Transcript Name of presentation

Practical Cardiology
Case Studies
Wendy Blount, DVM
Nacogdoches TX
Jake
Signalment
• 9 year old male Boxer
Chief Complaint
• Deep cough when walking in the morning, for
about one week
• Appetite is good
Jake
Exam
• Weight 81.9 – has lost 5 pounds in 3 months (BCS 5/9)
• Temp 101.4
• Mucous membranes pink, CRT 3.5 seconds
• Subtle dependent edema on the lower legs
• Jugular veins distended
• Harsh lung sounds
• 3/6 pansystolic murmur, PMI left apex (link)
• Heart rate 160 per minute
• Respirations 55 per minute
• Femoral pulses somewhat weak
Jake
Differential Diagnosis - Cough
• Respiratory Disease
• Cardiovascular Disease
• Both
Diagnostic Plan (B Client)
• Blood Pressure
– 150 mm Hg systolic (Doppler)
• Chest x-rays
Jake
Jake
Jake
Diagnostic Plan (B Client)
• Chest X-rays
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Massively enlarged heart (VHS 12.5)
Enlarged LA, LV (dorsally elevated trachea)
Enlarged pulmonary arteries and veins
Perihilar pulmonary edema
Left congestive heart failure
Right congestive heart failure (biventricular failure)
Jake
Immediate Therapeutic Plan (10 am)
• Furosemide
– 80 mg IM
• 4 hours later
– Respiratory rate is 36 per minute
Jake
Diagnostic Plan – 2nd Wave (2 pm)
• EKG
Jake
Diagnostic Plan – 2nd Wave (2 pm)
• EKG
• Rate – 140 bpm
• Rhythm – sinus rhythm – P wave abnormal
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Early and upside down
Followed by a normal QRS
Occurring 5 times a minute
APC – Atrial Premature Contractions
Supraventricular premature contractions
Jake
Diagnostic Plan – 2nd Wave (2 pm)
• EKG
• Echocardiogram
(video 1)
(video 2)
Jake - Echo
Transverse - LV Apex
• LV Looks Big
Transverse - LV Papillary Muscles
• LV looks REALLY big
• Myocardium is hardly moving
• Flat papillary muscles
Jake - Echo
Transverse - LV Papillary
Muscles
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IVSTD – 9.7 mm (n 10.8-12.3)
LVIDD – 72.1 mm (n 43-48)
LVPWD – 15.1 mm (n 8.7-10)
IVSTS – 11.9 mm (n 16.5-18.1)
LVIDS – 67.1 mm (n 27.4-30.4)
LVPWS – 13.0 mm (n 14-15.6)
FS = LVIDD – LVIDS
LVIDD
(72.1-67.1)/72.1 = 7%
(n 30-46%)
EF = 15%
(n >70%)
Jake - Echo
Transverse - Mitral Valve
• No increased thickness of MV
• No vegetations on the MV
• EPSS – 12 mm (n <6 mm) – myocardial failure
Transverse – Aortic Valve/RVOT
• LA at least Double Big
Jake - Echo
Transverse - Aortic Valve/RVOT
• AoS – 23.1 mm (n 27.4-30.4)
• LAD – 44.7 mm (n 25.8-28.4)
• LA:Ao = 44.7/23.1 = 1.9 (n 0.8-1.3)
Transverse – Pulmonary Artery
• No abnormalities noted
Jake - Echo
Long – 4 Chamber
• LV massively enlarged
• Poor systolic function
• LA 2x enlarged
• IVS is bowed toward the right, due to LV dilation
Long – LVOT
• No abnormalities in LVOT
Jake – Dx & Tx
Recommendations
• Congestive Heart Failure
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CBC, serum panel and electrolytes
Furosemide 80 mg PO BID
Enalapril 20 mg PO BID
Recheck mini-panel and electrolytes in 3-5 days
Recheck chest rads and BP 3-5 days
• Dilated Cardiomyopathy
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Thyroid panel (TSH, T4, FreeT4)
Pimobendan 10 mg PO BID (declined)
Carnitine 2 g PO BID
Recheck echo, chest rads, BP, EKG, mini-panel/lytes 60
days (sooner if respiratory rate >40 at rest)
Jake - Bloodwork
Carnitine for DCM
– Boxers with genetic defect need extra carnitine
– Plasma levels have low sensitivity
– Myocardial biopsy is usually required
CBC, Mini-panel - BUN, creat, glucose, TP, SAP, ALT
• Normal
Electrolytes, Thyroid panel
• Not done
Jake – Follow-Up
Recheck – 6 days
• BUN 30 (n 10-29)
• Creat normal
• Electrolytes not done
• Chest x-rays not done
No additional rechecks were done, owner did
not monitor respiratory rate at home
Jake – Follow-Up
4 months later…
• Chief complaint –
– Doing *very* well until last week
– poor energy, coughing again, not eating
• Heart sounds (audio file)
– Chaotic heart sounds with pulse deficits on
auscultation
– “tennis shoes in a dryer”
– Called “Delirium cordis”
Jake – Follow-Up
25 mm/sec
•Heart Rate
•200 bpm (tachycardia)
•Rhythm (NSR, RSA or arrhythmia)
•irregularly irregular - arrhythmia
Jake – Follow-Up
• P wave
(normal 1 box wide x 4 boxes tall)
• not present
• PR interval (normal 1.5-3.25 boxes)
• no P wave – can’t measure
• QRS
(normal 1.5 boxes wide x 30 boxes tall)
• 2 boxes wide x 26 boxes tall
• Wide QRS = LV enlargement
Diagnosis – Atrial Fibrillation
25 mm/sec
Jake – Treatment
• Recommended treatment
• Digitalis or Diltiazem for Afib
• Treatment was declined, and Jake was euthanatized 1
week later
• Most dogs with DCM are gone within 3 months of becoming
symptomatic, if treated with furosemide & ACE.
• Survival is likely much shorter – days to weeks – if untreated.
• Adding Pimobendan increases mean survival to 130 days.
• Median survival for dogs with DCM and Afib is 3 weeks,
without Pimobendan
Dilated Cardiomyopathy
Common Signalment
• Breed
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Doberman
Great Dane
Boxer
Newfoundland
Portuguese Water Dog
Dalmatian
Cocker Spaniel
• www.VetGen.com and NCState offer a DNA panel for
Dobermans to screen for DCM
Dilated Cardiomyopathy
Common Historical and PE findings
• Onset seems rather acute – signs of LHF
– Coughing, dyspnea, exercise intolerance, weak pulses, poor
appetite and energy
• Sometimes RHF also
– Ascites, pleural rubs, jugular vein distension, peripheral edema,
diarrhea
• Syncope
• Mitral murmur
– Holosystolic, PMI left apex
• Chaotic heart sounds with pulse deficits if A-fib
• Vegetarian diet (historical)
Dilated Cardiomyopathy
Common Historical and PE findings
• Chemotherapy
– doxorubicin
• DCM in a puppy
– Parvovirus at 2-4 weeks of age (historical)
– Chaga’s Disease – mostly right sided, with VPCs
• Trypanosoma cruzi
Dilated Cardiomyopathy
Common Radiographic Findings
• Generalized cardiomegaly - Increased VHS
• Enlarged LV – elevated trachea
• Enlarged LA – compressed left bronchus
• + RA/RV enlargement
• + Left Heart Failure – lobar veins > arteries,
pulmonary edema
• + Right Heart Failure – enlarged caudal vena
cava, ascites, pleural effusion,
hepatosplenomegaly
Dilated Cardiomyopathy
Common ECG Findings
• Wide P wave
– LA enlargement
• Tall R wave
– LV enlargement
• Atrial fibrillation
• VPCs
• Ventricular arrhythmias
Dilated Cardiomyopathy
Common Echocardiographic Lesions
• Dilation of all 4 heart chambers
• Large LVIDD (eventually large LVIDS also)
• Hypokinesis of LV wall and IVS
• Markedly Reduced FS & EF
• Paradoxical septal motion
• Increased EPSS
• Normal looking MV and TV leaflets
• Papillary muscle flattening
(Client Handout)
Dilated Cardiomyopathy
Treatment
• Pimobendan 0.2-0.3 mg/kg PO BID
– Inodilator – positive inotrope and vasodilator
• Treat left heart failure if present
– Diuretics
– ACE inhibitor if tolerated
• 0.5 mg/kg PO SID-BID
– Nitroprusside CRI if critical
– Dopamine or dobutamine CRI if critical
– Thoracocentesis if pleural effusion in cats
– Oxygen, of course
Dilated Cardiomyopathy
Treatment
• Furosemide boluses for fulminant LHF
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80% effective
6-8 mg/kg IV Q1-2 HR UNTIL RR<50
4 mg/kg IV q1-2h until RR<40
4 mg/kg PO q4-6 hr until RR<30
Then PO q6-12 hrs to maintain RR<30
Give IM if placing IV cath might be fatal
• Furosemide CRI may be more effective
– 0.5 to 1.0 mg/kg/hr
Dilated Cardiomyopathy
Torsemide
• *much* stronger diuretic than furosemide and
spironolactone
• Potassium sparing, like spironolactone
• 0.2-0.3 mg/kg PO BID
• For rescue – too powerful for routine use
• Will make ‘em a raisin, and create a swimming
pool in the living room
• Consider when >4mg/b/day furosemide is not
enough
Dilated Cardiomyopathy
Treatment
• Monitoring fulminant LHF
– Lactate (return to normal)
– blood gases (resolution of acidosis and
hypoxemia)
– Respiratory rate
– PROVIDE WATER & WATCH URINE
PRODUCTION
– Check BUN & electrolytes at least daily
– Central line can make blood draws easy
Dilated Cardiomyopathy
Treatment
• Taurine – if whole blood taurine levels low
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250-500 mg PO BID
Cats fed low taurine diets, or with genetic defect
American cocker spaniels, Newfoundlands
Dogs fed vegetarian diets
(Large and giant breed dogs fed lamb and rice diet)
Almost never Great Danes and Dobermans
• Carnitine – 500-1000mg PO BID
– Boxers with genetic defect
– Plasma levels have low sensitivity
– Myocardial biopsy is usually required
• Thyroxine – if hypothyroid
Dilated Cardiomyopathy
Beta Blocker Therapy
• Seems counterintuitive for DCM
– Negative inotrope
• In people, chronic stimulation of B1 receptors is
cardiotoxic
– Improved survival when people with myocardial
failure are put on beta blockers (carvedilol)
• No similar success with canine DCM
– Pharmacokinetics of carvedilol in dogs have been
studied, and are unpredictable
Dilated Cardiomyopathy
Monitoring patients in chronic LHF
• Chest x-rays and exam every 6 months
• Echocardiogram when chest x-rays change
– Every 6 months with cardiomyopathies
• ECG when arrhythmia ausculted, syncope, or if
disease which predisposed to arrhythmia
– Boxer cardiomyopathy
– Dilated cardiomyopathy
• Recheck sooner if RR at rest is >35-40 per
minute
Dilated Cardiomyopathy
Monitoring patients in chronic LHF
• BUN, creat
– 3-4 days after starting or increasing ACE inhibitor
– Every 6 months when doing well
– Sooner if things get worse
• Electrolytes and blood gases
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Every 6 months when doing well
Sooner if things get worse
Potassium supplementation is often necessary
Untreated hypokalemia can predispose to arrhythmia,
especially if on digitalis
Dilated Cardiomyopathy
Screening
• Predisposed dog breeds show decreased fractional
shortening for many years prior to onset of clinical signs
and/or murmur
– FS has to fall <15% to cause CHF
• Screening by echocardiogram at young adult to middle
age is effective.
– Interpretation of echo in mildly effected dogs can be challenging
• Some think a Holter monitor is more effective screening
– Especially for Boxers
• No one knows whether early intervention changes
outcome.
Atrial Fibrillation
What is it?
– Disorganized contraction of the atria
– Absence of effective atrial contractions
– AV node is bombarded
• Impulse makes it through to ventricles irregularly
• “irregularly irregular” rhythm
– Irregular ventricular rhythm
• More obvious at lower heart rates
– Irregular intensity of heart sounds due to erratic filling time
and volume
• More obvious at higher heart rates
• Pulse strength irregular with deficits
Atrial Fibrillation
What causes it?
– Anything that can cause enlarged LA
• Most common cause is DCM in dogs
• Also end stage MR progressing to myocardial failure
– Occasionally can be primary in very large dogs
• Very rare without underlying heart disease
– Less common in cats
• Advanced HCM with huge LA
Frequent APCs are a harbinger of Afib
Atrial Fibrillation
In people Afib comes in 4 flavors
– First detected episode
– Paroxysmal - terminates spontaneously in 2-7 days (2550%)
– Persistent - > 7 days, usually requires cardioversion to
stop (25%)
– Permanent - Fails to cardiovert or reverts within 24 hours
of cardioversion
Canine Afib is almost exclusively the permanent type
“Lone” Afib occurs in giant dogs with no cardiac defects
--12-30% of all, 20-45% of young dogs
--most go on to develop DCM
Atrial Fibrillation
– 30-35% of dogs with DCM and CHF have Afib at the time
of diagnosis
– Median survival for giant dogs with Afib on diagnosis of
DCM and CHF is 29 days
• Large breed dogs 36 days
• Spaniels 62 days
• Dobermans 9 days
– CHF + DCM with no Afib
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Giant – 64 days
Large – 164 days
Spaniels – 2 years
Dobermans – 56 days
Atrial Fibrillation
Treatment – Afib in unhealthy hearts
– Slow the heart rate at the AV node (goal 150 bpm)
– Digoxin
• Weak positive inotrope
– Beta blockers
• Negative inotrope
• Propranolol 0.1-0.2 mg/kg PO TID
• Titrate up to effect to 0.5 mg/kg PO TID
– Calcium channel blockers
• Diltiazem 0.5 mg/kg PO TID (titrate up to 1.5 mg/kg)
– Growing body of evidence that angiotensin II may promote
development of AFib
DON’T USE BETA BLOCKER AND CALCIUM CHANNEL
BLOCKER TOGETHER!!
Atrial Fibrillation
Why Treat??
• Heart rate around 250 beats per minute
– Myocardial failure will result within 3-6 weeks
– Ventricles can not fill properly – forward heart failure
Treatment
• Conversion would be ideal
• But this is not easy to accomplish in very sick hearts
• Can attempt in big dogs with normal hearts and primary
Afib, not dogs with DCM
– Can try medical conversion with quinidine
– Or Anesthesia and conversion with electric shock
Atrial Fibrillation
Atrial Fibrillation
Atrial Fibrillation
Boxer Cardiomyopathy
• Can be primarily ventricular arrhythmia
– VPCs or bursts of Vtach
• Can be primarily DCM
• Can have both
• If arrhythmia is primary, treatment of choice:
– Sotalol 1-3 mg/kg PO BID
– Beta blocker and class III antiarrhythmic
• Holter Monitor is more likely to diagnose than
echocardiogram
(Client Handout)
Jasper
Signalment:
• Middle Aged Adult Norwegian Forest Cat
• Male Castrated
• 13 pounds
Chief Complaint:
• Acute Dyspnea 1 day after sedation with ketamine
and Rompun for grooming
• Cannot auscult heart sounds well – muffled (audio)
• RR 75 per minute
Jasper
Immediate Diagnostic Plan:
• Lasix 25 mg IM – then in oxygen cage
• When RR <40, lateral thoracic radiograph
2 hrs later:
• RR 55 with oxygen off
• Put water and gel on hair over thorax, and
applied ultrasound probe
• Cat sternal on the table (video)
• Tapped 100ml pleural effusion (pink, opaque);
stopped when cat got stressed
Jasper
• Lasix 25 mg IM – back in oxygen cage
• Plan: When RR <40, lateral thoracic
radiograph, or tap more if we can’t get RR that
low with Lasix
4 hrs after intake (2 hrs later):
• RR 45 with oxygen off
• Tapped 100 ml more pleural fluid
• More stress – Jasper is angry 
• Lasix 12.5 mg IM – back in oxygen
Jasper
6 hrs after intake (2 hrs later):
• RR 35 with oxygen off
• Quick lateral chest x-ray allowed without too
much stress
• Regular vet tells me, “Oh, that cat is really
mean. We usually can’t touch him without
sedation.”
• I am glad we took an x-ray before I knew that
Jasper
6 hrs after intake (2 hrs later):
• RR 35 with oxygen off
• Quick lateral chest x-ray allowed without too
much stress
• Regular vet tells me, “Oh, that cat is really
mean. We usually can’t touch him without
sedation.”
• I am glad we took an x-ray before I knew that
Jasper
Differential Diagnosis – Pleural effusion
• Modified Transudate – Neoplasia, CHF
• Exudate – Blood, Pyothorax, FIP
• Chylothorax
(chart)
Jasper
Initial Therapeutic Plan:
• Thoracocentesis
• Tapped both right and left thoraces
• Removed 400 ml of pink opaque fluid that
resembled Pepto bismol
• Fluid had no “chunks” in it
Differential Diagnosis – updated
• Pyothorax
• Chylothorax
Jasper
Initial Diagnostic Plan:
• Fluid analysis
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Total solids 5.1
SG 1.033
Color- pink before spun, white after
Clarity – opaque, even after spun
Nucleated cells 8500/ml
RBC 130,000/ml
HCT 0.7%
Jasper
Initial Diagnostic Plan:
• Fluid analysis
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Lymphocytes 5600/ml
Monocytes 600/ml
Granulocytes 2300/ml
No bacteria seen
Triglycerides 1596 mg/dl
Cholesterol 59 mg/dl
chart
Likely Chylothorax (need to run serum TG/chol)
Jasper
DDx Chylothorax
• Trauma – was chewed by a dog 2-3 mos ago
• Right Heart Failure
• Pericardial Disease
• Heartworm Disease
• Neoplasia
– Lymphoma
– Thymoma
• Idiopathic
Jasper
Diagnostic Plan - Updated
• PE & Cardiovascular exam
• CBC, general health profile, electrolytes
• Occult heartworm test
• Post-tap chest x-rays
• Echocardiogram
Jasper
Exam
• Temp 100, P 180, R 48, BCS 3, BP 115
• 2/6 late systolic murmur (audio)
• Anterior mediastinum compressible
• Some pleural rubs still present
• No jugular pulses, no hepatojugular reflux
• Peripheral pulses slightly weak
• Mucous membranes pink, CRT 3 sec
Jasper
Bloodwork
• Occult Heartworm Test - negative
• CBC – normal
• GHP, T4 – normal except
– Glucose 134 (n 70-125)
– Cholesterol 193 & TG 137 (both normal)
Chest X-rays
• Post-tap chest x-rays
Jasper
Bloodwork
• Occult Heartworm Test - negative
• CBC – normal
• GHP –
– Glucose 134 (n 70-125)
– Cholesterol 193 & TG 137 (both normal)
Chest X-rays
• Post-tap chest x-rays
Jasper
Chest X-rays
• Minimal pleural effusion
• No cranial mediastinal masses
• Normal cardiac silhouette (VHS 7.5)
• Normal pulmonary vasculature
• Lungs remain scalloped
Jasper – Echo
Short Axis – LV apex
• No abnormalities noted
Short Axis – LV PM
Jasper – Echo
Short Axis – LV apex
• No abnormalities noted
Short Axis – LV PM
Jasper – Echo
Short Axis – LV apex
• No abnormalities noted
Short Axis – LV PM
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No abnormalities noted
IVSTD – 8.8 mm (n 3-6)
LVIDD – 16.2 mm (normal)
LVPWD – 7.2 mm (n 3-6)
IVSTS – 9.8 mm (n 4-9)
LVIDS – 10.5 mm (normal)
LVPWS – 10.1 mm (n 4-10)
FS – 35%
Jasper – Echo
Short Axis – MV
• No abnormalities noted
Short Axis – Ao/RVOT
Jasper – Echo
Short Axis – MV
• No abnormalities noted
Short Axis – Ao/RVOT
Jasper – Echo
Short Axis – MV
• No abnormalities noted
Short Axis – Ao/RVOT
• Smoke in the LA
• AoS – 11.7 mm ( normal)
• LAD – 10.5 (normal)
• LA/Ao – 0.9 (normal)
Jasper – Echo
Short Axis – PA
• Difficult to evaluate due to acoustic shadows
Long Axis – 4 Chamber
Jasper – Echo
Short Axis – PA
• Difficult to evaluate due to acoustic shadows
Long Axis – 4 Chamber
Jasper – Echo
Short Axis – PA
• Difficult to evaluate due to “rib shadows”
Long Axis – 4 Chamber
Jasper – Echo
Short Axis – PA
• Difficult to evaluate due to “rib shadows”
Long Axis – 4 Chamber
Jasper – Echo
Short Axis – PA
• Difficult to evaluate due to “rib shadows”
Long Axis – 4 Chamber
Jasper – Echo
Short Axis – PA
• Difficult to evaluate due to “rib shadows”
Long Axis – 4 Chamber
Jasper – Echo
Short Axis – PA
• Difficult to evaluate due to “rib shadows”
Long Axis – 4 Chamber
Jasper – Echo
Short Axis – PA
• Difficult to evaluate due to “rib shadows”
Long Axis – 4 Chamber
• Hyperechoic “thingy” in the LA, with smoke
Long Axis – LVOT
• Aortic valve seems hyperechoic, but not
nodular
• 2-3 cm thrombus free in the LA
Jasper – Echo
Short Axis – Ao/RVOT - repeated
• LA 2-3x normal size, with Smoke
• AoS – 11.7 mm ( normal)
• LAD – 29 mm (n 7-17)
• LA/Ao – 2.5 (n 0.8-1.3)
Jasper – Echo
Therapeutic Plan - Updated
• Furosemide 12.5 mg PO BID
• Enalapril 2.5 mg PO BID
• Rutin 250 mg PO BID
• Low fat diet
• Plavix 18.75 mg PO SID
• Lovenox 1 mg/kg BID
• Fragmin 1 mg/kg BID
• Clot busters may only send the clot sailing
Jasper – Echo
Recheck – 1 week
• Jasper doing exceptionally well –back to
normal.
• Lateral chest radiograph
Jasper – Echo
Recheck – 1 week
• Jasper doing exceptionally well –back to
normal.
• Lateral chest radiograph
Jasper – Echo
Recheck – 1 week
• Jasper doing exceptionally well –back to
normal.
• Lateral chest radiograph
• Jasper declined all other diagnostics, without
deep sedation/anesthesia
• Will do BUN, Electrolytes, BP, recheck echo to
assess thrombus in one month
Jasper – Echo
Recheck – 1 month
• Jasper doing exceptionally well
• Lateral chest radiograph – no change
• Jasper declined all other diagnostics, without
deep sedation/anesthesia
• Will do BUN, Electrolytes, BP, recheck echo to
assess thrombus at 6 month check-up.
Jasper – Echo
Recheck – 6 months
• Jasper doing exceptionally well
• BP – 140, chest x-rays no change
• Jasper declined all other diagnostics, without
deep sedation/anesthesia
• May never do BUN, Electrolytes, recheck echo
• Jasper hates my guts, forever
• He wants to kill me in my sleep
Jasper – Echo
Long Term Follow-up
• Jasper still doing well 18 months later
• On lasix & enalapril only
• At 2 years, owners decided Jasper didn’t need
heart meds anymore, so they stopped giving them
• Jasper was asymptomatic for one year after that
• Attacked and killed by dogs 3 years after initial
diagnosis
• On necropsy, Jasper’s heart weighed 31g
– The normal adult cat heart should be <20g
Hypertrophic Cardiomyopathy
Clinical Characteristics
• Diastolic dysfunction – heart does not fill well
• Poor cardiac perfusion
• Most severe disease in young to middle aged
male cats
• Can present as
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Murmur on physical exam
Heart failure (often advanced at first sign)
Acute death
Saddle thrombus
Hypertrophic Cardiomyopathy
Radiographic Findings
• + LV enlargement
– Elevated trachea, increased VHS
• LA + RA enlargement seen on VD in cats
• + LHF
– Pleural effusion
– Pulmonary edema
– Lobar veins >> arteries
Hypertrophic Cardiomyopathy
Echocardiographic Abnormalities
• Echo required in order to make diagnosis
• LV and/or IVS thicker than 8-10 mm in diastole
• LVOT view (video) – early HCM no LA enl
• Symmetrical or asymmetrical
– only a thick IVS (video)
– primarily very thick papillary muscles (video)
– Primarily apical
Hypertrophic Cardiomyopathy
Echocardiographic Abnormalities
• Echo required in order to make diagnosis
• LV and/or IVS thicker than 8-10 mm in diastole
• Symmetrical or asymmetrical
– only a thick IVS (video)
– primarily very thick papillary muscles (video)
– Primarily apical
Hypertrophic Cardiomyopathy
Echocardiographic Abnormalities
• Echo required in order to make diagnosis
• LV and/or IVS thicker than 8-10 mm in diastole
• Symmetrical or asymmetrical
– only a thick IVS (video)
– primarily very thick papillary muscles (video)
– Primarily apical
Hypertrophic Cardiomyopathy
Echocardiographic Abnormalities
• Echo required in order to make diagnosis
• LV and/or IVS thicker than 9-10 mm in diastole
• Symmetrical or asymmetrical
– only a thick IVS (video) (M-mode)
– primarily very thick papillary muscles (video)
– Primarily apical
• LVIDD usually normal to slightly reduced
• FS normal to increased, unless myocardial failure
developing (Jasper), or unclassified CM (UCM)
• LVIDS sometimes 0 mm
Hypertrophic Cardiomyopathy
Echocardiographic Abnormalities
• LA often enlarged
• RA sometimes also enlarged
• “Smoke” may be seen in the LA
• Rarely a thrombus in the LA
• Transesophageal US more sensitive at
detecting LA thrombi
• Borderline thickened LV should not be
diagnosed as HCM without LA enlargement
Hypertrophic Cardiomyopathy
Echocardiographic Abnormalities
• HOCM with SAM
– Hypertrophic Obstructive CardioMyopathy with
Systolic Anterior Motion
– Septal leaflet of the MV get sucked up into the LVOT
during systole rather than closing the MV caudally
– Results in two compounded systolic murmurs
• Aortic turbulence due to functional SAS
• Mitral regurgitation
– SAM and its murmur can be intermittent
(video B mode)
(video Doppler)
Hypertrophic Cardiomyopathy
DDx LV thickening
• Hypertension
• Hyperthyroidism
• (Chronic renal failure)
• Only HCM causes severe thickening of LV
• HCM due to hyperT4 resolves with treatment
– CHF is rare, treat with atenolol until resolved
Dogs can rarely have HCM
• Cocker spaniels
Hypertrophic Cardiomyopathy
Treatment
• Manage heart failure
– Therapeutic thoracocentesis in a crisis
– Diuretics
– ACE inhibitors
• Beta blockers – if persistent tachycardia
• Calcium channel blockers – if thickening
significant
• Treat hypertension if present
Hypertrophic Cardiomyopathy
Follow-Up
• Q6month rechecks
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Chest x-rays
CBC, GHP, electrolytes, blood gases
ECG if arrhythmia ausculted or syncope
BP
• Sooner if RR >40 at rest
• Sooner if any open mouth breathing ever
Hypertrophic Cardiomyopathy
Screening
• Genetic test is available at NCSU
• Auscultation not always sensitive
• Echocardiogram can detect early in breeds
predisposed
• No evidence that early intervention changes
outcome
(Client Handout)
Hypertrophic Cardiomyopathy
HCM and Pimobendan
• It seems counterintuitive to treat HCM cats with
pimobendan
• Positive inotrope *should* increase myocardial
oxygen demand, and is not necessary
• Case-control study of the effects of pimobendan on survival time in
cats with hypertrophic cardiomyopathy and congestive heart
failure. J Am Vet Med Assoc. September 1, 2014;245(5):534-9.
Yamir et al. NCSU.
Hypertrophic Cardiomyopathy
HCM and Pimobendan
• All cats had HCM and CHF - retrospective
• Those treated with pimobendan had
significantly longer survival than those treated
with other drugs
• Median survival for pimobendan cats 635 days
• Median survival for other cats 103 days
Hypertrophic Cardiomyopathy
HCM and Pimobendan
Mark Rishniw, DACVIM cardiology
• There are several major flaws with this paper -that's the consequence of a retrospective study.
• I would be very cautious about adopting this as
"standard of care" for cats with CHF.
Hypertrophic Cardiomyopathy
HCM and Pimobendan
Mark Kittleson, DACVIM cardiology
• as soon as pimobendan came on the market, veterinary
cardiologists started administering it to cats in heart
failure.
• Some avoided using it in cats with HCM while others
did not.
• Instead, when they found out it didn't kill these cats and
they perceived some benefit they initially tried to publish
data to show the drug was beneficial.
Hypertrophic Cardiomyopathy
HCM and Pimobendan
Mark Kittleson, DACVIM cardiology
• This latest paper is an attempt to do a clinical trial but in
a retrospective fashion, one that brings in all sorts of
potential bias.
• Layered on top of this is a pharmacokinetic paper that
shows that when you give a dog dose to a cat the
serum concentration of the parent compound
(pimobendan) is 10 times as high as that seen in dogs
and the active metabolite (desmethylpimobendan) may
not be present.
Hypertrophic Cardiomyopathy
HCM and Pimobendan
Mark Kittleson, DACVIM cardiology
• Pimobendan is a calcium sensitizer while
desmethylpimobendan is primarily a PDEIII inhibitor.
• A 10X dose of a calcium sensitizer should turn the heart
to stone (constant state of systole).
• Since the drug doesn't kill cats that it's reasonably clear
that pimobendan does something very different in cats
when compared to dogs.
Hypertrophic Cardiomyopathy
HCM and Pimobendan
Mark Kittleson, DACVIM cardiology
• In an ideal world we would go back to square one - do
the pharmacokinetic and pharmacodynamic studies in
cats that should have been done years ago and then do
a proper prospective clinical trial.
• Instead we're all sneaking in through the back door
that's been left open by the drug company and
regulatory agencies.
• The front door is closed because the drug company has
no incentive to fund a prospective clinical trial.
Pleural Effusion
• Usually caused by biventricular failure in the dog
– Parietal pleura veins drain into the R heart like the
systemic veins
– Visceral pleura veins drain into the L heart with the
pulmonary veins
• RHF alone can cause pleural effusion in dogs
• LHF alone almost never causes pleural effusion
in dogs, but often does in cats
– Cats in LHF will often have pleural effusion but no ascites
– Dogs in RHF will often have pleural effusion and ascites
Summary
• PowerPoint – Cases – Cardiomyopathies
• .pdf of PowerPoint – Cases Cardiomyopathies
• Fluid Analysis Chart
• Client Handouts
– Feline Cardiomyopathy
– Dilated Cardiomyopathy
– Boxer Cardiomyopathy