Test Laboratory Values Normal Values
K+ 3.31 mmol/L 3.5-5.1 mmol/L
SGPT 144 /L 39 /L

Drugs given were reevaluated and the prescription was modified. Enalapril,
which is usually the mainstay treatment for heart failure patients, was prescribed
using the same dose and preparation. Furosemide has been removed from the
prescription because of its hypokalemic effect. Jetepar replaced Liv 52 as liver
tonic because of its more potent effect. Taurine and L-carnitine may be prescribed
to make use of its cardioprotectant effects. However, since L-carnitine in its pure
form is not available in the market, only taurine was prescribed to the dog.

On September 13, 2008, Mocha went back to the hospital for her drug intake to
be revaluated. Upon seeing that her condition is improving, the attending
veterinarian decided to reduce the frequency of the enalapril intake from twice a
day to once a day only, using the same dose. Jetepar and Pet tabs are still being
given as supplements.

IV. Discussion

Cardiomyopathy is a disease that may be classified into two general forms:


hypertrophic and dilated. Hypertrophic form is where the walls of the myocardial
increase in thickness whereas the dilated form is the decrease in thickness of
myocardial wall but increase in volume capacity (Tilley and Smith, 1997).

Dilated cardiomyopathy is characterized by left and right sided dilation, normal


coronary arteries, normal (or minimally diseased), atrioventricular valves,
significantly decreased inotropic state and myocardial dysfunction occurring
primarily during systole. Breeds identified to be predisposed to disease include
Doberman Pinschers, Boxers, Cocker Spaniels and other giant breeds. 4 to 10 year
old patients have been commonly diagnosed with the disease.

Causes of dilated cardiomyopathy may include idiopathic causes, nutritional


deficiencies in taurine and/or carnitine, hypothyroidism and some viral, protozoal
and immune-mediated mechanisms. Clinical signs includes weakness, depression,
cardiogenic shock, weight loss, lethargy, anorexia, tachycardia, mitral
regurgitation and slow capillary refill time. Pathophysiology of the disease includes
reduced cardiac output and congestive heart failure which is a result of the failure
of the heart to advance blood from the right ventricle into the pulmonary arteries.

The disease has 3 clinical manifestations depending on the state of the animal.
Class I are animals that are asymptomatic but have arrhythmia detected on
physical examination, Class II have episodes of syncope weaknesses and Class III
may present congestive heart failure with arrhythmias (Meurs, 1998). Based on the
definition, Mocha may be classified as Class III patients because of the
enlargement of the heart on radiography and also typical signs which is suggestive
of congestive heart failure.

The hemogram, serum chemistry and urinalysis are usually normal unless
altered by severe heart failure (high alanine transferase), treatment for heart
failure and concurrent disease (Tilley and Smith, 1997). Anemia may have resulted
from the overhydrated status of the dog or due to the infection caused by the
underlying amoebiasis. Since the cause was possibly treated using a diuretic and
an anti-microbial, anemia have resolved. Leukocytosis and neutrophilia are
suggestive of infection and prompt therapy against the cause which is usually
bacteria is most significant. High alanine transferase levels have been correlated
with hypoxemia which causes increased hepatocyte destruction leading to seeping
out of the enzymes in the blood stream.
Other tests that should be checked routinely include creatinine, potassium and
calcium levels. A normally functioning kidney is a necessity in the treatment of
heart failure since diuresis is occurring in the kidney. Potassium levels need to be
constantly evaluated since it is excreted at high levels together with sodium and
water and hypokalemia should be prevented by giving supplements (Erling and
Mazzaferro, 2008). Pet-Tabs® with 5% potassium is used as the supplement for this
cause. Calcium levels need to be evaluated since it is a primary ion together with
ATP causing the contraction of the heart (Stephenson, 2007). Problems with
contraction of the heart may be a result with a decrease in calcium levels in the
extracellular fluid (ECF), normal levels of calcium but decreased in receptors or
normal calcium and receptors but the cascade in the contraction is disrupted.
Calcium:phosphorus ratio have to be evaluated to rule out possible
hypoparathyroidism. However, the exact cause of contractile problem will not
affect the treatment of the disease.

Diagnosis includes thoracic radiography, electrocardiography, echocardiography


coupled with good history taking and physico-clinical examination. Radiography is
used to diagnose cardiomegaly by evaluation of the cardiac silhouette (Root and
Bahr, 1998). In Dobermans, only left atrial enlargement may be evident whereas in
Boxers, thoracic radiographs may be normal, or there may be mild to moderate
cardiomegaly. As with the case, enlargement of the cardiac silhouette have been
observed and was interpreted objectively.

In the electrocardiogram, atrial fibrillation is seen in 75 to 80 per cent of giant-


breed dogs with dilated cardiomyopathy. There may be subtle changes such as
high amplitude or widened QRS complexes (left ventricular enlargement), or
widened P waves (left atrial enlargement). In Dobermans and boxers, one sees
ventricular premature contractions of variable frequency, singly or in runs, and,
later, paroxysms of ventricular tachycardia. Findings of the case are consistent
with typical findings like widened QRS complexes, coving of the S wave and
depression of the ST segment (Tilley and Smith, 1997).

In the echocardiogram, which is the gold standard for diagnosis, reduced


contractility and ventricular dilation may be observed, although this may not be
evident in Boxers (Tilley and Smith, 1997).

Upon physical examination, occasional to frequent premature beats, pulse


deficits, paroxysmal tachyarrhythmias or a totally irregular ventricular rhythm,
variability in femoral pulse strength is observed.

Therapy should be individualized based on presenting signs and findings during


physico-clinical examination (Meurs, 1997). Treatment includes the stabilization of
the patient with oxygen if hypoxemia is present, triple drug therapy for
maintenance and treating of arrhythmias with atenolol or diltiazem is indicated.
The treatment with taurine (500-1000 mg q8-12h) and L-carnitine (50-100 mg/kg
PO q8h) is still controversial since basal levels cannot be established in local
laboratories and is usually costly (Dove, 2001). It is thought that taurine works as a
cardioprotectant by regulating natriuresis and diuresis, exhibiting positive
inotropic effects on myocytes, and minimizing the adverse effects of angiotensin
II. Taurine has also been shown to decrease the level of lipid peroxides (and
hence, oxidative damage) in hypoxic tissues, and exert anti-arrhythmic effects in
cardiac muscle. L-carnitine can improve heart rate, lipid patterns, and exercise
tolerance, and protect against cardiac necrosis, all of which are important to
returning an animal to normal cardiac function. It is valuable to understand L-
carnitine in relation to taurine deficiency and supplementation, as the two
nutrients have interrelated roles in management of heart disease in dogs (Dove,
2001).

Triple drug therapy is recommended using furosemide, an ACE-inhibitor


coupled with digoxin. These three drugs is used as the mainstay in treating dogs
with congestive heart failure secondary to degenerative valve diseases and dilated
cardiomyopathy (Bulmer and Sisson, 2005). The first two drugs have already been
discussed above. Digoxin is a positive inotropic drug used to improve cardiac
output in conditions of congestive heart failure and cardiomyopathy (Erling and
Mazzaferro, 2008). However, it was not given since it potentiates the toxic ability
of furosemide. A potassium-sparing diuretic (spironolactone, triamterene and
amiloride) in lieu of a loop diuretic may be used so that hypokalemia may be
prevented (Landicho EF, 2006).

Outcome is based mainly on the class on which the animal belongs to: Class I
patients usually have a good prognosis and may be expected to live for more than
a year, Class II patients are at risk of sudden death and Class III patients with less
than 6 months (Meurs, 1997). However, the course of disease is always fatal and
that possible complications should always be noted (Tilley and Smith, 1997).

V. References

Allen DG, Dowling PM, Smith DA, Pasloske K and Woods JP. 2005. Handbook of
Veterinary Drugs. Baltimore: Lippincott Williams and Wilkins. pp. 156-157,
196-197, 209-210, 230-231.

Buchanan JW and Bucheler J. 1995. Vertebral scale system to measure canine


heart size in radiographs. Journal of the American Veterinary Medical
Association, 206(2): 194-199.

Bulmer BJ and Sisson DD. 2005. Therapy of Heart Failure. In Ettinger SJ and
Feldman EC (eds.). Textbook of Veterinary Internal Medicine: Diseases of
the Dog and Cat Volume II. 6th ed. St. Louis: Elsevier Saunders. pp. 948-
972.
de Morais HA and Scwartz DS. 2005. Pathophysiology of Heart Failure. In Ettinger
SJ and Feldman EC (eds.). Textbook of Veterinary Internal Medicine:
Diseases of the Dog and Cat Volume II. 6th ed. St. Louis: Elsevier Saunders.
pp. 914-940.

Dove, RS. 2001. Nutritional therapy in the treatment of heart disease in dogs.
Alternative Medicine Review, 6(Suppl):S38-S45.

Erling P and Mazzaferro EM. 2008. Left-sided congestive heart failure in dogs:
pathophysiology and diagnosis. Compendium, 30(2): 79-91.

Erling P and Mazzaferro EM. 2008. Left-sided congestive heart failure in dogs:
treatment and monitoring of emergency patients. Compendium, 30(2): 94-
104.

Landicho EF. 2006. Lectures in Veterinary Clinical Pharmacology. Department of


Basic Veterinary Sciences, College of Veterinary Medicine, University of the
Philippines Los Baños. pp. 71-92.

Meurs KM. 2005. Primary Myocardial Disease in the Dog. In Ettinger SJ and Feldman
EC (eds.). Textbook of Veterinary Internal Medicine: Diseases of the Dog
and Cat Volume II. 6th ed. St. Louis: Elsevier Saunders. pp. 1077-1082.

Meurs KM. 1997. Myocardial Disease. In Morgan RV (ed.). Handbook of Small


Animal Practice. Philadelphia: WB Saunders. pp. 103-111.

Root CR and Bahr RJ. 1998. The Heart and Great Vessels. In Thrall DE (ed.).
Textbook of Veterinary Radiology. 3rd ed. Philadelphia: W.B. Saunders. pp.
335-353.

Tilley LP and Smith FWK Jr. 1997. The 5 Minute Veterinary Consult – Canine and
Feline. Media: Williams and Wilkins. pp. 418-419, 422-423, 470-471, 474-
475, 550-551, 850-851.

Stephenson RB. 2007. Cardiovascular Physiology. In Cunninghum JG and Klein BG


(eds.). Textbook of Veterinary Physiology. 4th ed. St. Louis: Saunders. pp.
193-225.

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