Proposed major criteria for the diagnosis of canine DCM ~a dialogue about DCM

[Elaine]

Here - in sequence - is a discussion of DCM between Arthur (an M.D.) and Brenna related to an 2003 Journal article Arthur found of interest. Proposed major criteria for the diagnosis of canine DCM
I thought the discussion was interesting. It occurs to me that while this may not seem relevant to some of you now... given the DCM is in the Doberman breed (as well as in other breeds and in humans) some of this discussion may be of relevance to one of us in the future.

[Elaine]

Brenna,

I was reading this article tonight and was wondering if vets actually use these criteria. I just thought it was interesting. It was from 2003 and I cannot see where anyone follwed up on this.

-Arthur

[Elaine]

Re: ‏
From: Brenna
Sent: Fri 1/23/09 10:29 PM
To: Arthur Greenwood (arthurgreenwood@hotmail.com)

I have a few opinions about this.

First, they are making broad sweeping generalizations. There are easily documented left and right sided atrial or ventricular dilation forms.

Second, they do not even address the sudden death that presents as pericardial tampanade. The widow maker ruptures at the ventricular apex, pericardium fills, et viola, sudden death. I've seen a ton of those one the necropsy table.

Further, the numbers they present for low ejection fraction represent the category 3 and 4 (out of 4) in late stage heart failure.

Also, clinical symptomology often does not present until irreversible damage has be done to cardiac tissues.

The pathological findings made me giggle a bit as they only addressed a tiny fraction of a histopathologic evaluation. Wavy or vacuolated have entirely differing etiologies.

For my dogs, I have a very specific regime. I test for ejection fraction AND wall thickness AND pcvs occurring in a two sequence 72 hour holter, one routine and one under some stress. Further, I watch cpk (creat kinase) like a hawk. I watch from a human diagnostic angle.

Come on...even as a first year student, you knew the difference between pink puffers and blue bloaters. It seems that details like that are utterly disregarded by the veterinary community. They say "oh, clear cut case of dcm" which is like saying "oh its cancer" and then they KNOW the treatment regime? Whatever. As for treatment...haven't they learned about carvedilol, or the cardiac acorn implant? I just hate it when they use some of the right words, but not in a meaningful way. Want real diagnostics? Don't tell me about cardio clear. Not many 20 year old men have that, but is that the same when that man is 50? Show me the cardio strip. Then we'll talk.

As for males more often that females? They quote wrong. Human females actually have equal or greater cardiac pathology that men, its just that females are underdiagnosed and seldom go to autopsy for insurance purposes. Males of both dog and human, is also proportionately larger...so is the statistical skewing really off the numeric mean? Nope. Tell them to email me when they actually gather pathology based data. There's a phd dissertation for you!

[Elaine]

From: arthurgreenwood@hotmail.com
To: [email]]
Subject: RE:
Date: Sat, 24 Jan 2009 09:27:16 -0500

Brenna,

Wow. You spit that out pretty quickly. I'm not going to pretend to know much about DCM as for the most part it has been not been part of my practice. I can't say that it comes up much at all. Rarely we have a pregnant woman with a cardiac history that we need evaluated to determine if she can withstand labor. In reality the answer is she gets a cesarean delivery in a private hospital because they don't want the liability or don't have anesthesia in house and she labors without pushing (even though she is a New York Heart Association Class I) in a teaching institution because we all need practice with forceps deliveries. Sad but true.

I was looking at the paper from the perspective that people throw around the diagnosis of DCM because their dog who has never been to the vet died suddenly and everyone assumes it was DCM. I imagine that there are veterinarians who diagnose DCM the way physicians diagnose a upper respiratory infection and prescribe Z-Packs. It all seems to be without meeting diagnostic criteria. I thought this author attempted to establish some minimall criteria with the understanding that it is a diagnosis of exclusion.

Table 2
Exclusion Criteria Prior to Making a Diagnosis of Idiopathic Dilated Cardiomyopathy:

Congenital and other acquired heart diseases

Tachyarrhythmias which may result in a tachycardia induced cardiomyopathy

Systemic hypertension

Pericardial diseases (not mild pericardial effusion that may be secondary to heart failure)

Systemic diseases that might affect cardiovascular function (e.g. hypothyroidism)

History of use of drugs known to affect cardiac function (e.g. doxorubicin)

Metabolic deficiency (e.g. taurine, L-carnitine)

Presence of atrial fibrillation with a fractional shortening > 25% (mean of 5 to 10 beats)

Note, these criteria can be simply and practically excluded in the living dog. At post mortem, other criteria should actively excluded,

such as myocardial infarction, other coronary vascular disease, myocarditis etc. The authors recommend that, wherever possible,

post-mortem examination is carried out.

He also attempted to establish Major and Minor criteria that must be met. I agree that they fall short, but it puts into perspective how breeders are making breeding decisions based on utter observations with no physical findings, labs, or diagnostic testing.

If I took one of our dogs to NCSU Vet School, what diagnostic criteria woould they use? How many echos do they do in a week and have they ever done an echo on a doberman? I guess I need to find this out. Does your vet use breed specific ranges for wall thickness and ejection fraction or does she base it on body surface area. Or does she simply establishes a baseline and compares year to year? Do you know what the normal EF is for a doberman and what is the cuttoff? Is it two standard deviations? In this paper the author suggests using an EF of 40% as one of the major criteria. How many PVC's are normal in 72 hrs?

The DPCA isn't very helpful when it comes to defining DCM in dobermans. Their website says: CARDIOMYOPATHY - is suspected to be an inherited disease in Dobermans. Research is in progress in several institutions. An echocardiogram of the heart will confirm the disease but WILL not guarantee that the disease will not develop in the future.

I was surprised at how their breeders education web page is lacking. No wonder breeders are uneducated.
-Arthur


Proposed major criteria for the diagnosis of canine DCM

1. Left ventricular M-mode systolic or diastolic dimensions exceeding 95% confidence intervals for the individual based on regression equations or predicted reference values, or outside other established breedspecific reference ranges. Account should also be paid to the influence within specific breeds of body surface area, gender or age where these data are available and applicable.

2. Increased sphericity: LV length: M-mode LV diastolic dimensions is decreased. The authors propose that a ratio of LV diastolic length (from RPS long axis four chamber view) to the M-mode LV diastolic dimension <1.65 represents increased sphericity13.

3.a. EITHER:

M-mode fractional shortening of <20% or 25% (depending on breed-specific reference values).

3.b. AND / OR: Left ventricular ejection fraction less than 40%.

It is important that breed specific reference ranges are generated or consulted if available. The authors urge particular caution in assessing extreme breeds, or very athletic breeds (which, at rest, often have a low measured fractional shortening).

(From the conclusion paragraph) It is probable that certain criteria will be weighted differently in certain breeds (e.g. ventricular arrhythmias in Dobermanns and Boxers may represent a major criterion).

Proposed minor criteria for the diagnosis of canine DCM
1. The presence of an arrhythmia in a specific breed where the arrhythmia has been shown to be strongly associated with DCM (e.g. increased (for age) ventricular ectopy in Dobermanns or Boxers). Other (cardiac or systemic) causes for ventricular ectopy should be actively excluded.

2. Atrial fibrillation.

3. Increased mitral valve M-mode E point to septal separation (EPSS).

4. PEP:ET ratio increased over 95% confidence intervals (e.g. over 0.4)

5. M-mode fractional shortening in equivocal range (depending on breed-specific references).

6. Left or bi-atrial enlargement