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Links to DCM Information

10K views 29 replies 10 participants last post by  Skye 
#1 · (Edited)
In this thread I am going to post any information I find on DCM to create a 'got to' place where doberman owners can find out information about this horrible disease.
I'll start with this particular site which I found very helpful:

Enlarged Heart (Dilated Cardiomyopathy) in Dogs

Extract of note:

The gold standard for diagnosing DCM is echocardiography, which essentially is a highly sophisticated ultrasound of the heart. This is a completely noninvasive procedure, but it does usually require some degree of sedation so that the animal remains quiet and still. This technology is usually not available in a general veterinary practice; specialized referral centers and veterinary teaching hospitals usually have veterinary cardiologists on staff with the training and equipment necessary to perform an echocardiogram. An echocardiogram can reveal ventricular and atrial enlargement (dilation), as well as abnormal regurgitation of blood through the valves that separate the four heart chambers. An electrocardiogram can also identify erratic heart rhythms (arrhythmias). Atrial fibrillation and ventricular tachycardia are extremely common arrhythmias in Doberman Pinschers. Boxers more commonly have isolated ventricular arrhythmias that can be seen using echocardiography.
Feel free to post sites you know of or find, but please try not to repost sites that have already been posted.

Please keep posts to just links, not anecdotal evidence or opinions.

thanks
 
#3 · (Edited)
Yeah saw that one you have to trawl through loads of posts to find the actual links.
Hopefully people wont post opinions and just post links in this one.

Here is one particularly related to dobermans:

A Prospective Genetic Evaluation of Familial Dilated
Cardiomyopathy in the Doberman Pinscher

http://www.dobermandata.com/i0891-6640-21-5-1016MeursDCM.pdf

Edit: this is very interesting. In this study over eight years of a pedigree known to contain DCM they finally bred from two affected dogs and the whole litter was clear :confused:
 
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#4 ·
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#5 · (Edited)
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#7 ·
This is from another thread and I found it very useful so have decided to copy it here.

The Meur's gene is autosomnal dominant with incomplete penetrance. That means three things:

1) the trait is passed on through parentage.

2) The DCM gene is a dominant trait as opposed to recessive. Dominant meaning it's particulars will override the non carrying gene.

3) Incomplete penetrance means that for some reason the dominance of the particular trait is prevented from manifesting itself either fully or right away. Evidence is, some dogs develop cardio early, some later in life. Same disease different time frame. We do not know what other genetic factors create the incomplete penetrance. They could be good genes, totally benign genes or bad genes even.

Just like vWD or any other trait a dog carries two copies of the gene, but passes only one of the two to an offspring.

Parents:

Neg to neg = all puppies neg (homozygous)
Pos to pos = all puppies pos (homozygous)
Neg to pos = all puppies will carry one copy of the cardio gene (heterozygous)

Dogs that carry one copy of the cardio gene and are called heterozygous positive. These dogs are carrying the bad gene but also have the potential to produce negative dogs if bred to another heterozygous dog or to a negative dog.

The biggest problem with the test we have so far is that it is ONLY ONE GENE and we KNOW there are others that affect the heart and cause cardio. Evidence is that some dogs die of a fatal arrhythmia before going onto congestive heart failure. This is evidence of an "arrythmia gene". Also we do not know why some **** positive dogs never develop the disease. There is obviously other genetic factors at work protecting the heart.

This is a very complicated gene and very complicated research. We need to be proactive in SUPPORTING any research possible. Period.
 
#8 ·
#10 · (Edited)
did you know that DCM is a big problem in Turkeys too?

this is an interesting thesis to read................
http://scholar.lib.vt.edu/theses/available/etd-12192008-113226/unrestricted/XiTian.pdf




not sure if all this info. has been posted yet.

"Patent application title: METHODS AND COMPOSITIONS FOR DETECTING CANINE DILATED CARDIOMYOPATHY (DCM)
Inventors: Kathryn M. Meurs (Raleigh, NC, US)
IPC8 Class: AA01K6702FI
USPC Class: 800 8
Class name: Multicellular living organisms and unmodified parts thereof and related processes nonhuman animal
Publication date: 2011-12-15
Patent application number: 20110307965"

http://www.faqs.org/patents/app/20110307965
 
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#18 ·
#14 · (Edited)
#15 ·
Interesting:

t's obvious that new genes do evolve, but exactly how this happens has been unclear. Now researchers have shown for the first time how organisms can evolve new genes.

The previous idea was that a gene accidentally duplicates and then mutates to gain a new function, but there have been a few problems with this idea. One is the frequency of certain mutations. Ignoring neutral mutations (which have no effect on an organism's fitness), the likelihood of a mutation being harmful is much higher than of it being beneficial. So if a gene is duplicated by mistake, the chance of it then developing a beneficial mutation is very small compared to the chance of it developing a harmful one. There is more chance of it gaining a useful mutation if it is around for generations, but genes not positively selected for disappear from the gene pool. Natural selection does not wait around for genes to become beneficial.

Using salmonella bacteria, researchers from University of California (Davis) and Uppsala University (Sweden) tested a new model. This model suggests that the beneficial mutation comes first, giving the gene a weaker secondary function. There is no waiting around for a duplicate to develop a new useful function, and there is time for beneficial mutations to occur because the gene is selected for due to its primary function.

The research team grew a salmonella culture lacking the gene mainly responsible for synthesising tryptophan, forcing it to manufacture this amino acid using another gene's weak secondary ability. The bacteria was then placed in an environment without tryptophan. This put heavy selection pressure on any beneficial tryptophan-synthesis mutations or duplications. 3,000 generations later, the bacteria had a new gene for producing tryptophan working alongside the original gene. While this mechanism has not been tested on other organisms, this finding makes it highly likely it will be found eventually in other forms of life.
 
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#19 · (Edited)
ok, sorry Matt Vandart, I know you did not want discussion, just links, so this post can be edited if you want...........but i have cabin fever and my mind is on a roll. :)

now, working off this............ 1. Dobermans, free of heart disease, have hearts that are normally weaker than those of other dogs."

i wanta to add this link to this thread...........Thyroid Hormone Disorders

"TH imbalance has a profound effect on cardiovascular fitness because TH helps control heart rate and blood pressure. Under hypothyroid conditions, the heart can slow to 30 heart beats a minute and develop arrhythmia. Blood pressure may fall from normal levels of 120/90 to 70/50. Hypothyroidism also weakens muscles, including the diaphragm. As a result, breathing can become less efficient. A goiter impairs breathing even more. Snoring may start or become worse. Fatigue sets in easily; in fact it never quite leaves a person with symptomatic hypothyroidism. Muscles and joints often ache. With respiration impaired and oxygen in short supply, exercise takes a heavy toll on the body, and muscles do not strengthen in response to exercise; nor does stamina improve."

so, if a low thyroid, weakens the heart muscle, the diaphragm.....................

is the fact that so many of our breed is 'low normal' or 'lower', contributing to the dcm in our breed. Is it a 'trigger'?

and because the thyroid affects hormones.......is that why it seems that more males are affected with dcm than females.

does a female hormone somehow 'protect' the heart muscle?

my 2 longest lived dobes were both spayed females, on thyroid replacemant therapy most of their lives........i have always wondered if thyroid.....dcm....cvi and cancer were all linked in some way.
 
#21 ·
Interesting isn't this the Meurs gene?

Role of carnitine: Work performed by Dr. Bruce Keene a number of years ago suggested that a deficiency of carnitine may be responsible for DCM in some Boxers. Carnitine is essential to transport fatty acids into the mitochondria of the muscle cell. Without adequate carnitine, fatty acids cannot enter the mitochondria, and energy deficiency results. However, carnitine presently does not appear to be responsible for most cases of DCM observed in Boxers or other breeds. Rather carnitine deficiency is likely a secondary effect in heart disease and not a primary cause.[/QUOTE]
 
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#23 ·
Stem Cell Study

Wasn't sure where to post this and didn't want it to get lost in the "shuffle".

This was posted on Doberman DCM FB Group regarding the DCM stem cell study:

"No good news about DCM therapy
Stem-cell therapy for dilated cardiomyopathy: a pilot study evaluating retrograde coronary venous delivery
B. Pogue, A. H. Estrada, I. Sosa-Samper, H. W. Maisenbacher, K. E. Lamb, B. D. Mincey, K. E. Erger, T. J. Conlon
Journal of Small Animal Practice
Article first published online: 3 JUN 2013
DOI: 10.1111/jsap.12098
Objective
To evaluate retrograde coronary venous stem-cell delivery for Dobermanns with dilated cardiomyopathy.
Methods
Retrograde coronary venous delivery of adipose-derived mesenchymal stem cells transduced with tyrosine mutant adeno-associated virus 2 to express stromal-derived factor-1 was performed in Dobermanns with dilated cardiomyopathy. Cases were followed for 2 years and electrocardiograms (ECG), echocardiograms and Holter monitoring were performed.
Results
Delivery of cells was feasible in 15 of 15 dogs. One dog died following the development of ventricular fibrillation 24 hours after cell delivery. The remaining 14 dogs were discharged the following day without complications. Echocardiographic measurements of left ventricular size and function showed continued progression of disease. On the basis of Kaplan–Meier product limit estimates, median survival for dogs following stem-cell delivery was 620 days (range of 1–799 days). When including only the occult-dilated cardiomyopathy population and excluding those dogs already in congestive heart failure, median survival was 652 days (range of 46–799 days).
Clinical Significance
Retrograde venous delivery of tyrosine mutant adeno-associated virus 2-stromal-derived factor-1 adipose-derived mesenchymal stem cells appears safe. Stem-cell therapy in dogs with occult-dilated cardiomyopathy does not appear to offer advantage compared to recently published survival data in similarly affected Dobermanns."

Really not good news.
 
#26 · (Edited)
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