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Dilated cardiomyopathy, DCM, is the most common cause of heart disease leading to death before 10 years of age in larger dogs. In the general dog population, DCM ranks only behind mitral heart valve disease as an eventual cause of mortality. (ref1, ref2)
The diagnosis of dilated cardiomyopathy puts enormous emotional strains on dog owners. Unlike the situation with congestive heart failure (CHF) (rptref) for which many treatment options (and even surgery [ ref1, ref2]) exist, veterinarians like me must gloomily inform you that there are limited ways to buy more time for your pet. It is the hardest part of my being a veterinarian. You can read how grief affects us all here.
In dogs that develop DCM, changes are occurring in the muscles that form their heart that decrease the organ’s ability to forcefully contract. Although those changes are generally present in all of the heart’s four chambers, they are usually most severe in the lower left chamber, the left ventricle. That chamber is the most muscular of the four because its job is to force blood throughout the dog’s circulatory system of arteries and veins. When it can no longer do that efficiently, blood pools (congestion) in the lungs and various other organs and body cavities (eg ascites). (ref) As the dog’s heart struggles to meet its body's circulatory needs, its walls become thinner, its size enlarges (=dilation) and it assumes a more rounded shape.
No matter what the cause, be it an abnormally formed heart (ref), heart valve failure, obstructions to heart blood flow (ref), heartworms (ref), DCM or other electrical disturbances in your dog’s heart pumping mechanism (fibrillation), the heart changes that lead to debility and death are the same.
Your dog’s individual genetics account for a great deal of its susceptibility to dilated cardiomyopathy. I already mentioned that the larger dog breeds face DCM considerably more frequently than smaller dog breeds. But even large breeds do not suffer the problem with equal frequency. Of the 11 breeds most likely to develop DCM in a 2008 European study, Great Danes, St. Bernards, Newfoundlands, Leonbergers, Dobermans, Finnish hounds, Boxers, Giant Schnauzers, English cocker spaniels, and Flat-coated retrievers led the list in DCM frequency. (ref) Others put Irish Wolfhounds at the top. (ref) Dogs are usually, but not always, middle-age when conspicuous signs of the disease first appear. In the same European study I refed, the median survival time for all dogs after the disease had been diagnosed was 27-140 days. (rptref)
Even within those higher-risk breeds, some families, kennels and dog genetic lines are considerably more likely to develop dilated cardiomyopathy than others. It is only when the gene pool of the breed is dangerously small (too few originating dogs or "progenitors") that the whole breed tends to suffers. That is the case in Irish Wolfhounds (ref1, ref2)
According to the Purdue VMDB dog health database, in 2010 the prevalence of DCM in male dogs was nearly twice that of females (0.66% vs 0.34%) (ref)
As I mentioned, veterinarians believe that certain gene combinations present in large dogs predispose them to DCM. If lifestyle, nutrition or other unknown factors increase the risk of large dogs developing the disease is still unclear. But there is a group of dogs for which veterinarians are quite suspicious that nutrition does play a part. That is generally when dogs of smaller breeds that are not known to carry a DCM tendency develop cardiomyopathy. I’ll get to that under Nutrition. In all forms of DCM the heart muscle (the myocardium) and the nerve fibers within the heart are damaged. In some cases, nerve damage ("attenuated wave fibers") occurs first. In those dogs, heart rhythm defects occur before heart muscle damage is severe. In other cases, it is the reverse. With time, the size of the surviving individual heart muscle cells increase in an attempt to compensate for the muscle cells that have been lost. When that process is no longer adequate (volume overload) the walls of the heart chambers begin to stretch and thin. (ref) Space formerly occupied by healthy heart muscle cells is replaced by scar tissue (fibrosis). The amount of inflammation that accompanies this process is variable.
Dogs who are genetically predestined to develop DCM probably have destructive changes occurring in their hearts at an early age. But your are quite unlikely to notice them. The heart is a powerful organ created with a large reserve of muscle cells. For many years, it can often compensate for the loss of muscle fibers.
The first signs many dog owners notice is a decrease in their pet's activity level. The dogs don’t have the willingness to exercise as much as they used to. Their heart can no longer meet the increased oxygen needs of strenuous exercise. Some loose weight due to their poorer appetite. In breeds with a high incidence of DCM, even those subtle signs might prompt your veterinarian to have some electrocardiogram tests run - probably with a Holter halter.
But in most cases, early signs of DCM are overlooked and it is not until signs attributable to heart failure occur that these dogs are brought to their veterinarians. The signs then generally include coughing, a rapid irregular and weak pulse, rapid and difficult breathing (dyspnea), pronounced weight loss, and sometimes, fluid accumulation in their abdomen (ascites). Other dogs experience fainting spells due to disturbances in their heart's electrical system. Their gums are often pale and the tiny blood vessels in the gums more prominent (injected). Their heart beat can often be detected in their jugular vein (jugular pulse). (ref)
Sometimes the progress of DCM is rapid enough for dogs to die from an irregular heart beat before it was even noticed that they were ill.
Your veterinarian will quickly zero in on your dog’s heart as is probably problem. But there are a number of other heart diseases that can produce the same clinical signs. As I mentioned, all forms of heart disease produce quite similar symptoms; and other problems like pneumonia, chest tumors, toxin ingestion, heart developmental defects and autoimmune disease can too. (ref) I live in South Texas where Chagas disease in dogs also mimics DCM. (ref)
Once DCM has progressed to heart enlargement, x-rays of your dog’s chest will indicate that. Those x-rays will also help rule out some of the other causes of difficult respiration that I mentioned. An irregular pulse and heart murmurs detected with a stethoscope in non-anemic dogs help confirm heart involvement. If there is doubt, a proBNP test might be ordered as well.
At that point, your veterinarian will probably let you know that a board certified veterinary cardiologist has the specialized training required to delve deeper into your dog’s heart problem. Their tools are doppler ultrasound (echocardiography) that examines the thickness of your dogs heart chambers, abnormal distortions and the flow of blood through the heart. (ref) Veterinary cardiologists also have more experience utilizing some of the specialized medication cocktails in ways more likely to minimize side effects.
They closely examine your dog’s electrocardiogram– the electrical signals that fire the dog’s heart contractions on every beat. That might be done with a 24-hour Holter monitor ECG recording device. Rhythm defects are one of the main things cardiologists are looking for (eg atrial fibrillation, supraventricular tachycardia ventricular premature complexes and ventricular tachycardia). All predispose a dog to sudden death. (ref)
Your veterinarian or the cardiologist might suggest some genetic tests to determine if a dog carries gene combinations that predispose it to DCM - particularly if you are selecting an apparently health breeding or service dog (ref1, rptref2, ref3), or tests that detect telltale compounds an inapparently damaged heart might release. (ref) Most of these tests are still in their developmental stage. (ref)
Other than the proBNP or natriuretic peptide tests and confirmation that hypothyroidism is not compounding your dog's problem (ref) , blood serum chemistry and urine tests (ref) do not give much insight into organic heart problems - but your vet may want to run them just to be sure there are no coexisting liver, kidney or other problems that might affect the action of the heart medications he/she will dispense.
Veterinarians have known for a long time that a taurine amino acid deficiency can be responsible for dilated cardiomyopathy in cats. (ref) Turkey and chicken are particularly rich in taurine, as are shellfish. In dogs, carnitine deficiencies were once implicated as well. (ref) But more recent studies have not confirmed that.
With time, the prevalence of DCM in cats decreased as pet food manufacturers saw to it that their diets contained sufficient amounts of taurine after processing. Cases of taurine deficiency-induced DCM have also reported in dogs – particularly golden retrievers. (ref)
The incidence of DCM in which diet is suspected of playing a factor has been creeping up. That increase has paralleled the trend to feed dogs higher priced dog foods that base their acceptance on being grain-free or containing exotic ingredients. They are often among the “boutique premium brands” with trendy ingredients. There is more profit in selling these products than in selling traditional dog food, so many small companies manufacture them and sell them through groomers, pet superstores, the internet and the like. But these smaller companies rarely have veterinary nutritionists on staff or the resources for sophisticated nutritional analysis. Even the larger dog food manufacturers see financial opportunities in providing these untested products.
It may not be that these diets are deficient in taurine. But their formulas – especially the ones that advertise as “grain-free” might decrease taurine’s absorption. (ref1, ref2, ref3, ref4) One focus has been on golden retrievers. (ref) Many of these diets claim to meet the dog nutritional standards of the AFIA. But few if any have been tested in dog feeding trials that observed for later heart or other disease issues.
Your vet might suggest a blood taurine level test. But taurine supplementation in dogs - even with confirmed low taurine levels - does not necessarily revere the damage that DCM has already caused.
The best your veterinarian has to offer your dog are medications that might improve the remaining abilities of its heart to pump blood. Those are the same drugs that veterinarians use to treat all forms of heart failure in dogs. (ref)
Those medications include ACE inhibitors like enalapril and benazepril to lower resistance to blood flow. They also include pimobendan (Vetmedin®) to strengthen the force of each heart contraction. When the dog’s heart is no longer pumping forcefully enough to keep fluids from pooling in the lungs and abdomen, furosemide (Lasix®), a diuretic, is usually dispensed. Some of these heart drugs, like pimobendan, appear able to gain more time for dogs when DCM is discovered early than others. (ref) More exotic medications like carvedilol and metoprolol and drugs given in an attempt to correct heart rhythms such as mexiletine, atenolol and sotalol are sometimes given (with caution) as well. When furosemide no longer suffices to control pooled fluids in the lungs or abdomen, other diuretics such as spironolactone and hydrochlorothiazide can be added as well.
Some veterinarians dispense l-carnitine, taurine, omega-3 and Coenzyme Q supplements. But none have been proven to be of help other than those containing taurine when blood taurine levels were confirmed to be low. Both Hills and Purina make low-sodium dog foods. But none have been confirmed to extend the lives of dogs with DCM.
It varies from case to case but the end result is never favorable. Some breeds, like dobermans tend to go down hill rapidly – even with medications. Others, like cocker spaniels often go down hill slower. The outlook for dogs improves slightly when their heart is enlarged but no electrical (rhythm) abnormalities are detected. The only cases of DCM that have occasionally been reversed or halted are those that were due to a taurine deficiency that was corrected. Very few dogs survive more than 6 months to 1.5 years after a diagnosis of DCM has been made.
When contemplating the purchase of a high DCM risk breed, exhaustive research into the dog’s parents and their siblings for evidence of increased susceptibility (family history) to DCM is desirable. Some breeders go so far as to schedule yearly echocardiogram and Holter monitor screening of their breeding dogs. (rptref)
One needs to be certain that the family line from which the dog is selected was not prone to early death – regardless of the reported diagnosis.
There has been some progress in finding genes that are associated with doberman pinchers developing cardiomyopathy later in life. (ref) The problem is that some dogs that carry these genes will never develop the disease (incomplete or variable penetrance) while others that appear free of those genes develop cardiomyopathy (DCM) all the same. Others look for blood tests that might be specific for compounds released early in the disease. (ref)
Genetic tests for specific breeds are available. (ref)