BOXER CARDIOMYOPATHY

Cardiomyopathy usually presents differently in the boxer than in the other breeds at high risk for the disease such as Dobermans and Danes. Early in the course of the disease in boxers, there is an arrhythmia that may or may not be detected by listening to the heart with a stethoscope. Whether or not it is detected depends on the frequency of the abnormal rhythm. If it is frequent, it can easily be heard with a stethoscope. The arrhythmia usually consists of VPCs (ventricular premature contractions) that are heard as an extra beat or a skipped beat that do not have a corresponding pulse. To identify these, the listener therefore must have one hand on the stethoscope holding it to the chest and one hand feeling for a pulse. In the normal functioning heart, there is a pulse for every beat that is heard. When a VPC occurs, a beat is heard through the stethoscope, but there is no pulse to go with it. These VPCs have a characteristic pattern on an ECG and this is the way they are confirmed. Often this is the first abnormality noticed in a boxer with cardiomyopathy. Usually the dog is having no symptoms of heart disease when these are noticed by a veterinarian during a routine exam. If the frequency of these irregular beats increases, the animal may suffer "fainting" spells (called syncopal episodes). This happens because these abnormal beats do not pump the blood effectively (no corresponding pulse) to the vital organs like a normal beat does and the brain becomes oxygen deprived while the abnormal beats are occurring. Usually when an animal faints, they are having what is known as a run (several in a row) of VPCs. If the heart corrects itself, the animal regains consciousness in a matter of seconds to minutes. If the run of VPCs continues, this is then called ventricular tachycardia and can lead to the development of ventricular fibrillation which is fatal if the rhythm is not converted. This ventricular fibrillation (V-fib) is the cause of sudden death in most boxers with cardiomyopathy. There is no blood being pumped through the body when the animal is in V-fib. Many boxers with cardiomyopathy will live long enough to enter the next phase of disease where the ventricles of the heart start to dilate. The walls of the heart become thin, the heart muscle weakens and these animals can show symptoms of heart failure such as coughing (from lung congestion) and/or fluid retention in the abdomen (ascites) depending on which side of the heart is most affected. In time as the heart becomes very enlarged it begins to be an inefficient pump and the dogs so affected may require numerous medications to keep the heart functioning well enough to sustain life. Still, most boxers affected with cardiomyopathy will ultimately die of their arrhythmia, not of congestive heart failure. Any boxer that is apparently healthy and dies a sudden death should have a necropsy performed to determine the cause of death. The only way to definitively make the diagnosis of cardiomyopathy is to take tissue samples from the heart muscle for evaluation by a veterinary pathologist. The diagnosis is made by examining the heart tissue under a microscope. Cardiomyopathy can also be responsible for sudden death associated with anaesthesia.

Now, just because a boxer has VPCs does not absolutely mean it has cardiomyopathy IF there is another disease process at work. I have seen animals with severe infection have VPCs that resolved completely once the infection was cleared. If they are seen in an otherwise healthy boxer, one would have a high index of suspicion for cardiomyopathy, however, because of the prevalence of the disease in our breed. The best way to evaluate a boxer for arrhythmia is to use a 24 hour ECG called a Holter monitor. This will tell you if your dog has VPCs. Normal dogs of breeds that are not known to develop cardiomyopathy have none in 24 hours. Normal people can have several in 24 hours. Not enough boxers have been studied to know if a small number of VPCs may be normal, but what is known is that most boxers that go on to die of cardiomyopathy have lots of VPCs in a 24 hour period (thousands). The Holter also allows us to identify the likelihood of problems due to clusters of VPCs. For example, most asymptomatic animals have single VPCs interspersed with their normal beats throughout the 24 hour period. If a Holter shows many clusters or runs of VPCs, this means that this animal may be at more risk for syncope or sudden death and this can affect how the dog is treated (with anti-arrhythmic drugs, for example). An echocardiogram is also useful to determine if the heart is contracting properly. It will also help detect and identify the source of any murmurs that may have been heard on auscultation with a stethoscope. It can be used to rule out the inherited condition of sub-aortic stenosis which is known to affect the boxer and can also lead to sudden death. It can also show whether or not there is any enlargement of the heart chambers or any thinning (as seen in dilated cardiomyopathy) or thickening (as seen in hypertrophic cardiomyopathy) of the heart muscle walls. It is not a good tool for detecting an arrhythmia, unless the arrhythmia is very frequent.

As far as nutritional deficiencies go, it has been shown that dogs on commercial diets have adequate amounts of L-carnitine in their plasma and that 80% of dogs with cardiomyopathy that have a deficiency of L-carnitine in the heart muscle have normal to increased L-carnitine levels in their blood. Although there has been a correlation between a single family of boxers with cardiomyopathy and a response to supplementation with the L-carnitine, many more boxers have shown no improvement with supplemental L-carnitine. This family of boxers was found not to have a deficiency of carnitine in the diet, but most likely had an inability to utilize the carnitine present in the blood plasma and transport it into the heart cells where it must be actively concentrated so that it can be used for fatty acid metabolism, generation of energy and detoxification of certain metabolic compounds. This would be considered an inherited defect of the membrane transport of L-carnitine. While supplementation with L-carnitine improved the contractility of the hearts of these dogs and caused a temporary improvement, it did not decrease their arrhythmia. All of these dogs eventually died due to ventricular arrhythmias.

If you suspect your boxer may be affected with cardiomyopathy, I would urge you to find a board-certified internal medicine specialist with the subspecialty of Cardiology to rule out or confirm the disease. It is not easy to diagnose and will require special equipment and knowledge that is best found from someone who specializes in diseases of the heart.