I disagree with you on this.
"All but useless?" It measures abnormal electrical activity in the heart. How is that useless to know? If you have a 3 year old dog with 100+ abnormal heartbeats with doubles and triples but the Echo shows normal size heart, how is that useless? Breed it anyway because everything else is OK? The Echo measures one thing, the Holter measures another. A clear colonoscopy doesn't mean your liver isn't shot.
The whole issue with largely pointless diagnostics is that they're unlikely to find anything. Statistically speaking, what percentage of the time does a proactive Holter actually identify a concerning arrhytmia in a Doberman with an otherwise normal-appearing heart? That's what I'm wanting to see, it's a seemingly simple piece of resarch I'm not seeing anywhere. Everything is so vague, I want demonstrable clinical proof that there's value in proactive Holters in the general Doberman population.
There's plenty of research that says 48-hour holters have substantially more value than the standard 24-hour Holters. Of even more value would be a continuous, permanent Holter, but in reality, what we have is a brief snapshot and hopes & dreams of maybe finding a subtle indication that there might be a serious, chronic arrhythmia based on 24 hours of heart rhythm monitoring.
If, at some point, a relatively affordable heart implant monitor was made available that was like a permanent Holter that sent data to a smart collar, would I be interested? Absolutely.
There's also an interesting remark in the paper that implantable defibrilator devices may also produce meaningful survivability rates for a period of time in a dog diagnosed with DCM who are at risk of SCD (which is the more standard abbreviation, I don't know why Dobe folks often use just "SD").
You are comparing apples and oranges. Doberman DCM is almost entirely a genetic, inherited disease. Although DCM in humans does have some hereditary factors, it is mostly caused by lifestyle choices. How many of these preventatives can I use for my dog??? The average age for a first heart attack in a human is over 65. A 7 year old dog is thought to be equivalent to ~ 47 in human years. DCM strikes commonly in dogs under 7, especially the Euro dogs have countless dying before 4 years of age (think about a 35 year old human). The best preventions for humans is lifestyle changes because THAT is the biggest cause of it in humans.
Except I'm not-- we know a great deal about the disease and how to treat it. The paper I link discusses many different treatments for DCM and how much they may prolong lives of dogs receiving the treatments. Most of those medications listed are used in humans with heart issues as well.
Some of the pathology is different, in that a lot of human CHF is related to loss of aterial elasticity and constriction, which forces the heart muscle to work harder, and it gets damaged & weaker. This is obviously not a risk factor in Dobermans, and yes, it affects humans later in life & is due to poor lifestyle choices a lot of the time.
CHF is not SCD. The pathology can be related because, eventually, cardiac arrhytmia shows-up in an enlarged, failing heart, but generally not enough to cause random SCD in people with moderately healthy lifestyles and few comorbidities.
Genetic human DCM and associated arrhymias are quite similar to the corresponding condition in Dobes, which is what tends to cause SCD with normal-sized heart muscles in both species. That's what Holters are about identifying. If a dog or human experiences syncope, that's a prime indications that a Holter may be useful if there's not another obvious cause.
The genetic basis really all does come down to the same stuff. As has been discussed many times, "DCM1" is just a human genetic marker for the PDK4 mutation that also had an established coincidence relationship with DCM in humans, and was found to be a statistically-significant coincidence with DCM in Dobes in the NA cohort as well. Muers and her team were not starting from scratch, they started from human medicine and were throwing stuff at the wall using educated guesses and hoping something would stick. Researchers have been trying to establish a direct correlation between the PDK4 mutation and identifiable degradation in the heart muscle fibers that might actually prove causation of DCM for some cases, but they have precisely nothing except for there sometimes being a strong coincidence at this time.
Anyway, I don't think you reviewed the research I linked, it's pretty clear what they found, and it agrees with the general practical application for Holter testing in both humans and dogs, with the sole exception of suggesting there's possible early diagnostic value in dogs with familial history of SCD, but again, they found that VTach seems to matter the most and the VPC/PCVs aren't really that relevant.
This actually does make sense, because VTach often leads to VFib in humans, which typically results in SCD. That's often what defibrilator devices attempt to reset by hitting the heart with enough of a shock to stop it momentarily in hopes it can be restarted with a functional rhythm.
Again, from Mayo Clinic, referring to human PVC's:
Having frequent premature ventricular contractions (PVCs) or certain patterns of them might increase the risk of developing irregular heart rhythms (arrhythmias) or weakening of the heart muscle (cardiomyopathy).
Rarely, when accompanied by heart disease, frequent premature contractions can lead to chaotic, dangerous heart rhythms and possibly sudden cardiac death.
This is exactly what a Holter is for. In humans and dogs both, a handful of PVCs is not of concern. Over certain numbers or in certain patterns, it can indicate a risk of developing problems. If you know you (or your dog) has had zero or 5 or 10 in 24 hours and the next year you have 150, that is information to address.
I'm not saying that's incorrect information or wrong-- I'm saying it's apparently so rare as to be a pointless thing to look for under normal circumstances. Again, CHF and SCD are different things. There's a much lower risk of SCD across the board, both in humans and in dogs. That's why proactive Holters aren't performed in humans unless there's an indication calling for one, such as syncope or familial history.
It's 6 of one, half-dozen of the other. A personal, non-breeding companion dog without DCM positive close relatives? I don't push for these people to test if they don't want to. I will not every buy from a breeder who doesn't do both Holter & Echo yearly, but as you say even with best results showing healthy hearts, my girls sire died at 7 of sudden death. When it hits close to home - and the numbers are showing 50% of Dobermans will have this disease should be close enough to home for every one of us - you really wake up and want to find answers on prevention.
To offer a clarification, 50% or so of Dobes die of some form of DCM. It's maybe somewhere around half of that number who are at high risk of SCD. It's a much, much lower number who are at risk of SCD without exhibiting other clinical signs of DCM, such as an enlarged heart as seen in an Echosound.
So, at what percentage does a not-cheap diagnostic that's a bit of a hassle, such as a Holter, make sense? There is a good bit of statistical interpolation in the study I linked, since they were analyzing and ranking risk factors, but I think we're talking about single-digit percentages of Dobes in which a proactive Holter might catch an indication in the form of VTach episodes in dogs with hearts that appear to have normal size & function as seen with an Echo.
That's why I say it's kind of pointless.
I'd like to see research into:
1) The percentage of dogs in which a proactive Holter identifies an elevated SCD risk before heart enlargement is seen in an Echo.
2) The typical timeframe that the Holter identifies the elevated SCD risk in advance of it becoming apparent in an Echo.
3) The degree of increased risk of SCD in Dobes with familial history of SCD, how effective Holters are with identifying that specific condition, and how long in advance they're effective (since it's likely to be a substantially higher benefit over the general population).
I think these things are important in targeting diagnostics for maxium benefit and not just wasting effort & money. For example, if the typical advance notice a Holter gives over an Echo is a couple of months at best, then it's probably not at all valuable as a proactive diagnostic.
If it can give a year or more advance notice in targeted cases, that's absolutely huge, since, as the paper mentioned, implantable defibrilators can make a difference in survivability under arrhytmia which typically cause SCD, and beginning treatment to slow physical enlargement of the heart before it's even noticeable may also stave-off CHF substantially longer.
Again, I believe Echocardiography has the greatest proactive diagnostic benefit across all Dobes, which has had its value demonstrated again and again, including in that study I linked, and everyone who owns Dobes should strongly consider them regularly.
In your girl's case, yes, you should absolutely have heightened vigilance if her sire died of SCD-- that's the familial history factor which raises concerns and is an indication that there would be value in a proactive Holter for her and any half-siblings from that sire, especially any who may be bred at some point.
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