Cardiomyopathy: The Reality, Amanda Jinks Everyone will remember that there was a furore in the breed over cardiomyopathy a couple of years ago, but many of us really did not know what was going on. I read what appeared in the dog papers but it all seemed rather distant and unreal, certainly the implications of recognising it, dealing with it and most importantly, avoiding it, were hard to grasp. I hoped it would not happen to any of my boxers, but it has, and I have lost my young dog to this fatal disease. Here I describe what happened to us in the hope that it will help trigger some positive action to deal with Early this year, 2005, a fellow exhibitor at a show commented on how fit my boxer, Claude, looked. I looked at the dog and realised this was true, his muscles stood out plastically under his smooth, short, shiny coat. He was in hard condition. In March-April time he lost some weight, which I attributed to his girl being in season. He was eating as normal, however. A few weeks went by, with him on an increased amount of food, and indeed on three meals a day, all of which he ate quite readily, but still he did not seem to be regaining any weight. At the same time, I noticed that he was coughing occasionally. Again, I rationalised this by pinpointing the start of it to a day when he had been disturbed while eating; he barked and from the awful cough that followed I assumed the food had 'gone down the wrong way'. The coughing was not frequent, but happened now and then, usually when something disturbed him or just after he got out of the car, then it would stop again. I thought that the 'choking' incident had done some damage to his throat, causing him to cough on occasions. This went on for some time as well, but he was still bright and cheerful and eager to participate in normal dog activities. As the weather grew warmer he began to show a little reluctance to exercise quite so keenly. He would set off at normal high speed but within a few minutes, while the others were still getting rid of energy, he would hang around in the shady spots and watch or even sit down. An unrelated condition also arose at about this time, namely an epulis, which, being near a canine tooth, began to distort the shape of his muzzle, so I sought veterinary advice about it. The vet recommended that it be removed, but having also mentioned to him the other conditions outlined above, we agreed to err on the cautious side and carry out an ECG before proceeding with an anaesthetic and surgery. The ECG showed up some irregularities suggesting an increase in heart size and further investigations were recommended. I was away for ten days in July; on my return I saw Claude with fresh eyes and was concerned to see the extent of the changes that had taken place in his condition. Despite excellent care in my absence he was altogether thinner but his abdomen was noticeably extended. His backbones were now standing out, his back appearing to have become roached, his ribs stood out, his muscles had all but disappeared, and this heavy abdomen made him look almost pregnant. These conditions had been coming on for some time, but being away for a few days resulted in my seeing him afresh. He was still cheerful, active and eating well but his exercise tolerance had reduced. He had also fainted a couple of times. I took him back to the vet, to proceed with a heart X-ray and scan of his abdomen. In the event, the scan was hardly necessary, the X-ray was sufficient to show that his heart was greatly enlarged, taking up about half of the space within the rib cage. The muscles of his heart were 'flapping' - not functioning adequately to pump the blood at the required level. In the hope of giving him the best chance of as long a life as possible, with the best quality of life possible, I took Claude to one of the leading veterinary cardiologists. The verdict of cardiomyopathy was reconfirmed and various drugs were dispensed to assist his heart to function as well as possible under the circumstances and also diuretics to disperse the fluid in the abdomen. For the following six weeks or so Claude responded well to the drugs; he remained cheerful and retained his appetite, the size of his stomach decreased, but he continued to lose weight. Stroking his shoulder was stroking skin directly over bone - he had lost all his muscle, his collar hung loose and slack around his neck, his hindquarters looked withered and pathetic and his rib cage stuck out like two toast racks. His head also began to lose flesh, the occiput sticking out high and proud. But his eyes stayed bright and his expression was as alert and keen as ever. On Sunday morning the 25th September I walked him slowly round the paddock as usual, keeping him now on the lead so he couldn't rush off and damage himself. We were half way round and he stopped to sniff an interesting smell, then keeled over, briefly thrashed his front legs, and died. I tried to massage his heart but I could see in his eyes he had gone. He was three days short of his sixth birthday. In the hope of doing something to try and help to save other animals from this awful fate, I had Claude's heart sent off to research cardiologists, who have since confirmed that this was a classic case of boxer cardiomyopathy. This for me was the harsh reality; I hope that by recounting these sad events I can help to maintain the impetus for taking serious measures to tackle this dreaded disease in our beloved breed. Does anybody really want more people and dogs to experience this nightmare? Amanda Jinks November 2005 |
In the United States and Canada, an inarguable case has been made: We have a problem, and it’s a big one. For the better part of a century, the Boxer, whose fanciers followed the dictates of a standard that made it possible to create this breed in the first place, has been inbred on traits that are phenotypically desirable. The trouble with fixing type in a breed is that one also runs the all-too-difficult-to-avoid risk of fixing undesirable genotype as well. This, breeders in North America appear to have done in spades where one genetic disease is concerned. It’s called a number of names, but usually it’s known as Boxer Cardiomyopathy. We got where we are because more often than not, this disease presents with one symptom only: sudden death. In the past, if we were lucky, as an animal matured it might get through that asymptomatic stage and actually faint a time or two before the big event that ended its life. If they received this warning, they were able to relieve it of its breeding responsibilities. But mostly, they didn’t know that our Boxers had it. Thus, until they were presented with an option of a testing protocol only recently, breeders blithely and even ignorantly bred happily away, making sure that, over the decades, our dogs faced an uncertain future we’d never even imagined, much less intended. The test we have available now isn’t fool-proof. But is the only test we have. And although it cannot, yet, be said to clear any dog – it can most certainly condemn one. And therein lies the reason that we all must test. Every board-certified cardiologist studying the Boxer here is unequivocal on this point: Before breeding, Boxers must undergo the rigors of the Holter monitor, a twenty-four hour electrocardiogram that presents evidence (when evidence exists) of the premature contractions of the ventricle that, when occurring in multiples of four, five and six upward (ventricular tachycardia) can cause the sudden death of an otherwise healthy-appearing dog. A couple of studies are currently ongoing in the United States to discover the mode of inheritance of this gene – a dominant one with variable penetrance, according to the study funded by the American Boxer Club being conducted at Ohio State University by Dr. Kate Meurs. She would be the first to tell you that there is no hard-and-fast rule that allows her to look at a Holter result and declare the fitness for breeding of every dog tested. But she’d also be the first to tell you that the test must be done in spite of the remaining aura of uncertainty where results are concerned. In speaking with Dr. Meurs’ assistant two days ago (as I sent in the first of four Holter tapes with which I was faced recently), I heard the theme played again: Young Boxers in the study at OSU have been tested clear on a couple of yearly Holters, then suddenly evidence of BCM rears its ugly head. The converse is true as well: She suggested that an adverse reading on a young dog should not be sufficient evidence upon which to base his or her removal from a breeding program. One should hold off, and test in subsequent years to see what happens. This is because of the apparent variability of both symptoms and clinical signs – and because of their odd relationship to each other. Here, we’ve all heard of the dog with hundreds of VPC’s (confirmed to me by OSU) who never exhibits symptoms and lives to a ripe old age. On the other hand, dogs clear on Holter can keel over dead. So why do we test? We do it, and I believe we must do it, for two reasons: The first is that there is a certain percentage of severely affected dogs without symptoms who WILL keel over eventually – as will some of there unsuspecting get. If you don’t test, you don’t know your dog has thousands of VPC’s including the run of ventricular tachycardia that kill. Breed this dog at the rest of the Boxer-lover’s world’s peril. The second reason to test is simply to add to the increasing body of knowledge where this affliction’s concerned. If we don’t test and share our results, we will never find an answer, if an answer’s available to be found. I know that sometimes that last seems questionable. Researchers become increasingly vague about what dog is breeding material and what dog is not. But testing is the only way we’ll ever find a road out of this mire, if there is such a road. When I started out in Boxers over a decade ago, old-time Boxer breeders were in denial. Rumors were rampant because enough unexplained early deaths had occurred to be definitively noticeable. But “Its not in my line” was the mantra of the era. Fingers pointed in every direction attempting to shift suspicion elsewhere. Then the age of the internet arrived, and as novices like me entered the scene – folks who had no ways in which to be set and were, thus, less likely to dig in their heels and deny – eventually open discussion began to make clear the breadth of this problem, and even many experienced breeders came around, no longer having to feel so alone or maligned. After all, once you recognise that the boat in which finds one-self is full of sailors, the loneliness of a sad secret is lifted. Even in cases where breeders really believed there dogs had probably succumbed to allergic reaction to bee sting or any other such explanation, clarity flooded the pages of mailing lists; we all discovered reality and, once reality was clear to the leaders of the American Boxer Club, funding began to pour forth in hopes that the mysteries of this unfortunate genetic defect could be explained. Here in North America, the horse is long out of the barn. We had no wisdom to guide us when first our breed’s predilection for unexplainable early mortality (documented even half a century ago by Frau Stockmann) began to make itself painfully known. And once it was recognisable, the occasional naysayer still refused to see this particular forest for its trees. Given recent events in the United Kingdom, it appears that some breeders there are poised, themselves, to venture down that same lamentable road. Only doing so is totally unnecessary - because others have been there before you and blazed a clear and crucial trail. You have only to follow it. If you suspect that the gene for Boxer Cardiomyopathy may exist in your present breeding stock, it may not be too late to benefit from mistakes North American breeders made so long ago. If it is indeed concentrated in only a few places at present, and you know in your own heart that the hearts of some of your line’s best may be affected, difficult as it undoubtedly be to do it still I’d suggest you consider falling on the sword – for the literal survival of this beautiful breed in England. Consider adopting the testing regime we’ve been so clearly exhorted to follow here, or at least remove from your breeding program any dog you suspect may be implicated until you CAN test. Don’t wait until you’re where we here in the States and Canada are – coming to the conclusion that, given the inbreeding that’s been done for decades on this unfortunate trait, it’s possible that we may just have nowhere on this continent left to go. Some here still pin their hopes on the eventual discovery of a genetic marker. In so doing, I fear they may find that they have waited to long – that the marker will discover only that all of our dogs carry the gene. It truly appears to be pandemic here; it may not ever have to be where you are. The saying goes that when god closes a door somewhere he opens a window of opportunity in which to do the right thing. I wish for you the wisdom, and the generosity of spirit, to do it before the window slams tightly shut. Katherine Nevius, Minstrel Boxers, USA |
this horrible heart condition. 
The diagnosis that my vets had already suspected was now confirmed: cardiomyopathy. I was warned that the prognosis was poor: at best he might live for six months - or he could die the following week.