Myxomatous mitral valve disease is a degenerative condition in which the mitral valve, the one-way gate between the left atrium and left ventricle of the heart, gradually thickens and deforms. The disease involves profound changes in the cellular makeup and extracellular matrix of the valve tissue, particularly in collagen content and alignment. The spongy middle layer of the valve leaflets expands as proteoglycans accumulate, while activated myofibroblasts break down collagen and elastin through increased release of proteolytic enzymes. The result is a malformed valve apparatus that no longer seals properly, allowing blood to leak backward from the left ventricle into the left atrium with every heartbeat. This leakage, known as mitral regurgitation, drives progressive enlargement of the left-sided heart chambers and eventually culminates in congestive heart failure.

A key anatomical feature in this disease is the coaptation gap, the space between the anterior and posterior leaflets of the mitral valve when they should be meeting to form a seal. The larger this gap, the greater the volume of blood that escapes backward with each contraction. In most patients, once heart failure sets in, the only options are medications to manage the symptoms and, in some specialized centers, surgical valve repair. Without surgery, the valve condition deteriorates in nearly all cases, and as diuretic resistance develops and the ceiling effect of these drugs is reached, patients progress to Stage D of the American College of Veterinary Internal Medicine classification, a refractory state defined in dogs by a total daily furosemide dose of 8 milligrams per kilogram or an equivalent torsemide dosage. At that point, the prognosis is grim.

The three dogs in the report, all Maltese, arrived at the hospital with classic signs of left heart failure: coughing, breathing difficulties, and elevated sleeping respiratory rates. All three underwent echocardiography performed by a single experienced operator using the same ultrasound system, with standardized imaging views and measurement protocols applied consistently. Each dog showed severe mitral regurgitation, partial rupture of the chordae tendineae, the tendon-like strands that anchor the valve leaflets, and significant enlargement of the left atrium and left ventricle. Standard heart failure treatment was initiated, including furosemide, an angiotensin-converting enzyme inhibitor, pimobendan, and spironolactone, and in all cases the clinical symptoms improved. What happened next was anything but standard.

The first case, a 14-year-old spayed female Maltese, presented with a sleeping respiratory rate exceeding 35 breaths per minute for more than three consecutive days. Her initial echocardiogram revealed an anterior mitral valve leaflet thickened to 4.63 millimeters, a coaptation gap of 4.18 millimeters, and a regurgitant volume of 98.8 milliliters with a regurgitant fraction of 95.4 percent, figures consistent with catastrophic valve leakage. Her furosemide dose was eventually escalated to 8 milligrams per kilogram per day along with torsemide at 0.4 milligrams per kilogram per day. Yet 26 months after her initial visit, radiographs showed her heart had shrunk, with the vertebral heart size falling from 12.8 to 11.6 and the vertebral left atrial size dropping from 3.2 to 2.4. The valve had actually thickened further to 9.55 millimeters, but the coaptation gap had vanished, becoming too small to measure. Her regurgitant volume plummeted to 5.67 milliliters and the regurgitant fraction to 34.5 percent. She has now been managed with pimobendan alone for six months, free of diuretics.

The second case, a 9-year-old castrated male Maltese, arrived with dyspnoea and coughing and required intravenous furosemide and oxygen supplementation to stabilize. His initial echocardiogram showed a coaptation gap of 3.61 millimeters, a regurgitant fraction of 96 percent, and a regurgitant jet occupying 88.5 percent of the left atrial area. Twenty-eight months later, his vertebral heart size had decreased from 11.3 to 10.0, the coaptation gap was no longer measurable, and the jet area ratio had collapsed to 11.1 percent, indicating mild regurgitation. His regurgitant volume fell from 28.33 to 3.46 milliliters. He has been maintained on pimobendan alone for 22 months. The third case, a 12-year-old castrated male Maltese, followed a similar arc over 12 months: his regurgitant fraction dropped from 96.36 to 62.61 percent, his left atrial-to-aortic ratio improved from 2.53 to 1.55, and he has been diuretic-free for nine months.

The quantitative echocardiographic methods used to track these changes were rigorous. Regurgitant volume and regurgitant fraction were calculated from four key measurements: the diameter of the aortic valve during systole, the velocity-time integral of aortic outflow, the diameter at the tips of the mitral leaflets during early diastole, and the velocity-time integrals of the E and A waves of mitral inflow. A semi-quantitative measure, the ratio of the regurgitant jet area to the left atrial area, provided an additional cross-check. In all three dogs, every parameter moved in the direction of improvement, even as the valves themselves continued to degenerate and thicken, a paradoxical combination that has never before been documented at this stage of the disease.

The authors propose that the phenomenon may parallel rare human cases in which severe regurgitation caused by a flail mitral valve improves spontaneously. In human medicine, such improvement has been attributed to mitral valve adaptation, in which the anterior leaflet enlarges to close the coaptation gap, promoting reverse ventricular remodelling without surgery. This process has been suggested to involve the reactivation of embryonic developmental pathways, including endothelial-to-mesenchymal transformation, leading to increased leaflet area and thickness that restore coaptation and reduce leakage. Whether a similar mechanism operated in these dogs remains unknown, and the authors caution that the exact structural changes underlying their observations are unclear. The report also acknowledges an important limitation: the contribution of pimobendan, a drug known to improve haemodynamics, cannot be fully excluded, although there is currently limited evidence that it can induce marked and sustained reductions in regurgitation severity and cardiac remodelling in advanced disease.

The prognostic implications are striking. Using the Mitral INsufficiency Echocardiographic score, a tool for predicting severity and survival in dogs with severe mitral regurgitation, the expected median survival duration for these three dogs was approximately 623 days. Instead, all three survived well beyond that window, remaining alive without dyspnoea, coughing, or syncope months to years after discontinuing diuretics. The authors suggest the cases point to three remarkable possibilities: spontaneous healing of valve function despite ongoing degeneration, reversal of cardiac remodelling without surgery, and long-term survival that current prognostic models fail to predict. Recent evidence from surgical studies has shown that restoring coaptation length can reverse remodelling even in late-stage disease, but these dogs achieved similar outcomes naturally, as if they had undergone repair without ever seeing an operating theatre.

For now, the authors emphasize caution. The prognosis for myxomatous mitral valve disease accompanied by chordae tendineae rupture remains poor, and such spontaneous improvements are exceedingly rare. But the report opens a genuinely new avenue of inquiry: if the valve apparatus can, in some patients, remodel itself to close the leak, identifying the biological signals that drive this adaptation could transform how veterinarians and perhaps even human cardiologists approach degenerative valve disease. Further research is needed to uncover the mechanisms behind this phenomenon and to find markers that might predict which patients will experience such favourable outcomes. In the meantime, three elderly Maltese dogs are breathing easily on a single daily medication, living proof that even the most predictable of diseases can occasionally surprise the experts who study it.

Subject of Research: Spontaneous reduction of mitral regurgitation in dogs with severe myxomatous mitral valve disease

Article Title: Spontaneous Reduction in Mitral Valve Regurgitation in Three Dogs With Severe Myxomatous Mitral Valve Disease: An Unusual Case Report

Article References: Nam, H.-S., & Oh, Y. (2026). Spontaneous Reduction in Mitral Valve Regurgitation in Three Dogs With Severe Myxomatous Mitral Valve Disease: An Unusual Case Report. Veterinary Medicine and Science, 12(6), Article e71155. https://doi.org/10.1002/vms3.71155

Image Credits: AI Generated

DOI: 10.1002/vms3.71155

Keywords: myxomatous mitral valve disease, mitral regurgitation, dogs, veterinary cardiology, echocardiography, coaptation gap, chordae tendineae rupture, heart failure, pimobendan, diuretics, reverse remodelling, case report