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This is the
third article in a series addressing canine cardiac diseases, with
an emphasis on diseases that more commonly afflict Bichons Frises.
Refer to the first article in the series
www.bichonhealth.org/HealthInfo/CanineCardiac.asp
while you read this article, for descriptions of basic cardiac
anatomy and blood flow through the heart. A Bichon case study is
present at the end of this article. The next article will primarily
cover mitral valve disease.
Significance
Cardiac
disease in dogs is prevalent, accounting for about 11% of dogs seen
by veterinarians. At least 3 million dogs examined by veterinarians
via ultrasounds in the US have acquired heart disease and may be in
heart failure. Acquired heart diseases, both inherited and obtained
from influences outside the body such as infections, will be
addressed in the third article.
There are
basically 3 categories of heart disease in dogs that all progress to
heart failure if left untreated or interventions are ineffective:
-
Hereditary diseases that may appear later than birth, such as
valve diseases, dilated cardiomyopathy (disease of the cardiac
muscle), and sub aortic stenosis (a narrowing of the ventricle
below the aortic valve)
-
Congenital heart diseases that are present at birth and
genetically transmitted, such as patent ductus arteriosis (PDA)
-
Acquired
diseases such as coronary artery disease and chronic valve
diseases, which also may have an inherited component
The focus
of this article will be on dilated cardiomyopathy (DCM), the second
most common hereditary cardiac disease found in dogs. DCM tends to
strike larger breeds, but does occur in small breeds. There are
several reported cases of DCM in Bichons, and many reports of
clinical signs that may indicate DCM, but no definitive diagnosis
was obtained. In humans, 56 genes have been identified that cause
DCM, the most common reason for heart transplantation.
The
incidence of cardiac diseases in Bichons has risen significantly in
the last few years, moving from the #11 position to #7. My hope is
that this information will encourage Bichon breeders to obtain the
OFA cardiac certifications prior to breeding, reduce the incidence
of heart disease in Bichons, and help improve the health of our
beloved Bichons.
Clinical Signs of Heart Failure
Cardiac
diseases eventually lead to heart failure, also called congestive
heart failure (CHF), which is defined as failure of the heart as a
pump, meaning the heart is unable to supply the body and organs with
sufficient flow of oxygen-rich blood. The heart does not stop, but
functions less efficiently. This inefficiency is due to weakened
muscles in the ventricles, the major pumping chambers of the heart,
causing backup of blood into the venous system and the lungs. To
help you understand this process, see my toilet analogy in this
article posted on the Bichon health web site:
http://www.bichonhealth.org/HealthInfo/CanineCardiac.asp.
The heart
attempts to compensate for the reduced pumping ability by increasing
the heart rate, allowing more outflow of blood from more frequent
heartbeats. Despite many compensatory mechanisms in the heart and
body that preserve the balance short term, in time the stress on the
heart takes its toll.
Heart
failure ranges in severity from mild with minimal or no symptoms, to
severe. Initially, clinical signs of heart failure are mild, vague,
and easy to overlook. As time passes more blood backs up into the
lungs causing exercise intolerance, loss of appetite, rapid
respirations, and frequent coughing that can easily be mistaken for
a respiratory infection such as kennel cough. Blood also backs up
into the venous system causing engorged neck veins, liver
enlargement, and swelling in the abdomen and legs. Without adequate
blood flow, organs in the body malfunction and eventually fail, thus
causing more severe clinical signs, such as kidney failure.
Heart
murmurs, abnormal heart sounds, or irregularities in the heart beats
(arrhythmias) detected during a veterinary exam are the hallmark of
cardiac diseases and may be detected before any symptoms are
present, highlighting the importance of an annual veterinary exam,
OFA cardiac certification, and the last puppy exam before leaving
the breeder.
Symptoms
and clinical signs of heart failure include:
1.
Slow capillary refill in the gums (> 2 seconds is required
for the gums to regain the pink color after pressing with a finger)
2.
Weak and rapid pulses
3.
Cardiac rhythm irregularities (arrhythmias) that may cause
sudden death
4.
Abnormal heart sounds, murmurs
5.
Congestion heard in the lungs with a stethoscope
6.
Enlarged heart and lung congestion seen on xray
7.
Reduced stamina, weakness, lethargy, loss of appetite
8.
Shortness of breath, wheezing, coughing, rapid respirations
9.
Fainting episodes that may appear to be a seizure
10.
Confusion due to diminished blood flow to the brain
11.
Cyanosis (blue tint) in the white part of the eyes or gums
12.
Abdominal distension, jugular (neck veins) venous distension
13.
Enlarged liver palpated in the abdomen
14.
Elevated atrial natriuretic peptide (ANP or proANP) that
correlates with the severity of heart failure (blood test)
15.
Late stages: abnormal blood tests that indicate failure of
kidneys, liver, and/or other organs
Figure 2
A cross-section slice of the ventricles of the heart, exhibiting a
myocardial infarction and hypertrophic cardiomyopathy (left
ventricle is on the right side)
Figure 3 NOTE
the normal thickness of the muscle walls of the left ventricle in
the normal heart on the left, compared with the thickness of the
left ventricular muscle wall (hypertrophic cardiomyopathy) above in
figure 2. The diagram on the right depicts dilated cardiomyopathy (DCM),
showing dilatation and enlargement of atrial and ventricular
chambers with thinning of both ventricular walls. Note the overall
increased size of the heart with DCM as compared to the normal heart
on the left.
Pathophysiology of Cardiomyopathy
Cardiomyopathy is defined as a disease of the muscle of the heart
(myocardium), rendering the ventricles weakened and unable to pump
an adequate amount of blood to the body. Initially the thickness of
the myocardium increases (hypertrophy) to strengthen the
contractions to eject more blood, just as your bicep muscles
increase in size with exercise (see figure 2). In time, the
interior chamber of the ventricle dilates to allow increased
capacity for blood volume. Eventually these compensatory mechanisms
fail and heart failure ensues.
Dilated
cardiomyopathy (DCM) differs from classic cardiomyopathy in that the
walls of the ventricles do not hypertrophy. Instead, the
ventricular walls become thin and the ventricular chambers dilate,
resulting in considerable weakness of the ventricles and an enlarged
heart (see figure 3). In both types of cardiomyopathy, the
ventricles become stiff and difficult to fill with blood, which
alters the heart sounds that can be heard with a stethoscope.
The dilated
ventricles produce another consequence, dilation of the rings at the
base of the mitral and tricuspid valves (see figure 4), rendering
the valves incompetent. When blood flow is altered in the heart by
leaking valves, it produces turbulence that can be heard with a
stethoscope, called a murmur.
Figure 4
View of the heart valves from above the heart, showing the valvular
rings that surround the leaflets of the valves, which can dilate
with DCM
The
myocardium requires massive amounts of energy to be able to contract
at least every second, and to maintain its structural integrity,
similar to other muscles in your body during strenuous exercise.
The majority of the energy is derived from oxygen and glucose
contained in the blood that feeds the myocardium via the coronary
arteries. If blood flow is suddenly reduced to the myocardium
during a myocardial infarction (heart attack or MI), myocardial
cells die (infarction) causing weakness in the muscle. The dark
area of the myocardium of the left ventricle in figure 2 is an
infarction. If blood is chronically reduced to the myocardium
(ischemia) due to coronary artery disease, the myocardium will
weaken due to ineffective contractile cells. Once myocardial cells
die, they cannot be regenerated.
In addition
to oxygen and glucose, the myocardial cells utilize other nutrients
to function optimally, a deficiency of which may cause
cardiomyopathy. Carnitine is needed to transport fatty acids that
are required for energy into the myocardial cells. Taurine has
diuretic effects that help rid cells of excess water, plus it helps
maintain calcium balance in the myocardial cells, which strengthens
myocardial contractility. Adequate levels of Coenzyme Q10 promote
proper function of myocardial cells by assisting in maintenance of
cellular energy stores. These three nutrients are found in animal
proteins that are present in foods, smaller amounts in processed dog
foods and larger amounts in fresh raw foods, and can be purchased as
supplements. The levels of the electrolytes, especially Calcium and
Magnesium, must also be normal for effective function of the
contractile cells of the myocardium.
There are 2
classifications of cardiomyopathy, extrinsic and intrinsic.
Extrinsic cardiomyopathy is caused by factors outside of the
myocardium that lead to destruction of the muscle cells:
-
Coronary
artery disease that reduces blood flow to the myocardium
-
Hypertension (high blood pressure) causes excessive resistance to
outflow of blood from the left ventricle, leading to hypertrophy
(thickening of ventricular wall)
-
Nutrition
deficiencies such as reduced levels of Taurine, L-carnitine,
Coenzyme Q10, electrolytes, and Thiamine (vitamin B-1)
-
Endocrine
diseases such as diabetes, thyroid disease, Cushing’s disease
-
Viral or
bacterial infections that becomes systemic (spread throughout the
body) and attack the muscle cells of the myocardium
-
Autoimmune myocarditis (inflammation of the myocardium)
-
Toxins
that destroy the muscle cells of the myocardium, such as drugs or
poisons
-
Dental
disease: It is important to note that dental disease, the #4
disease in Bichons, can lead to cardiomyopathy. Diseased
gums/teeth release high levels of bacteria and pro-inflammatory
components (endotoxins). These bacteria and endotoxins gain
access to the systemic circulation via the very vascular oral
tissues and then travel to the heart muscle destroying myocardial
cells, as well as to other organs in the body.
Intrinsic
cardiomyopathy,
the second classification of cardiomyopathy, occurs without
identifiable external causes. In at least 50% of the cases of DCM,
no cause can be found (idiopathic), however DCM is suspected to be
genetic.
Diagnosis of DCM
DCM is an
adult-onset disease, so signs may not be apparent until well into
the breeding years. A definitive diagnosis of DCM can be obtained
by echocardiography (ultrasound) that will demonstrate the dilated,
poorly contractile ventricles. If echo is not available, a
presumptive diagnosis of canine DCM is based upon the physical
examination and clinical signs of heart failure; a chest xray that
reveals an enlarged heart with congested lungs; and an
electrocardiogram that reflects enlarged ventricles with possible
irregularities in the heart rhythm. In addition, any potential
extrinsic causes of cardiomyopathy must be ruled out via blood
samples, such as serum deficiencies of Taurine or Carnitine or
endocrine diseases such as diabetes, Cushing’s or thyroid disease.
An
additional blood test may reveal elevated atrial natriuretic peptide
(ANP or proANP) that correlates with the severity of heart failure.
Heart failure causes increased pressure in the atria (the heart
chambers above the ventricles) as the blood backs up from the
weakened ventricles that cannot empty properly. The increased
pressure in the atria stimulates the release of the hormone ANP.
Early detection of heart failure facilitates more effective
treatment, and screens dogs that may need further evaluation. A new
screening tool for proANP can be obtained from NationWide
Laboratories called “Canine Cardiac Screen” at this web address
http://www.nwlabs.co.uk/canine-cardiac-screen.html.
Treatment of DCM
Considering
the high mortality rate with survival at 1 year about 15%,
aggressive medical treatment is imperative. Up to 50% of affected
dogs die suddenly due to arrhythmias (irregularities in the heart
rhythm). If a cause for the DCM can be determined, treatment or
stabilization of that cause may improve the cardiac status of the
dog. Earlier treatment, prior to symptoms of heart failure, will
produce a better outcome.
Medications
that may be prescribed by the veterinarian to improve the efficiency
of the ventricles:
1.
Diuretics such as Furosemide (Lasix) that promote loss of
excess fluid
2.
Pimobendan (Vetmedin)
improves contractility of the ventricles
3.
ACE inhibitors such as Amlodipine, Enalapril, Benazapril
improve contractility of the ventricles
4.
Drugs to treat arrhythmias that may develop
Dietary
supplements that promote a healthy heart include fish oils, multiple
vitamins that contain minerals and the B vitamins, Vitamin E,
Taurine, L-carnitine, and Coenzyme Q10. Commercial lamb meal based
diets may cause a Taurine deficiency.
Sodium
restriction in the diet is essential to avoid stressing the heart
and lungs with excess fluid. Beware that high levels of sodium can
be hidden in cheese, lunchmeats, canned dog foods, and most dog
biscuits and treats. Many commercial dry kibbles do not indicate the
levels of sodium. The best diet to avoid sodium is fresh raw foods.
Limit
strenuous activities to allow for adequate rest. Maintain a normal
weight since extra pounds strain the heart. Seek veterinary services
for any signs of respiratory distress, progressive lethargy, or
fainting.
New
technology—stem cells:
Any disease that results from a premature loss of cells has the
potential for benefit from treatment with stem cells that can be
obtained from the dog’s intrinsic cells or a close relative.
Myocardial cells do not regenerate after injury, however stem cells
may be able to generate new myocardial cells to replace those that
died and to repair some of the damaged cells. The stem cells are
injected intravenously with hopes they will migrate to the heart, or
they are injected into the coronary arterial system, or directly
into the heart muscle.
A case study of a Bichon Frise with DCM
An
8-year-old female Bichon Frise presented to a veterinary internist
with a probable diagnosis of cardiomyopathy. During a pre-surgical
exam her primary veterinarian discovered an arrhythmia (irregular
heart beat), and then referred her to the internist for further
evaluation. DCM was then verified by echocardiogram.
Her past
history was negative for health issues. Her owner denies any
symptoms of heart failure. She completed her AKC championship and
was bred one time near the age of 4 years, producing 5 healthy
puppies via C-section. She tolerated pregnancy, the C-section, and
nursing well. Had she been bred again after her DCM had
progressed, she may not have tolerated this type of stress to her
body.
On exam at
the internist’s office, her pulses were normal, her color was normal
(pink), and there were no murmurs detected. Her blood tests were
all normal, ruling out diabetes, thyroid disease, kidney disease,
liver or pancreas disease, electrolyte imbalances, and anemia. Her
electrocardiogram revealed frequent premature beats (an
arrhythmia). Her echocardiogram (ultrasound) revealed dilatation of
both ventricles, mild leaking of the mitral valve, and an ejection
fraction (EF) of 18%. EF is calculated during the echocardiogram,
which indicates the average amount of blood ejected from the left
ventricle. A normal EF is 60-70%, so 18% is significantly reduced,
reflecting the weakness of the ventricular contractions.
She was
prescribed Benazapril and Pimobendan to strengthen myocardial
contractility, and Procainamide to treat the arrhythmia, which was
later discontinued due to stomach issues. Taurine, and L-carnitine
were also prescribed but may be discontinued soon since the vet does
not feel these supplements have made an impact on her cardiac
status. Her status remains stable with perhaps slight improvement
in her heart function after 9 months of treatment. Her owner still
does not discern any symptoms of heart failure.
Despite the
fact that this Bichon did not exhibit symptoms of heart failure, the
red flag that urged the veterinarian to investigate further was an
irregular heart rhythm (arrhythmia). The lesson that can be learned
from this case is to obtain the cardiac OFA certification prior to
breeding, which would detect arrhythmias and murmurs, and to obtain
annual vet exams for Bichons we are breeding in case an arrhythmia
develops.
Breeding Advice
Specific genes for DCM have not yet been identified in dogs, but
inheritance patterns in specific breeds have been established. DCM
is autosomal recessive in some breeds (not sex-linked and both
parents must be a carrier or affected), is sex-inked in some breeds
(found more often in males), and is autosomal dominant in other
breeds (only
one affected parent is needed to pass it to offspring).
56 defective genes that cause DCM have been identified in humans, so
in time the defective genes will be identified in dogs. We need to
consider that even if an extrinsic cause for DCM is identified, such
as a Taurine deficiency, that dog may have the genetic
predisposition to develop DCM when that trigger event occurs.
Affected
dogs and their parents should not be used for breeding. Siblings
should only be used after careful cardiac screening.
See the link below to Dr. Jerold Bell’s article for more information
on modes of inheritance.
The BFCA
Health Committee feels that this disease deserves vigilance. We
encourage you to share data with our committee on any Bichons with
DCM, which will remain confidential, so that we can be aware of
current trends in health problems in Bichons. Contact either a
committee member, or complete a health incident form located on
www.bichonhealth.org.
References:
-
Diseases
of the Heart by Charles K. Friedberg
-
Cardiovascular Nursing by Kernicki, Bullock, Matthews
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“Matters
of the Heart” by Mara Bovsun. AKC Gazette, October, 2005
-
“Facts on
Canine Cardiac Health” by Kevin Schargen. AKC Gazette, March,
2005
-
web
sites:
http://www.upei.ca/cidd/intro.htm
http://www.vetgo.com/cardio/concepts/concsect.php?conceptkey=78#78
http://vin.com/VINDBPub/SearchPB/Proceedings/PR05000/PR00034.htm
http://www.offa.org/cardiacinfo.html
http://www.bichonhealth.org/HealthInfo/Startegies.asp
(Dr. Bell’s article)
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