You’ve got a GREAT cardio that you are working with if you are able to watch echocardiograms done on your dogs. I’ve been able to do that for 20 years now, and I have learned so very much about understanding diagnostic tests and treatment options of acquired valvular disease from working with a cardiologist who loves to teach and allows clients to be present during the entire evaluation as well as from reading.
Your cardio is exactly right – and that is why I don’t pay a whole lot of attention to murmur grades except to use them as a signal as to when to get further diagnostic testing. My GP vet has graded my dogs’ murmurs the same as the cardiologist over all of these years, so I don’t bother to get an auscultation from my cardio (who is a two hour drive away) for a soft murmur when my GP vet hears one. (I will, though, shoot a baseline chest x-ray at some point after my GP vet first hears a murmur. I keep my x-rays at home so that I can take them to cardio appts. and it’s also nice to have them at home in the event I have a middle of the night ER visit for some crisis.) I do pay attention, though, if there is a significant increase in the grading of a murmur over a six month or one year period (i.e., a grade II murmur jumps to a IV quickly).
So knowing the grade of a murmur isn’t all that informative as it doesn’t give you a good picture of how the heart is actually functioning – but a color Doppler ultrasound (echocardiogram) when done by a specialist with training and experience (versus a GP vet simply with enough money to purchase an ultrasound machine) is very informative. That test will show the functioning of the valves, and you can see changes in the valve leaflets, whether or not there are ruptured chordae tendinae, whether there is valve prolapse; you can see the regurgitant flow and measure the velocity of the regurg, and you can get exact measurements of the cardiac chambers and compare them to normal measurements. Other complications such as whether or not pulmonary hypertension is present can also be measured by an echo. Another important measurement obtained from an echo is contractility or shortening fraction, which is given in a percentage (like 20% or 50%). This is a measurement of the pumping strength/ability of the heart. In acquired valvular disease, this usually remains normal until end stage heart failure whereas in DCM (dilated cardiomyopathy – the heart disease commonly found in large breeds) contractility is usually compromised early in the course of the disease.
Luka has leakage of his mitral and his tricuspid valves (very common to have leaking in more than one valve) and you will usually find on the report a description (trivial, mild, moderate, severe) and sometimes a figure measuring the velocity of the leak/regurg. Since she said subtle leakage and it appears that his heart chambers were not enlarged, she correctly prescribed watchful waiting/monitoring and no meds at this time. Generally, in the US anyway, cardios will prescribe an ACE inhibitor such as enalapril when there is moderate or greater chamber enlargement and moderate or worse regurg. even if the dog is not yet in active CHF. Once heart failure ensues, diuretics and other meds are added as needed to control overt symptoms. But all cardios don’t agree on exact time to start meds before CHF. (I tend to start an ACE inhibitor rather early in the game particularly if my dog is over 6 or 7.) Blood chemistry should be done before starting an ACEI and then again after 7-10 days and then periodically to watch for changes in kidney functioning, monitor electrolytes, etc.
It sounds as if Luka is in the early stage of the disease, and he could stay compensated for a long time. Have you taken a baseline chest x-ray? I would actually do that and then get another two-view chest x-ray in six months to look for changes. This isn’t too expensive, (not like an echo) and it will give you an idea if you are dealing with rapidly progressing or slowly progressing valve disease. As you go through the next year or two, you’ll have more of a prognosis/idea of how things will go for Luka. As for being more subdued, I can’t see any reason that this would be related to his heart disease.
Regarding the breeder’s comments – there is NO Cavalier breeder in the history of the world that has bred 300 litters (10 yr x 30 yrs) and has had only one Cavalier develop a murmur due to endocardiosis. (Are you saying she said “not at any age” or “not at Luka’s age”?) That person is either in denial, lying or is incredibly ignorant. There is no shame in producing a Cavalier with a murmur – 50% have them at age 5 and nearly 100% by age 10. It’s a fact of life. The way to approach the problem (IMO) is to simply breed to the protocol – only breed Cavaliers that reach age 2.5 with no murmur and have parents over 5 with no murmur. I have dear friends who are breeders; I know about proving a male early, etc, etc. But the way to minimize early onset endocardiosis and lengthen the lifespan of the Cavalier to one more normal for a breed of that size is to breed to the protocol. But even if you breed to the protocol, you’ll produce some Cavaliers that develop murmurs early and more that develop murmurs later – you’ll just start pushing the age of onset for the majority later and later.
I don’t know what the “throw back thing” means – endocardiosis is in the genes (we don’t know which ones obviously) of all Cavaliers. No “throw back” to anything – it’s there in all. It manifests itself in various ways depending on the combination of genes inherited in the particular Cavalier. Even within the same litter there will be differences. (i.e., the litter of 7 I described earlier where one died of CHF at age 8 and two others lived to 16+ and died of other causes.)
Sue, are you in the U.S.?