Myxomatous mitral valve disease

Question 1

What is the typical clinical course for smaller dogs (<20kg) with MMVD?

Answer 1

experience a long but unpredictable subclinical period

Median time to heart failure or cardiac death in untreated smaller dogs with clinically significant cardiomegaly is 2–3 years.

Question 2

What is the difference between MMVD in larger dogs compared to smaller dogs?

Answer 2

• often exhibit overt myocardial dysfunction
• faster progression
• more guarded prognosis

The reason for this is unknown.

Question 3

What is the etiology of MMVD?

Answer 3

Unknown, but hereditary factors are involved in some breeds

Question 4

What is the most common clinical finding in dogs with MMVD?

Answer 4

Heart murmur (incidental left-sided systolic)

Murmur intensity correlates with severity in smaller dogs with MMVD.

Question 5

What are the signs of CHF in dogs with MMVD?

Answer 5

Pulmonary edema or cavitary effusions, including:
* Tachypnea
* Orthopnea
* Dyspnea
* Cyanosis
* Abnormal lung sounds

Question 6

What can cause tachycardia in dogs with MMVD?

Answer 6

elevated sympathetic tone (—-> also causes loss of respiratory arrhythmia)

A normal or lower heart rate indicates heart failure is unlikely.

Question 7

What are common presenting signs of MMVD?

Answer 7

• Cough (not reliable - tracheobronchomalacia)
• Increased RR + effort (>30/min)
• Exercise intolerance
• Syncope/collapse (reduced CO + hypotension)

Question 8

Describe the pathophysiology of MMVD?

Answer 8

Myxomatous degeneration of the valve apparatus (valve thickening + irregularity, abnormal leaflet coaptation, chordae tendinae rupture, valve prolaps) characterized by dysregulation + subsequent weakening and disorganization of extracellular matrix –> systolic mitral valve regurgitation –> increased LA + LV filling pressures over time + reduced SV

This includes leaflets and chordae tendinae, leading to weakening and disorganization of the extracellular matrix.

Question 9

What compensatory mechanisms are activated due to decreased CO? Explain its consequences.

Answer 9

• Neurohormonal activation (RAAS, SNS)
• Increased norepinephrine, angiotensin II, and aldosterone

–> vasoconstricted, fluid retenetice state –> further increases LA, pulmonary venous + capillary pressures

Question 10

What are the long-term effects of neurohormonal activation in MMVD?

Answer 10

• Cardiomyocyte death
• Fibrosis
• Hypertrophy
• Myocardial failure
• fluid retention (–> postcapillary pulmonary hypertension)

Question 11

What complications can arise from MMVD?

Answer 11

• Chordae tendinae rupture
• LA tear (weakening of atrial wall)
• Pulmonary hypertension
• SVTs
• VTs
• Atrial fibrillation (more common in larger dogs; commonly associated with biventricular or R-CHF)

Question 12

What is a consequence of chordae tendinae rupture in MMVD?

Answer 12

Severe mitral valve regurgitation leading to acute, fulminant pulmonary edema.

Question 13

What type of pulmonary hypertension can develop in dogs with MMVD?

Answer 13

Chronic postcapillary pulmonary hypertension.

Question 14

What is the median time to HF or cardiac death in untreated smaller dogs with clinically significant cardiomegaly?

Answer 14

2-3y

Question 15

How does the prevalence of MMVD change with age?

Answer 15

up to 100% in >10y old CKCS, dachshund, miniature poodle and YST

Question 16

Does the murmur intensity correlate with the severity of MMVD in smaller dogs?

Answer 16

Yes

Question 17

How is CO initially maintained in MMVD?

Answer 17

Frank-Starling effect:
enhanced filling –> eccentric hypertrophy

Question 18

What is the pathomechanism of pulmonary hypertension in dogs with MMVD?

Answer 18

Chronic postcapillary PH –> reactive pulmonary arterial vasoconstriction + pulmonary vascular disease (combined postcapillary and precapillary PH)

Question 19

Name 2 different sequelae of atrial tear?

Answer 19

1. pericardial effusion + cardiac tamponade
2. acquired left-to-right shunt through atrial septal defect

Question 20

How can the causes of mitral valve regurgitation change with disease progression?

Answer 20

Progressive LV dilation –> displacement of papillary muslces + stretch of valve annulus –> progressive MV regurgitation

Question 21

What is Stage A in the ACVIM classification system for dogs with MMVD?

Answer 21

Dogs at high risk for developing heart disease with no identifiable structural disorder of the heart.

Example: Every CKCS without a heart murmur.

Question 22

What characterizes Stage B in the ACVIM classification system for dogs with MMVD?

Answer 22

Dogs with structural heart disease (e.g., heart murmur + typical valve pathology), but never developed signs of HF.

Question 23

What defines Stage B1 in the ACVIM classification system?

Answer 23

Asymptomatic dogs without radiographic or echocardiographic evidence of cardiac remodeling in response to MMVD, or only mild remodeling

–> not severe enough to meet current clinical trial criteria that have been used to determine that initiating treatment is warranted

These changes are not severe enough to meet clinical trial criteria for initiating treatment.

Question 24

What is the condition of dogs classified as Stage B2?

Answer 24

Asymptomatic dogs with advanced MVR that is hemodynamically severe and has caused radiographic and echocardiographic findings of LA and LV enlargement

–> benefit from initiating pharmacologic treatment to delay onset of CHF

Question 25

What defines Stage C in the ACVIM classification system for dogs with MMVD?

Answer 25

Dogs with either current or past clinical signs of heart failure caused by MMVD.

Question 26

What is Stage D in the ACVIM classification system for dogs with MMVD?

Answer 26

Dogs with end-stage MMVD where clinical signs of heart failure are refractory to standard treatment (e.g. furosemide > 12mg/kg/d)

Question 27

What hematologic changes can be seen in dogs with MMVD?

Answer 27

- Normochromic, normocytic nonregenerative anemia - Stress leukogram (neutrophilia, monocytosis, lymphopenia, eosinopenia) ## Footnote This indicates a lack of regeneration of red blood cells.

Question 28

What biochemistry findings can be present in MMVD?

Answer 28

Congestion: - Raised liver enzymes - hyponatremia - hypochloremia Poor renal perfusion: - azotemia ## Footnote These changes reflect liver stress and fluid balance issues.

Question 29

What are the blood gas analysis findings associated with MMVD?

Answer 29

- Hypoxaemia - metabolic acidosis secondary to peripheral vasoconstriction + poor perfusion (lactic acidosis) ## Footnote Reflects inadequate oxygen delivery and tissue perfusion.

Question 30

What are the significances of NT-proBNP in MMVD?

Answer 30

- Increases progressively with worsening MMVD and onset of HF - serial NT-proBNPs within the same dog most informative - normal/near normal NT-proBNP: severe cardiac disease not cause of respiratory distress - might aid in treatment decision + response evaluation ## Footnote This biomarker helps assess heart failure severity.

Question 31

What is the caviat of using NT-proBNP in dogs with MMVD?

Answer 31

renal dysfunction + pulmonary hypertension can increase NT-proBNP ## Footnote It provides insight into the effectiveness of therapeutic interventions.

Question 32

List 2 objective measurements on thoracic radiogrpahy supported by ACVIM consensus guidelines for assessing MMVD.

Answer 32

* VHS * Vertebral left atrial size (VLAS) ## Footnote These measurements help quantify heart changes associated with MMVD.

Question 33

What are some subjective criteria for assessing left atrial enlargement on thoracic radiographs?

Answer 33

* Straightening or loss of the dorsal caudal cardiac waist * Increased soft tissue opacity between the mainstem bronchi (VD/DV) * Bulge at the 2 to 3 o’clock position (VD/DV) * Widened cardiac silhouette --> > 2/3 of the thoracic width (VD/DV) ## Footnote These signs can indicate significant heart enlargement.

Question 34

What signs may indicate pulmonary venous distension on thoracic rafdiography in MMVD?

Answer 34

Pulmonary edema: interstitial pattern in the peri-hilar and caudodorsal lung fields (alveolar pattern if severe) ## Footnote This reflects fluid accumulation in the lungs.

Question 35

What are the signs of right congestive heart failure (R-CHF) seen in MMVD on thoracic radiographs?

Answer 35

* Pleural fissure lines or effusion * Distension of the CVC * Loss of abdominal serosal detail (ascites) ## Footnote These findings indicate fluid accumulation due to right heart failure.

Question 36

What is the purpose of echocardiography in diagnosing MMVD?

Answer 36

* Presence of MMVD? * Chamber size + function * LV filling pressures * Comorbidities or complicating factors * Staging ## Footnote Echocardiography provides detailed information about heart structure and function.

Question 37

How is left atrial size related to the severity of chronic mitral regurgitation (MR)?

Answer 37

LA size = robust surrogate for severity of chronic MR --> the bigger the LA, the worse the MR + more likely to experience or be at risk of L-CHF ## Footnote This relationship helps in assessing risk for heart failure.

Question 38

What is the goal of treating MMVD?

Answer 38

1. Decrease preload + venous congestion 2. Optimize CO 3. Improve tissue oxygenation -->Oxygen therapy (or CPAP, NiPS or PPV) ## Footnote Key variables include decreasing preload, optimizing cardiac output, and improving tissue oxygenation.

Question 39

List the standard emergency management treatments for MMVD.

Answer 39

* diuretic therapy: Furosemide 2mg/kg IV/IM/SC * positive inotropy: --> Pimobendan 0.25-0.3mg/kg PO q8-12hr (venodilator properties) --> Dobutamine 2.5-10mcg/kg/min * Oxygen therapy ## Footnote These treatments are essential for managing congestive heart failure.

Question 40

What are the risks associated with continuous rate infusion (CRI) of Furosemide?

Answer 40

* Increased risk of dehydration * Azotemia ## Footnote CRI has been shown to induce more potent diuresis compared to intermittent bolus therapy.

Question 41

What is the goal of optimizing CO in MMVD treatment?

Answer 41

To reduce afterload and improve forward stroke volume ## Footnote This can involve using arterial vasodilators and positive inotropes.

Question 42

In severe refractory cases of MMVD, what vasodilators can be used? What is the main side effect?

Answer 42

1. Sodium nitroprusside CRI 1-5mcg/kg/min for up to 48hr 2. clevidipine (calcium channel blocker) CRI 1mcg/kg/min 3. Oral vasodilators: --> hydralazine (0.5-2.5mg/kg PO q12hr) --> Amlodipine (0.1-0.2mg/kg PO q24hr) side effect: systemic hypotension ## Footnote This treatment is costly and has limited availability.

Question 43

What are the goals of long-term management in MMVD?

Answer 43

* Continue medications initiated for emergency management * Slow progression of disease * Improve survival ## Footnote This includes using RAAS blockers and ensuring adequate diet.

Question 44

What is the prognosis for most dogs with MMVD after the first onset of heart failure?

Answer 44

6 to 18 months of a good quality of life ## Footnote Recurrent or advanced heart failure secondary to MMVD has a median survival time of 9 months.

Question 45

What is the goal of managing pulmonary hypertension in MMVD?

Answer 45

Reduce postcapillary PH via reduction of LA pressures ## Footnote This can be achieved with diuretics and pimobendan.

Question 46

Which medications are used to manage pulmonary hypertension in MMVD?

Answer 46

* Diuretics * Pimobendan --> sildenafil (phosphodiesterase-5 inhibitor) not recommended as may worsen postcapillary pulmonary hypertension ## Footnote These medications help reduce left atrial pressures.

Question 47

Why is sildenafil not recommended as first-line therapy for pulmonary hypertension?

Answer 47

Due to risk of inducing/worsening pulmonary edema ## Footnote Sildenafil is a phosphodiesterase-5 inhibitor.

Question 48

What steps should be taken for a patient with LA tear and pericardial effusion?

Answer 48

* Lower LA pressures * Treat heart failure if present * Strict rest * Consider pericardiocentesis for life-threatening cardiac tamponade ## Footnote There is a concern of fatal hemorrhage with pericardiocentesis.

Question 49

What treatments are considered for ruptured chordae tendinae leading to acute left heart failure?

Answer 49

* Furosemide CRI * Consider arterial vasodilators (e.g. sodium nitroprusside) * Positive pressure ventilation if needed ## Footnote These treatments aim to stabilize the patient's condition.

Question 50

What should be monitored in MMVD?

Answer 50

- RR + effort Q1HR - Thoracic radiographs - BP - Volume status - Acid-base status (Metabolic alkalosis) - Electrolytes - Renal function ## Footnote RR stands for respiratory rate.

Question 51

How often should thoracic radiographs be assessed in MMVD?

Answer 51

Baseline + then q12-24hr

Question 52

What is the expected body weight decrease after diuresis in MMVD?

Answer 52

Usually by 5-8% compared to admission

Question 53

What renal function indicators require reevaluation of diuresis?

Answer 53

Creatinine >2.5mg/dl and BUN >50mg/dl

Question 54

What determines the recommendations for long-term management of MMVD?

Answer 54

Degree of left heart remodeling (determined by echocardiography) ## Footnote Echocardiography is a key diagnostic tool in assessing heart conditions.

Question 55

What is the dosing guideline for torasemide?

Answer 55

5-10% of desired daily furosemide dose or 0.1-0.3mg/kg PO q24hr ## Footnote This dosing is based on the patient's need for diuresis.

Question 56

What are the clinical indicators for using pimobendan?

Answer 56

- Loud murmurs (≥3/6) - LA:Ao ≥1.6 - LV internal dimension normalized to bodyweight (kg) ≥1.7kg (cm/kg0.294) - VHS ≥11.5 - VLAS ≥3 ## Footnote These indicators help identify patients who may benefit from pimobendan treatment.

Question 57

What are the options for slowing the progression of disease in MMVD management?

Answer 57

- RAAS blockers - dietary management - cardiologist assessment for: additional diuretics, arterial vasodilators, off-label up-titration of pimobendan ## Footnote Slowing disease progression is crucial for improving patient outcomes.

Question 58

What dietary considerations are important for patients with MMVD?

Answer 58

- Adequate calorie intake (prevent cardiac cachexia) - modest sodium restriction (control of edema) - omega-3 fatty acid supplementation ## Footnote These dietary changes aim to improve heart health and prevent complications.

Question 59

What is the MST according to Beaumier et al 2018 for recurrent or “advanced” HF secondary to MMVD?

Answer 59

9 months