All the information on these pages is just that - information - and does not take the place of proper veterinary attention for your animals.
The Canine Heart Disease Research Fund, which was started early in 1986, organised the testing of hearts of various breeds, but particularly Irish wolfhounds, at breed events and also purchased the equipment that was used for the testing.
The Canine Heart Disease Research Project came to an end when the Irish Wolfhound Health Group - http://www.iwhealthgroup.co.uk/ - which was started up in 2004 to deal with health problems in the breed, took over the organisation of heart checking at shows and other events. The following sections are details of how the Project worked over the twenty years of its early running.
How it came about
In late 1985 I received a telephone call from a very distressed wolfhound owner. His hound had been ill for weeks with what the vet said was an infection but, despite course after course of antibiotics, the dog was getting steadily worse. The list of symptoms he described informed me that the problem was the dog's heart, but the vet had checked the heart and said that, whatever else was wrong, the heart was as strong as an ox. I suggested asking the vet for a referral to the cardiologist at the Royal Veterinary College, which is what they did.
Two days later I had another call to tell me that they had come back from the College but without their hound. He had been found to be in such total heart failure that they had decided, on the cardiologist's advice, to have him euthanased there. They told me that the cardiologist had said what a pity it was that there was so little information available on cardiomyopathy and its early symptoms, so I wrote a letter to her (Dr. Serena Brownlie) asking if she would undertake the research if I found her the hounds. A few months later we set up shop at the Irish Wolfhound Club Championship show and offered free ECG testing, and so was born
The Project started in 1986, with Dr. Serena Brownlie, then cardiologist at the Royal Veterinary College (University of London), going to breed events and using an electrocardiogram (ECG) to check the hearts of hounds present. In the first year 64 hounds were studied - 24 dogs and 40 bitches - the average age of which was 2 1/2 years (ranging from 10 months to 8 years 8 months). This pilot study showed several interesting points, the main one being that the mean heart rate in both dogs and bitches was 107/minute and this did not alter to any extent when abnormalities were present. During this period, wolfhound owners donated enough money to the Fund to enable us to purchase our own portable ECG. A few years later, we added an ultrasound and computer to our equipment. A generous donation from the Canine Supporters Charity enabled us to buy monitoring equipment. We were testing hounds at all the main breed events, and other breeds were included in the scheme.
The most common heart disorder found in the Irish wolfhound is dilated cardiomyopathy, (DCM) which is a condition in which the heart muscle becomes weakened and the heart enlarged as a compensatory factor. The rhythm disturbance usually connected with the disorder is atrial fibrillation (AF). Cardiomyopathy eventually leads to heart failure, but there now appear to be two distinct types of cardiomyopathy. In one, the dog will show early signs of problems, with weight loss, exercise intolerance, possibly fluid retention and in some cases episodes which resemble heart attacks. ECG results will show rapid heart beat (tachycardia), maybe with atrial fibrillation and sometimes with ectopic beats, and other abnormalities will show up on ultrasound scan. The second type is where the dog shows no abnormalities on ECG or ultrasound, and there may be no symptoms of any problem with general health and demeanour, yet the dog suddenly goes into heart failure and fails to respond to treatment. A possible third type affects young animals, usually under two years of age, which leads to sudden death, often while exercising.
The first most noticeable symptom of the most common type of DCM is often weight loss, sometimes despite a huge appetite. Also exercise intolerance where the hound may just walk instead of galloping around when off leash but may sit down for a rest frequently while on walks. Pale gums are a not infrequent sign of poor circulation, and the heart beat can sometimes be seen when the hound is lying on its side. It can certainly be felt by putting a hand over the heart area, usually with a rapid and fluttery beat. If the pulse in the inside of the thigh is felt at the same time as the heart, it will be found that not all beats of the heart produce a pulse.
Further possible symptoms include a cough, which sounds rather as though the hound is clearing its throat; fluid retention in the abdomen and/or chest cavity, which can lead to abdominal discomfort, a disinclination to lie down, and breathing difficulties; loss of appetite; and general malaise.
A dog with any kind of a heart problem is not a healthy dog, which brings up the subject of vaccines. All the product information that comes with vaccines states they should only be given to a healthy animal. In the human field, the Merck Manual (published by a vaccine manufacturer) says that patients with heart disease should not receive live virus vaccines. It goes further, saying patients from families with a history of heart disease should not receive live virus vaccines. For further information on vaccinations, click here. For information on the homeopathic nosodes that can be used instead of vaccines, click here.
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The purchase of the ultrasound, which is capable of making quite sophisticated measurements of heart dimensions, has enabled us to obtain normal ultrasound cardiac measurements for wolfhounds, something which had previously been extrapolated from measurements made on much smaller dogs. It has also enabled us to document the progression of heart enlargement in dogs with previously diagnosed problems. In addition, it was (and still is) one of our objectives to find out which measurements alter first and therefore could be used as a prognostic indicator.
We are slowly building up a picture of the situation in wolfhound families. In 1994, 146 hounds were examined, some on more than one occasion, and there has been an encouraging increase in the number of littermates seen. The number of dogs with atrial fibrillation was 17, but 3 had been diagnosed in previous years. This means that the findings of our original survey have not changed, i.e. that we expect 10 per cent of the dogs to have atrial fibrillation. The total number with any ECG abnormality was 48, although this does not include dogs with mild notching of the CRS complex, which could indicate tiny areas of ventricular damage. The only group of dogs which consistently had heart enlargement on ultrasound were those with atrial fibrillation, all of which had left atrial and left ventricular measurements above the normal range. Dogs which had normal ECGs but whose ultrasound measurements did not fit our normal values will hopefully be re-examined in the future to monitor their progress.
Malcolm Cobb has been doing work on this project for his PhD studies, and his findings are very interesting but tantalising, as there are several avenues which need to be explored further. To understand the implications of this work, it is important to consider also findings from previous research into both human and canine cardiomyopathy, and work which is at present underway in other parts of the world, particularly the United States.
Cardiomyopathy is mainly a disease of young and middle-aged large and giant breeds of dog, particularly Irish wolfhounds, St. Bernards, Gt. Danes, Dobermann Pinschers, and Boxers. The fact that the disease is frequently seen in these breeds, whereas other common breeds such as Labrador Retrievers are rarely affected, suggests that there must be a genetic predisposition. Many reports in the human literature suggest that cardiomyopathy in man is a familial disease, although the mode of inheritance varies. However, there is general agreement that the cause is multifactorial. Previously reported causes of heart damage were viral (in the dog, distemper, parvovirus), bacterial, protozoal, and fungal infections, some hormonal diseases (particularly hypothyroidism), drug toxicity (some anticancer drugs [also alcohol] in humans), cancerous conditions and certain nutritional deficiencies.
Nutritional factors have attracted much attention in animals and there was great excitement a few years ago when taurine deficiency was discovered to be the major factor in the development of dilated cardiomyopathy in the cat. Around the same time, Bruce Keene from North Carolina demonstrated carnitine deficiency as the cause of the disease in a family of Boxers. However, although Dr. Keene has now shown that myocardial carnitine deficiency is present in more than 50 per cent of dogs with cardiomyopathy, it seems more likely that it is a result of the disease rather than a cause, except perhaps in the Boxer breed. It had always been assumed that dogs produced their own taurine and therefore would be unlikely to suffer from taurine deficiency, until Dr. Kittelson in California discovered a family of American Cocker Spaniels with cardiomyopathy due to taurine deficiency, probably due to an inborn genetic defect.
Microscopic examinations of the heart muscle after death tends to reveal only changes which are seen in end-stage heart failure, from any cause. The major debate, in both humans and animals, is whether or not there has been inflammation of the heart, or myocarditis, at an earlier stage of the disease. Inflammatory cells are seen in small numbers in many human cases, and this has led to the widespread belief that cardiomyopathy is the result of viral damage which leads to activation of the immune system, which then continues to attack the heart muscle. Although one might expect a virus to affect all individuals in the same way, it is very possible that heart damage may only occur in genetically susceptible individuals, and it has certainly been demonstrated in humans that many immune-mediated diseases run in families, often associated with particular tissue (HLA) types. Persistent viral antigen and antimyocardial antibodies have been detected in many, though not all, human patients, and these antibodies are not present in normal humans. However, there is much disagreement as to whether they are a cause of the disease or a result of it.
Much research effort in man has been directed at analysing myocardial proteins in normal and diseased heart muscle and finding out which proteins the antibodies are directed against. There has been no research previously into these aspects in the dog, which was why it was decided that Malcolm Cobbs project should be along these lines. The first set of results gave us a major surprise. Sera from dogs with cardiomyopathy and from normal dogs were tested for anti-heart IgG and IgM antibodies, and many autoantibodies were demonstrated in both normal and diseased dogs. It is not yet known why normal dogs should possess antibodies to heart muscle when humans do not.
In the second study, protein patterns from samples of left ventricular heart muscle, taken at post-mortem from dogs which had been put to sleep because of cardiomyopathy, were compared with heart muscle from large dogs of similar ages put to sleep because of non-cardiac causes. There were significant differences in the expression of a large number of proteins, and of these twenty have been tentatively identified. We do not yet know which altered proteins are found in all cases of heart failure, and which are specific to cardiomyopathy.
The third study was into the IgG auto-antibodies identified in the initial tests, as these are more likely than IgM to cause disease, and using more purified tissue. Again, sera from dogs with cardiomyopathy were compared with normal, and this time there was a significant difference in the prevalence of IgG reactivity, particularly to two specific proteins, one of which is recognised as an autoantigen in human patients with cardiomyopathy. However, its role in the development of the disease is not yet known.
It was decided that the project would not be complete without an attempt to study the role of viruses. Parvovirus is the main cause of proven myocarditis in dogs, and it was a suitable type of virus to work with. Therefore, heart muscle samples from affected and control dogs were examined for the presence of canine parvoviral DNA. This was detected in a number of dogs, from both diseased and control groups. These findings do little to support the theory that parvoviral damage causes cardiomyopathy, but the fact that the virus was in the heart muscle at all is a finding which may be worth pursuing. It may be possible to use the same technique to look for other viruses in the future.
Finally, Malcolm has applied genetic analysis to some specific Irish wolfhound families for which we have sufficient details. His conclusions are that, whilst the analysis suffers a number of limitations, it does provide evidence for genetic involvement in the development of cardiomyopathy in wolfhounds.
So, where do we go from here? We are not limiting our efforts to the projects described above, although much work remains to be done to determine the significance of Malcolms findings. We are in the process of studying thyroid hormone levels and amino acid profiles, and we are considering the possibility of a controlled trial of various nutritional supplements.
SERENA BROWNLIE and MALCOLM COBB
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The Irish wolfhound heart research programme began in 1986 with a study of apparently normal dogs at shows, rallies, and breeders kennels, and this has continued to the present day. Initially we listened to their hearts and carried out electrocardiographic (ECG) examinations, but in 1993 the acquisition of an ultrasound machine added further information about heart size and function. We reported on the prevalence of heart rhythm and conduction abnormalities in wolfhounds in 1991. Normal ultrasound heart measurements were established for wolfhounds, as the only previously available normal measurements were for dogs weighing less than 50 kg. bodyweight.
Over 250 dogs have been examined on a regular basis throughout their lives, and now we have data on several generations of many wolfhound families. The laboratory work carried out by Malcolm Cobb at the Royal Veterinary College has added much useful knowledge about the disease processes involved, particularly the identification of antimyocardial antibodies and parvovirus antigen in both normal and affected dogs and the types of proteins found in diseased heart muscle. Although Malcolms research sadly came to an end when he left the RVC, it seems likely that his place in cardiomyopathy research is being taken over by Jo Dukes-McEwen in Edinburgh. She is working principally with Newfoundlands but it seems that there are many similarities between dilated cardiomyopathy (DCM) in Newfoundlands and wolfhounds, and her results may be applicable to wolfhounds as well.
A generous grant from the Canine Supporters Charity enabled us to buy ECG monitoring equipment and this is available to wolfhounds. I am still interested in possible viral involvement in DCM and am making contact with research workers who may be able to help in this area.
What have we learned? It is important that wolfhound owners should now be aware of the most important conclusions which have been gained from the huge amount of data obtained so far.
1. The most common heart rhythm abnormality affecting Irish wolfhounds in Britain is atrial fibrillation (AF). This will affect at least 11% of the wolfhound population at some point in their lives. Age of onset of this rhythm disturbance has varied from 10 months to 11 years. In the dogs examined so far, the mean age at which AF was first detected was 45 months in males and 59 months in females. Surprisingly few dogs show any signs that they have this problem, although it reduces heart output by about 20 per cent. Occasional dogs may revert back to normal rhythm spontaneously but this appears to be unlikely. It is very difficult to convert AF back to normal rhythm in dogs, either because we do not know the right drug regimes to use or because the condition is usually well established by the time it is detected. Therefore it has to be assumed that, once a dog has AF, it will probably have it for the rest of its life.
2. The biggest question which we have had to answer was whether or not the presence of AF was an indication that the dog would develop DCM in the future. Reports from America initially suggested that AF was not an indication that a wolfhound would develop DCM. The presence of AF by itself does not normally cause deteriorating heart function in humans or in horses, and many wolfhounds with AF have heart measurements which initially are almost normal.. However, all wolfhounds with heart failure as a result of DCM have AF, therefore it always seemed surprising that people were saying there was no connection. The only way to find out was to re-examine these AF dogs regularly, preferably by ultrasound scanning, until they died to find out what happened to them. Unfortunately, I do not know if all dogs with AF develop heart failure because many owners have not brought them back for re-examination. Others have died of different unrelated diseases. At least six, to our knowledge, have died suddenly without warning signs. However, I now have evidence that over 40 dogs that developed AF have subsequently died of heart failure. I therefore conclude that AF must be considered an indication that an Irish wolfhound will develop DCM in the future.
3. The mean age at which heart failure develops in wolfhounds is 77 months in males and 86 months in females, but with a range of 28 months to 11 years. The mean time from detection of AF to development of heart failure is 27 months in males and 24 months in females, but five animals are known to have survived for four to six years before developing heart failure. This does not mean that they did not have DCM.
4. Throughout the project I have kept details of sire, dam and date of birth of all dogs examined, if their breeding was known. Many research projects cannot provide breeding information because the dogs are only identified by their pet names. In this study all the dogs, other than rescues, have been identified by their Kennel Club registered name. As a dog breeder myself, I actually hoped that we would find no evidence of genetic involvement, because wolfhounds could do without another inherited disease, and also because back in 1986 there was very little information suggesting genetic involvement in other species, particularly humans. However, research into human DCM now suggests that more than 30% of human cases are familial, and the tendency to develop AF may also be inherited. Sadly it seems that this is likely to be the case in wolfhounds too. The data shows that most affected dogs either have an affected parent and/or littermates. In those families in which we have been able to carry out genetic analysis, an autosomal dominant mode of transmission seems most likely. However, there may be modifier genes or environmental triggers which affect the age of onset and rate of progression.
5. Not all dogs which have died of DCM had AF earlier in life. There have been a small number of dogs which had no ECG abnormalities at all until they developed cardiac enlargement, although all had AF by the time they were treated for heart failure. These dogs are confusing but at least one had littermates with more typical wolfhound DCM, therefore we have no reason to believe that they had a different disease, only a different manifestation of it.
6. Because in many cases AF develops fairly late in life, it is important that abnormalities which may progress to AF and DCM are identified. Wolfhounds have many abnormalities detected on ECG other than AF. Ventricular premature contractions, supraventricular prematures, supraventricular and ventricular tachycardia, first degree atrioventricular block and left anterior fascicular block are all common. Supraventricular and ventricular dysrhythmias have been identified in dogs that subsequently developed AF and DCM. However, there are many others in which the rhythm disturbance apparently disappeared and the dogs lived to a ripe old age and died of other causes. Left anterior fascicular block is a very interesting abnormality which occurs in certain wolfhound families, and has been identified even in quite young dogs. The significance of this finding is still unknown. Occasional animals have more than one type of conduction block. The only abnormality which consistently seems to precede AF is first degree atrioventricular block, which indicates that the electrical impulse is taking longer to travel across the atria. I regard this abnormality with deep suspicion.
7. In my opinion, any wolfhound which has both an ECG abnormality and cardiac ultrasound measurements which are more than 10 per cent larger than our normal range for wolfhounds is likely to develop DCM. These conclusions may not be particularly welcome, or even helpful, to wolfhound breeders in Britain but at least you will be able to make informed decisions based on sound research and not on anecdotal evidence or hasty assumptions. I am very grateful for the patient co-operation and continued support of wolfhound owners and breeders. The research is still ongoing.
Q. What can I do to prevent my dog from getting DCM?
A. Unfortunately, if your dog is genetically programmed to develop it there is nothing you can do to prevent it, but good husbandry and a well-balanced diet containing L-carnitine, taurine, and vitamin E/selenium may help. Control his weight, have the heart checked regularly, vaccinate against Kennel Cough if in a risk situation and be alert for signs of illness.
Q. How often should I have my dogs heart checked by ECG/ultrasound?
A. At least once a year, and before every general anaesthetic.
Q. What can I do for my dog with AF?
A. Do not over-exercise him or let him get too hot. Monitor his heart rate and breathing at home. Your vet will show you how. If the heart rate rises to more than 140/minute at rest he may need treatment. The use of an ACE inhibitor (Cardiovet, Fortekor) has been recommended by some authorities but this treatment is expensive and still controversial. We are still hoping that there may soon be a trial which will give us answers to this question.
Q. Should I breed from a dog or bitch with AF?
A. It is up to you, but you may put the dogs life at risk and you are likely to produce puppies that will develop DCM later.
Q. In Cavalier King Charles Spaniels with mitral valve disease it has been shown that breeding from animals which develop the disease later is pushing up the age of onset and improving lifespan. Would this be the case with wolfhounds?
A. We do not know. The inheritance of MVD is thought to be polygenic, which may be different from DCM, and also we have not resolved the question of the effects of viruses, nutrition, environmental factors, etc. However, it is worth a try. The only reason to be concerned about wolfhound DCM is the number of dogs which die young. If they all died at ten years, no-one would be particularly worried about it.
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Research carried out into DCM (Dilated Cardiomyopathy) in another giant breed of dog brought up what seems to be a worthwhile area to check in the Irish wolfhound, which is to do with the amino acid Taurine. A deficiency of taurine was first found to be a cause of heart problems in cats who were fed commercial foods and led to the addition of taurine to all such foods, as it was found cats have to have it in their diet as they lack the ability to make it themselves. However, it was believed that dogs could manufacture their own taurine and that therefore any lack of it in their diet would not be a problem.
Taurine is a non-essential (excepting in cats) sulphur-containing amino acid that functions with glycine and gamma-aminobutyric acid as a neuroinhibitory transmitter. Taurine is found in the nervous system, including the retina, and muscles, especially the heart in which it is the most abundant free amino acid. The role of taurine is not properly understood but it is thought to help regulate heartbeat, maintain cell membranes, and affect the release of neurotransmitters in the brain. It also protects the heart from calcium overload and assists in calcium uptake by the heart cells during periods of hypoxia (reduced oxygen levels). In most animals taurine is derived from the metabolism of the amino acids methionine and cysteine.
The research into heart disease in Newfoundlands has found that some dogs do have a deficiency in taurine and that supplementing them with taurine had a noticeable effect on improving their condition. It was not a problem in all dogs affected with DCM and it is possible it is not the sole cause of the disease in those found to be deficient but it does seem to be an avenue worth exploring in the Irish wolfhound, especially as supplementing with taurine is easy to do and inexpensive. In Newfoundlands it was found that quite small doses worked best - larger doses had no greater effect and the excess taurine was simply excreted in the urine, as was discovered by testing the urine.
The Irish Wolfhound Club at its AGM, 2003 voted to donate £1000 from the Health Fund to the Canine Heart Research Project, and the Irish Wolfhound Society at its Rally held an auction to raise money for the Fund. It was decided to utilise these donations, plus some of the existing Fund, to set up a pilot study into taurine levels in the Irish wolfhound.
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I am sorry not to have been at the shows in 2004 due to personal circumstances but we have not forgotten our wolfhound friends and heart research is not dead, only having a rest. I am still available for consultation on ECGs and I am still coming "down south" once a month for work. Unfortunately these visits have not coincided with the shows but perhaps we can manage it next year. I am keen to catch up with news on Scottish wolfhounds, as I have not had the opportunity to see them for a few years now.
Recently I went to the autumn meeting of the Veterinary Cardiovascular Society and heard a report on the recent ACVIM conference in the States. One of the papers presented was a report on a large study of 1000 wolfhounds by Andrea Vollmar and others. I believe this was a multi-centre study and some of the co-authors were American, therefore presumably the dogs included were both European and American. I was pleased to learn that their conclusions were similar to ours - to summarise:
Serena E. Brownlie
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Methods of Heart Testing
If you have questions about the conditions screened for in your breed of dog, you should consult the relevant person in your breed club or the cardiologist attached to the breed club. The cardiologist testing your dog will be willing to discuss the results of the tests with you, which are summarised on the certificate of heart testing.
Heart testing is carried out at the
invitation of breed clubs and with the agreement of the RCVS
Information provided by the Veterinary Cardiovascular Society
|The Veterinary Medical Clinic article on DCM|
|Article on heart failure in your dog by Ron Hines DVM PhD|
|The AKC Canine Health Foundation page on Dilated Cardiomyopathy|
|The InTown Veterinary Group page on DCM|
|Proceeding of the NAVC North American Veterinary Conference, 2005 on Canine Dilated Cardiomyopathy (in .pdf format)|
Herbal and homeopathic treatments have been found to work well in many cases of DCM. Our first case of DCM was in a bitch which started to lose weight following having a litter, despite being ravenously hungry all the time. She then started having episodes of suddenly trying to run but only getting a few feet before she would brace herself with feet wide apart and go into a state of shakiness and even fall over. She was five years old when the vets finally diagnosed her as having cardiomyopathy. She was given six months to live. I took her to a homeopathic vet and she was put on various remedies. All her symptoms disappeared, she regained the lost weight, ran about with the other hounds as normal, and lived for a week under six years from her date of diagnosis, being eleven years of age when she suddenly went into complete heart failure.
Some of the homeopathic remedies found most useful in cases of DCM are Crataegus, Cactus grandiflora, Strophanthus hispidus, and Digitalis, but giving the constitutional remedy for the hound as well is also helpful. Flower remedies can also be useful. See the flower essences page for more information.
In some cases, diet can play a big part. Elsa came to us at four years of age, having been diagnosed with DCM the previous year. She was put on the BARF diet, to which she responded brilliantly, and she showed no symptoms of heart disease until the day she too went suddenly into complete heart failure just before her eighth birthday.
However, I would suggest that any dog diagnosed as having a heart problem should be given a chiropractic treatment, as this has been found to have beneficial effects in many cases and even to remove symptoms of heart failure. If you are in the U.K. I would suggest McTimoney chiropractic, which is a particularly gentle form of chiropractic. You can find your nearest animal chiropractor from the McTimoney Chiropractic Association, www.mctimoney-chiropractic.org. You will need a referral from your vet.
Supplements such as Magnesium, and the amino acids taurine and carnitine, plus some others less obvious, can often help. For more details on alternative treatments for DCM, click here and for nutritional treatment for DCM, click here.
|Page on Dr. Ihor Basko's book on Fresh Food and Ancient Wisdom|
|Animal Wellness Magazine article on Heart Disease in Dogs and Cats|
Do not use chemical flea treatments, and especially do not use organophosphate flea collars. Avoid chemicals as much as possible. Allow your hounds to have plenty of natural light each day. This means either having windows open if the hound is indoors (glass cuts out a vital part of the light spectrum) or the hound spending plenty of time outdoors. Alternatively (or as well) have full spectrum lighting in the house or kennel.
Beware of over-vaccinating. Do not have a puppy vaccinated at a very young age, but leave the puppy shots until as late as possible. The safest way to deal with this is to give the homoeopoathic nosodes (they may be given from two weeks of age) to cover the puppy early on and then vaccinate at three months or later, giving the puppy the nosodes again at a rate of one twice a day for five days before and five days after the vaccination. The Merck Manual for humans suggests that people with, or from a family with a history of, heart disease should not be vaccinated.
Do not give boosters every year. Many vets are now accepting that this is not only unnecessary but damaging. Some components of the vaccine should cover for life and others should cover for some years. The usual practice is to have blood titres tested annually and only revaccinate when these are low, and only for the specific disease/s for which the dog is no longer covered.
The Leptospirosis component of the vaccine only lasts for about three months but is, anyway, quite ineffective since it only covers a few varieties of the bacterium that causes the disease. Many dogs have contracted Leptospirosis within three months of being vaccinated. Dr. W. Jean Dodds, DVM (and many other holistic veterinarians) feels that the leptospirosis vaccine is not only useless but dangerous and is the part of the multivalent vaccine that is most likely to cause damage.
It should also be remembered that vaccines should only be given to dogs that are completely healthy. This is actually stated by the manufacturers on the product information sheet. A dog with dilated cardiomyopathy at whatever stage is not completely healthy.
See vaccines page for more information and links to other sites. Also see page on Geopathic stress.