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Cardiology - Myxomatous Mitral Valve Degeneration: What's New? By Rita Singh

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Cardiology - Myxomatous Mitral Valve Degeneration: What's New? By Rita Singh

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Cardiology - Myxomatous Mitral Valve Degeneration: What's New? By Rita Singh

  1. 1. Dr Rita Singh BSc, BVMS, DipVetClinStud, FANZCVS, Dip ACVIM (Cardiology)
  2. 2.  Most common heart disease of dogs  Toy poodle, Maltese, ShihTzu, Dachshund, Miniature Schnauzer, Chihuahua,Yorkshire Terrier,Whippet,  CKCS: 50% affected by 7 years  Large breeds: GSD, Doberman, ACD, Dalmation, X’s
  3. 3.  Mitral valve apparatus:  Valve leaflets  Annulus  Chordae tendinae  Papillary muscles
  4. 4.  Mucopolysaccarides  Appearance of embryonic mesenchymal tissue  Collagen degeneration  Endothelial proliferation
  5. 5. • Pathology alters valve motion: • Valve thickening • Prolapse • Annular dilation • Mitral regurgitation
  6. 6. Murmur Grading  Soft murmur (grades I-III) = mild disease  Loud murmur (grade IV-VI) = mild, moderate or severe disease
  7. 7.  Grading of murmurs:  I:Very soft. Only heard in a quiet room with concentration  II: Faint but easily heard  III: Moderately loud but localized to a single area  IV: Loud and radiates over the chest  V: Loud. Palpable thrill  VI:Thrill. Heard with stethoscope just off chest
  8. 8.  Location is important to differentiate cause  Mitral murmur: best heard at the left apex: where you can palpate the apex beat  Left basilar murmur: SAS, PS, hyperdynamic state
  9. 9.  Slow disease progression  558 dogs followed over ~ 3 yrs  60% alive or died of non cardiac related causes  Can be benign  CKCS?  Kvart et al JVIM 2002  Mean time to CHF 27 months
  10. 10.  Baroreceptors detect reduced CO  Stimulate SNS  HR and contractility  Arteriolar constriction  Normalizes haemodynamics
  11. 11.  β1 receptors down- regulate  CHF – approx 50% can’t stimulate  Improved rate and contractility diminishes  What now??
  12. 12.  BP  β1 stimulation  Renal perfusion  Na+ resorption Stimulates renal release of renin
  13. 13. Renin – Angiotensin – Aldosterone System Sympathetic efferent activity Diuretics Na to distal tubule Renal perfusion K+, Ca++ PGl ANP Renin release Angiotensinogen (liver) Angiotensin I (lung) Angiotensin II ACE Thirst Vasoconstriction Na retention Aldosterone secretion (adrenal) ADH secretion (pituitary)
  14. 14.  Progression forward SV  LA pressure  Pulmonary capillary pressure  Pulmonary oedema  Medication is essential
  15. 15.  CHF results from SEVERE heart disease  Treatment NOT required with mild disease  Exception: acute chordal rupture
  16. 16.  Once in heart failure:  Average survival 12 months  Large breed dogs: ~ 6 months?  Take Home Message!!  Reconsider diagnosis if your CHF patient is running around and happy 4 yrs later
  17. 17.  Penny  9y FS CKCS X Maltese, 8 kg  Presenting complaint: Coughing  1-2x/day for 2 years  8-10x/day for 6 months  Current treatment:  Frusemide 20 mg q 12 hrs  Pimobendan 2.5 mg q 12 hrs  Benazepril 2.5 mg q 24 hrs  Spironolactone 25 mg q 12 hrs
  18. 18.  T: 37.9  HR 100 bpm  PR 100 bpm  Resp sinus arrhythmia  RR 24, eupneac  MM pink, CRT 1 sec, tacky  Grade IV/VI left apical systolic murmur
  19. 19.  Signalment and murmur consistent with MMVD  IV/VI murmur could be consistent with CHF  HR, sinus arrhythmia, and RR are not consistent with CHF  Long history of cough suggests chronic airway disease  Plan: Chest xrays, Echocardiogram, Blood Work
  20. 20.  Stopped cardiac medications  Doxycycline 5 mg/kg bid 3 weeks  Theophylline 10 mg/kg bid 3 weeks  Bronchoscopy
  21. 21. 1. 100% collapse left cranial lobar bronchus 2. 100% collapse left caudal lobar bronchus 3. 100% collapse right middle lobar bronchus
  22. 22.  Staging disease  Assessing severity  Assessing cause cough  Assessing possibility and severity of CHF
  23. 23.  MMVD:  Diagnosis?  Severity  Chordal rupture  Pulmonary hypertension  Left atrial tear  NOW ALMOST ESSENTIAL for staging of the disease (EPIC)
  24. 24.  NYHA, ISACHC  ACVIM Consensus Statement*  A: High risk of developing MMVD but don’t currently have the disorder  B1: Has structural disease, asymptomatic, no cardiac remodelling  B2: Asymptomatic but has left heart enlargement  C: Has had congestive heart failure (past or current)  D: End stage disease. Refractory to standard therapy * Guidelines for the Diagnosis and Treatment of Canine Chronic Valvular Heart Disease, Atkins et al, JVIM 2009
  25. 25.  Stage A: Preclinical stage  Dogs such as the CKCS and other small breed dogs  At high risk of developing MMVD  Don’t yet have clinical evidence of the disorder  No treatment
  26. 26.  Stage B1: Has structural disease  Heart murmur  No clinical signs  No evidence of cardiomegaly (echo or rads)  No treatment
  27. 27.  Stage B2: Typical murmur of MMVD  Asymptomatic  BUT has evidence of cardiomegaly – radiographicAND echocardiographic  Treatment is now indicated  Pimobendan 0.25 mg/kg bid
  28. 28.  Stage C is the patient with clinical signs of CHF (past or current) associated with severe MMVD  Long term treatment is ALWAYS indicated
  29. 29.  Older than 7 yrs and < 15 kg  Loud murmur (IV/VI or >)  Sinus arrhythmia absent  Tachycardic (HR >120 bpm)  Dyspneac (sleeping RR > 30) **Cough on its own is not considered a sign of congestive heart failure** * Beijerink, Campbell, Gavaghan, Singh and Wooley. Published online via Vetforum, Boehringer Ingelheim, 2015
  30. 30.  O2 and frusemide before echo!  Body weight – need to lose 7-10% BW  Renal panel, urinalysis prior if possible
  31. 31.  Tachypnea (RR 40-60)  Dyspnea +/- cough  Tachycardic (>120 bpm)  Loud mitral murmur (>IV/VI)  Cardiomegaly and pulmonary oedema  Frusemide, ACEI, Pimobendan
  32. 32.  Loop diuretic  Effective  Many routes/doses  Mild –mod HF: 1-3 mg/kg q 8-12 hr  Severe/refractory: 4 mg/kg q 8 hr  Very few side affects
  33. 33.  Blocks conversion of AgI AgII  Decreases plasma aldosterone  Mild arteriolar/venous dilation  Less Na+/H2O retention  Reduces pathologic remodelling/ fibrosis  No evidence for use prior to CHF  Benazepril 0.25-0.5mg/kg sid Angiotensin I (lung) Angiotensin II ACE
  34. 34.  Increases binding affinity of calcium to cTNc  Inhibits cardiac PDE III → reduces breakdown of cAMP → increase ß stim  Improves myocardial contractility/ relaxation  Vasodilation  Antiplatet/ antiinflammatory?
  35. 35.  End stage disease  Refractory to standard therapy:  Frusemide 4mg/kg POTID  Pimobendan 0.25 mg/kg PO BID  Benazepril 0.25 mg/kg PO SID
  36. 36.  Sleeping RR > 40 breaths/min  Spironolactone 2 mg/kg bid  Hydrochlorothiazide 1mg/kg 2x/week* - 2 mg/kg bid  Pimobendan 0.3 mg/kgTID  +/- antiarrhythmics (AF, SVT,VPCs)  +/- hydralazine or amlodipine  +/- sildenafil (only if severe PHT) * Unpublished dose. Must monitor renal parameters
  37. 37.  Benazepril/ pimobendan (Fortekor Plus)  Benazepril/ spironolactone (Cardalis)  ‘Bespoke’ combinations (frusemide/benazepril/pimobendan)
  38. 38.  Medical emergency  Markedly dyspneac and hypoxemic  Coughing white/blood tinged froth  RR >100 breaths/min  HANDLE GENTLY
  39. 39.  O2  Baseline RR, body weight  IV frusemide 4-6 mg/kg q30-60mins or CRI till RR < 60 OR lost 10% BW  Delay radiographs/ echocardiography  Consider arteriolar dilators: oral hydralazine, IV nitroprusside (BP)  Positive inotropes: dobutamine or pimobendan (single daily dose IV)
  40. 40.  Procedure of choice – humans  Replacement - potential for thrombosis  Lifelong anticoagulant therapy  Repair preferred
  41. 41. Difficult in dogs:  Very few trained veterinarians  AU ~ $30,000 - $60,000  Requires cardiopulmonary bypass  High mortality* * Other than if performed by a single Japanese surgeon
  42. 42.  11 yo FS Poodle X  Presented to me for evaluation of a murmur  12 months ago grade II/VI  At presentation grade IV/VI  Needs surgical evaluation of left cranial cruciate rupture
  43. 43.  10 kg  HR 100 bpm, PR 100 bpm  Grade IV/VI left apical systolic murmur  RR 24 breaths/minute  Lame left hind  Hx and PE consistent with MMVD
  44. 44. LA:Ao 1.63 LVIDd 3.7 (2.7-3.4)
  45. 45.  3 weeks lethargy  Decreasing appetite  RR 100 breaths/minute  Soft gag/ cough  HR 160 bpm  Grade IV/VI murmur
  46. 46.  LA:Ao 2.4 (<1.5)  LVIDd 4.28 (2.5-3.2)  Severe MR  MildTR  MMVD stage C
  47. 47.  10 kg  Frusemide 20 mg bid (2 mg/kg bid)  Pimobendan 2.5 mg bid (0.25 mg/kg bid)  Benazepril 2.5 mg sid (0.25 mg/kg sid)  Renal profile 1 week later unremarkable  BAR, RR 24, HR 120 bpm
  48. 48.  Presented to ICU quiet, inappetant  RR 88 breaths/minute, cyanotic  HR 230 beats, irregularly irregular  O2  Frusemide 4 mg/kg hrly till RR < 60  Then 4 mg/kg 4 hrly  ECG
  49. 49. Discharged on frusemide 30 mg bid, pimobendan 2.5 mg bid, benazepril 2.5 mg sid
  50. 50.  Recurrence of dyspnea  Sinus rhythm  Increased frusemide to 30 mg po tid  Ebony doing well – owners reduced frusemide to 20 mg bid  ** DO NOT DOTHIS!!**
  51. 51.  5 months post initial presentation  3 months post initial CHF  Dyspnea  Inappropriately reduced frusemide  Medications 3 hrs late  Disease progression  RR 140 breaths/minute, dull, cynaotic  HR 100*, marked pulm crackles  No response to IV frusemide boluses  Critical, cardiorespiratory arrest close
  52. 52.  O2  Frusemide 6 mg/kg bolus IV  CRI 3 mg/kg/hr  Nitroprusside 5 ug/kg/min*  Gradually improved over 12 hrs  Weaned down overnight  Both CRI’s discontinued after 24 hrs  Frusemide 3 mg/kg IV q 3hr for 24 hrs  Ventilation? * Continuous BP monitoring essential
  53. 53.  Renal profile  K+ 2.8 (3.5-5.8)  BUN 22 (2.5-9.6)  Creat 145 (22-159)  Discharged  Frusemide 30 mg POTID  Pimobendan 2.5 mg PO BID  Benazepril 2.5 mg PO SID  Spironolactone 25 mg PO SID*  Kgluc 4 mEq BID* * New medications
  54. 54.  CHF  9.0 kg  Frusemide 40 mgTID*  Spironolactone 25 mg BID*  + Hydrochlorothiazide 6.25 mg PO EOD  2 weeks later – mildly increased RR  BP 154 mm Hg  + Amlodipine 2.5 mg po sid * Maximum dose
  55. 55.  Stage D MMVD, 9 kg dog  Frusemide 40 mg POTID  Spironolactone 25 mg PO BID  Hydrochlorothiazide 6.25 mg PO EOD  Pimobendan 2.5 mg PO BID  Amlodipine 2.5 mg PO SID  Benazepril 2.5 mg PO SID  Kgluc 4 mEq PO BID
  56. 56.  Stable for 3 months  Represented 6 months post initialCHF  Dyspnea (RR 60 breaths/minute)  FrusemideCRI 1 mg/kg/hr  Hydrochlorothiazide 12.5 mg PO sid  Recheck 1 week later – 1st syncopal episode  HR 120 bpm, RR 42 (stressed, post syncope), mm pale
  57. 57.  Arrhythmia - tachy or bradyarrhythmia  Severe MR - hypotension  Recurrence of CHF  Pulmonary hypertension  Left atrial tear
  58. 58.  ECG – sinus tachycardia 150 bpm  BP 80-100 mm Hg (systolic)  Echocardiogram  Severe MR: LA/Ao 3.0  LVIDd 5.0 cm (2.5-3.1)  Moderate pulmonary hypertension (TR PG 68 mm Hg)  No pericardial effusion (to suggest left atrial tear)
  59. 59.  Pulmonary arteriolar constriction secondary to pulmonary venous hypertension  Exacerbates mild right heart disease  Cx – diuretic refractory ascites, exercise intolerance, syncope  Dx: PA cath (gold standard) or echo (needTR or PI) 25 25 5
  60. 60.  Dyspnea  Renal profile:  BUN 76 (2.5-9.6)  Creatinine 243 (44-159)  Increased:  Frusemide 40 mg qid  Hydrochlorothiazide 25 mg am, 12.5 mg pm  K+ 4 mEq bid  Discontinue benazepril  Thin body condition – Omega 3 FA’s
  61. 61.  RR 28 breaths/min  Reducing appetite  Syncope with exertion  Current medications (8kg):  Frusemide 40 mg po qid  Pimobendan 2.5 mg po tid  Spironolactone 25 mg po bid  Hydrocholorthiazide 25 mg am, 12.5 mg pm  Kgluc 4 mEq bid  Amlodipine 2.5 mg sid
  62. 62.  Blood work  BUN 36 (3.8-7.9)  Creat 187 (44-159)  BP: 105 mm Hg  Echocardiogram  LA:Ao 3.2  LVIDd 5.15 (2.5-3.1)  TRVmax 4.5 m/s, PG 85 mm Hg (severe PHT)  + sildenafil 6.25 mg PO bid
  63. 63.  3 collapsing episodes today  Subdued  Inappetant and vomiting  HR 160 bpm, weak pulses  RR 60, moderate effort  MM muddy grey  Dull
  64. 64.  BP 88/40  BUN 90 (2.5-9.6)  Creat 240 (44-159)  Dehydration vs renal failure?  Treatment options:  Stop frusemide  IV fluids??
  65. 65. What now?

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