WSVMA Annual Conference
Small Animal Cardiology
Kathryn Meurs, DVM, DACVIM (Cardiology)
Washington State University
College of Veterinary Medicine
Spokane Convention Center
Spokane, Washington
October 1-3, 2010
Kathryn M. Meurs, DVM, PhD, Diplomate ACVIM (Cardiology)
Washington State University Pullman, WA
Biography:
Dr. Meurs is a Professor in the Department of Veterinary Clinical Sciences at Washington State University. She has a DVM from theUniversity of Wisconsin – Madison and completed a small animal internship at North Carolina State University in 1991. She completed a Cardiology residency at Texas A&M University and is board certified from the American College of Veterinary Internal Medicine (Cardiology).
Contact Email:
Radiographic/Echocardiographic Imaging in Cardiology
Kathryn M. Meurs, DVM,PhD Meurs@vetmed.wsu.edu Diplomate ACVIM (Cardiology)
Washington State University
In this session we will review thoracic radiology and echocardiography with an emphasis on normal and abnormal anatomic features.
Indications
Modern imaging technology (MRI, CT, echocardiography) has dramatically improved the veterinarian’s ability to diagnose cardiac and thoracic disease. However, it has not diminished the need for thoracic radiographs. Advanced imaging has not replaced thoracic radiography and thoracic radiography does not replace advanced imaging. Thoracic radiography
continues to be one of the most practical and best tests for identifying parenchymal disease (congestive heart failure, pneumonia, heartworm and Neoplasia).
Remember that dyspneic animals can be extremely fragile. In some cases, it may be reasonable to treat based on suspicion of the disease for 12-24 hours to try to stabilize the patients before taking radiographs.
Limitations
Remember that thoracic radiographs can not indicate cardiac or pulmonary function. Additionally, while they may be fairly specific for cardiac enlargement, they are not very
sensitive, or said another way- if significant cardiac enlargement is present it is likely real, if it is absent, it does not rule out cardiac disease. Significant breed variations are known and can complicate the interpretation of films even in normal patients. Finally it can be very difficult to interpret right ventricular enlargement patterns.
Technique for interpretation
In order to avoid misinterpretation it is ideal to examine every thoracic radiograph in a systemic fashion.
Technical quality
In almost all cases 2 views should be obtained. An exception to this would be a recheck radiograph taken within 24 hours after a thoracocentesis to determine the efficacy of a pleurocentesis. In this case it might be reasonable to just retake the lateral film.
Although different radiologists use different approaches, we generally evaluate the right lateral and a dorsoventral (DV) view. The use of a ventrodorsal approach is also acceptable, but may be more risky in animal with dyspnea or significant pleural fluid.
1. Thoracic space
The thoracic space should be evaluated for both pneumothorax and pleural fluid. Sometimes the most sensitive detection of pleural fluid is observed on a DV view in the costodiaphragmatic angles.
2. Cardiac anatomy
The cardiac silhouette should be evaluated for enlargement. If enlargement is identified, it is extremely important to then determine the specific chamber (s) enlarged. Unfortunately, breed and species differences can sometimes mislead and suggest the appearance of general cardiac enlargement even if it is not present.
The Vertebral Heart Score was developed to help reduce the confusion observed with these differences. The Vertebral Heart Score (VHS) is a method of normalizing cardiac size to body length or conformation by relating cardiac size to vertebral body (JAVMA 1995;206:194-199, Buchanan et al). The procedure is as follows:
1. Measure the long axis of the heart from the ventral border of the left mainstem
bronchus to the most distal ventral contour of the cardiac apex using calipers or a note card. Reposition the calipers or note card to the cranial edge of the fourth thoracic vertebrae and measure the number of vertebrae caudally to the nearest 1/10 of a vertebrae.
2. In the central third of the heart, measure the maximal width or short axis of the heart at the angle that is perpendicular to the previously measured long axis. Reposition the measuring device over the thoracic spine at the cranial aspect of the fourth vertebrae and record the number of vertebrae caudally to within the nearest 1/10 of a vertebra. 3. Add the 2 measurements together to equal the VHS.
4. The average VHS is 9.7, most dogs are less than 10.5. Most cats are less than 8. The Vertebral Heart Score is not very useful in cats since many cats with myocardial disease, including hypertrophic cardiomyopathy, can have normal VH scores and have very abnormal hearts.
Perhaps one of the best uses of the VHS is to study progression of known cardiac disease. For example, the VHS may be determined in cases where radiographs will be taken annually or every 6 months in patients with cardiac disease to help identify subtle size changes or different
interpretations between doctors.
After evaluating for global cardiac enlargement, the specific chambers of the heart should be evaluated for enlargement. Generally we use a clock face analogy.
Dorsoventral view 12:00- 1:00 aorta 1:00-2:00 pulmonary artery 2:00-3:00 left auricle 2:00-5:00 left ventricle 5:00-9:00 right ventricle 9:00-11:00 right atrium 2
Lateral view
12:00- 3:00 left atrium 3:00-5:00 left ventricle 5:00-9:00 right ventricle
9:00-11:00 right atrium, pulmonary artery or aorta
3. Vasculature
On the lateral view, the vessels are best evaluated in the cranial lobes where they are arranged dorsal to ventral as artery, bronchus and vein. On the dorsoventral view the vessels are best evaluated in the caudal lobes as they are arranged lateral to medial as artery, bronchus and vein. Pulmonary artery and vein are generally of equal size and have clear sharp edges. A rule of thumb is that the average vessel size is approx. 75% of the diameter of the proximal 1/3 of the fourth rib on the lateral view.
Enlarged pulmonary arteries may suggest pulmonary hypertension (heartworm disease, chronic pulmonary disease, thromboembolic disease).
Enlarged pulmonary veins may suggest pulmonary venous congestion with left heart failure.
Enlarged pulmonary arteries and veins may suggest over circulation, i.e.intravenous fluid overload or a left to right shunt (PDA, VSD, etc).
4. Parenchymal changes
Parenchymal patterns are generally divided into interstitial, bronchial and alveolar patterns. Interstitial patterns are generally described as “ground glass” and result from the accumulation of fluid in the connective tissue framework of the lung. This may be associated with aging changes, cardiogenic pulmonary edema, noncardiogenic pulmonary edema, interstitial pneumonia,
lymphoma or diffuse metastatic disease.
Bronchial patterns are associated with increased lymphatic flow in the peribronchial tissue as well as accumulation of fluid in the bronchial walls and peribronchial tissue. This pattern is characterized by the “doughnut” appearance of thickened bronchi in cross section. This may be associated with feline asthma, canine bronchitis, allergic pneumonitis or pulmonary infiltrates with eosinophils.
Alvelolar patterns are associated with the filling of the alveoli with fluid so that the fluid silhouettes the remaining air filled bronchi which appear as air bronchograms. This may be observed with severe heart failure, bronchopneumonia, pulmonary contusion, hemorrhage or other noncardiogenic edema.
It should be remembered that radiographs are good for suggesting cardiac enlargement and excellent for detecting vascular and parenchymal changes associated with heart failure. They are not specific for types of cardiac disease, therefore an echocardiogram is still needed to determine the type of cardiac disease that initiated the problem. Secondly, echocardiographs may tell us about the specific type of cardiac disease, but they can not tell us about the status of congestive
heart failure. Thus radiographs and echocardiography are BOTH needed in many cases, one does not replace the other.
Echocardiography
Echocardiography is not a particularly difficult technique, but it is very user dependent!!! It is similar in many ways to learning a sport or musical instrument in that it takes great dedication to practice to become skilled! Practice is crucial for the echocardiographer to develop the ability to obtain all of the images as well as to develop the ability to identify normal anatomical variations from disease states.
Equipment
There are many different types of machines. We will not discuss types of machines today, but minimally, the machine should come with multiple probes of different frequencies, a electrocardiogram that will run concurrently, printing ability and calculation packages to allow calculation of fractional shortening, pressure and shunt gradients, etc.
Transducers
High frequency probes (7.5 MHz) produce sound waves with a shorter wavelength which allows better reflection from smaller structures. This allows better detail and resolution but less tissue penetration than a lower frequency (3.5 MHz). So a small animal like a cat or puppy would be best approached with a 7.5 MHz, but a larger animal like a Doberman pinscher should be approached with a 3.5 MHz.
Types of echocardiography
M-Mode and two-dimensional echocardiography are used to evaluate cardiac chamber size anatomy and motion. The best images are obtained when the ultrasound beam is perpendicular to the heart structures. Doppler echocardiography is best to evaluate direction and speed of blood flow. Doppler information is most accurate when the Doppler waves are parallel to the blood flow,
Two dimensional (2D echocardiography)
Many cardiologists start with the 2D echo to begin the examination. The 2D study creates a pie or fan shaped image to display anatomic features and should be used to evaluate both the Long axis and Short Axis views.
M-Mode echocardiography
After the 2D study is completed, M-Mode images should be obtained from the short axis at the level of the left atrium, mitral valve, and left ventricle. The M-Mode evaluates a single “ice pick” beam over time. This is the mode generally used to evaluate the size and function of the ventricle. Measurements are made from leading edge to leading edge. After the wall thickness
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and ventricular lumen sizes are determined, the fractional shortening (FS%), an index of contractility, can be determined from the formula = Left ventricular dimension at diastole- left ventricular dimension at systole/left ventricular dimension at diastole.
Doppler echocardiograpy
Doppler echocardiography is used to evaluate blood flow direction and speed. It can be used to identify an insufficient valve as well as a congenital shunt. Color flow may be used to detect the direction of the valve, and Pulsed is generally used to detect flow velocity. The velocity is important since it can be used to identify the pressure gradient across an stenotic valve or shunt using the formula 4x (velocity)2 = Pressure gradient. It should be kept in mind that the accuracy of Doppler is best when the beam is parallel to flow and the lowest MHz probe should be used. In most evaluations, all three forms of echocardiography should be performed since they support each other and the study usually begins with a 2D study, followed by M- Mode and then Doppler.
However, in some cases, one can find sufficient information with just 2D or M-Mode. For example, 2D will be sufficient to diagnose pericardial effusion and cardiac tamponade. However, we may want 2D, M- mode and Doppler to evaluate the cat with hypertrophic cardiomyopathy.
The coughing dog- a comparative approach to coughing in the older dog (Valvular heart disease & chronic obstructive pulmonary disease)
Kathryn M. Meurs, DVM, PhD Meurs@vetmed.wsu.edu Dip ACVIM (Cardiology) Washington State University
Chronic obstructive pulmonary disease (COPD) and endocardiosis are both common problems observed in older small breed dogs. In this lecture, we will discuss the clinical presentation, diagnostic tests and treatment options of the two syndromes.
Coughing in the older dog
Common causes of coughing in the older dog may be a consequence of tracheal collapse COPD, endocardiosis with left atrial enlargement and mainstem bronchus compression (LAE) and/or endocardiosis with congestive heart failure (CHF). Careful evaluation of history, physical and radiograph findings will help differentiate which disease may be responsible in each
particular case, although it is not uncommon to have more than one underlying disease process. Echocardiography is not always needed.
The ability to differentiate the disease responsible in each case is dependent on evaluation of: Signalment
Physical examination The Cough
Thoracic radiographs
And sometimes BNP and Echocardiography
COPD Valve + MBC Valve + CHF
Signalment Overweight Normal Cachexia
Cough Dry Dry Productive
HR Slow Normal Fast
Radiographs Pulmonary Big LA CHF
BNP Normal May be Increased Increased
Chronic Obstructive Pulmonary Disease
Signalment
The signalment for the dog with COPD is typically an elderly, small breed dog, although the disease can be observed in larger breeds as well. Chubby to obese dogs are frequently seen with COPD.
Physical examination
The physical examination of the dog with COPD often includes an overweight dog with a pronounced sinus arrhythmia since the respiratory disease has led to increased vagal tone.
Auscultation may reveal pulmonary crackles that may be focal or diffuse.
Since many of the breeds that suffer from COPD also suffer from tracheal collapse and
endocardiosis, tracheal irritation and even a left apical heart murmur may be observed but may not be the cause of the cough.
The cough
In some cases, the characteristic of the cough and the timing of it may be of use to differentiate the underlying disease, however, significant overlap in the characteristic of the cough exists and so it should not be used as a definitive finding.
The dog with COPD has usually had a long history (often over 2 months, can be YEARS) of cough. In some cases, the cough can seem to be seasonal or episodic and some researchers think that there may be an allergic component. The cough usually has a dry and hacking nature. Thoracic radiographs
Thoracic radiographs for the dog with COPD may have an increase in interstitial or peribronchial infiltrates and/or peribronchial cuffing. However, in some cases, normal radiographs may be observed.
BNP
Measurement of Prohormone BNP (Idexx) has been shown to be helpful in differentiating respiratory from cardiac causes of dyspnea. Prohormone BNP is released when the cardiac ventricles are dilated, hypertrophic or subjected to increased wall tension. Therefore, BNP measurements can be used to help diagnose, or exclude a diagnosis of heart failure in dogs that presented for cough or dyspnea. Unfortunately, it is still a “send out “ so the results will take some time to obtain and false positives can exist (especially in the face of azotemia). However, BNP may provide helpful confirmatory results for a difficult case in which both cardiac and respiratory pathology exist and it is difficult to determine which process is the main cause of the dyspnea.
Echocardiography
In most cases, the cause of the cough can be determined from evaluating physical exam findings, the cough and thoracic radiographs. However, in some cases, echocardiography can be helpful. It may be indicated in cases where it is unclear if cardiac or pulmonary disease is the most important issue. If COPD is the cause of the cough, the echocardiograph should be within normal limits, except in rare cases where pulmonary hypertension develops or if concurrent valvular disease exists.
Treatment
Treatment for COPD is not curative. Clients should be advised of this at the time of diagnosis to avoid disappointment and false expectations. Treatment is aimed at control of the cough (palliation of signs). The clinical signs are often due to inflammation and an allergic component may exist. If an allergic component exists and is seasonal, therapy may be only needed on intermittent basis.
Glucocorticoids at an anti-inflammatory dose (Prednisone - 0.5mg/kg BID PO x 10 –14 days and then taper) are often very useful to get the cough under control. After 2 weeks at this dose it is generally reasonable to begin to slowly taper the dose to see if the control may be maintained at a lower dose. In some cases, dogs may even be intermittently removed from therapy. In some cases, it may be beneficial to add on a bronchodilator when therapy is iniated. However, bronchodilators alone are almost never sufficient to control a cough. Corticosteroids are almost always needed. A variety of bronchodilators exist, however Theophylline (15-18 mg/kg orally BID) is used frequently.
In some cases it may be reasonable to try inhalational therapy. An excellent website exists for the equipment and medication regimens for this type of therapy:
http://www.aerokat.com/ . Although this approach may be slightly more expensive, it has the advantage of allowing delivery of steroids to the lungs with minimal systemic effects.
Additionally, in some cases it may be more effective because of direct delivery to the lungs. If inhaled steroids will be used, it is a good idea to start the patient on oral steroids first or
simultaneously with the inhaled steroids since it often takes 3-4 weeks on inhaled therapy before a response is noted. After 3-4 weeks of simultaneous therapy the oral steroids can be gradually removed. The doses often used are: Corticosteroids (Flovent) 1 puff, twice a day and 1 puff bronchodilator (albuterol) twice a day.
A cough suppressant may also be added periodically to help break the coughing cycle. Hydrocodone- 0.22 mg/kg orally every 6-12 hours during difficult times can be prescribed and the frequency & dose decreased if lethargy develops.
If obesity is a problem, weight reduction should be discussed.
Endocardiosis with left atrial enlargement and main stem bronchus compression (MBC)
Signalment
The signalment is similar for dogs with endocardiosis – older small breed dogs (large breed dogs, especially Labradors can also be seen).
Physical examination
The physical exam for dogs with mitral valve endocardiosis and mainstem bronchus collapse (MBC) includes a systolic left apical heart murmur. A right apical heart murmur may also be heard since many cases of endocardiosis involve both the mitral and tricuspid valve. A dog that is coughing due to left atrial enlargement and mainstem bronchus compression should have a normal heart rate and normal lung sounds.
The cough
The dog with endocardiosis and MBC usually has a dry, nonproductive cough. Thoracic radiographs
Thoracic radiographs for dogs with endocardiosis and MBC have significant left atrial enlargement and compression of the mainstem bronchi.
Echocardiography
If endocardiosis with MBC is the problem, a thickened irregular mitral valve may be observed. Valve prolapse may be observed and left atrial enlargement will be present. Treatment
The cough in these cases is a direct effect of compression of the mainstem bronchi by the large left atrium. Unfortunately, there is no known pharmacological ability to reduce left atrial size. Some investigators believe that ACE Inhibitors (Enalapril, Enacard) or diuretics may help.
Enalapril may help decrease left atrial size by decreasing blood volume and afterload at a dose of 0.25-0.5 mg/kg PO BID.
Some individuals suggest furosemide to decrease blood volume and potentially decrease atrial size, however, furosemide has some potential to increase the neurohormonal cascade and should probably not be used alone (use with enalapril) if the possibility of concurrent heart failure exists.
Endocardiosis with congestive heart failure
Signalment
If endocardiosis has advanced to congestive heart failure (CHF), the animal may be thin to cachectic. If endocardiosis has advanced to congestive heart failure, the animal may be thin to cachectic.
Physical examination
The physical exam for a dog with endocardiosis and CHF should include a systolic left apical heart murmur and may have a right apical heart murmur (many have both mitral & tricuspid dz), but is typically tachycardic due to the high sympathetic tone observed with CHF. Dyspnea with tachypnea may be observed and moist crackles may be present.
The cough
Dogs with endocardiosis and CHF may have a soft, moist cough that is more commonly heard at night or first thing in the morning.
Thoracic radiographs
Thoracic radiographs for dogs with endocardiosis and CHF should have left atrial enlargement, an increased interstitial pattern (typically perihilar) and pulmonary venous congestion. With more advanced cases an alveolar pattern may be observed.
Echocardiography
If endocardiosis with CHF is present, a thickened irregular mitral valve (+/- prolapse) and left atrial enlargement will be observed. Left ventricular enlargement and systolic dysfunction may be observed.
Treatment
The trick to control of the cough with CHF is combination therapy !
Dogs with CHF benefit tremendously from manipulation of the RAAS system with ACE Inhibitors (Enalapril,Enacard). Control of these cases with a diuretic alone should not be
attempted because Furosemide may actually increase the neurohormonal cascade. I prefer to start with mid range doses of the following:
Enalapril - 0.25-0.5 mg/kg PO BID Furosemide - 1-3 mg/kg PO SID-TID Pimobenden – 0.25 mg/kg BID
Once control is obtained, the dose of Furosemide may be tapered to try to maintain at the lower end of the doses.
Additionally, Spironolactone, an aldosterone antagonist and weak diuretic, may be added. It has an additional RAAS effect and has been shown to decrease mortality in humans.
Spironolactone may be added at 1-2 mg/kg PO BID.
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Finally, digoxin is typically saved for cases with supraventricular tachycardias (most commonly atrial fibrillation as discussed in the ECG lectures.
Conclusions
A chronic cough can be caused by cardiac and/or respiratory disease in the older dog. In many cases, the dog may have several ongoing disease processes. Careful evaluation of the history, physical and radiograph findings may help differentiate the underlying cause.
Echocardiography is frequently not needed. Therapy is aimed at controlling the cough rather than curing it. It is imperative that owners understand this from the start, to avoid disappointment.
CANINE DILATED AND ARRHYTHMOGENIC CARDIOMYOPATHY
Kathryn M. Meurs, DVM, Ph.D. Meurs@vetmed.wsu.edu Diplomate ACVIM (Cardiology)
Washington State University College of Veterinary Medicine
In this lecture we will discuss canine dilated (DCM) and arrhythmogenic cardiomyopathy (ARVC). We will pay particular attention to breed specific findings.
Canine Dilated Cardiomyopathy - DCM
Strictly speaking, dilated cardiomyopathy (DCM) is defined as an idiopathic functional abnormality of the myocardium causing systolic dysfunction and/or arrhythmias. Definitive breed predispositions exist. Even though the disease is referred to as DCM in each breed, there are important clinical and pathological differences between the breeds mentioned. Although Boxer dogs can get dilated cardiomyopathy, most Boxers develop Arrhythmogenic Right
Ventricular Cardiomyopathy (ARVC), a very different disease.
Dilated cardiomyopathy is an adult onset disease, with the exception of the Portuguese Water Dog in which it is diagnosed between two and thirty-two weeks.
There appear to be two stages of DCM, an asymptomatic stage, referred to as occult, which may be detected by careful screening, and a stage at which symptoms appear, referred to as overt. There is some preliminary evidence that early recognition of the occult stage may slow progression of the disease therefore, being aware of early signs may be beneficial to patient management.
Clinical signs
Clinical signs may include coughing, dyspnea, tachypnea, syncope and occasionally, ascites.
Physical examination
A soft systolic murmur consistent with mitral valve regurgitation and/or a gallop rhythm (S3) may be ausculted at the left apex.
A tachyarrhythmia of sinus, supraventricular or ventricular origin may be noted. In some cases, a murmur or an arrhythmia may be the first signs of the occult form of the disease and should not be overlooked. Since primary valvular disease is relatively uncommon in large breed dogs, and the detection of DCM before the development of congestive heart failure (CHF) may be beneficial in the long-term management of the case, identification of a new murmur, gallop or tachyarrhythmia in suspect breeds should be considered a “red flag” and may warrant a thorough cardiac work-up. Although canine DCM is predominantly a left
ventricular disease, biventricular involvement and heart failure with jugular venous distension and ascites is frequently noted, particularly in the giant breeds.
Electrocardiography
Many dogs with DCM have normal electrocardiograms but atrial and/or ventricular enlargement patterns (R > 3.5 mV Lead II for the left ventricle) may be noted. Sinus tachycardia,
atrial fibrillation or ventricular arrhythmias are common. In some cases, ventricular
tachyarrhythmias can develop before any ventricular dilation or systolic dysfunction. Routine Holter monitoring may help detect these.
Radiography
Dilated cardiomyopathy is a progressive myocardial disease. If the disease is diagnosed in the early stages, radiographic findings may be subtle. Therefore, depending on the stage of the disease, thoracic radiographs may be within normal limits or may indicate atrial and ventricular enlargement (typically left) with or without pulmonary venous distension and pulmonary edema. In some cases, biatrial and biventricular enlargement may be noted.
Echocardiography
Echocardiography is the diagnostic test of choice for diagnosing canine DCM and is also an important test for occult disease. Echocardiographic findings in the patient with overt disease should include left and sometimes right atrial and ventricular dilation and decreased contractility as characterized by shortening fraction (FS%). Typically the decrease in contractility is quite severe with decreased fractional shortening % (< 20%).
A differential diagnosis for DCM is severe atrioventricular (AV) valve disease since severe ventricular dilation and systolic dysfunction may be occasionally observed in these cases. Consideration of the breed of dog may be helpful in differentiating between DCM and AV valve disease since it is uncommon for many of the large breed dogs to develop significant primary valve disease. An exception to this may be the cocker spaniel, a breed that has a high incidence of primary valve disease, and also is at increased risk of DCM.
Biomarkers
Prohormone BNP is released when the ventricles are dilated, hypertrophic or subjected to increased wall tension. Levels of BNP (Idexx) have been shown be increased in dogs with congestive heart failure and can be used to help diagnose, or exclude a diagnosis of heart failure in dogs that presented for cough or dyspnea. At this point it has not yet been shown to be
sensitive enough for detection of early disease. Etiology
It is clear that several breeds appear to be over represented and some breeds seem to have unique characteristics of the disease that may suggest that this is unique disease for their breed. A familial form of DCM has now been identified in several breeds and is suspected in others. Occasionally, atypical breeds of dogs develop DCM. The etiology of the disease in these cases is unknown and external factors that can insult the myocardium including infectious organisms or nutritional imbalances should be considered.
Doberman pinscher DCM
Etiology
Dilated cardiomyopathy is a familial disease in the Doberman pinscher and appears to be inherited in an autosomal dominant fashion.
Generally affected dogs are mature adults (average 6.5 years) although it has been reported as young as 1 year.
Clinical signs
Most affected Doberman Pinschers present for an initial diagnosis of DCM already in left heart failure (cough, respiratory distress). Syncope and sudden death are reported frequently due to the presence of ventricular premature complexes (VPCs). Most affected Dobermans will die from congestive heart failure and/or euthanasia due to refractory heart failure, although about 30% are believed to die from sudden death secondary to a lethal ventricular tachyarrhythmia. Screening for early (occult) DCM
Dilation of the ventricle may precede the development of systolic dysfunction and be an early indicator of DCM. It has been suggested that Doberman Pinschers with a left ventricular end diastolic dimension of greater than 4.6 centimeters and an end systolic dimension of 3.8 are at risk of developing DCM within a 1-2 year period. Caution- these numbers are based on average sized Dobermans (60-80 pounds) and may be less accurate if very large dogs (>100 pounds) Additionally, Holter monitoring has been suggested to be a good screening device for this breed. Adult Dobermans with greater than 10 VPCs per 24 hours, or couplets or triplets are suspect for the development of DCM.
Since dilated cardiomyopathy is an adult onset disease with a variable age of onset, screening should be performed every year and ideally include both an echocardiogram and a Holter
monitor. However, keep in mind that sometimes variations on the echocardiogram and Holter monitor can be due to other systemic diseases and if questionable should be repeated in 6 – 12 months
Prognosis
Affected Doberman pinschers have a poor prognosis. Once clinical signs have developed, death usually occurs due to heart failure or sudden death within 6 months, therapy is palliative at best. Preliminary work has suggested that starting enalapril when ventricular dilation has
occurred but before CHF develops, may slow rate of progression.Additionally, treatment with pimobenden as discussed below may have a significant positive effect on survival (increase survival to many months) but is still not a cure.
Great Dane Cardiomyopathy
Dilated cardiomyopathy in the Great Dane is a familial disease and appears to be inherited in an X- linked recessive mode of inheritance.
Clinical presentation
The Great Dane also typically starts with a left apical systolic murmur. However, there is some evidence to suggest that in some cases, the first sign of DCM is the development of atrial fibrillation, even before the development of left ventricular dilation and decreased systolic function. Additionally, Great Danes are much more likely to develop biventricular failure with ascites and jugular venous distension. Treatment for DCM and heart failure would be the same as for the Doberman pinscher. Although this is still a fatal heart disease, the prognosis is better than that for the Doberman pinscher.
Cocker Spaniel Cardiomyopathy
Cocker spaniels are at an increased risk of two forms of heart disease, endocardiosis (more common) and dilated cardiomyopathy. However since some of the cocker spaniels with dilated cardiomyopathy may be responsive to taurine and have an improved prognosis, differentiation is
important. If the taurine level is low, supplementation may be useful at 250-500 mg orally twice a day. Taurine is a safe supplementation so it may be started while waiting for the results of the plasma or serum levels. However, it is important to start other cardiac and heart failure medications as discussed above. Generally the prognosis is better for Cocker Spaniel
Cardiomyopathy than for some of the other breeds.
Taurine related cardiomyopathy
The development of dilated cardiomyopathy due to low taurine is much less common in the dog than in the cat since dogs have a much greater ability to synthesize taurine than cats. However, as mentioned above, a relationship between taurine and L-carnitine abnormalities and DCM has been previously described in the cocker spaniel. There have now been additional, reports of the development of DCM in the dog in which low blood or plasma levels of taurine have been documented. The dogs were all adult at the time of onset and were breeds that would be considered to be in the large breed dog groups. A common factor observed in several dogs that developed DCM and were determined to have low taurine was the feeding of a diet of a dry dog food with lamb meal, rice or both as the primary ingredient. It has been hypothesized that rice bran or whole rice products may result in decreased taurine levels in some dogs.
A diagnosis of taurine deficiency is indicated by a blood level of less than150 nmol/ml or plasma levels less than 40 nmol/ml. If taurine deficiency is suspected, taurine supplementation should be started while waiting for the results of the blood or plasma levels.
Published doses for taurine supplementation appear to vary slightly, although 1000 mg/day (divided or once a day) appears to be a consistent recommendation. Additional cardiac medications should be provided as needed including inotropic support such as pimobenden and treatment of heart failure if needed as discussed below. Taurine deficient dogs with dilated cardiomyopathy appear to respond to supplementation fairly rapidly and improvement in echocardiographic measurement should be observed in 3 - 6 months. Ideally blood levels of taurine should be reevaluated in 1-2 months to confirm that the levels have increased.
Treatment of the dog with occult (asymptomatic) dilated cardiomyopathy
Administration of angiotensin converting enzyme (ACE) inhibitors may have some benefit for the dog with early ventricular dilation, with or without systolic dysfunction. The use of ACE inhibitors in the Doberman pinscher with ventricular dilation was found to prolong the amount of time before the onset of CHF. Although this study was limited to evaluation of Doberman pinschers, the use of ACE inhibitors for other breeds of dogs with occult DCM may be considered (Enalapril, 0.5 mg/kg orally twice a day).
Administration of beta-blockers to the dog in the occult stage of DCM for a cardioprotective effect is still being evaluated and is not without risk. Further studies are needed before this can be safely used for the majority of our patients.
Treatment of the dog with dilated cardiomyopathy and congestive heart failure
Dogs with DCM and heart failure will benefit from inotropic support. Ideally, this would be with pimobenden, a phosphodiesterase III and V inhibitor with calcium sensitizing properties that acts as a positive inotrope as well as vasodilator (inodilator). Pimobenden has balanced vasodilatation and positive inotropic effects and has been shown to increase survival (median of 130 days versus a median of 14 days for the placebo in one study) in Doberman
pinschers with DCM. Additionally, it appears to be a mild appetite stimulant. Generally, it is dosed at approximately 0.25mg/kg orally q12 hours.
Additional medications for heart failure such as ACE inhibitors (Enalapril, 0.5 mg/kg orally BID) and diuretics (Furosemide, 1-4 mg/kg orally q 6-8 hours) should be started as needed.
Nonspecific treatments including nutritional supplementation by switching to a diet which contains supplements like taurine, L-carnitine and fatty acids (Royal Canin, Early Cardiac EC) should be considered.
Treatment of the dog with ventricular arrhythmias
There is little consensus for the decision of when and how to treat ventricular arrhythmias in the dog with DCM. Rapid ventricular tachycardia, complex ventricular arrhythmias or the combination of ventricular arrhythmias, ventricular dilation and systolic dysfunction are thought to be associated with a higher risk of sudden cardiac death and to be indications for treatment, but this has not been well studied. Additionally, some dogs die suddenly without having any of these arrhythmias documented. If treatment is warranted, consideration might be given to the use of one of several ventricular antiarrhythmics. Sotalol, a combination beta-blocker and potassium channel blocker, may be beneficial in some cases, but should be used a bit more cautiously (Sotalol, low dose, 1.0 mg/kg BID) if systolic dysfunction is present. Mexiletine at a dose of 5-6 mg/kg, q8hr, orally can be very effective at decreasing the arrhythmia. In a small number of cases it can cause nausea but this can be significantly reduced if it is given with at least a small meal, so it should never be given on an empty stomach. Although the goals of treatment include decreasing the number of ventricular premature complexes, decreasing symptoms and decreasing the risk of sudden death, the ability of any antiarrhythmic to reach these goals has not been well studied.
Boxer Cardiomyopathy (CM)
There are two forms of myocardial disease in the boxer, DCM and Arrhythmogenic right ventricular cardiomyopathy (ARVC) (most common).
Dilated Cardiomyopathy (less common myocardial disease in the boxer)
Boxers with DCM present with similar clinical signs to other breeds (syncope, cough, dyspnea). They may have a soft left apical murmur, an arrhythmia and sometimes have biventricular heart failure (ascites, jugular venous distension). Diagnosis is confirmed by echocardiography.
CAUTION!!!- Many boxers have a left basilar systolic murmur, this is more suggestive of a potential aortic stenosis or physiologic flow murmur than cardiomyopathy!
The treatment is similar to that in other breeds with DCM (as above) except that some Boxers with DCM may benefit from L- Carnitine (50 mg/kg orally three times a day) available at most health food stores) as well as possibly switching to a supplemented food such as Royal Canin early cardiac EC.
Arrhythmogenic right ventricular cardiomyopathy
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The more common form of boxer myocardial disease is arrhythmic and is named Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC). This is a familial (autosomal dominant) disease in the boxer.
The classical presentation is an adult boxer with VPCs. The dog may be asymptomatic, or symptomatic with episodes of syncope. The VPCs are typically wide and upright QRS in leads I, II, III, and AVF. The arrhythmia may be quite intermittent and in many cases, may require a 24 hour Holter monitor for documentation. Interpretation of the Holter results can sometimes be challenging because strict criteria for this diagnosis does not exist. However the observation of > 100 VPCs, or periods of couplets, triplets or runs of ventricular tachycardia are abnormal. A larger number of VPCs or a greater complexity of the arrhythmia (ventricular tachycardia, bigeminy, etc) has been associated with the development of clinical signs. Supraventricular premature complexes may be seen but not frequently, and are more commonly associated with the myocardial dysfunction form of the disease.
Treatment
Asymptomatic dogs with ventricular tachyarrhythmias
If an arrhythmia is detected on routine examination, a Holter monitor should be performed to evaluate for the frequency and complexity of the arrhythmia. Although a strict relationship between the development of symptoms and the number of VPCs does not exist, treatment is generally started if > 1000 VPCs/24 hours, runs of ventricular tachycardia or evidence of the R on T phenomenon exist. Owners should be advised that ventricular antiarrhythmics have the potential for proarrhythmic effects.
Dogs with syncope
Dogs with syncope and ventricular arrhythmias are generally started on treatment.
Sotalol (1.5-2.0 mg/kg, q 12hr, orally) is well tolerated and have been shown to decrease VPC number and complexity. In some cases, sotalol and mexiletine (5-6 mg/kg, q 8hr, orally WITH FOOD) may be needed.
Prognosis
Sudden death is always possible. However, many dogs may live for years on
antiarrhythmics without symptoms, some of these may eventually develop ventricular dilation and systolic dysfunction.
Feline Cardiomyopathy
Kathryn M. Meurs, DVM, PhD Meurs@vetmed.wsu.edu Diplomate ACVIM (Cardiology)
Washington State University
This session will focus on the most common form of feline cardiomyopathies which is hypertrophic. We will touch briefly on the much less common forms dilated, restrictive and arrhythmogenic. We will also discuss thromboembolic disease.
Myocardial disease, particularly hypertrophic cardiomyopathy, is the most common heart disease in the adult cat. Remember that valvular disease in the cat is very rare!!!! Cats do not develop endocardiosis and endocarditis is very rare, so always consider myocardial disease first when considering differentials for feline heart disease.
There are several forms of feline cardiomyopathy, hypertrophic (HCM), restrictive (RCM), dilated (DCM), arrhythmogenic (ARVC) and unclassified. In many cases, there is significant overlap between these different forms of cardiomyopathy with regard to clinical signs, ECG and radiographic findings. Echocardiography is needed to complete the diagnosis.
Feline Hypertrophic Cardiomyopathy (HCM)
Hypertrophic cardiomyopathy is defined by left ventricular hypertrophy w/o causative systemic or other cardiac disease. It is the most common form of heart disease in the cat! The etiology for the majority of cases is unknown. However, it is inherited in Maine Coon and Ragdoll breeds and is believed to be in the American Shorthair, Sphynx, Norwegian Forest and a few others. In the Maine Coon it has been shown to be an autosomal dominant trait (both genders are equally affected). In the Maine Coon and Ragdoll breeds a mutation has recently been identified as causative for the disease. Genetic tests based on a buccal swap are now available for these breeds (http://www.vetmed.wsu.edu/deptsVCGL/felineTests.aspx). It is a different mutation in both breeds and does not appear to be causative in other breeds.
Hypertrophic cardiomyopathy is typically characterized by hypertrophy of the left ventricular free wall and/or interventricular septum. This results in myocardial stiffness and decreased ventricular lumen size and therefore is a diastolic dysfunction disease. Mitral regurgitation may develop from distortion of the left ventricular cavity and from systolic anterior motion of the mitral valve (SAM). An increased left atrial pressure develops to fill the stiffened left ventricle. Elevated pulmonary venous pressure and pulmonary edema may result. In some cases,
pulmonary hypertension and right ventricular enlargement may occur secondary to the left sided heart disease and pleural effusion may develop. Thrombi may develop in the stretched, dilated atria and subsequently break free and lodge in the systemic circulation (typically the distal aorta).
The clinical signs of affected cats are quite variable. Affected cats may be asymptomatic, but dyspnea, and shortness of breath may be presenting complaints due to congestive heart failure. Acute hindlimb paralysis suggests distal aortic embolization. Sudden death can occur.
Physical exam findings may include a systolic murmur consistent with left ventricular outflow tract obstruction and/or mitral regurgitation. A gallop rhythm may be ausculted indicating abnormal left ventricular filling. Since asymptomatic cats may be affected, we recommend screening with an echocardiogram if a murmur or gallop is ausculted. Tachypnea and dyspnea may be observed if heart failure is present but crackles are uncommon.
The ECG is often within normal limits but conduction disturbances and arrhythmias (ventricular and supraventricular) may be noted.
Radiographs may be useful to evaluate for cardiomegally, chamber enlargement patterns, and evidence of heart failure, but are NOT diagnostic for the specific form of feline heart disease. Radiographic findings may range from normal to significant cardiac enlargement depending on the stage of disease and may have evidence of heart failure with pulmonary venous distension and patchy pulmonary edema present.
Echocardiography is the best diagnostic test !!! Generalized concentric left ventricular hypertrophy may be observed and localized left ventricular free wall and / or interventricular septal hypertrophy may be noted. Most clinicians use a cut-off of a wall thickness at diastole of greater than or equal to 6 mm as diagnostic in the absence of other causes of left ventricular hypertrophy such as hyperthyroidism, or systemic hypertension. Wall thickness measurements may be made on M-mode echocardiogram or by measurement of the wall on long axis. Multiple modes of echocardiography should be used for a thorough study including 2D echo to scan for regions of asymmetric hypertrophy, M-mode for LV measurements and Doppler to look for evidence of SAM and document obstruction. Left atrial or biatrial dilation may be noted.
Since left ventricular hypertrophy can occur secondary to hyperthyroidism and systemic hypertension, these diseases should always be considered when evaluating a cat with left ventricular hypertrophy.
BNP is a test that is being discussed with increasing frequency in both canine and feline cardiology.Prohormone BNP is released when the ventricles are dilated, hypertrophic or
subjected to increased wall tension. However it is most specific for identifying cats that are in heart failure. It has NOT been found to be reliable for assessing the presence or absence of heart disease in asymptomatic cats or cats with heart murmurs.
Treatment
Treatment of hypertrophic cardiomyopathy is directed at decreasing the heart rate to allow for maximum filling time, decreasing the left ventricular outflow tract gradient if SAM is present and controlling CHF if present.
The optimal therapy for asymptomatic cats is uncertain. In general, mildly affected cats are not treated.
Cats that are tachycardic (>220) and/or have outflow obstruction (SAM) on echo should probably be treated.
The most commonly recommended treatment is a beta blocker (atenolol, B1 selective).
Atenolol (approximately 3 mg/kg orally, twice a day) should decrease heart rate and left
ventricular outflow tract gradient if SAM is present. However, atenolol should never be started in cats with congestive heart failure (CHF). Supportive treatment for CHF should be given to these cats and once pulmonary edema is resolved (Furosemide, enalapril) atenolol may be started. Calcium channel blockers (Diltaizem) are another option but these are not frequently used any more. They may be used to decrease heart rate (perhaps less than beta blockers) but the ability to decrease left ventricular outflow tract gradient (SAM) with oral medications is unclear. Calcium channel blockers should also probably be withheld until the congestive heart failure is resolved.
In one study, the only drug that increased survival in HCM cats with CHF was enalapril (0.25-0.5 mg/kg q 24 hours) and atenolol actually decreased survival- but this was in cats with CHF. Atenolol (beta blockers) should never be started in a cat in CHF but can be used once the heart failure is controlled. However, if the cat is already on Atenolol when CHF develops, the Atenolol should not be withdrawn.
The prognosis for HCM may vary dependent on etiology and some cats progress rapidly to CHF while others plateau and never progress and live with mild disease for years. It may be best to advise owners that prognosis may be best determined after observing progression over months and that cats with CHF or thromboembolic episodes have a poorer prognosis.
Feline Dilated Cardiomyopathy (DCM) and Feline Restrictive Cardiomyopathy (RCM) These are both fairly uncommon forms of cardiomyopathy and will not be discussed at length today. The following information is provided to you as additional reference
material.
Feline Dilated Cardiomyopathy (DCM)
Feline dilated cardiomyopathy is a functional abnormality of the myocardium causing
systolic dysfunction – similar to the canine form. It is uncommon in cats but can be associated with Taurine (an essential feline amino acid) deficiency. Although most commercial cat foods today are well supplemented, special diets or owner created diets may be deficient. A small percentage of cats have dilated cardiomyopathy and normal plasma taurine levels, the cause in these cases is unknown. Myocarditis may have preceded development of DCM in some of these cases.
Radiographs may provide information about cardiomegaly and heart failure but the
echocardiogram is needed for diagnosis. Additionally taurine levels should be evaluated. Whole blood taurine levels should always be measured (normal mean is >200 nmol/ml) even if the diet is thought to be balanced. Taurine levels are typically low (< 100 nmol/ml) with taurine
deficiency. Since taurine supplementation is safe and inexpensive, Taurine supplementation should be given until Taurine deficiency is ruled out by blood levels. Taurine is given at 250 -500 mg PO q 12 hours, orally. Additionally, medications for heart failure (Lasix,enalapril) should be provided as needed and a positive inotrope should be started. Pimobenden
(Vetmedin) could be provided (although not yet FDA approved for use in cats) at a dose of 1.25 mg/cat orally twice a day.
The prognosis for cats that are Taurine deficient and that are supplemented is actually quite good and many cats will eventually be able to be removed from cardiac medications. The
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prognosis for cats with dilated cardiomyopathy that are not Taurine deficient is not good and many progress into advanced heart failure.
Feline Restrictive Cardiomyopathy - (RCM)
Restrictive cardiomyopathy is an uncommon myocardial disorder characterized by endomyocardial fibrosis, stiffened ventricular wall and impaired ventricular filling. This is mainly a diastolic disorder. Systolic function may be normal or decreased. Etiology is unknown. Biventricular CHF with pleural effusion and thrombi commonly develop in the markedly dilated atria.
***** In many cases, there is significant overlap of clinical signs, ECG and radiographic findings between cats with hypertrophic, dilated and restrictive cardiomyopathy.
Echocardiography is needed to complete the diagnosis.
Arterial Thromboembolism
Thromboembolism can occur with all forms of feline cardiomyopathy. Three factors are typically required for clot formation. Endomyocardial injury, blood stasis and altered
coagulability. Endomyocardial injury is likely due to injury and fibrosis in the large dilated left atria. Exposed collagenous fibers as well as reactive substances that occur with fibrosis act as reactive substances for platelet adhesion and large, dilated atria may have areas of decreased contractility where blood pools. Finally, cats have large, sticky platelets and platelets release serotonin, as well we other factors that lead to a hyperaggregable state. Other coagulation abnormalities may be present in cats with cardiomyopathy
Historically, treatment was directed towards removal or lysis of clot. This is no longer recommended due to high mortality associated with rapid clot removal that is likely a result of reperfusion injury and hyperkalemia among other factors. Now, treatment is directed towards
PAIN RELIEF that might includeButorphanol (+/- acepromazine as tranquilizer) and Epidural (requires skill in local anesthesia) or Fentanyl patch (does not provide immediate relief)
The prognosis is frequently poor, but approximately 35-40% regain use of limbs. Although many cats will regain use of motor function within 1-2 weeks, risk of a second episode is high. Many owners elect euthanasia due to the patient’s discomfort and concurrent heart disease The best method for prevention is not known but one could consider a platelet inhibitor such as clopidogrel (Plavix) 18.75 mg/cat q24 hrs (more potent than aspirin, described in
JAVMA, 2004;225:106-1411). For cats that have had one episode, many suggest adding a low molecular weight heparin. A less expensive, but likely weaker option would be aspirin (81 mg every 72 hours). There is no clear evidence yet that clopidogrel is any more effective than aspirin although studies are ongoing. Generally, some type of anticoagulant preventative therapy is recommended for all cats with atrial enlargement and any form of
