Canine Cardiac Disease Flashcards
What is cardiac cachexia and how is it treated
Cardiac cachexia is defined as a loss of muscle or lean body mass associated with heart failure, with or without clinically relevant accompanying weight loss. Cachexia has substantial negative prognostic implications and is much easier to prevent than to treat.
Maintain adequate calorie intake (maintenance calorie intake inStage C should be approximately 60 kcal/kg BW) to minimize weight loss that often occurs in CHF
Address anorexia/hyporexia secondary to medications
Ensure adequate protein intake and avoid low-protein diets designed to treat chronic kidney disease, unless severe concurrent renal failure is present
Supplement K+ if indicated
recommendations for stage D MMVD
Few clinical trials have addressed drug efficacy and safety in this patient population. This deficiency leaves cardiologists treating heart failure refractory to conventional medical treatment with a perplexing variety of treatment options.
Torsemide can be used in place of frusemide (1/20th of dose) but has an increased risk of causing electrolyte imbalances, prerenal azotaemia and hypotension increases with more aggressive diuretic treatment. Some degree of disturbances during treatment will have to be accepted, as they seldom cause clinical problems.
An arterial vasodilatory or venodilator may be considered in the critically ill patient to reduce afterload and stabilise the CHF.
Because afterload reduction may increase cardiac output substantially in the setting of severe MR and heart failure, administration of an effective arterial dilator drug in this setting does not necessarily compromise blood pressure sodium nitroprusside (for afterload reduction) or dobutamine (for inotropic support), especially in hypotensive patients) or both is recommended by a majority of panelists
Sildenafil if complicated by PHT
B-blockers - only indicated as adjunct to control HR in patients with atrial fibrillation and used cautiously due to their negative inotropic effects
Complications of MMVD and CHF
cough due to mainstem bronchi compression/concurrent malacia
RSCHF from pulmonary hypertension from concurrent tricuspid regurg or persistent elevation in LA pressure
Arrhythmia usually supraventricular.
Chordae tendineae rupture - acute decompensation
LA rupture and cardiac tamponade
development of renal dysfunction (CvRDH)
for and against ACEi in MMVD
ACEi: JSAP 2022 review: based on current evidence the there is unlikely efficacy of ACEi in preclinical Dz to delay CHF onset or change CV related mortality. current publications the good responses seen are within margin of error for the same risk of negative response.
ACVIM - clinical trials in B2 dz have mixed results still recommended but weak LoE
VALVE trial - no difference in cardiac death or MST in triple vs double therapy. Again recommended in ACVIM consensus
Evidence for/against VLAS
2021 comparison to VHS found was superior at identifying LA:Ao >1.6), less issues with positioning, less affected by breed conformation, less inter-observer variability.
Both can be affetected by ability to see landmarks
2020 - comparison of VHS and VLAS and combined found no difference in ability to differentiate
2023 - comparison in ability to differentiate dogs with CHF vs resp signs.
VLAS cutoff >2.4 Sens 93%, Spec 82.5%
Associated with CHF
VHS - more false positive in non-CHF dogs
2020 - VLAS optimal cut off
2018 - VLAS only, good interobserver agreement
Evidence for diet in MMVD
JAVMA 2022 key nutrients summary
Long-chain omega-3 fatty acids provide anti-inflammatory, antithrombotic, and other benefits.
Medium-chain fatty acids and ketones derived from MCT provide an alternative energy source for cardiac mitochondria and help reduce free radical production.
Magnesium supports mitochondrial function, normal cardiac rhythm, and provides other benefits.
Both vitamin E and taurine counter oxidative stress, and taurine also has direct cardiac benefits.
Methionine and lysine are important for carnitine production as well as other functions. Dogs with MMVD have reduced plasma methionine
JVIM 2023 - effect of specialised diet no difference in 12 months
Goals of therapy in stage C MMVD
Reduce venous pressure
Maintain cardiac output
Reduce workloads and regurgitation
Protect from negative long-term effects of neurohormones.
Role of selective breeding in MMVD
A mandatory breeding scheme based on auscultation and echocardiography findings significantly decreased the prevalence of MMVD over the 8- to 10-year period.
Diagnostic criteria for stage C
Clinical signs of left-sided CHF and a history that can include tachypnea, restlessness, respiratory distress, or cough
Cardiac ultrasound examination can confirm the presence of MMVD, quantify chamber enlargements and cardiac function, pro- vide general estimates of LV filling pressures, and identify comorbidities and complications of chronic MR (PHT, atrial rupture, neoplasia).
As a group, dogs with clinical signs caused by heartfailure have higher serum NT-proBNP concentrations than do dogsin which clinical signs are caused by primary pulmonary disease,although the positive predictive value of any single specific NT-proBNP concentration has not been adequately characterized
Systemic causes of DCM
chronic volume overload,
hypoTH,
myocarditis,
nutritional insufficiency (taurine),
toxins;
chronic tachyarrhythmia
Criteria for DCM Dx
left ventricular dilation (systole and diastole);
depressed systolic function;
EITHER: M-mode fractional shortening of <20% or 25% (depending on breed-specific reference values).
AND / OR: Left ventricular ejection fraction less than 40%. Using breed specific references
increased sphericity of ventricle (altered geometry)
overt disease
Atrial enlargement (wihtout other cause) Increased EPSS
Arrhythmia
Consideration of the breed of dog may be helpful in differentiating between DCM and AV valve disease since it is uncommon for many of the large breed dogs to develop significant primary valve disease
Recommended screening in Dopbermans
Genetic testing PDK4 might be useful in USA but not in europe
Screening starting at 2 years old
Annual screening
Echo and 24 hour Holter ECG
< 50 single VPCs/24 hours is considered to be normal in Dobermans. Note: Some Doberman Pinschers might have only a few VPCs/24 hours, but < 50 VPC/24 hours. If the VPCs have a short coupling interval (Vmax > 250/min), this could be also suspicious of being affected.
NT-proBNP result > 500 pmol/l (especially to predict echocardiographic changes) cTnI > 0.22
Evidence for cardiac biomarkers in DCM and Sens/Spec (Dobermans)
JSAP 2022 - for DCM in Dobermans: When both Se and Sp were optimised for all forms of dilated cardiomyopathy, N‐terminal proBNP cut‐off was 626 pmol/L (Se and Sp 0.79) and high‐sensitivity cardiac Troponin I cut‐off was 0.056 ng/mL (Se and Sp 0.84).
JVIM 2019 Dobermans only: A cutoff value of hs‐cTnI concentration >0.113 ng/mL had a sensitivity of 81.2% and a specificity of 73.2% to identify the presence of DCM
hs‐cTnI assay identified more dogs (21/29 dogs, 72%) in the last‐normal group compared to the conventional cTnI test (18/29 dogs, 62%).
Difference in American and English Cocker Spaniel DCM
In American dogs some of those affected with DCM are suffering from taurine (+/- L-carnitine) deficiency and have responded to supplementation.
Blood and plasma levels of taurine should be measured in these patients, and supplementation (500mg taurine, 1g L-carnitine q12h) combined with supportive treatment for CHF or other consequences of dilation
A small clinical trial including 11 American cocker spaniels with DCM showed that all dogs were found to have low plasma taurine concentrations at baseline (<50 nmol/mL)
The group supplemented with both taurine and carnitine showed significant echocardiographic improvement, whereas dogs receiving a placebo did not.
No association with dietary insufficiency is reported in English Cocker Spaniels, although the course of disease in affected dogs is typically prolonged (aside from some who die suddenly)
Pathogenesis of ARVC and pathophys
fibro- fatty replacement of the right ventricular myocardium which results in ventricular arrhythmias and syncope. Myocardial dysfunction and CHF can occur.
Causes loss of mechanical coupling between myocytes
Autonomic dominant genetic inheritance, variable penetrance
