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AFGHANS ARE US -HEALTH
Canine Cardiomyopathy
John Bonagura United States
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Myocardial diseases are a common cause of
heart failure, arrhythmia, and cardiovascular mortality in the dog. The most
common of the canine myocardial diseases represent “primary” disorders of
the myocardium. These are manifested as idiopathic dilated cardiomyopathy (DCM),
arrhythmogenic cardiomyopathy (ACM), or both problems. ACM is characterized
by recurrent atrial arrhythmias, lone atrial fibrillation (AF), or by
ventricular ectopia without obvious echocardiographic evidence of myocardial
failure. DCM is typified initially by asymptomatic decreases in left
ventricular ejection fraction (so called occult DCM) followed by progressive
left ventricular dysfunction culminating in congestive heart failure (CHF).
Sudden cardiac death can occur in either form. Most cases of cardiomyopathy
are influenced by genetic factors, including breed, body size, and sex.
Aside from DCM and ACM, most other forms of cardiomyopathy are considered
relatively rare in dogs. Persistent atrial standstill in Springer Spaniels
and other canine breeds is diagnosed sporadically. Primary hypertrophic
cardiomyopathy is rare in dogs but is a differential diagnosis for sudden
death. Hypertrophic cardiomyopathy is also encountered with some regularity
in mature Boston Terrier dogs. Secondary causes of canine myocardial disease
include hypertrophy or injury from systemic hypertension, hypothyroidism,
iatrogenic hyperthyroidism, catecholamines, doxorubicin, brain-heart
syndrome, ischemia, Duchenne’s myopathy, and myocarditis (including Chagas
disease). Chronic volume or pressure overloads (as with congenital shunts or
chronic valvular disease) can progress to the “cardiomyopathy of overload,”
wherein the ventricle is hypertrophied and myocardial function impaired.
Cardiac tamponade, transient myocardial ischemia, and relentless
supraventricular or ventricular tachycardias are causes of reversible
myocardial failure.
Arrhythmogenic Cardiomyopathy
The term “arrhythmogenic cardiomyopathy” (ACM) is a useful term that refers
to recurrent or persistent arrhythmia in the setting of a normal left
ventricular ejection fraction. While some dogs affected with ACM clearly go
on to develop classic DCM, many do not, and in some, the key to clinical
management is control of the cardiac arrhythmia. ACM is particularly common
in the Boxer (and some English Bulldogs) where the term arrhythmogenic right
ventricular cardiomyopathy (ARVC) is sometimes used to indicate the presumed
origin of arrhythmia. The Doberman Pinscher is another breed that often
manifests ventricular ectopics prior to the development of overt myocardial
failure (DCM). Another common example is the Irish Wolfhound (and other
giant breeds); these dogs are prone to atrial fibrillation (AF) without
obvious impairment of LV contractility, a condition sometimes referred to as
lone AF. Other atrial arrhythmias may be recognized in ACM including ectopic
atrial tachycardia and atrial flutter.
ACM must be distinguished from other causes of cardiac arrhythmia such as an
atrial tumor (hemangiosarcoma), electrolyte imbalance (hypokalemia), splenic
tumor, or post-operative ventricular arrhythmia (probably caused by ischemia
and reperfusion). Similarly, a medication history should be obtained to
insure the arrhythmia is not caused, for example, by ongoing treatment for
respiratory disease (using sympathomimetic airway dilators) or by therapy
for hypothyroidism (excessive supplementation resulting in iatrogenic
hyperthyroidism). Some breeds that are prone to DCM are also predisposed to
hypothyroidism and may be receiving supplemental L-thyroxin. Successful
management of ACM includes 1) assessing the rhythm disturbance using routine
and ambulatory (Holter) ECG; 2) measuring LV ejection fraction by
echocardiography; 3) reviewing relevant clinical signs; and 4) judging the
clinical significance of the arrhythmia.
In dogs with lone AF, the Holter data provide insight about the daily heart
rate and the exercise heart rate. Average daily heart rates that exceed
90–95/min or moderate-level exercise heart rates that exceed 250/min are
reasonable grounds for slowing the heart rate response to AF. This can be
done with a beta-blocker such as atenolol (6.25 to 25 mg PO q12h) or
metoprolol (12.5 mg PO q12h in giant breeds). The initial dose of the
beta-blocker should be low to prevent lethargy, but it can be titrated up
over two to four weeks to achieve an appropriate average daily rate
(generally in the range of 70 to 80/min). Digoxin can be prescribed for lone
AF, but cardiac glycosides are less effective for controlling excessive
exercise-related rates and are not recommended by the author unless there is
congestive heart failure. Diltiazem (0.5 to 1.5 mg/kg PO q8h) is very
effective in controlling heart rate, but does not confer the
“cardioprotection” of beta-blockers should the arrhythmia represent occult
DCM.
Grading the severity of ventricular arrhythmias in terms of relative risk
for sudden death is more difficult. Clearly, the presence of clinical signs
(collapse, syncope) is an indication to control ventricular tachycardia if
the clinician is certain that a tachyarrhythmia is the basis for the spells.
If uncertain, an event monitor (client activated ECG) should be prescribed
and worn by the dog. The more common problem is when there are no overt
clinical signs but frequent ventricular ectopic beats. Here the clinician
must attempt to judge the seriousness of the arrhythmia. If the Holter ECG
shows rapid runs of ventricular tachycardia (exceeding 225/min), frequent
ectopics (such as more than 7,000 per 24 hour period), or “warning”
arrhythmias (such as short-coupled PVC’s, or flutter-like runs of
ventricular tachycardia), antiarrhythmic therapy is recommended.
Treatment depends in part on personal preference. For frequent single VPC/PVCs,
a simple beta-blocker may be effective in controlling the rhythm (see doses
above). For ventricular tachycardia, either sotalol (40 to 80 mg PO q12h for
a large dog) or the combination of mexiletine (5–8 mg/kg q8h) plus a
beta-blocker represent effective therapy for reducing the frequency of
ventricular beats and runs. The value of these in preventing sudden cardiac
death has not been proven however. In difficult to manage cases, amiodarone
may be tried. Procainamide plus a beta-blocker is used by some, but appears
to be less effective and more pro-arrhythmic. It should be emphasized that
beta-blockers, sotalol, and amiodarone are negative inotropic drugs. Sotalol
in particular is a class III drug with potent beta-blocker effects and it
must be used with great care—if at all—in the setting of congestive heart
failure or when LV ejection fraction is substantially depressed. In dogs
with obvious CHF, mexiletine is the preferred treatment to control serious
ventricular arrhythmias. Once CHF is treated (see below), the gradual upward
titration of a beta-blocker may confer better control of the rhythm and
protection against sudden death.
Dilated Cardiomyopathy
Dilated cardiomyopathy (DCM) is an idiopathic, genetic, or familial
myocardial disease characterized by cardiac dilatation and reduced
myocardial contractility. Histologic lesions include absence of
inflammation, attenuated wavy fibers, loss of myocytes, and the presence of
increased myocardial fibrosis. Coronary arteries are normal and the valves
unremarkable, except in older dogs with concurrent mitral or tricuspid valve
endocardiosis. Deficiency of metabolic substrates (such as L-carnitine or
taurine) is found in a minority of dogs, but the exact cause and effect
relationship between these substrates and DCM is incompletely understood.
There is no published evidence for deficiency of co-enzyme Q10 in this
disorder. The onset of myocardial failure and limited cardiac output is
followed by an assault of neurohormones and cytokines released to support
arterial blood pressure. However, neurohormonal activation is associated
with further myocardial damage. The left ventricular ejection fraction
continues to decrease, the heart dilates, and ventricular diastolic
dysfunction can be recognized by detailed echocardiographic studies.
Secondary atrioventricular valvular regurgitation often develops leading to
murmur of mitral or tricuspid regurgitation. Renal retention of sodium and
water combines with reduced left ventricular performance to produce CHF.
Arrhythmias can occur at any time during the course of disease. Syncope,
sudden cardiac death, or CHF are potential consequences of these events.
Frequently, biventricular CHF is precipitated by development of AF in a dog
with previously “compensated” DCM.
Dilated cardiomyopathy occurs most often in middle-aged, male, large and
giant breed dogs, such as the Doberman Pinscher, Great Dane, and Irish
Wolfhound, but DCM can affect dogs of any age and many other these breeds.
Often males are predisposed or more likely to be affected at a young age. In
addition to the large-breed dog, DCM is recognized regularly a variety of
spaniel breeds, and the condition occurs sporadically in small canine
breeds. The precise genetic basis for DCM has not been demonstrated. The
four most common clinical presentations of DCM are 1) occult DCM; 2) cardiac
arrhythmia (see above); 3) sudden cardiac death; and 4) congestive heart
failure (CHF).
Occult DCM indicates an overtly healthy dog with echocardiographic evidence
of systolic dysfunction by echocardiography. Most diagnoses are made when a
breeder requests screening of an important dog or after a veterinary
examination uncovers a murmur or arrhythmia. In most cases the “diagnosis”
of occult DCM is based on a minor axis measure of LV systolic function (the
shortening fraction). Values below 25% are considered suspicious in most
laboratories, but there is no unanimity about one specific figure that
indicates myocardial failure. This single linear approach can be questioned
because larger dogs shorten relatively more in the apical to basilar
direction and this motion is not assessed by the shortening fraction
measure. Before rendering a diagnosis of occult DCM, the clinician should
request more detailed echocardiographic measures of systolic function
including LV short-axis shortening area, apical-to-basilar mitral annular
motion, and volumetric estimates of LV ejection fraction using the method of
discs or a prolate ellipsoid model. Serial examinations also can be helpful
in establishing a downward trend in LV function. Holter ECG is a useful
adjunct for establishing the diagnosis in breeds prone to DCM with cardiac
arrhythmias. Most would consider >50 VPC/PVC’s per day abnormal. When the
diagnosis of occult DCM is certain, cardioprotection should be considered.
This can be initiated with an angiotensin converting enzyme inhibitor (ACEI)
such as enalapril, benazepril, ramapril (ramipril), or quinapril given once
daily. If persistent arrhythmias are evident, a beta-blocker or sotalol
should also be considered (see above for doses).
Advanced cases of DCM are presented with exercise intolerance and clinical
signs of CHF. There can be marked weight loss and cachexia. Syncope related
to ventricular arrhythmia or neurocardiogenic syncope (inappropriate
bradycardia and vasodilation) may be related by the owner. Clinical signs of
left-sided CHF include tachypnea, respiratory distress, and coughing related
to pulmonary edema. Right-sided CHF is characterized by jugular pulses and
jugular venous distension, hepatomegaly, and ascites. Biventricular failure
includes the above findings along with pleural effusion. Auscultation may
reveal atrial and ventricular gallops, systolic murmurs, or arrhythmias. The
arterial blood pressure usually is normal owing to vasoconstriction and
neurohormonal activation, but will be decreased in profound DCM with
cardiogenic shock. The intensity of the first heart sound and strength of
the arterial pulse are often diminished, indicating reduced LV contractility
and stroke volume. Crackles of pulmonary edema or a pleural fluid line may
be evident.
Laboratory studies support the diagnosis in advanced cases of DCM. The EKG
may demonstrate abnormalities typical of cardiomegaly (wide or tall P-waves;
wide or increased amplitude QRS complexes) or myocardial disease (wide QRS,
slurred R-wave descent, and ST-segment coving). One or more of the
aforementioned cardiac arrhythmias may be evident, though an ambulatory EKG
is needed to assess the frequency of ventricular ectopic rhythms. The signal
averaged EKG may demonstrate late potentials indicating increased risk for
ventricular fibrillation. Thoracic radiography reveals cardiomegaly and may
demonstrate typical radiographic features of heart failure. The
echocardiogram shows ventricular dilation, reduced left ventricular
shortening fraction, increased E-point to septal separation, decreased wall
excursion, left atrial dilation and variably right-sided cardiomegaly.
Doppler evidence of mitral regurgitation and tricuspid regurgitation,
pulmonary hypertension, and diastolic ventricular dysfunction are common.
Routine laboratory tests are usually normal or reflect intercurrent disease,
consequences of CHF, or complications of CHF therapy. Specialized blood
tests for L-carnitine or taurine may be performed in selected cases.
Initial hospital therapy of CHF caused by DCM includes diuresis with
furosemide (2–4 mg/kg IV, IM q6-8h), supplemental oxygen, nitroglycerin
ointment (1–1.5 inches for a large breed dog q12h), and rest.
Life-threatening pulmonary edema can be managed with furosemide and infusion
of sodium nitroprusside (0.5–2.5 mcg/kg/min) with careful attention paid to
arterial blood pressure (titrate the infusion to a systolic value of 85 to
90 mm Hg). Thoracocentesis is indicated for moderate to large pleural
effusions. When there is CHF with systemic hypotension, the treatment should
be furosemide, oxygen, and dobutamine (2.5 to 10 mcg/kg/min). Dobutamine can
have relatively long-term benefits and is continued for at least two days,
at which point the drug is tapered over a 6–12 hour period while assessing
blood pressure. In the setting of hypotension, vasodilators are avoided
until the pressure is stabilized by dobutamine for at least two hours after
which therapy with either sodium nitroprusside or an ACEI can be initiated
(see below). In dogs with atrial fibrillation, digoxin (0.005 mg/kg PO q12h)
is prescribed to control the ventricular rate response.
Home therapy for CHF caused by DCM includes furosemide, an ACE-inhibitor,
digoxin, and sodium-restricted diet. Fluid retention is controlled with
furosemide (2–4 mg/kg PO q8-12h) and sodium restriction if possible. Digoxin
therapy is initiated unless there is a contraindication (moderate renal
failure, complicated ventricular ectopics). An ACEI is prescribed for once
daily use (with a typical dose of 0.5 mg/kg PO for enalapril or benazepril),
and the dose increased to twice daily after one or two weeks of home care.
Where available, pimobendan (a phosphodiesterase inhibitor-calcium
sensitizing inotropic drug with vasodilating properties) should be
considered based on limited but promising clinical studies. Spironolactone
(12.5 to 25 mg PO q12h in a large dog) may be added to block the cardiotoxic
effects of aldosterone and impede sodium retention in the distal nephron. A
beta-blocker may be considered to blunt the cardiotoxic effects of the
sympathetic nervous system; however, heart failure must be well controlled
first. The beta-blocker of choice in human patients is carvedilol. This drug
is both a beta-blocker and alpha-adrenergic blocker (which helps to reduce
the afterload on the left ventricle). Carvedilol also had anti-oxidant
properties that may benefit the myocardium. Unfortunately, the prescription
drug (Coreg) is expensive. Dosing can be difficult even in large dogs that
may not tolerate the negative inotropy of any beta-blocker. Thus, low
initial dosages are mandatory (start with ¼ to ½ of a 3.125 mg carvedilol
tablet q12h). Drugs such as propranolol (0.1–0.25 mg/kg PO q8-12h) are
easier to dose, but have the disadvantage of greater “inverse agonism”
(inactivating the active state of beta receptors) and causing greater
negative inotropy. Metoprolol long acting (3–12.5 mg q12h) has been studied
in experimental canine heart failure, but the drug is difficult to dose at
less than 12.5 mg, which is too large for an initial dose. While there are
clear theoretical benefits of beta-blockers in canine DCM, one’s practical
ability to initiate and maintain treatment may be very limited and CHF can
worsen (often with pleural effusion). Certainly, when AF complicates CHF,
either a beta-blocker or diltiazem (0.25 to 1.0 mg/kg PO q8h) is prescribed
to control ventricular rate. Nutraceuticals (taurine or L-carnitine) are
used empirically in selected cases. When DCM occurs in spaniels or small
breed dogs, taurine supplementation (500 mg q12h) is recommended. Fish oil
supplements containing omega-3 fatty acids may improve appetite and reduce
cardiac cachexia (EPA–30 to 40 mg/kg PO q24h; DHA 20 to 25 mg/kg PO q24h).
Serious ventricular arrhythmias in the setting of CHF are managed with
mexiletine (5–8 mg/kg q8h) plus a low dose beta-blocker. Sotalol can be
tried in larger dogs (40 mg q12h) but can worsen CHF. A Holter EKG should be
used to assess therapy. |
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