Page 291 - Clinical Small Animal Internal Medicine

26 Canine Myocardial Disease 259

(NT‐proBNP), or substances released from myocardial these two mutations do not account for all DCM cases in
VetBooks.ir tissue in response to injury (cardiac troponin‐I [cTnI]). Dobermans, a negative test does not assure a dog will not
develop DCM, nor does a positive test assure the dog will
Note that biomarker testing is never intended to be used
in isolation and should not replace gold standard testing
cannot replace standard clinical screening. Appropriate
(e.g., echocardiography, thoracic radiography for CHF); develop clinical disease. With this in mind, genetic testing
rather, it may be a tool to complement, and in some sample types include EDTA whole‐blood or buccal swabs.
instances justify, other indicated diagnostics. Diagnoses Results may be:
and therapeutic recommendations cannot be made on negative – individual does not carry that particular
biomarker results alone. ● mutation (but there may be other mutations so not
The utility of NT‐proBNP in identifying likelihood of
guaranteed to never develop DCM)
occult disease has been examined in the Doberman. NT‐ positive heterozygote – individual carries one copy of
proBNP >550 pmol/L had a sensitivity of 78.6% and ● the mutated gene and may or may not develop clinical
specificity of 90.4% for detecting echocardiographic disease
abnormalities in one study. It is more sensitive in the positive homozygote – individual carries two copies of
detection of structural disease than arrhythmic disease. ● the mutated gene and may or may not develop clinical
Another study in Dobermans suggests that the combined disease but if so, may be more severe.
use of Holter monitoring and NT‐proBNP >457 pmol/L
(either being abnormal) yields increased sensitivity (94.5%) The greatest utility of genetic testing is determining suit-
and specificity (87.8%). A cTnI >0.22 ng/mL (Immulite®, ability for breeding. It is recommended that homozygous
Troponin I, Diagnostics Products Corporation, Los dogs not be bred, and heterozygous dogs should be bred
Angeles) yielded 79.5% sensitivity and 84.4% specificity for only to negative dogs and only so long as they do not
detection of DCM in another study. Dobermans with express the phenotype.
NT‐proBNP or cTnI greater than these values should be
evaluated with echocardiography. Therapy
For the differentiation of CHF from primary respira-
tory disease in dogs presenting with respiratory signs, Preclinical DCM (ACVIM Stage B)
plasma NT‐proBNP >2447 pmol/L (using second‐ Goals of therapy in preclinical cases include slowing sys-
generation assay) was 81.1% sensitive and 73.1% specific tolic dysfunction, preventing ventricular remodeling and
in a study including 8% DCM cases in a variety of breeds. disease progression, and delaying CHF or SD. Two drugs
This may have utility when physical exam and thoracic for which there is evidence of these benefits are
radiography are ambiguous and echocardiography is not pimobendan and angiotensin converting enzyme inhibi-
available, but otherwise may not provide added value. tors (ACEI). See Table 26.2 for all drug doses.
Pimobendan, a calcium sensitizer with positive ino-
Plasma Taurine tropic and vasodilatory effects, delayed the progression
Whole‐blood or plasma taurine should be measured of preclinical disease in Dobermans in a multicenter,
(using heparinized samples) in cocker spaniels, retrievers, placebo‐controlled, double‐blinded clinical trial. The
Dalmatians, any atypical DCM breed, or any case with a PROTECT trial enrolled 76 Dobermans with preclinical
history of lamb‐based diet, vegetarian diet, low‐protein DCM. The pimobendan group had a significantly longer
diet, grain‐free diet (currently being investigated), or any time to the composite endpoint of onset of CHF or SD
unbalanced home‐made diet. Whole‐blood concentration compared with the placebo group (63% increase in time
<150 nmol/mL or plasma concentration <40 nmol/mL to endpoint, nine months longer). Additionally, the
indicates significant taurine deficiency. Note that taurine pimobendan group had significantly longer overall sur-
deficiency is not necessarily related to amounts of taurine vival time compared with the placebo group. There was
consumed, but may be due to abnormal absorption or no increase in VA noted on one‐month recheck Holter
excretion of taurine or its precursor amino acids (methio- monitoring and no increase in SD in the pimobendan
nine and cysteine), abnormal taurine synthesis, or reduced group. It is important to note that all dogs in this study
protein digestibility limiting availability of precursors. had presence of echocardiographic systolic dysfunction,
so these results are not necessarily applicable to
Genetic Tests Dobermans presenting with VA alone. Pimobendan was
Tests are available for two genetic markers associated with also shown to prolong the time to CHF or SD in IWs with
DCM in Dobermans in North America (PDK4 and titin preclinical DCM, AF, or both. The similarity in pathol-
mutations) through the Veterinary Genetics laboratory at ogy and pathophysiology among different breeds would
North Carolina State University (https://cvm.ncsu.edu/ suggest potential benefit in breeds other than Dobermans
nc-state-vet-hospital/small-animal/genetics/). Note that and IWs, but specific studies are required.