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ACVIM literature 2015-2019 > Cardiovascular > Flashcards

Cardiovascular Flashcards

Papers 2015-2019 JVIM, VCNA, JFMS,JVECC

1
Q

What drugs are used for rate control of Afib?

A

Beta- blockers (class II)

  • Atenolol
  • Esmolol

K+ channel blocker (class III)

  • Sotolol
  • Amiodarone

Ca++ Channel blockers Class IV)
- Diltiazem

And digoxin

VCNA 2017. AFib Pariaut

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2
Q

What options are used for rhythm control of Afib?

A

Electric cardioversion

Lignocaine Na++ channel blocker ( class 1b)
Amiodarone k+ channel blocker (class III)

VCNA 2017. AFib Pariaut

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3
Q

What are the causes of Afib?

A 
Structural heart disease
Lone AFib (giant and large breed dogs, structural normal heart with erratic rhythm with significant exercise +/- GA)
High vagal tone (shortens the refractory period)
Hypothyroidism
Anaesthesia/opiates
Rapid, large vol pericardial effusion
GI disease
Vol overload causing atrial stretch

VCNA 2017. AFib Pariaut + ettinger

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4
Q

Diltiazem mechanism of action?

A

Class IV antiarrhythmic; calcium-channel blocker (like verapamil or nifedipine).

  1. Inhibits the transmembrane influx of extracellular calcium ions in myocardial cells and vascular smooth muscle but does not alter serum calcium concentrations.
    => inhibit the cardiac and vascular smooth muscle contractility, thereby dilating main systemic and coronary arteries.
    => Decreased Total peripheral resistance, blood pressure, and cardiac afterload
  2. Effects on cardiac conduction.
    - slows AV node conduction
    - prolongs refractory times.

Diltiazem rarely affects SA node conduction, but in patients with sick sinus syndrome (contraindicated) resting heart rates may be reduced.

Although diltiazem can cause negative inotropic effects, it is rarely of clinical importance (unlike verapamil or nifedipine). Diltiazem apparently does not affect plasma renin, aldosterone, glucose, or insulin concentrations.

Reduction in ventricular response rate is dose dependant.
Risk of hypotension
Plumbs

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5
Q

Sotolol : What is the mechanism of action?

A
  1. Non-selective beta-blocker
  2. Class III antiarrhythmic agent - potassium channel blocker:
    selectively inhibiting potassium channels => prolongs repolarization and refractoriness without affecting conduction.

In supraventricular tachycardias, sotalol may be more effective in preventing recurrence of the arrhythmia rather than terminating it.

Plumbs

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6
Q

Where does an AV block originate from?

A

Conduction abnormalities along the AV nodes, bundle of His/Purkinje system or both.

Santilli JVIM 2016

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7
Q

What are the causes of AV nodal conduction abnormalities in dogs?

A
  • Chronic fibrous or fibrous-fatty replacement of av bundles and branches
  • Acute lymphoplasmacytic myocarditis (young dogs - Lev’s disease) with mild fatty-fibrous replacement
  • infectious disease (Borrelia burgdorferi, bartonella vinsonii, bacterial endocardititis, parasitic - Trichinella spiraliz
  • Immune med disease (MG, SLE)
  • Neoplasia
  • non-penetrating chest trauma

Santilli JVIM 2016

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8
Q

What proportion of dogs with AV nodal conduction disturbances had unchanged or progressed AV blocks after pacemaker implantation?

A

87%

Santilli JVIM 2016

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9
Q

In what dogs with AV conduction disturbances should pacemaker be considered the first line treatment?

A

High second degree AV block
Third degree AV block
2:1 second degree AV block

Santilli JVIM 2016

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10
Q

What proportion of dogs with AV noda conduction disturbances showed regression after pacemaker implantation?
What proportion of these returned to a normal sinus rhythm

A

13%
67%
consider acute lymphocytic myocarditis as a possible cause for these?

Santilli JVIM 2016

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11
Q

What drug is most effective at reducing progression to CHF or sudden death in Irish Wolfhounds with preclinical DCM, Afib or both?

A

Pimobendan > digoxin > benazepril

Vollmar JVIM 2016

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12
Q

What is the median time to CHF or sudden death in Irish Wolfhounds with preclinical DCM, Afib or both treated with:

  • Pimobendan?
  • Digoxin?
  • Benazepril?
A

P: 1991 days (65m or ~5.5years)
D: 1263 days (41m or ~ 3.4 years)
B: 997 days (32m or ~ 2.6 years)

Vollmar JVIM 2016

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13
Q

Is there any evidence for starting pimobendan in preclinical DCM in Irish Wolfhounds?

A

Yes - Vollmar JVIM 2016 found improved survival and significantly longer to sudden death or CHF in wolfhounds receiving pimobendan preclinical DCM and/or Afib

Vollmar JVIM 2016

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14
Q

For every 10 bpm increase in HR with dogs with Afib, what is the risk of all cause mortality increased by?

A

35%

Pedro JVIM 2018

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15
Q

What is the median survival time of dogs with AFib and a mean heart rate (measured by Holter)

  • <125 bpm
  • > 125bpm
A

<125 bpm = 1037 days
>125 bpm = 105 days

Pedro JVIM 2018

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16
Q

What is a benefit of Holter monitoring of Afib over ECG?

A

Holter monitoring allows ambulatory montiroing outsite the hospital setting, more accurately representing the dogs normal daily HR flucutations in its usual routine/environment.

ECG tents to over-estimate mean HR compared to Holter recordings in dogs with AFib

Pedro JVIM 2018

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17
Q

What Heart rate target should be aimed for with Holter readings in dogs with Afib?

A

<125 bpm

Pedro JVIM 2018

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18
Q

What are the options and aims for control of AFib?

A

Rhythm control: abolish the arrhythmia and restore sinus function:

  • Electrical cardioversion
  • Lignocaine
  • Amiodarone

Rate control: - slow ventricular rate to reduce clinical signs and minimize deteriorationg of ventricular function

  • Atenolol
  • Esmolol
  • Sotolol (mild)
  • Diltazem
  • Digoxin (mild)

VCNA 2017. AFib Pariaut

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19
Q

What does lignocaine do?

A

Lidocaine may also have benefit in dogs to terminate supraventricular tachycardia in the presence or absence of an accessory pathway and paroxysmal atrial fibrillation initiated by elevated vagal tone in large breed dogs with normal cardiac function

Class IB antiarrhythmic agent (membrane-stabilizing).
- combines with inactive fast sodium channels, => inhibits recovery after repolarization.

rapid rates of attachment and dissociation to sodium channels in ventricular conducting tissue more so than atrial tissue.

At therapeutic levels, lidocaine causes phase 4 diastolic depolarization attenuation, decreased automaticity, and either a decrease or no change in membrane responsiveness and excitability. These effects will occur at serum levels that will not inhibit the automaticity of the SA node, and will have little effect on AV node conduction or His-Purkinje conduction.

Plumbs

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20
Q

What is the mechanism of action of Atenolol?

What are the effects of Atenolol?

A

Relatively specific β1-blocker. At higher dosages,β2 blockade can occur.

Effects:
- no intrinsic sympathomimetic activity or membrane-stabilizing activity

  • Negative inotropic and chronotropic actions =>
  • decreased sinus heart rate,
  • slowed AV conduction,
  • decreased cardiac output at rest and during exercise,
  • decreased myocardial oxygen demand,
  • decreased blood pressure,
  • inhibition of isoproterenol-induced tachycardia

Plumbs

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21
Q

What is the mechanism of action of Esmolol?

What effects does this drug have?

A

Class II antiarrhythmic drug.
Short acting beta1-adrenergic receptor blocker
- antiarrhythmic effect is thought to be due to its blockade of adrenergic stimulation of cardiac pacemaker potentials
- no intrinsic sympathomimetic activity or membrane-stabilizing activity

Cardiovascular effects include:
- negative inotropic and chronotropic activity
=> reduced myocardial oxygen demand.
- reduced systolic and diastolic blood pressures

  • increases sinus cycle length,
  • slows AV node conduction,
  • prolongs sinus node recovery time.

Plumbs

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22
Q

What is the mechanism of action of Amiodarone?

A

Class III

  • potassium channel blocker
  • also blocks sodium and calcium channels and beta-adrenergic receptors.

Causes:
- prolongation of myocardial cell action-potential duration and refractory period.

Plumbs

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23
Q

What is the mechanism of action of Digoxin?

A

Suspected:
- increase the availability of Ca++ to myocardial fibers and to inhibit Na+-K+-ATPase with resultant increased intracellular Na+ and reduced K+

This leads to:

  • decreased conduction velocity through the atrioventricular (AV) node
  • prolonged effective refractory period (ERP).

+/- increase the PR interval, decrease the QT interval, and ST segment depression on ECG.

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24
Q

What are the effects of digoxin?

A

In patients with a failing heart includes:

  • increased myocardial contractility (inotropism) with increased cardiac output;
  • increased diuresis with reduction of edema secondary to a decrease in sympathetic tone;
  • reduction in heart size, heart rate, blood volume, and pulmonary and venous pressures; and (usually) no net change in myocardial oxygen demand.
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25
Q

What is the mechanism of action of Pimobendan?

A

Pimobendan is an inodilator, with both positive inotropic and vasodilator effects via inhibition of PDE-3 and increasentracellular calcium sensitivity in the cardiac contractile apparatus.

  • decreases heart rate (negative chronotrope)
  • Increased contractility without increased myocardial oxygen consumption, as pimobendan does not increase intracellular calcium levels.

Pimobendan’s vasodilator effects are via vascular PDE-III inhibition, +/-
activity against phosphodiesterase V and increase cGMP

Slight antithrombotic activity

Plumbs

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26
Q

What is the best technique to measure HR in dogs with AFib?

A

24h Holter monitor

VCNA 2017. AFib Pariaut

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27
Q

What are urgent rate control drugs for dogs with AFib?

A
  • Diltazem IV boluse or CRI * risk hypotension
  • Esmolol CRi. * less effective.

VCNA 2017. AFib Pariaut

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28
Q

Long term rate control drugs for dogs with AFib?

A
  • Diltazem
    +/- Digoxin or Sotolol
  • Atenolol (cats)
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29
Q

What are the rhythm control strategies for dogs with AFib?

A
  • Lignocaine Bolus (first line for acute termination of vent. tachycardia)
  • Amiodarone CRI or oral * allergic reactions or increased ALT
  • Synchronised electrical cardioversion.
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30
Q

What is the benefit of using a biphasic shock with cardioverter-defibrilators as opposed to monophasic shocks to convert AFib?

A
  • less energy

- Higher success rates than monophasic shock

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31
Q

What needs to be done before cardioversion can be performed?

A
  • IV access
  • Airways management
  • Lignocaine for V tachy
  • Adropine ofr unexpected bradycardia
  • Correct electrolyte impances including Mg
  • adequate oxygenation
  • GA (no opioids due to effect on vagal tone)
  • paddles attached (dorsal recumbency at level of atria not ventricles)
  • shock delivered at peak of R wave.
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32
Q

If an electrical cardioversion shock is delivered at the peak of the T-wave, what can occur?

A

Increased risk of V-Fib

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33
Q

What phase of the ECG should the electrical cardioversioin be synchronised with?

A

Peak of the R-wave.

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34
Q

How much energy is required for cardioversion?

A

1-2 J/kg for 1-2 to 10 shocks.

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35
Q

What is the KCNQ1 gene mutation associated with?

A

Sudden death during exercise due to QT interval prolongation in English springer spaniels. (increased symp stimulation = increased risk)
Single heterozygous base pair mutation from threonine to lysine => change in protein structure to slow and fast outward potassium channels and fast inward sodium channel.

Ware JVIM 2015

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36
Q

What are causes of prolonged QT interval?

A
  • inherited
  • Drugs
  • Electrolytes disturbances
  • toxins
  • Infectious
  • inflammatory
  • autonomic impanance
  • metabolic disease.

Ekectrophysioloigcially:
factors that delay repolarization prolong the QT interval including
- reduced outward K+ during phases 2 and 3, esp slow K+ or rapid K+ components => can trigger VPC
- increased inwards NA+ or Ca++ current during depolarization.

Ware JVIM 2015

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37
Q

What does the QT interval represent?

A

The time of ventricular depolarization and repolarization on the ECG

Ware JVIM 2015

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38
Q

What drugs may be helpful in precenting syncope and sudden death in patients with QT interval prolongation?

A

Beta blockers - used in people.

Ware JVIM 2015

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39
Q

What are the major complications commonly seen with pacemaker implantation?

A
  • Lead dislodgement
  • lead or generator infection
  • lead or generator migration
  • pacing failure

Ward JVIM 2015

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40
Q

What circumstances have been associated with higher risk of complications with pacemaker implantation?

A
  • At night
  • pre-existing structural heart disease
  • post-op infections
  • previously used generators
  • inexperienced operators.

Ware JVIM 2015

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41
Q

What are the most common indications for pacemaker implantation in dogs?

A
  • High grade second degree AV block (3:1 conduction or less)
  • third degree AV block

Ware JVIM 2015

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42
Q

What is the inicidence of sudden death in dogs with high grade AV block without pacemaker?

A

up to 40% within 6 months of diagnosis.

Ware JVIM 2015

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43
Q

Familial boxer ARVC is associated with a deletion in which gene? What is the method of inheritance

A

Striatin gene. Autosomal dominant.

Meurs VCNA 2017

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44
Q

What treatment is generally used for boxer ARVC?

A 
Sotalol +/- Mexiletine 
or Amiodarone INI with above
\+/- Fish oil
 If CHF treat as for DCM
- pimobendan
- ACEi
- diuretics
- L-Carnitine

Meurs VCNA 2017

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45
Q

What is the most common age of onset for boxer ARVC?

A

Adult between 5-7 years, however homozygous dogs may present between 1-3 years old.

Meurs VCNA 2017

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46
Q

Striatin gene deletion mutation causes what disease?

A

ARVC - Boxers

Meurs VCNA 2017

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47
Q

What is Striatin and how does it cause ARVC?

A

Striatin is localizedin the intercalated disks of cardiac myosytes where it co-localizes to 3 desmosomal proteins. Desmosomes help adhere myocytes in the heart => structural integrity
Abnomal desmosomal adhereance => myocyte death, inflam and replacement with fibrous tissue.

Thus ARVC is a degenerative myocardial disease with RV myocoyte atrophy and fatty infiltration.

Meurs VCNA 2017

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48
Q

What are the different types of ARVC?

A
  1. Asymptomatic with occasional VPC
  2. Tachyarrhythmia and clinical signs such as syncope or exercise intolerance
  3. Myocardial systolic dysfunction and ventricular dilation +/- CHF. Least common, more likely homozygous form

Meurs VCNA 2017

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49
Q

Are biomarkers useful in detection of ARVC in boxers?

A

Troponin I: inconsistent but when elevated can correlate with VPC number and grade or complexity of the arrythmia
BNP: only useful in boxers with myocardial dysfunction

Meurs VCNA 2017

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50
Q

ARVC: what is the diagnostic screening criteria for ARVC based on Holter monitoring?

A

Asymptomatic dog:
0-20 single VPC per 24h = wnl
20-100 VPC per 24h = indeterminate. repeat in 6-12m
100-300 single VPCs per 24h = suspicious
100-300 VPC per 24h with increased complexity (couplets, triplets, V.tach) = likely affected.
300-1000 single VPC per 24h = likely affected
>1000 VPC per 24h = affected, consider treatment

Meurs VCNA 2017

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51
Q

ARVC: What screening tests are recommended?

A
  • Holter monitor
  • Genetic test for striatin deletion.

Meurs VCNA 2017

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52
Q

ARVC: what does a negative striatin genetic test mean?

A

This dog does not carry the Striatin deletion mutation and thus will not develop ARVC because of the striatin deletion but can still develop ARVC or heart disease.

Meurs VCNA 2017

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53
Q

ARVC: What does a positive heterozygous Striatin genetic test mean? What monitoring is recommended? What breeding is recommended?

A

At risk of developing ventricular arrhythmia and sudden death. Variable expression => only 40-60% of dogs will develop clinical signs.

Recommended monitoring:

  • annual Holter monitor after 4 years of age,
  • avoid breeding or only breed to negative

Meurs VCNA 2017

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54
Q

ARVC: WHat does a positive homozygous Striatin genetic test mean? What monitoring is recommended? What breeding is recommended?

A 
2 copies of Striatin gene mutation. 
Most likely to:
- develop the disease 
- develop at younger age. 
- develop ventricular dilation and systoilci dysfunction stage of the disease

Recomended monitoring:

  • annual holter +/- echo from 3 years old.
  • do not use for breeding.

Meurs VCNA 2017

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55
Q

What criteria are used for prognostic significance on Holter ECG?

A

For dogs with structurally normal hearts >50VPC per 24h, polymorphic VPCs and the presence of VTach have been associated with shorter survival times.

Meurs VCNA 2017

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56
Q

ARVC: Are TXR likely to be abnormal?

A

No unless generalized cardiomegaly and CHF - pulmonay oedema and or pleural effusion.

Meurs VCNA 2017

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57
Q

What echocardiographic finding may be a useful prognostic factor in ARVC?

A

TAPSE - tricuspid annual plan systolic excursion.
Lower in boxers with >50 VPC per 24h.
Lower TAPSE associated with more severe disease and shorter survival times.

Meurs VCNA 2017

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58
Q

Is echocardiography generally useful in diagnosing ARVC?

A

Not generally as most myocardial changes are histological only, however may see:

  • right ventricular enlargement
  • right ventricular dysfunction
  • lower TAPSE (tricuspid annual plane systolic excursion)

Meurs VCNA 2017

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59
Q

What are the histological findings of ARVC?

A

Fibrofattym segmental or diffuse replacement of the right ventricular free wall from the epicardium towards the endocardcium +/- IVS and LVFW.

Meurs VCNA 2017

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60
Q

What Holter findings in an asymptomatic dog would indicate commencing treatment for ARVC?

A
  • Sustained VTach > 30 seconds.
  • increased complexity of arrhythmia including frequent couplets, triplets, bigeminy and/or Ront.
  • > 1000 VPC

Meurs VCNA 2017

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61
Q

What level of day to day variability has been noted with VPC in affected, untreated boxers with ARVC?

A

83% change in VPC number from day to day.

Meurs VCNA 2017

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62
Q

ARVC: On post treatment holter monitor, what % reduction in VPCs is aimed for?

A

80% reduction in VPCs and reduction in complexity

Meurs VCNA 2017

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63
Q

ARVC: What does an increase in symptoms or increase in number of VPCs per 24h on post-treatment Holter monitor suggest?

A

Proarrhythmogenic effects of medications. must compare to pre-treatment holter.

Meurs VCNA 2017

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64
Q

What are prognostic indicators for boxer ARVC associated with shorter survival times?

A
  • Echo: - left vent systolic dysfunction and TAPSE <15.1mm
  • Holter: - increased frequency and complexity of VPCs inc VTach and Polymorphic VPCs

Kaye JVIM 2015

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65
Q

Is TAPSE lower or higher in Boxers with ARVC or dogs with left ventricular dysfunction?

A

lower

Kaye JVIM 2015

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66
Q

TAPSE ……… mm in boxers with >5o VPC/24h on Holter is associated with ……. cardiac survival times and is an independant predictor of …… irrespective of the presence of CHF, echo evidence of LV systolic dysfunction and Holter detection of VT.

A

TAPSE <15.1 mm is associated with shorter cardiac survival times and is an independant predictor of time to cardiac death irrespective of the presence of CHF, echo evidence of LV systolic dysfunction and Holter detection of VT.

Kaye JVIM 2015

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67
Q

MMVD: What clinical signs have been identified as negative prognostic indicators?

A
  • cough,
  • exercise intolerance,
  • decreased appetite,
  • breathlessness/difficulty breathing
  • syncope
  • Mumur > III/VI
  • absence/loss of respiratory sinus arrhythmia

lopez-alvarez JVIM 2015

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68
Q

MMVD: What other changes (apart from clinical signs) have been associated with higher risk of CHF?

A
  • increase NT-proBNP
  • enlarged heart size
  • LA enlargement

lopez-alvarez JVIM 2015

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69
Q

What histopathological changes are seen with MMVD CHF in the lungs?

A
  • Thickened alveola septum (all ISACHC classes)
  • Increased Type II pneumocytes (All ISACHC classes)
  • Increased heart failure cells (alveolar macrophages with phagocytosed extravasated RBCs) in class III and above.

Lee JVIM 2015

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70
Q

What histopathological changes are seen with MMVD in the left atrium?

A

Fatty replacement
Inflammatory cell infiltration
fibrosis

secondary to metachic strech and schear stress by regurg jets => inflamm and thus

  1. Migration of leukocytes (chemotaxis for phagocytosis)
  2. Formation of scar tissue (fibrosis for healing)
  3. Fatty replacement (lipomatous metaplasia)

Lee JVIM 2015

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71
Q

What histopathological changes are seen with MMVD in the left ventricle?

A
  • few inflammation related change
  • increased cellular hypertrophy secondary to compensatory myocardial hypertrophy,

May effect LVEDd and EF.

Lee JVIM 2015

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72
Q

What are the most common breeds in the UK to be diagnosed with MMVD?

A 
CKCS
King Charles Spaniel
Chihuahua
Whippet
Poodle

Mattin JVIM 2015

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73
Q

What are the most common breeds in the UK t be diagnosed with a heart murmur?

A 
CKCS
King Charles Spaniel
Chihuahua
Boxer
Whippet

Mattin JVIM 2015

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74
Q

What is the prevalence of MMVD in the UK?

A

0.35%

Mattin JVIM 2015

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75
Q

What is the prevalence of heart murmur in the UK?

A

3.54%

Mattin JVIM 2015

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76
Q

Do males or females have higher odds of developing MMVD in the UK?

A

Males OR 1.40

Mattin JVIM 2015

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77
Q

Do insured or uninsured dogs have higher odds of developing MMVD in the UK?

A

Insured - OR 3.56

Mattin JVIM 2015

78
Q

Do dogs >20kg or <20kg have greater odds of developing MMVD?

A

<20kg - OR 1?

Mattin JVIM 2015

79
Q

Does the presence of AFib in medium to large breed dogs with MMVD affect prognosis?

A

Yes - associated with shorter MST (142 d) compared to those without AF (234d)

Jung JVIM 2016

80
Q

What is the MST for medium to large breed dogs with MMVD and:

  • no AFib
  • AFib with HR <160 bpm via medication
  • AFib with HR >160 bpm with medication
A
  • no AFib: 234d (7.5m)
  • AFib with HR <160 bpm via medication: 171d (5.5m)
  • AFib with HR >160 bpm with medication: 61d (2m)

Jung JVIM 2016

81
Q

Is diltiazem or diltazem + digoxin recommended for control of Afib in medium to large breed dogs with MMVD?

A

MST for digoxin + Diltazem = 130d (3m)
Diltiazem alone = 35d (1m)

Jung JVIM 2016

82
Q

Why is it important to control the heart rate in medium to large breed dogs with MMVD and AFib?

A

Increased heart rate associated with shorter MST and higher rate of mortalities

Chronic tachycardia >180bpm for 2-4 weeks least to tachycardia induced myocardial failure.
Cut off of HR <160bpm was associated with significantly better outcomes.

Jung JVIM 2016

83
Q

What are the 5 types of cardio-renal syndrome?

A
  1. Acute cardiorenal syndrome: rapidly worsening cardiac function leading to AKI
  2. Chronic cardiorenal syndrome: chronic abnormalites in cardiac function causing progressive CKD
  3. Acute renocardiac syndrome: abrupt and primary worsening of kidney function leading to acute cardiac dysfunction
  4. Chronic renocardiac syndrome:characterized by primary CKD leading to decreased cardiac function, ventricular hypertrophy, diastolic dysfunction, increased of adverse cardiovascular events.
  5. Secondary cardio-renal syndrome: combined cardiac and renal dysfunction associated with acute or chronic systemic disorders.

Martinelli JVIM 2016

84
Q

In regards to cardiorenal syndrome and MMVD in dogs, what factors were associated with shorter survival times?

A
  • Severe heart disease
  • severe renal disease
  • both severe heart and renal disease
  • frusemide administration
  • advanced age at diagnosis of heart disease.

Martinelli JVIM 2016

85
Q

The presence of cardiorenal disease + MMVD is associated with shorter/longer survival times that dogs with MMVD alone?

A

Shorter

Martinelli JVIM 2016

86
Q 
True or False:
The class of MMVD heart disease and IRIS stage are correlated?
A

True

Martinelli JVIM 2016

87
Q

True or False:

Dogs being treated for heart failure had higher prevalence of CKD compared to dogs that had not received treatment?

A

True

Martinelli JVIM 2016

88
Q

True or False:
Advanced ACVIM class of MMVD could be predictive of advanced IRIS stage?
And Vice Versa?
IRIS stages directed correlated with echo variable of heart enlargement including La/Ao and LVEDDn?

A

True
True
True

Martinelli JVIM 2016

89
Q

Does body size influence CKD severity?

Does it influence heart failure severity?

A

No
Yes

Martinelli JVIM 2016

90
Q

True or False:
The amount of frusemide administered during CHF for MMVD was directly correlated with Urea but not IRIS stage or serum creatinine?

A

True:
Decreased renal blood flow => decreased flow rate in renal tubules => increased reabsorption of urea, thus urea increases disproportionately to creatinine (not reabsorbed)

Martinelli JVIM 2016

91
Q

True or False:

Hb was negatively correlated with serum creatinine and IRIS stage but not with classes of heart failure?

A

True

Martinelli JVIM 2016

92
Q

Do MMVD breeding schemes in CKCS work to reduce the prevalence of this disease?

A

Yes - over 8-0 years, mandatory auscultation, echo and registration.
Dogs were assessed at 1.5yrs old and excluded from breeding if they had a:
- murmur >grade III/VI
- Mitral valve prolapse >7.5mm
- Grade II/VI murmur and mitral valve prolapse >4.5mm

Birkegard JVIM 2016

93
Q

What is the estimated heritability of MMVD in CKCS in the UK?

A

0.33

Birkegard JVIM 2016

94
Q

What is the estimated heritability of MMVD murmur grade in CKCS in UK?

A

0.67

Birkegard JVIM 2016

95
Q

What are adipokines?

A

Biologically active substances derived from adipose tissues that play a role in obesity and related conditions in people.
Included adiponeckin and leptin

Kim JVIM 2016

96
Q

What role does leptin play in the body and in particular , in relation to the heart and cardiac disease?

A

Body:

  • modulates the immune system
  • proinflammatory
  • regulates energy homeostasis

Regulates baseline physiology of the heart including

  • myocyte contractility
  • hypertrophy
  • apoptosis
  • metabolism

Thus in heart disease contributes to the pathogenesis of heart failure and LV dysfunction.

Kim JVIM 2016

97
Q

What role does adiponectin play in relation to the heart and cardiac disease?

A

Capabple of slowing the progression of cardiovascular diseases including hypertrophy, ischaemic injury and athelerosclerosis in people.

Kim JVIM 2016

98
Q

In dogs with MMVD, when and what change would you expect to see in leptin concentrations?

A

Increased with ISACHC class 3 but not class 1 or 2

Kim JVIM 2016

99
Q

Would you expect serum adiponectin to be higher or lower in MMVD dogs than healthy dogs?

A

lower in ISACHC class I, but ISACHC class III was higher than class I.

Kim JVIM 2016

100
Q

Is moderate to severe mitral regurgitation in CKCS <3 years associated with increased hazard of:

  • all cause mortality
  • cardiac death
A

Yes
Yes
and for intermittent moderate to severe mitral regurg in dogs <3 years of age

Reimann JVIM 2017

101
Q

Are increased LV systolic dimension at 1-3 years of age in CKCS associated with
- increased cardiac mortality later in life

A

yes

Reimann JVIM 2017

102
Q

Are flow murmur in CKCS between ages 1-3 associated with increased cardiac mortality later in life?

A

No

Reimann JVIM 2017

103
Q

Is mild mitral regurg in CKCS between ages 1-3 associated with increased cardiac mortality later in life?

A

No

Reimann JVIM 2017

104
Q

For dogs with MMVD (ACVIM staging) would you to see a difference in:

  • LA strain between B1 and B2?
  • LA longitudinal strain during atrial contraction (EA) between B1 and B2?
  • LA longitudinal strain during atrial contraction (EA) between B and C/D?
  • LA longitudinal strain during ventricular systole (ES) between B1 and B2?
  • LA longitudinal strain during ventricular systole (ES) between B and C/D?
A
  • LA strain between B1 and B2? No
  • LA strain during atrial contraction (EA) between B1 and B2? No
  • LA strain during atrial contraction (EA) between B and C/D? Yes - C/D were lower
  • LA strain during ventricular systole (ES) between B1 and B2? No
  • LA strain during ventricular systole (ES) between B and C/D? Yes - C/D were lower

Nakamura JVIM 2017

105
Q

What echo measurement was the best predictor of the presence or history of CHF?

A

EA - LA longitudinal strain during atrial contraction

Nakamura JVIM 2017

106
Q

What echo measurements were identified as independant indicators of stage C/D?

A

EA (LA longitudinal strain during atrial contraction) and peak early diastolic mitral inflow velocity

Nakamura JVIM 2017

107
Q

Are markers of oxidative stress (plasma malondialdehyde, oxidized LDL and Vit E) associated with clinical stages of MMVD?

A

No

108
Q

What are plasma malondialdehyde, oxidized LDL and Vit E associated with?

A

All are positively associated with serum cholesterol concentration.
Ox-LDL associated with lowere in females
Vit E y-tocopherol were higher in neutered

109
Q

What is the PV/PA measurement used for?

A

discrimination of dogs with MMVD and CHF from MMVD and aymptomatic.
>1.7 in 2D = CHF

Merveille JVIM 2015

110
Q

How is PV/PA measured?

A
  • Right parasternal long view
  • trace line perpendicular to the medial PV passing through the center
  • Use M mode to measure inner edge to inner edge at the end of the Twave

Merveille JVIM 2015

111
Q

What is the cut off used for PV/PA measurement for CHF in dogs with MMVD?
What is the sensitivity and specificity of this?

A

> 1.7 = CHF
Sens 96%
Spec 91%

Merveille JVIM 2015

112
Q

What is tissue Doppler imaging-derived E/Emsept a predictor of?

A

load independant CHF in dogs with MMVD

Kim JVIM 2015

113
Q

What is the cut off used for tissue Doppler imaging-derived E/Emsept for CHF?
What is the sensitivity and specificity of this?

A

> 18.7 = CHF
Sens 56%
spec 90%

Kim JVIM 2015

114
Q

What is tissue doppler imaging?

A

Form of doppler that measures the velocity of the heart muscles through different phases of the heart cycle.

Kim JVIM 2015

115
Q

What does the E/Emsept measure?

A

the ratio of the transmitral peak early diastolic velocity to the tissue doppler-derived peak early diastolic velocity at the interventricular septal basal segment

Kim JVIM 2015

116
Q

What is the Tei Index used for? (TX)

A

TX - index of global myocardial function including systolic and diastolic performance.

Nakamura JVIM 2016

117
Q

What is the right ventricular Tei Index used for? (RVTX)

A

RVTX - evaluate the RV systolic and diastolic function in dogs with right heart disease including tricuspid regurg, pulmonary hypertension and secondary to MMVD.

Provides an independent correlate of cardiac - related death within 1 year.

Nakamura JVIM 2016

118
Q

What view is RVTX measured in?

A

left parasternal short axis. dual phased doppler to measure tricuspid inflow and PA flow simultaneously.

Nakamura JVIM 2016

119
Q

do dogs with pulmonary hypertension have higher or lower transmitral E-wave peak velocity?
What is the cut off for this?
What is the sensitivity and specificity of this cut off?

A

Higher
>10
Sens 84%
Spec 71%

Toaldo JVIm 2016

120
Q

Do dogs with pulmonary hypertension have higher or lower E/e’ ratio of septal (sMV) and lateral (pMV) mitral annulus?
What is the cut off for this?
What is the sensitivity and specificity of this cut off?

A

higher
>9.33
Sens 72%
Spec 80%

Toaldo JVIm 2016

121
Q

True or False?
MMVD - as the disease progresses (increases ACVIM stages) you would expect left atrial areas to increase and left atrial function to increase?

A

Left atrial areas increase
LA function decreases.

Toaldo JVIm 2017

122
Q

Using 2D speckle tracking in dogs with MMVD, what would you expect to see change between stages B2 and C/D?

A
  • Left atrial area - increase
  • fractional area change
  • Peak atrial logitudinal train
  • peak atrial contraction strain
  • contraction strain index - decrease

Toaldo JVIm 2017

123
Q

What is the effective regurgitant orifice area (EROA) in dogs with MMVD calculated from?

A

Using 3D echo from the vena contracta width as the narrowest portion of the proximal regurgitant jet

Tidholm 2017

124
Q

What is the best view for measuring calculated EROA using vena contracta width measurements?

A

2 chamber view

Tidholm 2017

125
Q

What are some of the limitations to 3D EROA?

A

High beat to beat variability
patient induced variablity
non-circular EROA

Tidholm 2017

126
Q

What changes would be expected to be seen in echo measured right ventricle systolic function as the disease progresses from stage B2 to stage C?

A

B2 - increased compensated remodelling = increased RV systolic function
C - CHF = reduced RV systolic function.

Chapel JVIM 2018

127
Q

Do dogs in stage B2 MMVD have increased or decreased TAPSE?

A

increased

Chapel JVIM 2018

128
Q

Do dogs in stage C MMVD have increased or decreased TAPSE?

A

decreased

Chapel JVIM 2018

129
Q

Peak tricuspid regurgitant pressure gradient (TRPG) of what pressure is associated with worse outcomes in dogs with MMVD?

A

> 55mmHg

Borgarelli JVIM 2015

130
Q

La:Ao greater than what value is associated with worse outcomes in dogs with MMVD?

A

> 1.7

Borgarelli JVIM 2015

131
Q

What proportion of dogs with MMVD stage B2 have pulmonary hypertension?

A

Approx 1 third

Borgarelli JVIM 2015

132
Q

What echo indicies may be used to assess for pulmonary hypertension if tricuspid regurg is not present?

A

a combination of

  • decreased pulmnary arterial AT/DT (acceleration time/deceleration time)
  • increased RVIDDn (RV end diastolic internal diameter corrrected for body weight)
  • increased La/Ao
  • small or great LVIDDn (left ventricular end diastolic internal diameter corrected for body weight)

Tidholm JVIM 2015

133
Q

Does butorphanol sedation impact peak tricuspid regurgitant flow velocity (when measured for pulmonary hypertension)?

A

Yes

Rhinehart JVIM 2017

134
Q

What proportion of dogs have their tricuspid regurg flow velocity affected by burorphanol sedation?
Does it increase or decreased?
By how much?

A

78%
sedation increased TRFV
increased by >0.4m/s in 42% of dogs indepednant of stroke vol.

Rhinehart JVIM 2017

135
Q

Doessonographer, body position or 6 minute walk test significantly impact the measurement of tricuspid regurgant flow velocity when measuring for pulmonary hypertension?

A

no

Rhinehart JVIM 2017

136
Q

What is the most repeatable measure of pulmonary hypertension?

A

Vtr - peak velocity of tricuspid valve regurgitation.

Abbott JVIM 2017

137
Q

When tricuspid regurg is absent, what other mentions cna be sured to measure pulmonary hypertension?

A
  • acceleration time of pulmonary ejection
  • acceleration to ejection time ratio.

Abbott JVIM 2017

138
Q

A change in peak velocity of tricuspid regurg greater than what is likely to be outside the range of expected within-operator variation?

A

> 0.3m/s

Abbott JVIM 2017

139
Q

How is the right atrial area index calculated?

A

Right atrial are divided by BSA

Vezzosi JVIM 2018

140
Q

What is the utility of right atrial area index?

A

Used to evaluate size of right atrium and may be more effective than peak tricuspid regurg flow velocity in predicting R-CHF in dogs with pulmonary hypertension.

Vezzosi JVIM 2018

141
Q

Is right atrial index higher in dogs with:

  • mild pul. hypertension
  • moderate pul. hypertension
  • severe pul. hypertension
  • R-CHF
A
  • mild: 6.7 cm2/m2
  • moderate 13.3 cm2/m2
  • severe 12.1 cm2/m2
  • R-CHF: 17.5 cm2/m2

Vezzosi JVIM 2018

142
Q

What cut off value of right atrial area index can be used to determine R-CHF?
Sensitivity?
Specificity?

A

> 12.3 cm2/m2
Sens 100%
Spec 89.5%

Vezzosi JVIM 2018

143
Q

What is the main determinant of right atrial area index in dogs with pulmonary hypertension?

A

severity of tricuspid regurgitation

Vezzosi JVIM 2018

144
Q

What criteria were used for dogs for inclusion in the EPIC study? preclinical MMVD - stage B2

A 
Evidence of cardiomegaly:
- La/Ao > or = 1.6
- normalized LV internal diameter in diastoles > or = to 1.7
- vertebral heart sum >10.5
- grade III/VI murmur or above
reduced by approx one third.

EPIC JVIM 2016

145
Q

Approximately how many months does administration of pimobendan prolong preclinical period (stage B 2) in dogs with MMVD?

A

15 months compared to non treatment
reduced by approx one third.

EPIC JVIM 2016

146
Q

Was the risk of experiencing a cardiac related death or progression to CHF increased or decreased in dogs with stage B2 receiving pimobendan compared to controls?

A

reduced by approx one third.

EPIC JVIM 2016

147
Q

Where does Frusemide act in the kidneys?

A

Na+:K+:2Cl- cotransported in the thick ascending loop of henle.

Plumbs

148
Q

Where does Torsemide act in the kidneys?

A

interfers with the chloride binding site of the Na+/K+/2CL- cotrasnporter in the thick ascending loop of Henle

Plumbs

149
Q

What does Frusemide increase the excretion of?

A

Furosemide can increase renal excretion of

  • water,
  • sodium,
  • potassium,
  • chloride,
  • calcium,
  • magnesium,
  • hydrogen,
  • ammonium,
  • bicarbonate.

Plumbs

150
Q

What is the bioavailability, half life and duration of action of oral:

  • frusemide
  • torsemide
A

Frusemide: 77%, 1-2h, 6h
Torsemide: 80-100%, 8h, 12h

Chetboul JVIM 2017

151
Q

Apart from renal effects, what else does Torsemide do?

A
  • vasodilating properties
  • improves cardiac cunction and reduced cardiac remodelling secondary to anti-aldosterone effect.

Chetboul JVIM 2017

152
Q

Is Torsemide q24h non-inferior to Frusemide?

A

Yes

Longitudinal EPIC JVIM 2018

153
Q

Does Pimobendan treatment in preclinical MMVD change heart size?
What difference is seen?

A

Yes reduce by day 35
LVIDDN - 0.06
La:Ao - 0.08

Longitudinal EPIC JVIM 2018

154
Q

Does treatment with pimobendan in stage B2 change survival after the development of CHF?

A

No. only prolongs stage B2

Longitudinal EPIC JVIM 2018

155
Q

Is change in heart size associated with a change in survival in dogs with stage B2 MMVD?

A

Yes - reduction in heart sieze was associated with increased time to CHD for cardiac related death

Longitudinal EPIC JVIM 2018

156
Q

What is orthodromic AV reciprocating tachycardia?

What are the ECG findings?

What treatment may be beneficial?

A

When the accessory pathway is reached
=> able to retrograde re-enter the atrium causing a negative P-wave immediately after the QRS
=> starts next complex early => loop => tachycardia

Regular narrow QRS complex tachycardia that terminates in teh face of a second degree AV block/
Rarely have a wide QRS if also had bundle branch block.

Lignocaine total dose 2mg/kg cardioverts in 84% of cases.
More likely to cardiovert if have a right free wall accessory pathway affected tharther than right posteroseptal accessory pathway.

Wright JVIM 2019

157
Q

What % of dogs with CHF had cardiac cachexia?

What clinical findings are associated with cardiac cachexia?

A

Base on muscle loss - 48%
based on weight loss 42%

Clinical findings:

  • older
  • arrhythmia
  • lower BCS

Ineson JVIM 2018

158
Q

What are the laboratory findings associated with cardiac cachexia?

What factors in dogs with CHF were associated with shorter survival times?

A

Lab findings with cachexia

  • increase chloride
  • lower HCT and HB
  • lower albumin

Assoc with shorter survival times:

  • Cardiac cachexia
  • clinical tachyarrhythmia
  • azotaemia
  • under or over weight

Ineson JVIM 2019

159
Q

What is the sensitivity and specificity of high sensitivity cardiac troponin 1 to detect the presence of DCM in dobermans?

A

Sens: 81%
Spec:73%
- identified more in the “last normal” group

Kluser JVIM 2019

160
Q

What additional echocardiographic indices may be used to quantify mitral regurg severity in dogs with preclinical MMVD?

A
  1. Regurgitation fraction >/= 50%
  2. Effective regurgitant orifice area (EROA) to BSA >/= 0.347
  3. Ratio of mitral regurg to aortic flow rate >/= 0.79

all strongly associated with
La:Ao >/= 1.6
LVIDdN >/= 1.7

Larouche-Lebel. JVIm 2019

161
Q

What effects does brain naturic peptide (BNP1-32) have on dogs with compensated MMVD?

A

No change in measured cariorenal values suggestive that dog with chronic CHF may have a reduction in naturic peptide responsiveness.

Yata JVIM 2019

162
Q

What type of PDA is most commonly seen in german shepherds?

What factors associated with this may change the approach to management?

A

Type II most common but type 1 and IV also noted.

Generally larger minimal ductal diameter of 4.4-4.9mm

Given abnormal changes can be seen and larger minimum ductal diameter, transoesophageal echo may be benificial for procedure planning.

Wesselowski JVIM 2019

163
Q

What care should be taken when interpreting cardiac troponin 1 in cats?
What additional test can be used to help evaluate this further??

A

Cats with compromised renal function can have higher cardiac troponin 1 due to reduced excretion.

Cardiac troponin 1 in urine was more common in cats with renal disease than in cardiac disease.

Langhorn JFMS 2019

164
Q

Do cats with preclinical HCM have altered all cause death compared to apparently healthy cats?
Why?

What are the most common non-cardaic causes of death in cats?

A

Increased all cause death (65%) compared to healthy (40%) as incidence rates of non-cardiac related death was similar in both groups but the preclinical HCM group also had higher cardiovascular mortality => increased total morality.

Most common non cardiac causes of death were:

  • cancer
  • CKD
  • chronic weight loss/V+/D+/anorexia associated

FOX JVIM 2019

165
Q

What is the cut off, sensitivity and specificity of cardiac troponin 1 for detecting:

  • Cats with HCM
  • Asymptomatic cats with HCM
A

HCM:
Cut off: 0.06ng/ml
Sens: 91%
Spec: 95%

Asymptomatic HCM
Cut off: >0.06 ng/mL
Sens: 87%
Spec: 95%

Hertzsch JVIM 2019

166
Q

What is the median age of cats diagnosed with RCM?
What % are symptomatic at diagnosis?
What is the most common clinical sign?

A

8.6 years
70% symptomatic at diagnosis
90% of these had dysponea secondary to CHF.

Chetboul JVIM 2019

167
Q

what is the MST of cats wtih RCM from diagnosis?

What echo features were associated with shorter survival time?

A

MST 667d
with 20% experiencing cardiac death in the first 24h after diagnosis due to ATE or CHF

Shorter survival associated with increased La:Ao, and severe LA enlargement (La:Ao >/= 2)

Chetboul JVIM 2019

168
Q

Is there a benefit to the use of benazepril in cats with heart disease for:

  • reducing all cause treatment failure
  • reducing time to treatment failure related to heart disease
  • reducing LA diameter, LV wall thickness or QOL?
A

No benefit from placebo in any category but was well tolerated.

King JVIM 2019

169
Q

Does the use of tissue plasminogen activator in cats with ATE:

  • improve survival?
  • reduce repurfusion injury
  • reduce AKI
  • clinical improvement?
A

survival:
TPA - discharge rate 44% but short term survival 56% vs 29% and 30% with standard of care but not statistically significant.

Repurfusion injury: no difference between groups
AKI - no difference between groups

Clinical improvement - TPA 56%, Standard of care 31% - not statistically significant

Guillaumin JFMS 2019

170
Q

What is the benefit of focused cardiac utlrasound in cats?

What areas does the focused cardiac ultrasound assess?

A
  • detection of occult heart disease, especially moderate (93%) to marked (100%) disease in cats but non-specialist practitioners.

Focused cardiac ultrasound assesses:

  • LA enlargement
  • LV hypertrophy
  • Cavitary effusion
  • decreased contractility

Loughran JVIM 2019

171
Q

What is the average reduction in systolic blood pressure seen in seen in cats with telminsartan?

A

-23mmHg at days 14 and 30

Coleman JVIM 2019

52% had SABp <150mmHg at day 28 and was effective at reducing severe and moderate nypertension
Glaus JVIM 2019

172
Q

What effects does sacubil/valsartan (Entresto) have in dogs with cardiomegaly secondary to MMVD?

What are they.

A
  • increased urinary aldosterone to creatinine ratio

Combines ATRB with a neprilusin inhibitor
neprilysin (NEP) cleaves natriuric peptides that antagonize RAAS and increased levels are assoc with cardiac death and hospitalization in people.

Aims to reduce stimulus for RAAS activation and inhibit RAAS hormones

Newhard JVIm2018

173
Q

What % of puppies have an innocent murmur?
What are the characteristics of this?
What may explain the presence of an innocent murmur?

A

15% had an innocent murmur

Systolic
muscial
maximum 2/6 intensity
PMI left cardiac base

Anaemia was noted in these and may contribute to initial murmur that resolves with age and improvement in HCT.

Szatmari JVIM 2015

174
Q

Is there a difference in NT-proBNP in puppies with congenital heart disease vs innocent murmur?
What changes are suggestive of abnormality instead of innocent murmur?

A

NTproBNP was higher in puppies with congenital heart disease but not consistently. Elevation is likely abnormal, but normal doesn’t rule out an abnormality

Murmurs longer than 80% of systole are likely abnormal. shorter may be normal or abnormal.

Marinus JVIM 2017

175
Q

What is the benefit of multidector CT in the assessment of dogs with pericardial effusion?

A
  • not better then echo for detection of masses but is better at detecting pulmonayr and extracardaic leions with a single modality

Scollan JVIM 2015

176
Q

where should the CVC be measured and what are the normal values?

A
  1. transverse 11-13th right hepatic intercoastal view
    Insp: 6.16 x BW^0.762
    Wxp: 7.24 x B^0.787
  2. longitudinal right paralumbar view
  3. 79 x BW^0.390

Darnis JVIM 2017

177
Q

what changes are expected to be seen on echo after PDA closure?

A
  1. reduced preload
    - reduction in LVIDd
    - reduced La:Ao
  2. Transient reduction in LV systolic function
    - reduced FA
    - LV dyssynchrony

Hambe JVIM 2015

178
Q

Does butorphanol affect evaluation of pulmonary stenosis?

What about atenolol?

A

Butorpnahol does not affect

Atenolol might reduce mean and max pulmonary valve pressure gradient but doesnt alter other methods of assesmsen tof pulmonary stenossis severiyt.

Nishimura JVIM 2018

179
Q

What is the sensitivity and specificity of NTproBNP on pleural fluid to detect if is primary cardiac?

A

Sen: 100%
Spec: 76%
- higher in pleural fluid than plasma/

180
Q

what is the sens and spec of the point of care ELISA NTproBNP on serum to detect cardiac disease from healthy cats?

A

Sens 65%
spec 100%

Negative doesn’t rule out, but positive is most likely cardiac disease

Harris JVIM 2017

181
Q

What are the cut offs, sens and spec of cardiac troponin 1 to detect:

  • cats with asymptomatic heart disease withouth LA dilation
  • cats with heart failure
A

Asympotmatic:
Cut off: 0.163mg/mL
Sens: 62%
Spec: 100%

Heart failure:
Cut off: 0.234ng/mL
Sens: 95%
Spec: 77%

Hori JVIM 2017

182
Q

What % of cats with preclinical non obstructive or obstructive HCM develop:

  • CHF
  • ATE
  • cardiovascular death
A

CHF, ATE or both occured in 30% of cats
CV death in 28%

risk at 1, 5 and 10 years

  • CHF 7%, 20%, 24%
  • ATE 3.5%, 10%, 11%
  • cardiovascular death 6%, 22%, 28%

Fox JVIM 2017 REVEAL study

183
Q

How does SDMA vary in cats with HCM or DM?

A

HCM - no change
DM - lower

Langhorn JVIM 2018

184
Q

What is the MST for cats with RCM presenting

  • with resp distress
  • without resp distress
A

With resp distress MST 64 days (majority of cats)
Without resp distress MST 466 days.

Locatelli JFMS 2018

185
Q

What factors are associated with survival in cats with CHF?

A

NTproBNP that decreased significantly before discharge liver longer

Cats with active CHF at re-evalation and whos owners had difficult administering meds had shorter survival times

Pierce JVIm 2017

186
Q

What is the common presentation and clinical progression for cats with transient myocardial thickening associated with heart failure?

A
  • young
  • associated with anticedent events
  • LVWT normalized and La:AO decreased from 1.8 to 1.45 over approx 3 months
  • HCF generally does not return
  • Cardiac meds can generally be discontinued.
  • much better (100%) sruvival

Matos JVIM 2018

187
Q

What is timolol and what can it be used for in cats?

A

Timolol is an opthalmic nonselective beta blocker

Can be used in cats to reduce HR and resolve dynamic outflow tract obstruction => better diastolic assessment

Gunther-Harrington JVIm 2016

188
Q

What tests may be benifitial in diagnosing CHF in cats with resp distress?

A 
1. Lung ultrasound with >1 site having >3 B-lines. 
Sens 78%, 
spec 83%
2. Subjective La enlargement - 
sens: 97%, 
spec 100%
3. Presence of pericardial effusion
sens60%
spec 100%
4. Positive serum NTproBNP
sens 93%
spec 72%

Ward JVIm 2017

189
Q

What is the recommended treatment for AV accessory pathways in dogs?
What is the success rate from this?
What breed is it most seen in?
what changes are seen on echo post treatment?

A
  • radiofrequency catheter abalation
  • suscessful in 98%, currence in 3/89 but resolved with second treatment
  • labradors
  • post abalation echo show resolution or significant improvement in tachcardia induced cardiomyopathy.

Wright JVIM 2017

190
Q

At what cut off, what is the sensitivity and specificity of NTproBNP for discriminating between CHF and non-cardiac resp distress in dogs?

A

> 2447 pmol/L
sens 81%
spec 73%

Fox JVIM 2015

ACVIM literature 2015-2019 (12 decks)

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