Canine Valvular Heart Disease: ACVIM Staging Notes for Veterinary Teams
These are the clinical notes for the 1-hour continuing education lecture “Understanding Canine Valvular Heart Disease: Classification, Diagnosis and Management,” presented by veterinary cardiologist Dr. Matthew W. Miller for the Dr. Fossum’s Pet Care veterinary CE series. They are written for veterinarians and technicians: the staging criteria, the cutoff numbers, the prognosis figures for client conversations, and the stage-driven therapy logic, with primary references. The full lecture carries 1 hour of RACE-approved CE credit.
Clinical bottom line
Degenerative mitral valve disease is the most common cardiac disease of small animal practice, and the ACVIM staging scheme is the working tool: it converts a murmur into a prognosis, a diagnostic plan, and a therapy decision.
The pivotal distinction is B1 versus B2, asymptomatic disease without versus with significant remodeling, because B2 is where pimobendan has trial-proven benefit (about 15 more symptom-free months in EPIC) and B1 is where routine drug therapy for the valve disease itself is not recommended.
Radiographs plus NT-proBNP can carry most of the staging load when echo is out of reach, and a substantial share of murmur-plus-cough seniors are not in failure and need airway workup, not more furosemide.
About the lecturer
Matthew W. Miller, DVM, MS, DACVIM (Cardiology) trained at The Ohio State University and served 26 years on the faculty of Texas A&M University before moving to specialty private practice in Arizona, where he is medical director and cardiologist at Thrive Pet Healthcare Specialists North Scottsdale. Financial disclosure: Dr. Miller formulated a cardiac support supplement sold by Dr. Fossum’s Pet Care, which sponsors this CE program. These notes are educational.
The disease, and who gets it (2:13)
Degenerative (myxomatous) mitral valve disease, also called endocardiosis, is presented in the lecture as roughly 70 percent of the canine cardiac caseload, far ahead of congenital disease, pericardial disease, dilated cardiomyopathy, and heartworm.
It is a degenerative and heritable process, not an infectious one, and Miller spends a moment on the dental-disease question: dental disease is not established as a cause of valve degeneration, which shows up in dogs with pristine mouths. (Dental health still matters for vascular reasons, and, usefully, most murmur dogs that have never been in failure tolerate anesthesia for dentistry well; assess cardiac stage and anesthetic risk when planning dental care rather than deferring it on the murmur alone.)
Signalment: predominantly small breeds, typically under 10 kg. Cavalier King Charles Spaniels are the classic breed; Havanese, Shih Tzus, Lhasa Apsos, and Dachshunds follow. Among larger dogs, sighthounds and Labradors appear, while Dobermans mostly belong to the dilated cardiomyopathy story instead. A practice seeing small-breed seniors sees this disease weekly if not daily.
Heart disease is not heart failure (7:32)
The lecture’s central distinction. Heart disease is any cardiac abnormality: a leak, an arrhythmia, an elevated pressure. These notes use heart failure to mean congestive heart failure, which is fluid: pulmonary edema when the left side fails, ascites (in dogs) when the right side does.
A large fraction of dogs with valvular disease never become clinical and never need a cardioactive drug. Miller’s own estimate: about 20 percent of his clinical day goes to reducing or stopping cardiac medications, not starting them, mostly in murmur dogs whose respiratory signs came from inflammatory airway disease, tracheobronchial collapse, or bronchomalacia rather than failure. The murmur got them referred; the airway was the problem.
Two physical-exam anchors from the lecture. Dogs with hemodynamically important mitral disease have obvious murmurs; the EPIC trial required at least grade 3 of 6 for entry. And, in the lecture’s experience, an aged small-breed dog with no murmur at all is very unlikely to be hiding clinically significant valvular disease.
Diagnostics and the numbers that stage a dog (9:22)
Radiographs: vertebral heart score (VHS), VLAS, and the progression sequence
Thoracic radiographs answer the first staging question: is the heart remodeled? Mitral regurgitation is a volume load; an important leak enlarges the heart, and a normal cardiac silhouette in a murmur dog argues the leak is inconsequential. VHS and VLAS are measured on the lateral view; for the orthogonal view pick one convention (VD or DV) and have your team shoot it consistently, because you read change better against a consistent baseline.
- Vertebral heart scale (VHS): long axis (carina to apex) plus perpendicular short axis, summed in vertebral-body lengths starting at T4. Normal is under about 10.5, with some breeds legitimately running to 11. Many digital systems now compute it, including AI-assisted versions Miller considers usably accurate.
- Vertebral left atrial size (VLAS): carina to the caudal intersection of the left atrium with the caudal vena cava, in vertebral lengths. The lecture’s working rule: above about 2.5, the dog is usually entering stage B2 territory, and the primaries agree. In Stepien’s 2020 series 2.5 was the optimal B2 cutoff (sensitivity 70 percent, specificity 84 percent); a VLAS of 2.3 or more predicts left atrial enlargement (Malcolm 2018); and 3.0 or more is the rule-in threshold (specificity 96 percent in Stepien 2020; the Cardiac Education Group flags a VHS of 11.5 or more or a VLAS of 3 or more as likely B2). Treat VLAS as a strong screen that echo confirms.
- The progression sequence worth memorizing, because it is what serial films show: left atrial enlargement first, then left ventricular elongation, tracheal elevation, with or without left mainstem bronchus compression (a proposed driver of chronic cough even out of failure; airway disease and left atrial enlargement often coexist), then distended pulmonary veins, and finally perihilar-patterned edema: congestive failure.
Echo, ECG, and where they actually rank
Echocardiography is the gold standard for severity, staging precision, and the prognosis-changing complications (pulmonary hypertension, ruptured chordae, falling systolic function, pericardial effusion from left atrial tear). Characteristic findings: nodular thickened AV valves, prolapse of the anterior leaflet into the left atrium, and, early on, normal to hyperdynamic systolic function; myocardial failure is a late-disease event in survivors of long management.
ECG plays a minor role at diagnosis (these dogs rarely start with important arrhythmias) but matters in the long-managed stage C dog who decompensates: atrial fibrillation, fast and irregular with absent P waves, is the classic late complication.
NT-proBNP: the working bands (29:04)
| NT-proBNP (pmol/L) | Asymptomatic murmur dog | Dog with clinical signs |
|---|---|---|
| Under 900 | Clinically significant disease less likely; monitor | Failure unlikely; look elsewhere for the signs |
| 900 to 1,800 | Clinically significant disease likely (the IDEXX threshold is 900 or more); image to assign the stage | Indeterminate: this band does not separate failure from other causes; radiographs, ideally plus echo |
| Over 1,800 | Significant disease likely; image | Failure likely in a compatible clinical picture; radiographs (ideally plus echo) are indicated |
The cutoffs are the IDEXX Cardiopet proBNP bands and the interpretations follow IDEXX’s published criteria; the lecture’s practical gloss is that the middle band in an asymptomatic dog usually means remodeling worth staging. Two usage notes from the lecture: day-to-day biologic variability runs 25 to 30 percent, so 800 today and 900 tomorrow is the same number; and trend-based monitoring (BNP as a therapy-response gauge) is an active research area rather than settled cutoffs.
Where finances rule out serial imaging, BNP plus radiographs carry a real share of the staging and monitoring load. Canine-specific assays are available both in-house and through reference labs.
ACVIM stages A to D: prognosis and therapy in one table (36:37)
Adapted by the 2009 ACVIM panel from the human ACC/AHA heart-failure stages (Atkins 2009), and the reason classification “matters” is in the two right-hand columns: each stage carries a prognosis you can say out loud to a client and a therapy decision with evidence behind it.
| Stage | Definition | Prognosis (as presented in the lecture) | Therapy (2019 ACVIM consensus) |
|---|---|---|---|
| A | At-risk breed, no structural disease (born a Cavalier) | May never develop clinical disease | None; auscultate at every wellness visit |
| B1 | Murmur, regurgitation on echo, minimal or no remodeling | Less than a 1-in-3 chance of ever reaching failure | No cardioactive drugs; the consensus recommends no drug or dietary treatment; re-image in 6 to 12 months |
| B2 | Asymptomatic with significant remodeling: murmur at least 3/6 plus LA/Ao at least 1.6, LVIDDN at least 1.7, and breed-adjusted VHS above 10.5 (the EPIC-derived consensus definition) | About 50 percent reach failure within 2 years | Start pimobendan (EPIC evidence, below); mild sodium restriction; ACE inhibitor or spironolactone here is still an open question |
| C | Past or present congestive heart failure | About 13 to 20 months in the lecturer’s managed population (as presented). Published CHF trials report shorter medians to composite endpoints (QUEST: 267 days on pimobendan, 140 on benazepril), which include treatment failure, not only death | Consensus quadruple therapy: furosemide, pimobendan, ACE inhibitor, spironolactone; moderate sodium restriction with adequate calories and protein |
| D | Failure refractory to standard therapy | Typically weeks | Escalated diuretics, pimobendan up to three times daily (an off-label frequency the consensus lists as a weak-evidence option), rate control for atrial fibrillation (diltiazem, often with digoxin; the lecture also lists sotalol), amlodipine for additional afterload reduction |
On nutrition the table follows the consensus, not the lecture: the 2019 consensus recommends no drug or dietary treatment at B1, mild sodium restriction from B2, and at stage C considers omega-3 supplementation reasonable in selected dogs (Class IIa, expert opinion). The part of the lecture’s supplement teaching that matters clinically is the supportive-versus-active distinction in the section below.
The B1-to-B2 transition is the moment that matters most in this disease: clinically the dogs look identical, and the diagnostics (radiographs, VLAS, BNP, echo) are the only way to catch the change. Catching it is what the EPIC benefit depends on, which is the next section.
Stage B2 and the EPIC pimobendan evidence (51:21)
Pimobendan is an inodilator: a calcium sensitizer (stronger contraction without a proportional oxygen bill) plus a phosphodiesterase-3 inhibitor (peripheral vasodilation). The vasodilation is not a side note in mitral disease: regurgitant volume is set by orifice size, which medical therapy does not change, and by the resistance ratio between forward and backward flow, which vasodilation improves.
In the EPIC trial, stage B2 dogs started on pimobendan went a median of 1,228 days to the composite endpoint of congestive failure, cardiac death, or euthanasia versus 766 days on placebo: roughly 15 more symptom-free months (the FDA label’s analyses of the same program span about 13 to 15.6 months, which is why we quote a range rather than one number). Vetmedin’s B2 indication, delaying the onset of congestive heart failure, moved from a 2022 conditional approval to full FDA approval in December 2025. In the lecture Dr. Miller rounds the EPIC benefit to about 18 months; these notes use the published medians.
Once dogs are in failure, pimobendan beat benazepril head-to-head on top of standard background therapy (QUEST: median 267 vs 140 days to the composite of cardiac death, euthanasia, or treatment failure).
US forms: chewable tablets in 1.25, 2.5, 5, and 10 mg, which the lecture recommends giving on an empty stomach (the US label gives no food instruction and says the effect of food on tablet absorption is unknown), plus an FDA-approved oral solution (1.5 mg/mL, syringed into the mouth, not mixed into food) for small or hard-to-pill dogs. A generic pimobendan chewable (Pimomedin) has been FDA-approved since April 2024 for the heart-failure indication only, not the B2 delay indication. The full dosing and label detail lives in our heart medications guide.
Note what the lecture does not do: it does not start pimobendan at B1. Routine therapy for the valve disease itself is not recommended before remodeling, and that is exactly why the staging diagnostics earn their cost.
Nutrition and supplements: supportive versus active (44:06)
Diet: moderate sodium restriction, not severe (severe restriction risks inappetence in patients who are already a nutritional challenge). The lecture names the veterinary cardiac diets from Royal Canin and Purina Pro Plan as examples, with the explicit caveat that they are supportive, not therapeutic.
The supplement chapter is built on one clinically useful distinction. Cardio-supportive ingredients, in the lecture’s framing, are nutrients that supply substrate for myocardial energy metabolism and vascular tone: amino acids, omega-3 fatty acids and antioxidant cofactors. The one trial the lecture cites for the category studied six weeks of fish oil in Boxers with arrhythmogenic right ventricular cardiomyopathy (Smith 2007), a different disease in a different population, and none of these nutrients is a treatment for valve disease.
Cardioactive ingredients change rhythm, contractility, or volume status, and they do not belong in an over-the-counter supplement stacked on top of prescription cardiac drugs.
The screening rule Miller gives: read combination supplement labels for digitalis-like botanicals and for herbal diuretics, dandelion root being the classic example, because an uncounted diuretic in a preclinical dog, or added to prescribed furosemide in a stage C dog, is an interaction you did not plan for. That checklist, not any particular brand, is the takeaway. (See the disclosure above; product specifics are out of scope for these notes.)
When medical management is not the ceiling (42:35)
Most dogs are managed medically, but the interventional options are real and growing. Open surgical valve repair under bypass: the Japanese groups the lecture credits, and in the US the University of Florida program (launched August 2023; it considers stage C, D and advanced B2 dogs and excludes B1, early B2 and dogs 14 or older; UF’s own page, read September 2026, quotes 8 to 10 weeks for record review, 3 to 4 months of preparation, and surgery “as far as 1 year out”).
Transcatheter edge-to-edge repair (TEER, the V-Clamp): Colorado State was the first established center and has the largest published series (111 dogs from 2021 to 2025: in-hospital mortality 6.3 percent, one-year survival 75 percent, two-year 67 percent) but had paused new case reviews for volume as of September 2026; the lecture also names Texas A&M and Illinois and two Los Angeles private practices (VCA West Los Angeles was the first private practice to do it, in February 2023), and more private programs have opened since.
Left atrial decompression, a created atrial septal defect as a pressure pop-off for advanced stage C dogs, is offered by several private practices including the lecturer’s own; the first 17-dog series reported a median 195 days of survival after the procedure (Allen 2021).
Referral-worthy candidates are typically B2 and C dogs whose owners want an option beyond pills; the practical move is knowing which centers within reach are taking cases this year. Center status as of September 29, 2026.
Frequently asked questions
A murmur dog is coughing. Failure until proven otherwise?
No, and this is one of the lecture’s loudest points. Murmur plus cough in a small-breed senior is compatible with failure, with airway disease (inflammatory, collapsing, or malacic), and with mainstem bronchus compression from a big left atrium in a dog not in failure.
Radiographs answer most of it: an unremodeled heart makes failure very unlikely, and a normal-lung film with a large left atrium raises compression cough as a differential, though airway disease and left atrial enlargement often coexist. BNP helps discriminate cardiac from non-cardiac respiratory distress when the picture stays murky.
Can I stage without an echocardiogram?
To a working degree, yes: murmur grade, radiographic remodeling (VHS, VLAS, the progression sequence), and NT-proBNP bands will sort most dogs into not-remodeled versus remodeled versus probably-in-failure. Echo remains the reference standard, sharpens the B2 call (LA/Ao, LVIDDN), and finds the prognosis-changing complications, so it is the right answer where owners can elect it, and before committing a dog to lifelong drugs on a borderline call.
The 2019 consensus allows a radiographic substitute when echo is out of reach: clear cardiomegaly (a general-breed VHS of 11.5 or more, or the breed-adjusted equivalent) or accelerating interval change on serial films can stand in for quantitative echo to identify B2, and a VLAS of 3 or more carries minimal false-positive risk (Stepien 2020).
What actually changes at each stage boundary?
A to B1: disease now exists; still no cardioactive therapy. B1 to B2: remodeling crossed the thresholds; start pimobendan, backed by EPIC. B2 to C: fluid arrived; add the consensus stack (furosemide, ACE inhibitor, spironolactone) around the pimobendan. C to D: standard therapy no longer holds the line; escalate diuretics and frequency, manage the arrhythmias, and discuss prognosis, treatment burden and quality of life with the owner.
Each boundary is also a prognosis update for the client, which is why stage, findings and uncertainties are the right vocabulary in the exam room.
Earn the CE credit
The full hour includes the radiograph series (the same dog crossing from B1 to B2 to C with matched BNP values), the echo clips, and the complete therapy walk-through. Watch it free and earn 1 hour of RACE-approved CE: Understanding Canine Valvular Heart Disease: Classification, Diagnosis and Management (1 CE hour). Watch at least 75 percent, pass the six-question quiz at 70 percent, and the certificate is issued on the spot and emailed to you.
This program has been RACE approved for 1 hour of continuing education credit in jurisdictions that recognize RACE approval. RACE program number 20-1291735 (provider 50-29133), approved through 2027-04-23; category Medical; delivery method Non-Interactive-Distance. RACE does not accredit, endorse, or certify any program or person, nor does RACE approval validate the content of the program.
References
- Keene BW, Atkins CE, Bonagura JD, et al. ACVIM consensus guidelines for the diagnosis and treatment of myxomatous mitral valve disease in dogs. J Vet Intern Med. 2019;33(3):1127-1140. PMID 30974015.
- Boswood A, Haggstrom J, Gordon SG, et al. Effect of pimobendan in dogs with preclinical myxomatous mitral valve disease and cardiomegaly: the EPIC study. J Vet Intern Med. 2016;30(6):1765-1779. PMID 27678080.
- Haggstrom J, Boswood A, O’Grady M, et al. Effect of pimobendan or benazepril hydrochloride on survival times in dogs with congestive heart failure caused by naturally occurring myxomatous mitral valve disease: the QUEST study. J Vet Intern Med. 2008;22(5):1124-1135. PMID 18638016.
- Buchanan JW, Bucheler J. Vertebral scale system to measure canine heart size in radiographs. J Am Vet Med Assoc. 1995;206(2):194-199. PMID 7751220.
- Stepien RL, Rak MB, Blume LM. Use of radiographic measurements to diagnose stage B2 preclinical myxomatous mitral valve disease in dogs. J Am Vet Med Assoc. 2020;256(10):1129-1136. PMID 32364449.
- Malcolm EL, Visser LC, Phillips KL, Johnson LR. Diagnostic value of vertebral left atrial size as determined from thoracic radiographs for assessment of left atrial size in dogs with myxomatous mitral valve disease. J Am Vet Med Assoc. 2018;253(8):1038-1045. PMID 30272515.
- Cardiac Education Group. Canine cardiac diagnostic scheme: ABCDs of myxomatous mitral valve disease. Updated January 2021. cardiaceducationgroup.org (PDF).
- Atkins C, Bonagura J, Ettinger S, et al. Guidelines for the diagnosis and treatment of canine chronic valvular heart disease. J Vet Intern Med. 2009;23(6):1142-1150. PMID 19780929.
- Smith CE, Freeman LM, Rush JE, Cunningham SM, Biourge V. Omega-3 fatty acids in Boxer dogs with arrhythmogenic right ventricular cardiomyopathy. J Vet Intern Med. 2007;21(2):265-273. PMID 17427387.
- Allen JW, Phipps KL, Llamas AA, Barrett KA. Left atrial decompression as a palliative minimally invasive treatment for congestive heart failure caused by myxomatous mitral valve disease in dogs: 17 cases (2018-2019). J Am Vet Med Assoc. 2021;258(6):638-647. PMID 33683957.
- Potter BM, Orton EC, Scansen BA, et al. One-year echocardiographic follow-up and two-year survival in 111 dogs undergoing mitral transcatheter edge-to-edge repair. J Vet Cardiol. 2025; online ahead of print, doi 10.1016/j.jvc.2025.12.002. PMID 41513577.
Related resources on this site: the owner-facing heart murmur guide and congestive heart failure guide, which cover the same staging ground in client language your team can hand out. Educational content provided by Dr. Fossum’s Pet Care.
These notes summarize a recorded continuing-education lecture for veterinary professionals. They are educational, not clinical guidelines; decisions about an individual patient belong to the attending veterinarian.