251 Adult Onset Valvular Disease Flashcards
(42 cards)
1
Q
What is MMVD?
A
= a progressive myxomatous degeneration of the mitral valve apparatus with subsequent left atrial and ventricular dilation. The other four valves can be affected
2
Q
What is the prevalence of MMVD?
A
- 75-80% of canine cardiac disease
- in all breeds, but highest in small-medium sized dogs, such as CKCS, daschunds, miniature poodles, and Yorkshire terriers
- increases with age, and higher in males
3
Q
How is MMVD inherited?
A
- studies of CKCS and daschunds provide evidence that inheritance is polygenic; and multiple traits influence the trait and certainty threshold is reached for MMVD to develop
4
Q
What is the pathology of MMVD?
A
- the edges Of the leaflets become thickened, irregular, with bulging/ballooning towards the LA side.
- Chordae tendinae might also be affected
- budging of leaflets worsens with progressions.
- late stages = fibrosis causes marked thickening and contraction of leaflets and chordae tendinae.
- Jet lesions might also be observed
- atrial rupture might be present
5
Q
What is the pathogenesis of MMVD?
A
Not much is known but it is thought that:
- Endothelial damage induces release of vasoactive peptides such as endothelin-1, which is involved In transforming subendothelial valvular interstitial cells (VICs) from predominantly fibroblast phenotype into more active myofibroblast and smooth muscle cell phenotypes.
- 5-HT is suggested to initiate VICs, as it is higher in CKCS and those dogs with MMVD
6
Q
What is the pathophysiology of mitral regurgitation caused by MMVD?
A
Distortion to valve and chordae tendinae -> leads to systolic atrial displacement of mitral valve leaflets, and abnormal coaptation, of mitral valve leaflets during systole. = percentage of stroke volume is ejected into LA
- Elongation and potential rupture of chordae tendinae worsens MR by causing leaflets partially or completely prolapse (valve flail) into LA
- Left-sided cardiac dilation is linked to MR severity, suggesting that MR volume is major determinant for left sided cardiac dilation.
- The extra pathway for stroke volume into LA reduces LV afterload, here as the increased volume load leads to an increased preload. This absorption of the regurgitation volume protects the pulmonary vascular bed from hypertension. The increased LA pressure results in pulmonary venous congestion and oedema.
- The LV compensates for loss of forward stroke volume by increasing end diastolic volume, and to allow for increased preload, the LV undergoes compensatory responses:
- LV Eccentric hypertrophy (also stimulated by neurohormonal activation such as angiotensin II)- Dilation
7
Q
What is the pathophysiology of tricuspid regurgitation caused by MMVD?
A
- Occurs concomitantly with myxomatosis degeneration of mitral valve as consequence of primary valvular changes, +/- secondary to pulmonary hypertension due to left sided myxomatosis degeneration
- same changes described for mitral valve
- TR is of significance if pulmonary hypertension is present
- RV is designed to contract against low pressure artery, it is vulnerable to increase in pressure
8
Q
What are the clinical signs of mild/moderate MMVD (ACVIM stage A and B)
A
- usually no signs of disease
- exercise intolerance may be noted
- Cough is common presenting complaint but not heart failure specific. Dogs with mainstream bronchial compression, but pulmonary congestion or oedema, may have coughing spells at any time during the day, especially during physical activity or excitement.
9
Q
What are the clinical signs of decompensated (stage C) CHF?
A
The clinical signs relate to the pathophysiological events listed in order of importance:
1) increased LA and pulmonary venous pressure, which result in respiratory (tachypnoea and dyspnea) distress and cough due to pulmonary oedema and main stem bronchial compression
2) reduced LV or RV forward flow, result in weakness and reduced stamina
3) increased RA and systemic venous pressure resulting in pleural effusion and ascites
4) acute decompensation due to rupture of chordae tendinae, atrial rupture, or ventricular fibrillation which can cause sudden death.
10
Q
What is the expected finding on physical examination?
A
- systolic murmur is prominent finding
- PMI over mitral valve on left side thorax, and may be intermittent
- Progression of disease, results in a murmur of ‘harsher’ and more intense quality, and longer duration (holosystolic)
- with pulmonary congestion/oedema the RR at rest is expected to breast >30 bpm
- advanced CHF can have MM cyanotic, greyish, or ashen
- tamponade - pericardial haemorrhage due to LA tear; weak pulses; and jugular distension
- progressive MMVD -> leads to RSCHF due to pulmonary hypertension +/- tricuspid degeneration +/- tachyarrhythmia. Results in venous distension with signs of hepatomegaly +/- splenomegaly, pulsating jugular veins, ascites, muffle heart sounds.
11
Q
What are the expected findings on ECG of MMVD?
A
- vary from normal tracing to a marked abnormalities in rate, rhythm, or configuration.
- Useful to identify arrhythmia
12
Q
What are the expected radiographic findings of a dog with MMVD on the left side?
A
Left sided cardiac chambers:
- Assess LA, LV, mainstem bronchi, pulmonary vessels, and lung field
- LA enlargement is earliest and most consistent radiographic finding
- VHS is most likely to be enlarged 6 months prior to CHF
- lateral projection: LA + LV enlargement signs include dorsal elevation of caudal portion of trachea and carina, dorsal displacement of left mainstem bronchus, and visible prominence of LA causing caudal border of heart to appear straight or bulge dorsocaudally
- VD: enlarged LA appendage identified as bulge in left cranial part of cardiac border (2 & 3 o’clock position)
- pulmonary congestion (veins are greater than artery size and tortuous) and oedema may develop
13
Q
What are the expected radiographic findings of a dog with MMVD on the right side?
A
- lateral projection: moderate to severe RA enlargement would show bulging of RA in craniodorsal direction, and this also elevates trachea. Dilation of caudal vena cava, signs of RV enlargement include increased eternal contact and rounding of right hear border.
- DV projection: enlarged RA inn 9-12 o’clock position. Cardiac apex shifts to the left. May have pleural effusion, abdominal effusion, hepatomegaly, and splenomegaly.
14
Q
what are the echocardiographic findings of the mitral valve and left side cardiac chambers in a dog with MMVD?
A
- mitral valve leaflet thickening and systolic leaflet protrusion (prolapse)
- valve regurgitation on colour-flow Doppler to find regurgitating fraction
- LA size. The parasternal short axis view will allow for comparison between LA + auricle, with the aortic root.
15
Q
what are the echocardiographic findings of the tricuspid valve and right side cardiac chambers in a dog with MMVD?
A
- mitral valve leaflet thickening and systolic leaflet protrusion (prolapse)
- valve regurgitation on colour-flow Doppler to find regurgitating fraction
- RA is hard to access due to anatomy and orientation. Signs indicating pulmonary hypertension include hypertrophy and dilatation of RV, dilation of pulmonary artery , and flattening or paradoxical motion of interventricular septum
- assess pulmonary hypertension and stroke volume with spectral Doppler.
- pulmonary hypertension can be diagnosed if peak TR velocity is >3m/sec corresponding to a peak TR gradient >36 mmHg
16
Q
What is stage A?
A
Dog at risk for developing heart disease but currently no identifiable structural disorder of heart.
- e.g. CKCS without heart murmur
17
Q
What is stage B?
A
Dogs without clinical signs but present in with systolic click +/- systolic heart murmur
18
Q
What is stage B1?
A
Dogs with evidence of mild MR (heart murmur and echocardiographic signs of AV valve regurgitation) but no signs of cardiomegaly
19
Q
What is stage B2?
A
Asymptomatic dogs that have hemodynamically significant AV valve regurgitation, as evidenced by radiographic or echocardiographic findings of cardiomegaly
20
Q
What is stage C?
A
Dogs with past or current clinical signs of CHF associated with structural heart disease.
Severity of clinical signs of CHF range from mild to severe, the latter requiring aggressive therapy that would normally be reserved for those the refractory disease (stage D).
21
Q
What is stage D?
A
Dogs with end stage disease presenting with clinical signs of heart failure caused. By AV valve regurgitation that are refractory to standard CHF therapy. Such patients require advanced or specialised treatment strategies in order to remain clinically comfortable with their disease
22
Q
What are the differential diagnosis of mitral valve regurgitation?
A
Apart from myxomatosis degeneration:
- DCM or other myocardial disease
- bacterial endocarditis
- lesions of the valve are thickened but more echogenic and isolate. Patient will have fever, arthritis, systemic disease, murmur, and clinical signs of thromboembolic disease - congenital : mitral valve dysplasia or PDA
23
Q
What are the differential diagnosis of tricuspid regurgitation?
A
Occur as consequence of V dilatation in conditions associated with acquired increase in RV pressure
- heartworm disease
- pulmonary thromboembolism
- pulmonary hypertension secondary to left sided heart disease
- idiopathic pulmonary hypertension.
- biventricular or DCM
- incongenital pulmonic stenosis
- cats with cardiomyopathy and hyperT
- unusual for it to be affected by infective endocarditis or chordae tendinae rupture
24
Q
How do you manage dogs without signs of CHF (ACVIM stage B)?
A
- VETPROOF and SVEP - large multicentre trials did not show ACE inhibito enalapril to have an effect on MMVD when dogs are B1 or B2
- Beta receptor antagonists have shown benefits in experimental situation by improving the hemodynamic situation and myocardial contractility, but they fail in a clinical setting.
- Arterial vasodilators (amlodipine) suggested beneficial ins rage B2 MMVD, due t reduction of aortic impedance may theoretically reduce MR. Dose 0.057mg/kg PO q 12h in dogs studied and although clinical documentation is scars a non-blind echo study found improvement in stroke volume and 10% reduction in blood pressure
- EPIC study found pimobendan beneficial at stage B2, and prolong time of develop CHF.
- ## monitor disease progression at regular checks at 3-12 months if cardiomegaly present
25
How do you manage dogs with mild-moderate signs of CHF (ACVIM stage C)?
Therapy should be directed toward:
1) reduce venous pressure to alleviate oedema and effusions
2) maintain adequate CO to prevent weakness, lethargy, and prerenal azotemia
3) reduce cardiac workload and valvular regurgitation
4) protect the heart from negative long-term effects of neurohormones
Diuretics:
Furosemide= 2-4 mg/kg IV, IM, SQ, q 8-12h for 2 - 3 days; then reduced to maintenance of 1-2 mg/kg PO q 12-48h or lower.
Torsemide = 1/10 dose of furosemide
Pimobendan: 0.25 mg/kg PO q 12 h
- QUEST (91% longer) and VetSCOPE trials indicate longer survival time.
- benefit is mediated through vasodilation and increased contractility, which reduce MR by decreasing size of LV and mitral valve annulus through improved forward stroke volume.
ACEinhibitors
- give in combination with diuretics as they have less severe clinical signs of disease, better exercise tolerance, and live longer than those not receiving ACEi.
- decrease fluid retention and counteract the peripheral vasoconstriction and other negative effects on the heart
Spironolactone
- aldosterone antagonise and potassium-sparing agent
- reduces risk of primary endpoint of study which was cardiac related death, euthanasia or worsening CHF.
Digoxin
- Controversial as there is lack of scientific evidence
- weak positive ionotrope, but reduces reflex tachycardia by normalising baroreceptor activity by reducing sympathetic activity.
26
How is dogs with recurrent CHF managed (stage C or D)?
When furosemide has reached 4-5 mg/kg PO q 8-12 h, hen switch to torsemide.
- Also sequential blocking of the nephron by using Spironolactone (1-3 mg/kg PO q 12-24h)
- Thiazides such as hydrochlorothiazide (2-4 mg/kg PO q 12h) or amiloride (0.1-0.3 mg/kg PO q 24h)
-
The risk of inducing prerenal azotemia, hypotension and acid-base and electrolyte imbalances increases with the intensity of the diuretic treatment
27
How are dogs with severe and life-threatening (fulminant) CHF (ACVIM stages C or D)?
- Require immediate hospitalisation
- No stress
- sedative : butorphanol 0.25 mg/kg IM, IV repeated every 30-60minutes, or combined with buprenorphine (0.0075-0.01 IM mg/kg) and acepromazine (0.01-0.03 mg/kg IV, IM, or SC)
- Furesomide Iv 1-4 mg/kg IV q2-6h or higher; or IM if IV is not possible.
- Pimobendan 0.15 mg/kg IV single dose and repeated q 12h PO at 0.25-0.3 mg/kg q 12h
- Oxygen therapy
- vasodilator - nitrogen glycerin ointment (4-12 mg topically q 12h) to unload the heart, and arterial vasodilators such as amlodipine PO to reduce afterload
- Amlodopine 0.1 mg/keg q 24h reduces LA pressure in dogs with experimental MR, and severity in dogs with MMVD
-Reflex tachycardia can develop in response to hypotension, and GIT problems then oral medication wont work. Use nitroprusside (for afterload reduction in life-threatening pulmonary oedema) or dobutamine (for inotropic support of the hypotension patient) must be administered by IV CRI.
-
28
How is coughing due to left mainstem bronchial compression managed?
Significant coughing caused by left mainstem bronchial compression, therapy is aimed at suppressing cough reflex or reduce the influence of the underlying cause for compression.
- Couugh suppressants: hydrocodone bitartrate (2.5-10 mg/dog PO q 6-12 h), butorphanol (0.55-1.1 mg/kg PO q 6-12 h) or dextromethorphan (0.5-2 m/kg PO q 6-8 h)
If tracheal ist ability or chronic small a irway disease then a bronchodilator and brief course of glucocorticoids.
- Aminophylline (8-11mg/kg PO q 6-8h), theophylline (sustained duration) 20mg/kg PO q 12h, an oxitryphilline (sustained) 25-30 mg/kg PO q 12h are commonly used bronchodilators.
29
How is right sided CHF due to pulmonary hypertension managed?
- A pressure gradient >55mmHG recently shown to be independent negative predictor of outcome.
- sildenafil 0.5-2 g/kg q 8-12h
- Bronchodilator therapy my be indicated, and methylxanthines and beta-2 selective agonists may be considered.
30
What is infective endocarditis likely to occur in?
Prevalence = 0.09-6.6% in necrotised dogs
- medium-large breeds, mainly purebred, middle-aged male dogs
- Prevalence in cats is 7-10 times lower than dogs
31
What is the aetiology and pathogenesis of IE?
- A transient or persistent bacteremia results in bacteria either making direct contact with endocardium from the bloodstream or from capillaries within the valve (vasculitis).
- A predisposing factor is depressed immune system or endothelial damage, sometimes associated with depositions of platelet-fibrin complexes to adhere to valve and create IE
- Extracellular matrix proteins, thromboplastin, and tissue factor all trigger coagulation. -> Coagulant forms on damaged endothelium and inflammatory factors are activated. - >The inflammatory processed together with enzymes released from bacteria contribute to degradation of valve tissue
- Organisms causing IE include staphylococcus and streptococcus spp.
- Staphylococcus aureaus and Bartonella become internalised in endothelial cells and remain undiscovered by the immune system. Bacteria are also protected from immune system and from antibiotic substances by being embedded within coagulum
- Gram negative bacteremia often results in peracute or acute clinical manifestations.
- Gram positive bacteremia results in subacute or chronic conditions.
- Depositions of immunocomplexes can cause glomerulonephritis, myositis, or polyarthritis.
- Thromboembolic complications causing CS is 30-40% of dogs, with most common site lungs, kidneys, and distal part of aorta.
32
What are some predisposing actors that could raise suspicion of IE?
- Immunosuppressive drug therapy
- non-oral surgery within 3 months
- trauma to mucosal surfaces in oral or genital tract and infections in these body regions
- indwelling catheters
- infected wounds
- abscesses
- pyoderma
33
What are the clinical signs associated with IE?
- Variable
- lameness
- lethargy, anorexia, resp abnormalities, weakness, fever, weight loss, and GI disturbances.
- muscle stiffness or joint pain due to immunomediated responses
- abdominal pain caused by secondary renal or splenic infarction
- septic embolisation
- abscess formation
- CHF and syncope from arrhythmias (ventricular arrhythmia 62% of cases)
34
What are physical examination findings IE?
- lack of specific clinical signs
- heart murmur, pyrexia (50-90%), and lameness are considered classical signs
- Aortic insufficiency - diastolic murmur and bounding peripheral pulse
- Sytolic Murmur due to destruction of mitral valve causing Mitral Regurgitation, or vegetation’s obstructing the aortic outflow tract leading to stenosis.
- 26% don’t have murmur
- 34% lameness
- pain
- cold extremities
- cyanosis
- Skin necrosis
- neurological problem
35
What are the echo findings of a dog with IE?
- hyperechoic valvular vegetation’s, irregularly outlined, and can move independent of the alive.
- erosive lesions are hard to see, but aortic regurgitation should raise suspicion of aortic IE
36
What are the ECG findings of IE?
- Arrhythmia in 50-75% of dogs with IE
- VPC’s & tachyarrhythmia but is usually not life-threatening
- ST-segmentdeviation guest myocardial hypoxia and indicate coronary artery embolism or myocardial is he is of other aetiologies
37
What are the radiographic findings of IE?
- no specific findings
- chronic IE with aortic or mitral insufficiency, left sided cardiac enlargement may be detected
- 50% of dogs with IE present with CHF, as indicated by perhilar and caudodorsal pulmonary infiltrates
- LA enlargement absent in comparable large proportion of dogs with CHF (acute onset of valve leakage)
38
Why are blood cultures negative when trying to diagnose IE?
- 60-70% of blood cultures in dogs with IE reported to be negative.
- high proportion of negative samples can be due to dogs receiving antimicrobials, chronic ‘enacpsulated’ infections, non-infectious IE (only platelets and fibrin in vegetation) or failure to grow organisms from samples.
- bartonella can take 4 weeks to culture
- of positive cultures 90% of cultures will be in 72 hours, but some may take 10days
- PCR could be used to identify bacterial nuclei acid in blood, and increase likelihood of bacteremia
- microorganisms known to cause IE include:
Staphylococcus : S. Aureus, S. Intermedius, coagulate-positive, and coagulase-negative
Streptococcus: S. Canis, S. Boris, and beta-haemolytic
Bartonella
E.Coli
Pseudomonas Aeruginosa
Corynebacterium
Erysipelothrix rhusiopathiae
39
What are the expected laboratory findings for dogs with IE?
- 50-60% mild regenerative anemia
- Leukocytosis - 80% of dogs with IE, usually from neutrophilia and monocytes is (left shift)
- increase BUN +/- creatinine due to embolisation, metastatic infection, CHF, or immune-mediated disease
- increased ALP and hypoalbuminemia due to circulating endotoxins and reduced hepatic function.
- possibly decreased glucose and serological tests for immune-mediated diseases such as Coombs test, may be positive.
- Urinalysis reveal hemoglobinuria, hematuria, pyuria, bacteruria, +/- proteinuria
- urine culture should be performed
40
How is IE diagnosed?
Definite diagnosis is based on histopath; 2 major; or 1 major and 2 minor
Major criteria:
- echocardiogram: vegetative/erosive lesion or abscess
- Valvular insufficiency: > mild aortic insufficiency with our sub-aortic stenosis or annuloaortic ectasia
- Positive blood culture: 2 or more positive blood cultures, or 3 or more if common skin contaminant
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Minor criteria:
Fever
Med-large breed dog
Subaortic stenosis
Thromboembolic disease
Immune mediated: polyarthritis, glomerulonephritis
Positive blood cultures
Bartonella serology >1:1024
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41
How is IE managed?
IV broad-spectrum AB:
- timentin (ticarcillin and clavulanate) 50g/kg IV q 6h or impenetrable 10mg/kg IV q 8h
- Aminoglycoside: amikacin 20mg/kg q 24h combined with above. Patient should be supported with IV fluids.
- Furesemide is contraindicated as it enhances nephrotoxicity
- Enrofloxacin if gram negative IE suspected, or so furesemide can be given
- AB’s for at least 6weeks.
- If bartonella is cause then repeat serology in 1 month
42
What is the prognosis of IE?
Poor prognosis: late diagnosis and late treatment, aortic valve involvement, valvular vegetation, Bartonella, gram-negative infections, heart or renal complications, septic embolisation or metastatic infection, thrombocytopenia, increased ALP and hypoalbuminemia, treatment with steroids, bacteria static antibiotics, premature termination of ABs
Better prognosis: mitral valve involvement, gram-positive infections, infected skin, abscess, or wound
