Congenital heart defects are relatively common in dogs, a study in excess of 34,000 found that about 0.9% were affected. The worrying thing was that more purebred dogs were affected than were crossbred dogs. There is much evidence that many conditions are heredity. The problem is that during development of first the embryo and then the foetus, the heart develops through several stages and a two chamber organ eventually develops into the classical four chamber mammalian heart. Because of this change, there are a number of weak points that must be overcome for the final product to be perfect. Holes in the dividing walls must close, various tubes become redundant and must seal themselves off. Not all this happens in the foetus, but some stages carry on into the separate being of the puppy, not finalizing for a week or more. In some cases the actual closing may be purely physiological, relying on interchamber pressures, rather than truly anatomical. So the presence of a small so called hole in the heart of a puppy at post mortem may be normal rather than the actual cause of its death.
Because of the intricacies of the heart development there are a number of different defects which occur. These may be totally separate conditions, or they may be related to a single characteristic with different forms of expression. All of these problems make the decision as to whether the condition is heredity or not complicated. There is no single gene which may be labelled as the `bad guy’.
The types of abnormalities seen in their order of frequency are: patent ductus arteriosis, pulmonic stenosis, subaortic stenosis, persistent right aortic arch, interventricular septal defect, atrial septal defect, and tetralogy of Fallot. There are some others as well but their incidence is minimal.
In mild conditions some affected animals may reach advanced age without showing signs of heart disease. But when the condition is more serious, young whelps in the nest may show weakness, difficulty in breathing, blueness of the tongue and growth rate will quickly lag behind the litter mates. The most severely affected will die within the first few weeks of life.
Surgical correction of certain defects are within the scope of most competent veterinary surgeons, and specialist veterinary surgeons may attempt the correction of even more complicated malformations.
But having stated the last paragraph, please never ever include such animals who have been successfully treated, in any breeding programme whatsoever. Ideally their parents should also be removed from any breeding programme.
Such defects may be the result of environmental influences. These may include nutrition of the dam (and not just during pregnancy), the presence of extraneous chemical fumes at certain stages during the pregnancy, as well as treatments that the bitch had to receive for some reason other than her pregnancy.
If the animal shows signs of congestive heart failure, such as enlarged veins, enlargement of the liver, fluid in the abdomen, lung congestion and generalized oedema, he/she may respond to rest, low salt diets, diuretics and cardiac drugs. But the response is usually only short lived, and surgery is more permanent.
1) PATENT DUCTUS ARTERIOSIS
An important communication exists between the aorta and the lung artery. This is known as the ductus arteriosis. This duct normally closes within the first few days after birth. If it fails to do so, the patent ductus arteriosis occurs. It is one of the most common heart abnormalities in dogs, and may occur by itself or in conjunction with other abnormalities.
It may be suspected if there is a continuous heart murmur, and often the water hammer pulse. There is usually no blueness of the head mucous membranes. Sometimes the earliest physical sign is weakness or even collapse of the hindquarters during exercise.
Surgery may be entirely successful except in the case of `right to left shunt’ and there is hypertension of the lungs.
2) PULMONIC STENOSIS
This condition occurs when there is a `bottleneck’ within the right ventricle of the heart. The narrowing may occur in the valves, below the valves or in the body of the ventricle. In dogs the most common condition is that of the valves. It is stated to be hereditary in certain breeds of dog.
There is a heart murmur and a `thrill’ may be felt (heard) in the chest area over the heart.
Surgery is possible, but the results are unpredictable.
3) SUBAORTIC STENOSIS
Here again there is a narrowing, but this time in the left ventricle, occurring as a fibrous ring just below the valves. The condition occurs in familial aggregations in several breeds of dog. There is a systolic murmur which may be felt in the neck in some cases. Fainting and sudden death are not uncommon.
Surgery is not recommended for this condition. Some medical treatment is available.
4) PERSISTENT RIGHT AORTIC ARCH
This like the first condition is where there is a failure to change from the foetal system to the real mammalian state. The problem arises as the arch encircles and displaces the gullet and the windpipe, in some cases causing constriction of the oesophagus (gullet). This may lead to difficulty in swallowing and also to regurgitation of food.
5) INTRAVENTRICULAR SEPTAL DEFECT
This indicates a flaw in the wall between the right and left ventricles. It is sometimes associated with one or more of the other congenital defects. If the hole is small there may be no signs of heart disease, but there is usually a murmur present. Many animals with such small defects lead perfectly normal lives. However if the hole is large, the animal will tire quickly and easily, be thin, weak and have difficulty breathing, as well as showing markedly blue mucus membranes. Treatment for these animals should not be contemplated.
6) ATRIAL SEPTAL DEFECTS
This indicates failure of the wall of the two atria to become patent. Small openings may be present without any clinical signs whatsoever. In larger openings there is a harsh heart murmur, as well as difficulty breathing, palpitation and blue mucus membranes.
Surgical correction is possible.
7) TETRALOGY OF FALLOT
This is a complicated malformation which consists of pulmonic stenosis, interventricular septal defect, right positioning of the aorta with overriding of the interventricular septum, and right ventricular hypertrophy. It is reported to be inherited in some breeds of dogs. Cyanosis (blue mucus membranes) is present from birth and is worsened by exercise which precipitates difficult breathing and often collapse. There is usually a loud harsh murmur.
Open heart surgery is required to relieve the condition. It is really not recommended.
These are the most common problems with congenital heart conditions. Some other minor ones do occur, but you as a dog breeder and vendor should be fully aware of the above conditions. Before you offer any puppy for sale, you should have its heart checked by your veterinary surgeon. This is most easily done when the puppies are presented for vaccination. If the puppies have grown normally and well and do not huff and puff or have blue grey tongues, there should be nothing to worry about. But if a puppy is found with any heart murmur, it would be wisest to have it painlessly destroyed before even you can become too fond of it. It certainly should never be offered for sale, even at a markedly reduced price.
You should consider having the dam spayed, you should contact the owner of the sire and quietly and nicely inform him that you have a puppy with a defective heart. Never blame the sire, he is only half responsible, if that. You chose to use him, so any responsibility for the condition is yours, not the owner of the sire. The exception to this is when the sire had already produced puppies with heart defects, and the owner did not inform you of the fact before your bitch was served.
The only way to eliminate the inherited faults of congenital heart defects is to remove from the breeding programme any dog or bitch that has produced puppies that are defective. The brothers and sisters of such puppies should also never be used as breeding stock. This is simple in the more populous breeds, but in breeds with few individuals in the community, it may cause a lot of hardship and financial loss. But it should still be done, certainly before the breed comes into disrepute for carrying these defects genetically. The loss will be much less if you, the breeder, take the long view, rather than try to cover up the problem. The latter course may solve your immediate problems, but in the long run it will severely damage the breed, and certainly break you the breeder.=