<<

2019 SUMMER MEETING

Friday June 21, 2019 Burlington Hilton Hotel

Suzanne Cunningham, DVM, DACVIM and Emily Karlin, DVM, DACVIM Tufts University, Cummings School of Veterinary Medicine [email protected] [email protected]

UPDATES IN SMALL CARDIOLOGY

Generously sponsored by:

HOLD THE DATES!

2020 Winter Meeting – Saturday and Sunday, February 8-9 – Burlington Hilton Hotel • Small Animal Speakers TBA • Equine Ophthalmology – Saturday, February 8 – Dr. Alison Clode • Bovine Speaker TBA

2020 Summer Meeting – Friday, June 19 – Burlington Hilton Hotel

Stay tuned for more details

Thanks for being a VVMA member! We are pleased to welcome the following members who joined since our 2019 Winter Meeting

Kathryn Hazzard – Norwich Regional Animal Hospital Laura Jesseman – Ryegate Small Animal Hospital Amanda LaCroix – River Cove Animal Hospital Allana Mather – Mt. Mansfield Animal Hospital Samuel Scheu – Riverbend Veterinary Clinic Elizabeth Wheeler – River Road Veterinary Clinic

VVMA Mission: Promoting excellence in veterinary medicine, animal well-being and public health through education, advocacy and outreach.

VVMA Vision: VVMA Values: To be the preeminent authority on Integrity, Service, Dedication, Compassion, veterinary medicine and animal well- Inclusivity, Visionary Thinking, Life-Long being in Vermont. Learning

For questions or more information on the VVMA, visit www.vtvets.org or contact Executive Director Kathy Finnie at [email protected] 2019 Summer Meeting Vendors Thank you for your support of our Meeting!

Bank of America Sean Coyle [email protected]

Blue Buffalo Nat Lacey [email protected]

Boehringer-Ingleheim Paige Willson [email protected] Heather Tarmey [email protected]

Burlington Emergency & Whitney Durivage [email protected] Veterinary Specialists

Christian Veterinary Mission Dr. Amy St. Denis [email protected]

Companion Animal Health by LiteCure Kevin Gouvin [email protected]

Eastern States Compounding Pharmacy Kim Johnson [email protected]

Hill’s Nutrition Dr. Andrew Hagner [email protected]

IDEXX Carmelita Castellon [email protected] Colin Dudunake [email protected] Dr. Maryse Osborn-Doser [email protected]

Jorgensen Laboratories Marnie Ciquera [email protected]

MWI Animal Health Danielle Preece [email protected]

Nestle Purina Lauren Koron [email protected]

Nutramax Laboratories Connie Hayes [email protected]

Stokes 503b Tamara Langreich [email protected]

U.S. Drug Enforcement Administration Christopher Paquette [email protected] George Lutz [email protected]

Universal Imaging Michael McElhinney [email protected]

VetCor Jessica Bird [email protected] Bryan Brackett [email protected]

Vetri-Science Laboratories Kelley Lucarell [email protected] Steve Parent [email protected]

Wilcox Pharmacy Tina Rotella [email protected]

Wingate Pharmacy & Compounding Gary Wingate [email protected]

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Suzanne Cunningham,DVM, DACVIM (Cardiology) 2019VVMA Summer CE Conference June 21,2019

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. Brief review . Current diagnostic recommendations . Is “heat treatment” worth the hype?

. Treatment update 1 . and . Traditional vs “slow-kill”approaches . Feline Heartworm AssociatedRespiratory Disease (HARD) . Treating complications of heartworm disease

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. Patent infections . – definitive . . Wild canids and felids . 2 . . Other hosts . Man . Horse . . Orangutan

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DIAGNOSIS &STAGING

 History  Physical Examination  Antigen (Ag) tests  Primary screening test for dog  Antibody (Ab) tests  Primary screening test for cat  Microfilarial concentration tests(MCT; “Knotts Test”)  Thoracic radiography (CXR)  (Echo)  Minimum database

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ANTIGEN (AG)TESTING

 ELISA test for glycoprotein released fromthe adult female reproductive tract  Usually positive if 3 or more female worms  False negative if low worm burden, all male, prepatent inf,or Ag bound up in immune complexes 4  Detectable by 6-7 months post-infection  Semiquantitative  repeat test if weak +  High specificity,good sensitivity in dog  Main screening test for  Dogs should be tested annually in late spring (~ 7 months following peak exposure)  Puppies < 6 mos old cannot be antigen +

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ANTIBODY (AB)TESTING

 Detects feline HW associatedAb – may become + as early as 2-3 mo post-infection; usually + by 5mo  More sensitive,less specific thanAg tests  Indicates exposure, not active infection!  + Ab test  pre-patent infection, live adult infection or persistent Ab following death of immature or adult worms  Antibodies persist for ~6 mo post larval or worm death  Initial screening test of choice in the cat  90% + ofcatswithHW disease will have + Ab test  Ag testing and/or echo needed to confirm diagnosis!

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. Modified Knott’s, blood smear,microhematocrit tube . are rarelymicrofilaremic . In dogs,ifAg -  confirm species as immitis . Rule out (formerly Dipetalonema)reconditum

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From CE Atkins, Canine Heartworm Disease. In Textbook of Veterinary InternalMedicine, Ettinger and Feldman Eds. 6th Ed, 2005

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 Pulmonary disease is theprimary manifestation of HWD

 CXR arean essential component of the pretreatment evaluation

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The relative frequency of cardiovascular radiographic findings in heartworm disease (Losonsky JM, Thrall DE, Lewis RE: 6 Thoracic radiographic abnormalities in 200 dogs with heartworm infestation. Vet Radiol 24:120, 1983.)

From CE Atkins, Canine Heartworm Disease. In Textbook of Veterinary Internal Medicine, Ettinger and Feldman Eds. 6th Ed, 2005 12 6/17/2019

ECHOCARDIOGRAPHY

 Double linestructures (worm exoskeleton) in PA or right heart  In dogs,echo is a supplemental diagnostic (to serology) – Evaluate for:  Parasite burden  Presence and severity of PHT – RVE, PAE, septal flattening  Cor pulmonale (PHTN + RCHF)  Caval syndrome  Concurrent heartdisease  In cats,echocardiography is of primary diagnostic importance  sometimes able to detect a single adult parasite!

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. In cases where soluble antigen is bound to endogenous antibodies in insoluble immune complexes, the antigen can be 9 blocked from detection . Heat treatment denatures the proteins within the circulating immunecomplexes so that antibodies precipitate and the antigen is freed, making it available for detection by commercially available HW Ag kits

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. 16 dogs experimentally infected with heartworm - 8 dogs in both control andtreated group . Treated dogs received 10 months of topical administration ofAdvantage Multi® for Dogs (10% Imidacloprid + 2.5% ) every 4 weeks and 30 days of 10 mg/kg doxycycline BID . Blood samples were collected from all study prior to surgical transplantation of adult heartworms, on study days 0, 1, 3, 7, 14, 21, 28, and every 4 weeks thereafter for the duration of thisstudy. . Concentration of HW antigen was tested using DiroCHEK® test kit using serum samples both pre- and post-heat- treatment. . Total of 4 instances in 3 treated dogs in which a serum sample converted from negative for the detection of heartworm Ag prior to heat-treatment to positive post-heat- treatment. . At necropsy,these dogs had no adult heartworms recovered and were all negative on antigen testing.

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. CONCLUSIONS: . Ag testing accurately diagnosed all dogs with live adults recovered at necropsy as heartworm Ag + and all those dogs with no live adults recovered at necropsy as heartworm Ag - without the use of heat-treatment. . Heat-treating serum samples did not provide data of any additional value in the diagnosis of heartworm-positive dogs in this study. 11 . Conversion of serum samples fromAg negative to positive with heat-treatment may not always accurately diagnose live adult heartworm infections since no adult heartworms were recovered at necropsy for those dogs in which a conversion eventoccurred. . Conversion events may be detecting residual antigen leftover after all adult worms have died or may even be detecting off-target antigens, which have been denatured during heat-treatment.

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. Conclusion: . It is not necessary to heat-treat every sample that tests negative, but if heartworm infection is suspected and the Ag test result is negative, heat treatment can be considered to ensure an appropriate diagnosis

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. Kill Wolbachia . Eliminate microfilaria . Prevent disease transmission . Kill adult worms 12 . Minimize pulmonary parenchymal & arterial pathology . Exercise restriction . Corticosteroids forpneumonitis . Treat RCHF and significant PHTN if present

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. Obligate, intracellular gram negative . Wolbachia surface protein (WSP), endotoxin

. Critical for certain stages of filarial life cycle . Aid development from L3 → L4 . Increase worm fecundity . Research shows that targeting Wolbachia in addition to D.immitis may greatly decrease pathology and improve outcome in HW infected dogs . Treatment with and doxycycline suppresses HW embryogenesis and weakens adult worms

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https://www.heartwormsociety.org/veterinary-resources/american-heartworm-society-guidelines

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 AHS Recommendations: 1. Confirm diagnosis!! 2. Administer doxycycline 10mg/kg BID for 1month 3. Administer monthly HW preventative for 1-2 months to kill L3 and L4 larvae and MF 4. Melarsomine after ~2 months

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. Electronic medical records from a large veterinary practice in northeast Alabama were searched to identify dogs treated with melarsomine from January 2005 through December 2012. . The dogs were then divided into those that also were treated with doxycycline 10 mg/kg BID for 4 weeks (Group A, n =47) and those thatdid not receive doxycycline (Group B,n = 47).

. Results:Dogs from Group A receiving doxycycline had fewer 15 respiratory complications (6.52%) and heartworm disease- related deaths (0%) than Group B (19.14% and 4.25%, respectively). . Conclusions: Although there are not enough cases to indicate statistical significance, the results strongly suggest that including doxycycline into canine heartworm treatment protocols decreases post-treatment complications and mortality in naturally infected clinical cases.

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PRE-TREATMENT ALSO DECREASES THE “SUSCEPTIBILITY GAP” BETWEEN MACROCYCLIC LACTONES ANDADULTICIDE

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. Initial single injection followed in 1-3 months by 2 injections 24 hoursapart . Required for symptomaticdogs . Recommended by AHWS for all HW infected dogs needing adulticide . Allows for controlled, staged worm k i l l  50% of worms (males > females) killed following 1st injection – then have 1-3 months to recover before remainder of worms killed by final 2 injections . Kills 98% of heartworms . Downsides? . lengthier exercise restriction,increased $, increased total arsenicaldose  http://www.marvistavet.com

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. Typically administer tapering course of prednisone . Peak worm death occurs 1-3 weeks post Rx . ALWAYS accompanied by pulmonary 17 thromboembolism (PTE) . Strict exercise restriction/cage rest absolutely necessary for 6-8 weeks postRx! . Wait 6 months to repeatAg test

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. 50 dogs treated with AHWS recommended adulticideprotocol . 52% minor complications after melarsomine (vomiting,diarrhea, lethargy, pain) . 54% respiratory signs associated with worm death . 14% dogs died withinthe treatment period . Most adverse events in dogs with more severe disease

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. Candidates for conservative “slow-kill” Rx: . Geriatric,inactive dogs with low (or extremely high) worm burdens . Dogs with severe systemic disease (renal,hepatic,etc.) . Dogs who have had an adverse reaction tomelarsomine 19 . Ivermectin at preventative doses will kill all adult heartworms within 30 mos. . Unacceptable  progressive pulmonary pathology, prolonged exercise restriction

. Doxycycline (10-20 mg/kg/day) given in addition to avermectins may greatly expedite worm due to its anti-Wolbachia effects . ~ 80-95 % reduction in adult worm burden in 9-12 months . Ivermectin vs moxidectin?

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. 16 HW-infected Beagledogs . 8 non-treated and 8 treated with 10 mg/kg of Doxy BID for 30 days and monthly IMD + MOX (Advantage Multi™) for 10 months . Echocardiograms, radiographs, CBC/chemistry profiles, heartworm Ag and MF evaluated every 4 weeks

. Dogs euthanized and necropsied at 10 months…

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. No MF were detected in treated dogs after 21 days post-treatment . At necropsy,adult heartworms recovered from all non-treated control dogs -range of 10–12 adult worms/dog . In treated group, the range of adult heartworms recovered at 10 months was 0–2 adult worms/dog, with 5 dogs having no adult heartworms present 21 . Treatment regimen demonstrated a 95.9% efficacy in eliminating adult heartworms (P < 0.0001)

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. This treatment regimen successfully eliminated D.immitis MF by 21 days post- treatment, reduced heartworm antigen concentration over time,and had a 95.9% efficacy in the elimination of mature adult heartworms at 10 months

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. Minimum database . CBC, Chem,UA,CXR . Doxycycline at5-10 mg/kg BID for 30 days . IMD + MOX (Advantage Multi™) 23 every 2 weeks for 3 months, then monthly thereafter . Recheck exam and heartwormAg, +/- CXR every 4-6 months . Not recommended by the AHWS but reasonable for dogs that are not good candidates for arsenical

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. Cats are resistant to infection compared with dogs . Prevalence correlates geographically with that of canine infection (~10%) . Many L5 larvae don’t survive in the catbut immature 24 worms can result in clinical disease . Ectopic infection more common than in dogs (brain, subcutis,abdomen) . Intense respiratory distress results from acute pulmonary injury  may lead to respiratory failure

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From CE Atkins, Feline Heartworm Disease.In Textbook of Veterinary Internal Medicine, Ettinger and Feldman Eds.6th Ed,2005

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70-90 days PI 25 L 5  lung

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. Often confused with . Pulmonary insult/pneumonitis coinciding with the arrival of immature worms to the pulmonary vasculature (~2-3 months post infection) . Occlusive medial hypertrophy of small pulmonary arterioles . Additional inflammatory changes in small airways, alveoli and pulmonary arteries . Easily misdiagnosed as asthma given radiographic changes, dyspnea and coughing

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. 3 groups of cats (n=10) infected with 100 L3 larvae . Group A treated with topical (Revolution™) at 28 days,then once monthly . Group B treated with ivermectin PO at 70 days, then every 2 weeks for 5months . Group C untreated post infection(PI) . Peripheral blood (CBC,AB),BAL,radiographs collected at 26 specified intervals, euthanasia and necropsy at 8 mos. . Results: Cats from Group A had no radiographic changes and no worms at necropsy.Group B had no adult worms at necropsy, but Groups B and C could not be differentiated based on severity of rad changes, Ab titers, CBC changes, or BAL cytology throughout thestudy… . Conclusions: Cats that become infected with immature adult HW often do not develop fully mature HW and are only transientlyAb + but still develop HARD.

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B C

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. No adulticide! . Heartworm extraction may be considered for high worm burden/caval syndrome . Risk of fatalanaphylaxis . Corticosteroids - prednisone,prednisolone . MAINSTAY of symptomatic therapy in the cat! . Used to treat asthma-like signs (HARD), PTE

. Macrolide HW preventative monthly . Antiplatelet agents? . Doxycycline? . Keep indoors, minimize stress & activity . Guarded prognosis . 10-20% of cats may die suddenly

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. Asymptomatic . Caval syndrome . Pulmonary vascular . Glomerulonephropathy disease . Disseminated intravascular . Thromboembolic disease coagulation . Cor pulmonale / right sided . Wolbachia associated congestive pathology . Eosinophilic pneumonitis . Aberrant infection . Feline HWinfection . HARD

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. Severe diffuse interstitial to alveolar infiltrates associated with eosinophilic pneumonitis in a HW positive dog . Furosemide will nothelp!

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. Tapering courseof prednisone . 0.5 mg/kg BIDfor 1st week . 0.5 mg/kg SID for 2nd week 31 . 0.5 mg/kg EOD for 3rd +/- 4th week

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. Associated with worm death, either spontaneous or 2-3 weeks post-adulticide . Clinical signs: acute onset dyspnea, cough, collapse, sudden death

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. Antiplatelet agents . **Corticosteroids** . Clopidogrel – loading vs . Dexamethasone, prednisone maintenance dose . Only for HW-associated PTE! . Anticoagulants . Pulmonary vasodilators . Heparin . Oxygen . Low molecular weight heparin . Sildenafil – 1-2 mg/kg BID . Enoxaparin or dalteparin . Pimobendan – 0.2-0.3 mg/kg BID . $$ . Rivaroxaban . Oral Factor Xainhibitor . $$

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. Right-sided CHF secondary to chronic pulmonary hypertension 33 . Jugular & hepatic venous distension, ascites, pleural effusion, cachexia

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. Oxygen . Sildenafil – 2 mg/kg TID . RCHF therapy: . Furosemide . Pimobendan . ACE-I . Spironolactone . Abdominocentesis or thoracocentesis as needed

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. Acute onset anorexia, weakness, collapse (cardiogenic ) . Complicated by concurrent pulmonary arterial disease/cor pulmonale 34 . Hemolysis from shearing forces imposed by worms w/in the heart .  Hemoglobinemia, hemoglobinuria, anemia . Requires immediate surgical removal of adults

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. Recommended for dogs with caval syndrome or ↑↑ worm burden seen on echo – prior to melarsomine . Jugular venotomy . Sedation or lightanesthesia

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QUESTIONS? [email protected]

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1. Dillon AR,Blagburn BL,Tillson M, et al.Heartworm-associated respiratory disease (HARD) induced by immature adult Dirofilaria immitis in cats.Parasit Vectors. 2017 Nov 9;10(Suppl 2):514.

2. Kramer L,Crosara S,Gnudi G,et al.Wolbachia,doxycycline and macrocyclic lactones:New prospects in the treatment of canine heartworm disease.Vet Parasitol. 2018 Apr 30;254:95-97.

3. Maxwell E,Ryan K,Reynolds C,Pariaut R.Outcome of a heartworm treatment protocol in dogs presenting to Louisiana State University from 2008 to 2011: 50 cases.Vet Parasitol. 2014 Nov 15;206(1-2):71-7.

4. Nelson CT,Myrick ES,Nelson TA.Clinical benefits of incorporating doxycycline into a canine heartworm treatment protocol. Parasit Vectors. 2017 Nov 9;10(Suppl 2):515.

5. Savadelis MD, Ohmes CM, Hostetler JA. Assessment of parasitological findings in heartworm-infected beagles treated withAdvantage Multi® for dogs (10% imidacloprid + 2.5% moxidectin) and doxycycline. Parasit Vectors. 2017 May 19;10(1):245.

6. Savadelis MD, Roveto JL,Ohmes CM, et al.Evaluation of heat-treating heartworm-positive canine serum samples during treatment with Advantage Multi® for Dogs and doxycycline. ParasitVectors.2018 Feb 20;11(1):98.

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Suzanne Cunningham,DVM,DACVIM-Cardiology 2019 V MASummerCEConference June 21,2019

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Update on arrhythmogenic right ventricular cardiomyopathy (ARVC) Background Screens and genes Treatment Prognosis Ongoing research

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History Recognized since the late1960s 1983-Harpster described a primary myocardial disease in 64Boxer dogs from the NEarea Distinguished from idiopathicDCM Ventricular arrhythmias of right ventricular (RV)origin and sudden death more common thanCHF ARVCdesignation Basso, , Meurs etal. Circulation 2004

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ARVC

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Progressive degeneration of the RV,+/-LVmyocardium Replacement byfat/fibrosis Inflammation Electrical instability Sudden death Frequent in juvenilesand athletes Geographic/familial incidence Autosomal dominant inheritance Several different geneticmutations As many as50 %of affectedpeople are “mutationnegative”

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Gros RVdilation, LVinvolved later indisease RVaneurysms Atrialdilation

Microscopic Fatty or fibrofattyinfiltration Inflammatory infiltrates (myocarditis) Primary or secondaryresponse?? Predominant RVinvolvement Active and chronic myocardialdamage and repair

Basso,et al. Circulation.2004 7

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Incidence up to 30-35% Average age of onset 5-8 yrs(variable) Equal sexdistribution Familial occurrence Meurs, et al(1999) Autosomal dominanttrait Meurs et al.(2010) Identified mutationin desmosomal protein

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Striatin – desmosomal protein involved in calcium handling 8 bp deletionassociated with ARVCinBoxers Incomplete penetrance Variable expressivity

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Meurs et al. J Vet Intern Med 2013

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Similar to the disease in Boxers Affected dogs tend to be older at the time of diagnosis CHFmore likely May have refractory VT “storms”

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Annual ECG/Holter Annual echo (breedinganimals) Genetic testing -NCSU Striatin mutation One of many?? Biomarkers? C-BNP,Troponin-I not helpful NT-proBNP? Inflammatory markers? MicroRNAs?

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Three main categories(Harpster) Type I: Asymptomatic arrhythmia Sudden death may be first sign… Type II: Ar r h yt h m ia Syncope/weaknes Type III: “DCM”/congestive heart failure With or withoutarrhythmia Least common form in the U.S.

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Usually associated with excitement Attributed to runs of rapid R-on-TVT Possible precursor to sudden death

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62 Boxers with ARVC,no DCM (2000-2010) Evaluated effect of age, syncope, Holter class, treatment options on median survival time (MST) Probability of death 5x greater in dogs w/ syncope MST with syncope 365days MST without syncope 693days

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Syncope vs. No Syncope

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Complete physicalexam ECG Echocardiogram Holter monitor Minimum database Basicbloodwork +/-Thoracic radiographs +/-Abdominal ultrasound

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Arrhythmia VPCs Pulse deficits

+/-Murmur and/or gallop +/-Weakpulses +/-Signs of CHF

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Upright RV-origin VPCs

Monomorphic ventricular tachycardia Origin: RVfree wall Kraus, Moise, et al.(2002) Pacemapping comparison Supraventricular tachycardia (rare)

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Harpster. Vet ClinNAm Small Anim Pract19 1 Advocated Holter monitoring for assessing efficacy of anti- arrhythmic therapy Meurs etal. JAVMA 2001 Holter vs. in-houseECG In-hospital ECGis a specific but insensitive test for arrhythmia detection inBoxers Spier et al. JAVMA2004 80%daily spontaneous variation in arrhythmia frequencyon Holter! ≥80%change neededto document antiarrhythmic efficacy

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Tyler

-HR 40-45 -Long sinus pauses -No VPCs,VT

Presu med vasovagal syncope

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Vasovagal syncope is arelatively common (and benign) cause of collapse in excitable (i.e., all) young Boxers…

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Echo Type I/II (Arrhythmic form) Normal or RVenlargement TAPSE? Type III (DCMform) Biventricular dilation Severely depressed contractile function Concurrent MR Marked LAE in dogswith clinical signs MRI/NMR?

From: Baumwart et al. JVIM 2009 37

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I. Treatment of the asymptomatic patient

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Totreat or not totreat? Controversial! Not a “numbersgame”… Criteria forinitiation of medical treatment: Malignant arrhythmia >1ectopic focus(polymorphism) Pairs or runs ofVPCs Paroxysmal or sustainedtachyarrhythmia Rapid R-on-T Exercise restriction, Omega-3FA?

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From: Smith etal. JVIM 2007

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II. Treatment of the dog with symptomatic arrhythmia

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Acute treatment Hospitalization with continuousECG IV lidocaine or procainamideinfusion Start sotalol at 1-2mg/kgBID Echo first

Chronic therapy andmonitoring Sotalol alone or Sotalol +mexiletine Mexiletine + atenolol? Amiodarone Exercise restriction Omega 3FA Follow-up Holter, echo

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Presented for 1episodeof collapse during awalk Marked arrhythmia with soft grade II/VI murmur at heart base (“Boxer murmur”) Normal contractile function, mild right heart dilation on echo

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• Rhythm diagnosis? • Malignant “R-on-T” ventriculartachycardia • RVorigin VPCstypical for BoxerARVC • Underlying cause? • ARVCuntil provenotherwise… • Any further tests? • Teststo rule out systemic disease • Minimum database, +/-AUS • Echocardiogram • Holter monitor • Genetic testing forstriatin?

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Treatment options? Intravenous lidocaine Sotalol Mexiletine plusSotalol Mexiletine plusatenolol Meurs et al. JAVMA2002 ♥ Fish oilsupplementation Smith et al.JVIM2006

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Arrhythmia well-controlled for almost 5 years on atenolol/mexiletine combination Presented forrecurrent “collapsing episodes” Normal ECG Advanced i m a g i n g meningioma (brain tumor ) Treated with radiation and chemotherapy for 3 months before euthanasia forrecurrent 52

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10yr SFBoxer w/ARVC Verywell controlled on sotalol and mexiletine for 2 years Presented for vomiting &lethargy; collapsed in CPAin hospital exam room Successfully resuscitated with defibrillation, emergencydrugs, amiodarone (NexteroneTM) and >15minutes ofCPR…

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Amiodarone Indications: Malignant or refractoryVT,SVT Atrial fibrillation with ventricular ectopy IV– use with caution!! 3-5mg/kg diluted, slowIV Risk of anaphylaxis – usepremixed! No polysorbate 80 Oral Difficult dosing – long half life Loading: 5-8 mg/kg BIDx 5-7days Maintenance: 5-8 mg/kg q 24h

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Premixed amiodarone

Bolus of 2-5 mg/kg IVover~10min 1/2–1premixed 150mg bag for a Boxersized dog CRI of 0.8 mg/kg/hr for 6 hours, followed by 0.4 mg/kg/hr Then proceed with oralloading

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Amiodarone Side-effects • Hepatopathy • Dose-dependent • More frequent inDobies? • Usually reversible • Others: • Thyroid dysfunction, pulmonaryfibrosis , blood dyscrasias,neuropathy • Monitoring • Frequent bloodwork • Serum levelsuseful? • ECG/Holtermonitoring

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Discharged 3 days following resuscitation Amiodarone, sotalol, mexiletine, carvedilol, pimobendan

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Nelson OLJVIM2006

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II. Treatment of the dog with DCMand CHF (congestive heart failure)

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Pimobendan Diuretic (Furosemide) ACE-inhibitor (Enalapril, benazepril) Spironolactone Low-salt diet Royal Canin Boxer orEarlyCardiac? Digoxin or diltiazem if atrial fibrilation Other diuretics Torsemide, thiazides L-carnitine?

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Presented for 3 week Hx of cough with excitement, increased panting, and decreasedinterestin running/playing withtoys Cough not responsiveto antibiotics History of soft murmur since birth Physicalexam III/VI murmur and gallop FastHR, frequent runs of arrhythmia Weak pulses Increased respiratory effort

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Hospitalize to get heart failure and arrhythmia undercontrol Continuous ECGmonitor inICU Antiarrhythmics IV lidocaine drip Amiodarone in lieu ofsotalol Mexiletine Heart failure medications Pimobendan-$$ Furosemide Eventually enalapril & spironolactone Recheck Holter & CXRin 1wk.

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Inodilator Calciumsensitizer PDEIII-inhibitor Quick onset ofaction Oral absorption w/in1hour Possible side-effects (rare) ♥ Diarrhea ♥ Tachycardia or arrhythmia Approved in dogswith CHFdue to CVDor DCM

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Increased survival in every published canineCHFstudy From 3 months to15months PROTECTstudy (Boswood ACVIM2012) Delayed CHFby 9 months in76 Dobies with preclinical DCM EPICStudy (Boswood JVIM2016) CHFdelayed by 15months in 360 dogs with MMVD and LAenlargement

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?

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Doing well atrecheck; cough resolved; improved energy and appetite Holter monitor: good arrhythmia control Overall good quality oflife with some medication adjustments over next several months Lived for >9 months; PTS for progressive heart failure and inappetance

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ARVC in both and Boxers (& English Bulldogs) substrate predisposed to sLuodndgetnerdmeaptrhognosis is poor for dogs withheart failure (CHF) Severe myocardial structuraldisease Serious ventricular arrhythmias 6-9 months a “good” outcome Dogs without CHFmay do well for years ! Anti-arrhythmic therapy may improveQOL and prolong survival (Harpster1991) Avg > 1-2yrs after diagnosis; some > 5yrs Avg survival to 10-1 years

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Screening of breeding animals: Annual Holter, echo, genetic testing Role of biomarkers? hsTnI, NTproBNP, Antidesmosomal Abs? Novel echo parameters? 4D volumetric assessment RV Genetic Studies Genetic modifiers? Other mutations? New drug therapies? Role of inflammation? Immunosuppressants? Implantable cardioverters? Electroablation

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Current Tufts ARVCStudy

Antidesmosomal antibodies as a potential biomarker for ARVCinBoxers Enrolling normal dogs and affected Boxers with >100 VPC/24hrs. Study pays for exam,ECG,Echo, Holter monitor, full bloodwork (including CBC/Chem, genetic testing, biomarkers) Contact: [email protected] or [email protected]

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Overview

• Review • Clinical approach to cardiomyopathy,CHF,ATE

• Diagnostics Emily Karlin DVM,DACVIM (Cardiology) • Treatment • Follow up • Owner expectations(prognosis)

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What is cardiomyopathyagain? FelineCardiomyopathy

• Diseaseof the heart muscle • Hypertrophic Cardiomyopathy(HCM) • Often has a geneticcomponent • Some known genetic mutations in cats, dogs, people • DilatedCardiomyopathy • Phenotype usually not expresseduntil later in life • RestrictiveCardiomyopathy

• Abnormal heart muscle  CongestiveHeart Failure (CHF) • UnclassifiedCardiomyopathy (eventually)

• ARVC

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Cardiomyopathy =CHF? Hypertrophic Cardiomyopathy(HCM)

• Canhave “occult” cardiomyopathy for years • Spectrum of disease

• Eventually the heart can not compensate

 Elevated ventricular filling pressures Thick left ventricle Thick left ventricle Thick left ventricle  Elevated atrialpressures Normal left atrium Big left atrium Big left atrium  Passivecongestionof pulmonary veins or vena cava Normal actingcat Normal actingcat Symptomaticcat  Fluid spills out into lungs or pleural space/peritoneal space =CHF

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Middle age to older cats • Early clinical signs might be subtle (hiding, decreased appetite) • (but can be anyage) • Male >female • Dyspnea (CHF) • Big? • ArterialThromboembolism • Breed • Collapse/syncope • Sudden death

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Physical Examfindings

• Often no PEsigns in occult phase

• Murmur • S4/summation Gallop • Arrhythmia

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Physical Examfindings • Diagnostics… for whatreason?

• Often no PEsigns in occult phase • Heard something on PE(murmur, gallop, arrhythmia)… • Want to anesthetize… • Murmur • Want togive IV fluids… • S4/summation Gallop • Cat in ERfor open mouth breathing… • Arrhythmia • Cat unable to move back legs… • Jugular vein distension

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Diagnostics… for whatreason? • Heard something on PE/want to anesthetize/want to give IVF

• Heard something on PE (murmur,gallop, arrhythmia)… • Want toanesthetize… • Want to give IV fluids… Thick left ventricle Thick left ventricle Thick left ventricle • Cat in ERfor open mouth breathing… Normal left atrium Big left atrium Big left atrium • Cat unable to move back legs… Normal actingcat Normal actingcat Symptomaticcat

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Searching for occultHCM  Ownerconversation What tests areavailable? . What tests areavailable? . Possible results/action steps? • Thoracic radiographs • NT-proBNP • TFAST • Echocardiogram • ECG

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Searching for occultHCM • Searching for occultHCM

Possible results/action steps? Possible results/action steps?

• Thoracic radiographs – Looking for cardiomegaly • Thoracic radiographs • NT-proBNP Canbe low yield if asymptomatic • NT-proBNP – Snap test (could miss mild disease) • TFAST Clear cardiomegaly echocardiogram • TFAST Quantitative • Echocardiogram • Echocardiogram Abnormal might promptreferral • ECG • ECG

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NT-proBNP (pmol/L) Asymptomatic cat with murmur Quantitative SNAP (0-1500) (+ at ~140-200)

. <50-100 = likely normal . – = likely not severe heart dz Versus . >100 = consider moretesting (mild heart dzpossible) . + = consider more testing

. < 100= likely not CHF . – = likely notCHF . 100-270 = maybeCHF . + = possibleCHF . > 270 = likelyCHF

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Searching for occultHCM • RecentStudy Possible results/action steps? • Detectionof occult heart disease in cats

• Brief “2-minuteechocardiogram” • Thoracic radiographs in primary caresetting • NT-proBNP • TFAST– Assess left atrial size • Echocardiogram Look for LV wallthickening Determine need for referral or medication • ECG https://www.youtube.com/watch?v=I4U8AoxYmok&feature=youtu.be

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Searching for occultHCM

Possible results/action steps?

• Thoracic radiographs • NT-proBNP • TFAST Gold standard fordiagnosing HCM • Echocardiogram – Assess left atrial size • ECG Assessfor outflow tract obstruction Determine need formedication

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Hypertrophic Cardiomyopathy Obstructive Hypertrophic Cardiomyopathy(HCM) (HOCM) • Searching for occultHCM • Systolic anterior motion(SAM) of the mitral valve Possible results/action steps? • Obstructs leftventricular outflow  pressure gradient between LV • Thoracic radiographs and aorta • NT-proBNP • TFAST • Prevents MV from closing  MR • Echocardiogram • ECG– Especially if arrhythmia Determine need for referral or medication

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Dyspneic cat • Spectrum of disease

Thick left ventricle Thick left ventricle Thick left ventricle Normal left atrium Big left atrium Big left atrium Normal actingcat Normal actingcat Symptomaticcat

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Dyspneic cat • Dyspneic cat

What tests areavailable? What tests areavailable?

• Thoracic radiographs • TFAST • NT-proBNP • NT-proBNP • TFAST • Thoracic radiographs Only when stableenough • Echocardiogram • Echocardiogram

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Hypertrophic Cardiomyopathy(HCM) Dyspneic cat

• Dyspneic cat

Possible results/action steps?

• TFAST– Assess left atrial size • NT-proBNP Look forpleural effusion Versus • Thoracic radiographs • Echocardiogram

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Dyspneic cat Hypertrophic Cardiomyopathy(HCM)

• Dyspneic cat

Possible results/action steps?

• TFAST– Big LA  Furosemide& clopidogrel! • NT-proBNP Pleural effusion Thoracocentesis! • Thoracic radiographs (and furosemide,clopidogrel) • Echocardiogram

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Hypertrophic Cardiomyopathy(HCM) NT-proBNP (pmol/L) Quantitative SNAP • Dyspneic cat (0-1500) (+ at ~140-200)

Possible results/action steps? . <50-100 = likely normal . – = likely not severe heart dz . >100 = consider moretesting (mild heart dzpossible) • TFAST . + = consider more testing • NT-proBNP – Snap BNP Normal – dyspnea is probably not CHF • Thoracic radiographs . < 100= likely not CHF Abnormal – dyspnea might be from CHF . – = likely notCHF • Echocardiogram . 100-270 = maybeCHF . + = possibleCHF . > 270 = likelyCHF

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Dyspneic cat Hypertrophic Cardiomyopathy(HCM)

• Dyspneic cat

Possible results/action steps? Reference Sample Reference Sample

• TFAST • NT-proBNP Versus • Thoracic radiographs – Best test for pulmonary edema • Echocardiogram Lungs obscured ifpleural effusion *Only when stable enough (might need some furosemidefirst)*

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Dyspneic cat Hypertrophic Cardiomyopathy(HCM)

• Dyspneic cat

Possible results/action steps?

• TFAST • NT-proBNP Versus • Thoracic radiographs • Echocardiogram – Gold standard for diagnosing HCM Assessfor outflow tract obstruction Confirm that dyspnea is resulting from CHF

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Cat unable to move back legs • Cat unable to move back legs

1.Tests? 1.Tests?

• Physical exam • Physical exam • Differential BG/lactate • Differential BG/lactate • Assessments for HCM andCHF • Assessments for HCM andCHF

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Cat unable to move back legs • Cat unable to move back legs

1.Tests? 1.Tests?

• Physical exam – Cold, painfullimbs • Physical exam • Differential BG/lactate Firm gastrocnemius muscles • Differential BG/lactate – Not always necessary • Assessments for HCM andCHF Absent/weak femoral pulses • Assessments for HCM andCHF Low BG& high lactate in Cyanotic pawpads affected limbs

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Cat unable to move back legs • Other tests

1.Tests? • Kidney values (fullCBC/chemif possible) • T4 (especially if >6 years old) • Blood pressure • Physical exam • Heartworm (antigen +antibody) • Differential BG/lactate • Assessments for HCM andCHF – TFAST, Radiographs, NT-proBNP, echo Determine if cardiomyopathy likelyATEcause Determine if dyspnea is from pain orCHF

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Owner conversation – have a diagnosis, now what???

• What does it mean? • Occult HCM • What do we do now? • HCM +CHF • Meds? (owners able togive them?) • ATE • Monitoring at home? • Follow up? Treatment, follow-up,prognosis… • What should theyexpect? • Possible outcomes • Prognosis

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Treatment – OccultHCM • Treatment – OccultHCM

• Clopidogrel? • Clopidogrel? – yes if bigLA • Pimobendan? • Pimobendan? 18.75 mg POSID • ACEinhibitor? • ACEinhibitor? • β Blocker? • β Blocker?

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Treatment – OccultHCM • Treatment – OccultHCM

• Clopidogrel? • Clopidogrel? • Pimobendan? –we do not do this routinely yet in cats • Pimobendan? • ACEinhibitor? • ACEinhibitor? –sometimes • β Blocker? • β Blocker?

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Hypertrophic Cardiomyopathy(HCM)

• Treatment – OccultHCM

• Clopidogrel? • Pimobendan? βBlocker • ACEinhibitor? • β Blocker? – often done if outflow obstruction is present (but we aren’t certain that it improves outcome)

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Follow up –Occult HCM • Follow up –Occult HCM

• Recheck echo timing depending on degree of LAE or if β blocker • Recheck echo timing depending on degree of LAE or if β blocker

• Owner expectations… • Owner expectations… How long will mycat What might • Possible outcomes: Remain occult; CHF; ATE; sudden death happen to live? • Prognosis: Can remain occult for years my cat?

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Treatment – HCM +CHF • Monitoring – HCM + CHF

• Furosemide ~1-2 mg/kg POS-BID • Owner tools: • DVM tools: • Clopidogrel 18.75 mg POSID • Resting respiratory rate • Blood work • Pimobendan? • Appetite • Kidneys, electrolytes • ACEinhibitor? • Attitude • BNP? • β Blocker? • Echo/TFAST(effusions) • Thoracic radiographs (edema)

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Follow up– HCM + CHF • Follow up– HCM + CHF

What might • 7-14 day recheck • Owner expectations… How long happen? will they • Seehow cat is doing at home (breathing, appetite, attitude, meds) live? • Check kidney values andelectrolytes • Check for pleural effusion (TFAST) or pulmonary edema (radiographs) How will I know? • Recheck every 2-4months

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Follow up– HCM + CHF • Treatment –ATE

• Owner expectations… • Pain control (usually an opioid at first) • Clopidogrel 75mg PO loadingdose • Heparin/low molecular weightheparin • Possible outcomes: Recurrent CHF; ATE; Azotemia; Suddendeath • Tissue plasminogen activator? • Prognosis: ~6-12months • Rivaroxaban? • Goal: Breathing well, eating well, good energy,purring (i.e. “normal”) • Furosemide ONLY IF DOCUMENTED pulmonary edema

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Hypertrophic Cardiomyopathy(HCM) Hypertrophic Cardiomyopathy(HCM)

• Follow up–ATE • Follow up –ATE

• 7-14 day recheck • Owner expectations… • Limb assessment • Monitor CHF if present • Possible outcomes: Recurrent ATE; CHF; Sudden death;Azotemia • Prognosis: ~6 months? ~11-12 months? longer?

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Referral is not always an option….

• Thoracic radiographs? • NT-proBNP? • TFAST? • ECG?

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Asymptomatic cat Asymptomatic cat

• Convinced there is a big LA? • Convinced there is a big LA?

• Clopidogrel

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Dyspneic cat Dyspneic cat

• Convinced there is a big LAandCHF? • Convinced there is a big LAandCHF?

• Furosemide • Clopidogrel • Probably not pimobendan without an echo…

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Dyspneic cat

• Starting furosemide?

• Monitor: Questions?

• Breathing [if ↑ might need ↑ furosemide] • Appetite/energy [if ↓ might need ↓ furosemide] • Kidney values [if ↑ might need↓ furosemide]

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CanineCardiomyopathies

• Primary cardiomyopathies • Dilated cardiomyopathy (DCM) • Arrhythmogenic RightVentricular Cardiomyopathy (ARVC) • Hypertrophic cardiomyopathy Emily Karlin, DCM, DACVIM(Cardiology) • Secondarycardiomyopathies • Tachycardia induced cardiomyopathy (TICM) • Sepsis • Toxin/drug induced • Nutritional

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Overview CanineCardiomyopathies

• DCMphenotype • Canine cardiomyopathy review • Nutritional cardiomyopathyknowns and unknowns • Outcomes andexpectations • DCMStudy atTufts • Current recommendations

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Dilated Cardiomyopathy(DCM) DCM – PhysicalExam

• Big dogs (Doberman, Great Dane,Wolfhound, Newfoundland…) • Soft left apical systolic murmur (II-III/VI) • CockerSpaniel, Portuguese • S3Gallop • Maybe male >female • Arrhythmia • Middle age • Pulmonary crackles • Poor arterial pulses+/- pulse deficits • Jugular vein distension • Occult stage can lastyears

• Sometimes cardiogenic shock

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DCM – PresentingComplaints DCM –Diagnostics

• “ADR” • Reason for doingtests? • Owners want tobreed • Cough • You want to anesthetize • Dyspnea • Hear something onPE • Weakness/syncope • Clinical signs (syncope, cough, dyspneaetc.) • Sudden death

• Healthy with PE abnormalities

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DCM –Diagnostics DCM –Diagnostics

• Reason for doingtests? • Occult DCM • Owners want tobreed • You want toanesthetize Looking for “occult”disease • 24 hour Holtermonitor • Hear something onPE • Echocardiogram • Clinical signs (syncope, cough, dyspneaetc.) • 5 minute ECG • Biomarkers • TFAST

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DCM –Diagnostics DCM –Diagnostics

• Reason for doingtests? • Occult DCM • Symptomatic (collapse,cough,dyspnea) • Owners want tobreed • You want to anesthetize • 24 hour Holtermonitor • Thoracic radiographs • Hear something onPE • Echocardiogram • TFAST/AFAST • Clinical signs (syncope, cough, dyspneaetc.) • 5 minute ECG • Echocardiogram • Biomarkers • ECG Looking for CHF +/- • TFAST • NT-proBNP significant arrhythmia

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DCM –Treatment DCM –Treatment

• Occult DCM • Occult DCM

• +/- Pimobendan 0.25 – 0.3 mg/kg POBID • +/- Pimobendan • +/-Antiarrhythmics • +/-Antiarrhythmics vs.

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DCM –Treatment DCM –Treatment

• Occult DCM • DCM +CHF

• +/- Pimobendan • Pulmonary edema: Furosemide +pimobendan • +/-Antiarrhythmics vs. (+ ACE inhibitor +/-spironolactone) • Significant effusions: -centesis (and abovemedications) • +/-Antiarrhythmics

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DCM–What to Expect Nutritional Cardiomyopathy

• Occult DCM • Why is thissuch a big deal?? • Can remain asymptomatic foryears • Outcomes: Develop CHF,collapse, sudden death first sign • Potentially avoidable • Potentially reversible

• DCM +CHF • >6 months =Success • Outcomes: Recurrent CHF, azotemia, suddendeath • Goal: Feeling well

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NutritionalCardiomyopathy – History

• Cats Nutritional Cardiomyopathy • Taurine is an essential aminoacid • Deficiencycan  DCM, retinal degeneration, reproductive issues

• Describedin the ‘80s  taurine requirement increased

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NutritionalCardiomyopathy – History NutritionalCardiomyopathy – History

• Taurine functions • Dogs • Should be able to make taurine from methionine and cysteine • Conjugation of bileacids • Taurine is not considered an essential amino acid • Antioxidant BUT… • Positive inotrope (calcium) • Osmoregulation • Membrane stabilization

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NutritionalCardiomyopathy – History NutritionalCardiomyopathy – History

• Dogs • Dogs • Should be able to make taurine from methionine and cysteine • Should be able to make taurine from methionine and cysteine • Taurine is not considered an essential amino acid • Taurine is not considered an essential amino acid BUT…

• Breed variation • Dietary content/processing can influence absorption & excretion • GIbacterial composition caninfluence enterohepatic circulation • Precursor content variation

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NutritionalCardiomyopathy – History NutritionalCardiomyopathy – History

• 1995–Certain breeds have low taurine & DCM • 2019 –Dogs with DCM • Golden , AmericanCocker • Most dogs with DCM had normaltaurine • Various breeds with DCM eating a grain-free diet • Several unrelated house-mates • 1997–CockerSpaniels with DCM were found to have low taurine • Improvement with taurine & carnitine supplementation • Not taurinedeficient • But some werelow-normal • 2003& 2005 – Dogs with DCM eating lamb and rice-based diets • Improvement with diet change & taurine supplementation • Improvement with diet change& taurine supplementation • Including 2 who switched to a major brandgrain-free • 2013– Many Wolfhounds with & without DCM had low taurine • More low taurine dogs went on to develop DCMor atrial fibrillation Adin 2019

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NutritionalCardiomyopathy – History Nutritional Cardiomyopathy– BEG Diets

• 2018 –Golden Retrievers with DCM & taurine deficiency • Boutique • Exotic • 24/24 were eating a “BEG” diet • Most grainfree • Grain-free • Most had legumes in top 5ingredients • 23/24 improved after diet change& taurine +/- carnitine • Many were consuming

• Adequate taurine concentrations may behigher in Goldens

Kaplan 2018

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NutritionalCardiomyopathy – Knowns NutritionalCardiomyopathy – Unknowns

• Some dogs have developed cardiomyopathy & CHFwhile eating BEGdiets • Lack of grain? • But notall • Deficiency? • Some dogs have been taurine deficient • Change in nutrientmetabolism? • But most arenot It’s not just taurine… • Lentils/legumes? It’s not just grainfree… • Many diets have beengrain-free • But not all (though all havebeenBEG) • Toxin or toxiccombination? • Some dogs have had convincing improvement (clinical & echocardiographic) • Breed predisposition? after changing diet & supplementing taurine • But notall • Other factors?

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NutritionalCardiomyopathy – Unknowns NutritionalCardiomyopathy – Diagnostics

• Lack of grain? • Occult • Symptomatic • Deficiency? • Change in nutrientmetabolism? • Lentils/legumes? • Toxin or toxiccombination? • Breed predisposition? • Other factors?

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NutritionalCardiomyopathy – Diagnostics Nutritional Cardiomyopathy –Treatment

• Occult • Symptomatic • Occult

• NT-proBNP • +/- Pimobendan • Troponin • +/-Antiarrhythmics • Taurine levels • +/-Taurine supplementation • Thoracic radiographs • Diet change • Echocardiogram • ECG

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NutritionalCardiomyopathy – Diagnostics Nutritional Cardiomyopathy –Treatment

• Occult • Symptomatic • Symptomatic

• NT-proBNP • Thoracic radiographs • Treat CHF& arrhythmia asfor DCM • Troponin • TFAST/AFAST • Taurine supplementation • Taurine levels • Echocardiogram • Diet change • Thoracic radiographs • ECG • Echocardiogram • NT-proBNP • ECG • Taurine levels

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Nutritional Cardiomyopathy –Outcomes Nutritional Cardiomyopathy –Outcomes

• Daisy #1 –Radiographs

• Cases: The TwoDaisies

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Nutritional Cardiomyopathy –Outcomes Nutritional Cardiomyopathy –Outcomes

• Daisy #1 • Daisy #1 – Initialecho • 9-year-old SF GoldenRetriever • Presented for evaluation of cough and weight loss

• 2/6 left apical systolic murmur • No jugular veindistension • Normal femoralpulses • No overt dyspnea

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Nutritional Cardiomyopathy –Outcomes Nutritional Cardiomyopathy –Outcomes

• Daisy #1 – Initialecho • Daisy #1 –Treatment plan

• Pimobendan • Furosemide asneeded • Enalapril • Taurine • Diet change

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Nutritional Cardiomyopathy –Outcomes Nutritional Cardiomyopathy –Outcomes

• Daisy #1 – Initialecho • Daisy #1 –Taurine levels

• Plasma: 105 [normal 60-120nmol/mL] • Whole blood: 229 [normal 200-350 nmol/mL] • Normal forGolden ?

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Nutritional Cardiomyopathy –Outcomes Nutritional Cardiomyopathy –Outcomes

• Daisy #1 – 9-monthRecheck • Daisy #1 – 9-month Recheck Echo

• Doing well • Gained weight, no longer ravenous • Cough resolved • Not onfurosemide

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Nutritional Cardiomyopathy –Outcomes

• Daisy #1 – RecheckRadiographs

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Nutritional Cardiomyopathy –Outcomes Nutritional Cardiomyopathy –Outcomes

• Daisy #2 • Daisy #2 – Radiographs • 3-year-old SF LabradorRetriever • Presentedfor evaluation of cough

• 3-week duration cough, sometimes gag • Progressivelethargy • Labored breathing

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Nutritional Cardiomyopathy –Outcomes Nutritional Cardiomyopathy –Outcomes

• Daisy #2 • Daisy #2 – Echo • 3-year-old SF LabradorRetriever

• 2/6 left apical systolic murmur • Pronounced gallop • Jugular veindistension • Weak femoral pulses • Moderate dyspnea

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Nutritional Cardiomyopathy –Outcomes Nutritional Cardiomyopathy –Outcomes

• Daisy #2 – Echo • Daisy #2 – NT-proBNP

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Nutritional Cardiomyopathy –Outcomes Nutritional Cardiomyopathy –Outcomes

• Daisy #2 – Echo • Daisy #2 –Treatment plan

• Pimobendan • Furosemide • Enalapril • Taurine • Diet change

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Nutritional Cardiomyopathy –Outcomes Nutritional Cardiomyopathy –Ongoing Study

• Daisy #2 – Outcome • Tufts DCM Study

• Did well at home for 2 days • Any dog withDCM • Returned to ERwith lethargy and dyspnea • 3, 6, 9 monthrechecks • Must change to an approved diet • Cannot have already changeddiet

[email protected]

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Nutritional Cardiomyopathy –Outcomes Our CurrentRecommendations

• Daisy #2 –Taurine levels • All animals should get a full nutritional assessment

• Plasma: 125 [normal 60-120nmol/mL] • Weight • Whole blood: 296 [normal 200-350 nmol/mL] • Body condition score • Muscle condition score • Diet history

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Our CurrentRecommendations Our CurrentRecommendations

• Healthy dog eatinga BEG diet • Change diet to a well-establishedcompany Normal PE • With grains,no exotic ingredients, no lentils in top 5 No clinicalconcerns

https://vetnutrition.tufts.edu/petfoodology/ • Submit NT-proBNP (toIDEXX) • Change diet

https://vetmed.tufts.edu/heartsmart/

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Our CurrentRecommendations Our CurrentRecommendations

• NT-proBNP • Symptomatic dog eatinga BEG diet

• < 900 pmol/L– Generally normal • Dx & tx CHF,arrhythmia asfor DCM • Submit taurine levels to UCDavis • Dobies run low (normal< 500?) • Change diet to a well-establishedcompany • Labradors run high (normal< 2000?) • Supplement taurine • Report to FDA • Screenhousemates

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Our CurrentRecommendations Our CurrentRecommendations

• Taurine supplementation • Don’t overlook the classic“DCM breeds” • Brands: NOW,Solgar,Twinlab, Thorne, PetAg(Consumerlab review)

• Doses: < 10 kg: 250 mg q12h 10-25kg: 500 mg q12h >25kg: 1000 mg q12h

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Our CurrentRecommendations Our CurrentRecommendations

• Avoid: Same diet +taurine • Doberman eating a BEGdiet Same diet +grains

6mo

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Our CurrentRecommendations

• Doberman eating a BEGdiet Questions?

6mo

Emily Karlin [email protected] NT-proBNP: 1703 NT-proBNP: 629

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Selected References Conclusions • Pion PD, Kittleson MD, RogersQR, et al. Myocardial failure in cats associated with low plasma taurine: a reversible cardiomyopathy. Science 1987;237:764–768

• KramerGA, Kittleson MD, FoxPR,Lewis J,Pion PD. PlasmaTaurine Concentrationsin Normal Dogs and in Dogs with Heart Disease. JVet Intern Med. • Nutritional cardiomyopathy 1995;9:253–8.

exists, but the current issue is • Kittleson MD, Keene B, Pion PD, Loyer CG,InvestigatorsS. Resultsof the MulticenterSpanielTrial(MUST): Taurine- and Carnitine-Responsive Dilated yet to be fully understood Cardiomyopathy inAmericanCockerSpanielsWith Decreased PlasmaTaurine Concentration. JVet Intern Med. 1997;11(4):204–11. • FascettiAJ,Reed JR,RogersQR, BackusRC.Taurine deficiencyin dogs with dilated cardiomyopathy: 12cases(1997-2001).JAm Vet MedAssoc. • Diagnose & treat similar to DCM 2003;223(8):1137–41. Available from:papers2://publication/uuid/11D30A52-27D1-4EA7-B7D6-9F55E8EF07D1 • Bélanger MC,Ouellet M, Queney G, MoreauM.Taurine-deficient dilated cardiomyopathy in a family of golden retrievers. Journal of theAmericanAnimal • Taurine testing, HospitalAssociation. 2005 Sep;41(5):284-91. • Vollmar AC, Fox PR, Servet E, Biourge V. Determination of the prevalence of whole blood taurine in Irish wolfhound dogs with and without supplementation, diet change echocardiographic evidence of dilated cardiomyopathy. JVet Cardiol. 2013;15(3):189–96.Availablefrom: http://dx.doi.org/10.1016/j.jvc.2013.03.005

• Freeman LM, Stern JA, Fries R,Adin DB, RushJE.Diet-associateddilated cardiomyopathy in dogs: what do we know? Journal of theAmericanVeterinary • Outcomes are variable, butcan be MedicalAssociation. 2018 Dec 1;253(11):1390-4. better than typicalDCM • Kaplan JL,Stern JA, FascettiAJ,Larsen JA,Skolnik H, PeddleGD, et al.Taurine deficiencyand dilated cardiomyopathy in golden retrievers fed commercial diets. PLoS One.2018;13:1–19.

• Adin D, DefrancescoTC, Keene B,TouS, Meurs K,Atkins C, et al. Echocardiographicphenotype of canine dilated cardiomyopathy differs based on diet type. JVet Cardiol.2019;21:1–9.Availablefrom: https://doi.org/10.1016/j.jvc.2018.11.002

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