Cardio. MMVD. Chap 48

Question 1

incidence

Answer 1

• approximately 10% of dogs presented to primary care veterinary practices have heart disease
• MMVD is the most common approximately 75% in NA
• small breed dogs, with up to 85% showing evidence of the valve lesion by 13 years of age

Question 2

most commonly affects MV, ____% TV:
males vs females:
large vs small:
inheritied and genetic component in some breeds

Answer 2

30%
1.5X more common in males
large dogs have faster progression

Question 3

Pathophys. disease consistently is characterized by:

Answer 3

• changes in collagen and alignment of collagen fibrils within the valve
• changes in the proteoglycan content = expansion of the spongiosa layer
• activated myofibroblasts & matrix metalloproteinases, which degrade collagen and elastin faster than they can be produced
• hypothesized that abnormal numbers or types of mitogen receptors (ie, any of the subtypes of serotonin, endothelin, or angiotensin receptors) on fibroblast cell membranes in the valves of affected dogs play a role in the pathophysiology of acquired valvular lesions

Question 4

increased risk of sequelea?

Answer 4

no, no increased risk of PTE or infective endocarditis

Question 5

Pathopys. leading to CHF

Answer 5

• progressive deformation of the valve structure
• prevents effective coaptation, allowing regurgitation
• valvular regurgitation increases cardiac work = ventricular remodeling (eccentric hypertrophy of both the atrium and ventricle, and intercellular matrix changes)
• eventually to ventricular dysfunction - volume overload and CHF

Question 6

What factors are moderately predictive of the rate of progression of MMVD and can help identify dogs at risk for impending heart failure:

Answer 6

• progressive heart enlargement (of the left atrium [LA] and ventricle)
• increased transmitral E wave blood flow velocities
• increased serum NT‐proBNP
• increases in resting HR

Question 7

Define “heart failure”:

Answer 7

“heart failure” refers to CS caused by heart dysfunction.

• such that either venous pressures increase so severely that fluid accumulates in the lungs or a body cavity (congestive heart failure [CHF]/ “backward” failure)
• pumping ability is compromised such that it cannot meet the body’s, in the face of either normal or increased venous pressures (sometimes called “forward heart failure”)

Question 8

2009 consensus:

staging system for MMVD describes 4 basic stages

staging system, applied to dogs with MMVD, remains useful, although recent clinical trial results necessitate a more critical clinical evaluation of dogs in Stage B to facilitate sound therapeutic decision making

Answer 8

Stage A: identifies dogs at high risk but no identifiable structural disorder (eg, every Cavalier King Charles)

Stage B: identifies dogs with structural heart disease (eg, the typical murmur), never developed clinical signs

Stage B1

• asymptomatic dogs that have no radiographic or echocardiographic evidence of cardiac remodeling
• as well as those in which remodeling changes are present, but not severe enough to meet current clinical trial criteria that have been used to determine that initiating treatment is warranted

Stage B2
-asymptomatic dogs w more advanced mitral valve regurgitation caused radiographic and echo findings of left atrial and ventricular enlargement that meet clinical trial criteria that clearly should benefit from initiating pharmacologic treatment

Stage C denotes dogs with either current or past clinical signs of heart failure caused by MMVD.

Stage D end‐stage MMVD, clinical signs of heart failure are refractory to standard treatment (defined later in this consensus statement). Such patients require advanced or specialized treatment strategies to remain clinically comfortable

Question 9

In a change from the 2009 recommendations:

Answer 9

strong evidence now supports initiating treatment to delay the onset of clinical signs of heart failure at stage B2 patients with more advanced cardiac morphologic changes

Question 10

Diagnostic and theraputic guidelines/ stage:

Stage A:

Answer 10

unchanged from 2009 - 2019 consensus

• predisposed breeds (eg, Cavalier King Charles Spaniels, Dachshunds, Miniature, and Toy Poodles)
• yearly auscultation

Question 11

Diagnostic and theraputic guidelines/ stage:

Stage B:

Answer 11

unchanged from 2009 - 2019 consensus

Dx: baseline radiographs, BP, echo

Question 12

Diagnostic and theraputic guidelines/ stage:

Stage B1:

Answer 12

unchanged from 2009 - 2019 consensus
Dx: baseline radiographs, BP, echo
Tx: not recommended
Reeval: echo (or radiography) in 6‐12 months

Question 13

Diagnostic and theraputic guidelines/ stage:
Stage B2:
Stage B2 criteria for treatment before the onset CHF: (Class I, LOE: Strong):

In the absence of echocardiographic measurements…

Answer 13

Stage B2 criteria for treatment before the onset CHF: (Class I, LOE: Strong):

• murmur intensity ≥3/6;
• echocardiographic LA : Ao ratio in the right‐sided short axis view in early diastole ≥1.6
• Left ventricular internal diameter in diastole, normalized for body weight (LVIDDN) ≥1.7
• vertebral heart score (VHS) >10.5.

..clear radiographic evidence of cardiomegaly (eg, a “general breed” VHS ≥11.5, or a comparable “breed‐adjusted” VHS in cases where breed‐specific VHS normal values are available) or evidence of accelerating (increasing) interval change in radiographic or echocardiographic cardiac enlargement patterns can substitute for quantitative echocardiography to identify Stage B2. (Class I, LOE: expert opinion)

Question 14

newer index of radiographic left atrial enlargement:

explain how to perform it and what normal is:

Answer 14

VLAS (vertebral LA size) - quantitative method of estimating left atrial size

• right or left lateral radiograph
• line from the center/ventral carina
• to most caudal aspect of the LA
• intersects with the dorsal border of the caudal vena cava,
• line then is transposed to the cranial edge of the 4th thoracic vertebral body

-Studies are ongoing to determine a VLAS value that accurately predicts B2 remodeling, but in the absence of echocardiography, VLAS values of ≥3 likely identify Stage B2 MMVD. (Class 1, LOE: moderate)

Question 15

Stage B2 treatment:

Answer 15

Pimobendan -0.25‐0.3 mg/kg PO q12h (Class I, LOE: strong)

Mild dietary sodium restriction and provision of a highly palatable diet with adequate protein and calories (Class IIa, LOE: weak)

ACEI on either initial examination, or in which the LA has increased markedly in size on successive monitoring examinations, 5 (of 10) panelists recommend treatment with ACEI (LOE: weak)
Clinical trials addressing the efficacy of ACEI for treatment of dogs in Stage B have shown mixed results

+/- cough suppressants - when their cough is thought to be the result of pressure from cardiac enlargement on adjacent bronchi. (Class IIa, LOE: expert opinion)

Question 16

Logistical difficulties associated with the stability of B-type natriuretic peptide have been overcome with pro-BNP:
What is it?
What other factors influence it?

Answer 16

more stable amino terminal portion of the cleaved pro-hormone (NT-proBNP)
These assays have been validated and demonstrate
good sensitivity and specificity in differentiating patients with dyspnea secondary to cardiac disease versus primary respiratory

numerous other factors e.g., pulmonary hypertension, renal dysfunction

Question 17

What is P mitrale
P pulmonale
ECG evidence of left ventricular enlargement

Answer 17

P wave width >40 msec
P wave height >0.5 mV
evidence of left ventricular enlargement = R wave amplitude >2.5 mV or duration >60 msec

Question 18

Describe radiographic finding of MMVD

Answer 18

• loss of the caudal cardiac waist (left atrial enlargement)
• tall cardiac silhouette (left ventricular enlargement)
• dorsal deviation of the trachea
• pulmonary venous congestion in cranial lobar veins on the lateral projection and caudal lobar veins on the orthogonal projection
• dorsoventral better visualization of the caudal pulmonary vasculature and is less stressful
• severe TR: changes consistent with right-sided heart enlargement (reverse D on dorsoventral films, increased sternal contact)
• global or generalized cardiomegaly

-pulmonary edema mild, perihilar, or central
interstitial infiltrate. As the severity of the infiltrates increases in

heart failure or biventricular disease, pleural fissure lines or overt effusion may be visible and there may be a loss of serosal detail in
the abdomen.

Question 19

Classic echo fingings

Answer 19

left ventricular and left atrial dilation
hyperdynamic left ventricular wall motion
and thickened mitral valve leaflets

Question 20

Diagnosing Stage C:

S and PE plus labs:

Answer 20

• obese dogs with no history of weight loss
• marked sinus arrhythmia and relatively slow heart rates = less likely to have clinical signs attributable to MMVD
• BW, radiographs, echo., proBNP

Question 21

Diagnosing Stage C:
benefit of echo:
comorbidities:

Answer 21

• confirm the presence of MMVD
• quantify chamber enlargements and cardiac function,
• estimates of LV filling pressures
• identify comorbidities and complications of chronic MR
• pulmonary hypertension, acquired atrial septal defect, and pericardial effusion from an atrial tear or unrelated cardiac tumor
• i.e. pretreatment finding of a low‐velocity E‐wave on pulsed‐wave Doppler strongly argues against a diagnosis of left‐sided heart failure
• Conversely, most dogs in Stages C and D have high‐velocity early filling waves

Question 22

normal or near normal NT‐proBNP

Answer 22

normal or near normal NT‐proBNP concentration in a dog with clinical signs of cough, dyspnea, or exercise intolerance strongly suggests that heart failure is not the cause of the clinical signs

Question 23

Acute Stage C tx:

Answer 23

1. Furosemide 2 mg/kg administered IV (or intramuscularly [IM]), followed by 2 mg/kg IV or IM hourly until the patient’s respiratory signs are substantially improved
   - or total dosage of 8 mg/kg has been reached over 4 hours. (Class I, LOE: expert opinion)
2. life‐threatening pulmonary edema (ie, expectoration of froth associated with severe dyspnea, radiographic white‐out lung, poor initial response to furosemide over 2 hours), furosemide also may be administered as a CRI 0.66‐1 mg/kg/hour after the initial bolus (Class IIa, LOE: weak)

***Allow the patient free access to water once diuresis has begun. (Class I, LOE: expert opinion; humane considerations apply)

3. Pimobendan, 0.25‐0.3 mg/kg administered PO q12h. Although the clinical trial evidence supporting the chronic use of pimobendan in the management of Stage C heart failure from MMVD is stronger than for the acute presentation, the recommendation to use pimobendan in acute heart failure treatment is strongly supported by hemodynamic and experimental evidence as well as the anecdotal experience of the panelists
   - outside of the United States, pimobendan for IV administration is available. (Class I, LOE: weak)
4. Oxygen supplementation
5. Sedation‐anxiety with dyspnea should be treated Butorphanol 0.2 to 0.25 mg/kg administered IM or IV was the narcotic most often utilized for this purpose; combinations of buprenorphine (0.0075‐0.01 mg/kg) and acepromazine (0.01‐0.03 mg/kg IV, IM, or SC) (Class I, LOE: expert opinion)

Provide optimal nursing care, patients in sternal posture.

6. Dobutamine (2.5‐10 μg/kg/min as a CRI, starting at 2.5 μg/kg/min and increasing the dosage incrementally) may be used in addition to the above treatments to improve the left ventricular function in patients that fail to respond adequately to diuretics, pimobendan, sedation, oxygen, and comfort care measures.

Continuous ECG monitoring is recommended where available during dobutamine infusion, with dosage reduction indicated if tachycardia or ectopic beats occur. (Class I, LOE: expert opinion)

Question 24

When to consider nitroprusside:

Answer 24

CRI sodium nitroprusside 1 to 15 μg/kg/min for up to 48 hrs useful for life‐threatening, poorly responsive pulmonary edema

this medication is currently (2018) expensive
PO titration of additional arterial dilators (eg, hydralazine or amlodipine, specific dosing recommendations also in Class D below) also may be useful in patients when administration of nitroprusside is not feasible. (Class I, LOE: weak)
ACEI, for example, enalapril or benazepril, 0.5 mg/kg PO q12h. Although treatment with an ACEI is a Class I recommendation for chronic Stage C heart failure (see below) and some panelists also treat acute heart failure with ACEI, the evidence supporting ACEI efficacy and safety in acute treatment, when combined with furosemide and pimobendan, is less clear. There is, however, clear evidence that the acute administration of enalapril plus furosemide in acute heart failure results in significant improvement in pulmonary capillary wedge pressure when compared with the administration of furosemide alone.70 (Class IIb, LOE: weak)
Nitroglycerin ointment, approximately half an inch paste/10 kg BW, applied to an unhaired or shaved area of skin, can be used for the first 24 to 36 hours of hospitalization.71, 72 Some panelists recommend administering the ointment at intervals (12 hours on, 12 hours off). Other panelists do not use nitroglycerin in this setting. (Class IIb, LOE: weak)