Left Atrial Rupture Secondary to Myxomatous Mitral Valve Disease in 11 Dogs

Introduction

Left atrial rupture (LAR) has been described in the veterinary literature as a rare consequence of myxomatous mitral valve disease in dogs.^1–3 A study reported that only 5 of 14 dogs diagnosed with LAR secondary to myxomatous mitral valve disease survived to discharge and 3 of those 5 dogs were euthanized within 35 days of diagnosis. Consequently, the study concluded that dogs with LAR have a poor short- and long-term prognosis.³ The authors’ experience in the management of LAR secondary to myxomatous mitral valve disease has been inconsistent with the results of that previously published study.³ As such, the purpose of this current study was to evaluate the long-term survival of LAR secondary to myxomatous mitral valve disease in dogs diagnosed via echocardiographic evaluation.

Materials and Methods

The medical records database at VCA Advanced Veterinary Care Center in Lawndale, California was searched for all dogs with a diagnosis of a LAR secondary to myxomatous mitral valve disease between January 1, 2009 and May 1, 2012. Dogs were included in the study if they had a complete echocardiographic examination diagnosing the LAR. The echocardiogram had to be performed by a board-certified cardiologist or a cardiology resident under the supervision of a board-certified cardiologist to be included in the study. The echocardiographic diagnosis of a LAR was based on the presence of the following four criteria: (1) myxomatous mitral valve disease and severe mitral regurgitation defined as >50% of the atrium filled by aliased flow of regurgitation on color Doppler interrogation; (2) left atrial/ aortic root ratio >1.5:1 on two-dimensional measurement on the right parasternal short-axis view; (3) pericardial effusion; and (4) organized echogenic material in the area of the left atrium within the pericardial space suggestive of a thrombus on any echocardiographic view.^3–5 Dogs were excluded from the study if the medical record was either incomplete/missing or the echocardiographic evaluation did not fulfill the criteria for a LAR.

Medical records of the dogs were reviewed. Data collected from the medical records included signalment, history, physical examination findings, results of radiographic and echocardiographic findings, treatment, and long-term outcome. Median survival time was reported for the 11 dogs from the day of diagnosis of LAR. The dogs were then divided into the following two groups: dogs with a previous history of congestive heart failure (CHF) at the time of diagnosis of the LAR and those without a previous history of CHF. The survival data for the two populations were compared.

Results

A total of 13 dogs were identified. One was excluded because the medical record could not be located, and another was excluded because a complete echocardiographic evaluation was not performed. Consequently, 11 dogs met the criteria for inclusion in the study. There were 6 castrated male dogs and 5 spayed female dogs. Breeds included were the Chihuahua (n = 2), toy poodle (n = 1), whippet (n = 1), papillon (n = 1), Welsh springer spaniel (n = 1), shih tzu (n = 1), miniature schnauzer (n = 1), Jack Russell terrier (n = 1), Cavalier King Charles spaniel (n = 1), and mixed-breed (n = 1). Median age was 11.6 yr (range, 8.3–17.8 yr) and median body weight was 5.8 kg (range, 3.8–15.2 kg). Reported clinical signs included weakness or collapse (n = 7), rapid respiratory rate (n = 6), coughing (n = 4), vomiting (n = 1), and loud borborygmi (n = 1). Five of the 11 dogs had been treated for decompensated left-sided congested heart failure prior to the diagnosis of a LAR for a median duration of 160 days (range, 47–710 days). Treatment of those 5 dogs included furosemide^a (n = 5), angiotensin converting-enzyme inhibitors^b (n = 5), pimobendan^c (n = 2), and potassium supplementation^d (n = 1).

A systolic heart murmur was identified over the left apex in all 11 dogs. They were graded as III/VI (n = 3), IV/VI (n = 5), and V/VI (n = 3). Muffled heart sounds were noted in 2 of the dogs. One of the 11 dogs had evidence of tachycardia (heart rate was >160 beats/min). Six dogs were described as tachypneic (respiratory rate was >60 breaths/min). Femoral arterial pulse quality was described as weak in 5 dogs and pulsus paradoxus was identified in an additional dog. Jugular venous distension was noted in 4 dogs.

Thoracic radiographs were performed in seven dogs. A globoid cardiac silhouette was identified in five of the dogs, and severe left atrial and left ventricular enlargement was identified in two other dogs. Perihilar infiltrates assessed as consistent with decompensated left-sided CHF was identified in four of the seven dogs.

The median left atrial/aortic ratio was 2.14 (range, 1.69–2.59). Mitral valve prolapse was identified in 5 dogs.^6,7 Myxomatous tricuspid valve disease was identified in 10 dogs, which was subjectively assessed as mild in 9 dogs and moderate in the other dog. Median estimation of peak systolic pulmonary artery pressure based on the maximum tricuspid regurgitant velocity via the modified Bernoulli equation was 29 mm Hg (range, 16–48.8 mm Hg). Cardiac tamponade defined as collapse of the right atrium during diastole was visualized in 8 dogs. One dog demonstrated evidence of a ruptured chordae tendineae and another dog was subjectively assessed as having trivial aortic insufficiency.^8,9

Of the 11 dogs, 4 dogs were discharged from the hospital and 7 dogs were hospitalized for treatment of the LAR. Two of the 4 dogs that were not hospitalized had a systolic blood pressure measured via Doppler measurement and both were normotensive (systolic blood pressure >90 mm Hg). Pericardiocentesis was performed in 2 of the 4 dogs, in both instances hemorrhagic effusion was evacuated from the pericardial space. In 1 dog the volume removed was 28.96 ml/kg and in the other dog the volume of pericardial effusion collected was not recorded. One of the 4 dogs had a previous history of treatment of left-sided CHF.

Of the seven hospitalized dogs, one died in the hospital shortly after echocardiographic evaluation while two others had an episode of cardiopulmonary arrest; both of these latter two dogs were successfully resuscitated and survived to discharge. Of the six remaining dogs, two were hypotensive (defined as a systolic blood pressure <90 mm Hg via Doppler measurement) on admission to the hospital. In both hypotensive dogs, cardiac tamponade was evident on echocardiogram. One dog was hypotensive for approximately 5 hr while the other dog was hypotensive for approximately 8 hr. In the latter case, the dog was treated with IV crystalloids at 1 ml/kg/hr. In both cases after the elapsed time, systolic blood pressures increased to greater than 100 mm Hg. Of the six dogs that survived the initial 24 hr of hospitalization, treatment consisted of furosemide^e (n = 6), pimobendan (n = 6), oxygen supplementation (n = 4), hydralazine^f (n = 2) and intravenous crystalloid therapy^g (n = 1). None of the dogs that were hospitalized had a pericardiocentesis performed. The median duration of hospitalization for the six dogs was 2 days (range 1–4 days).

Long-term treatment of the 10 dogs that survived 24 hr after diagnosis included furosemide (n = 10), pimobendan (n = 9), angiotensin converting enzyme inhibitors (n = 8), potassium supplementation (n = 4), aldactazide^h (n = 2), amlodipineⁱ (n = 2) and hydralazine (n = 2).

All dogs that survived the initial 24 hr after diagnosis survived for at least 30 days after initial diagnosis. Of the 10 dogs, 5 of the dogs were still alive at the conclusion of the study. The median survival of all dogs in the study was 203 days (range 0–760 days). The 5 dogs with a previous history of CHF had all died by the end of the study and had a median survival time of 160 days (range 0–252 days). The cause of death in these 5 dogs was euthanasia due to renal failure (n = 2), euthanasia due to recurrent heart failure (n = 1), death in the hospital (n = 1) and 1 dog died at home from an unknown cause but suspected to be secondary to recurrent heart failure. Of the 6 dogs with no previous history of CHF prior to diagnosis of LAR, 1 dog developed recurrent CHF and was euthanized. The remaining 5 dogs were alive at the conclusion of the study. The median survival time of the 6 dogs with no previous CHF was 345 days (range 40–760 days) which was significantly longer (P = 0.0038) compared with dogs with a previous history of CHF.

Discussion

The primary finding of this study was that 10 of 11 dogs survived more than 24 hr after initial diagnosis of a LAR secondary to myxomatous mitral valve disease and all 10 dogs survived for at least 30 days after the initial diagnosis, which is an improved survival duration from the previous study of LAR in dogs.³ The difference in survival to discharge recorded in the current study compared with previously could be explained by differences in patient selection criteria. In our report dogs needed to be clinically stable enough to permit a complete echocardiographic evaluation.

However, the long term survival of dogs in this study was also improved compared with the previous study.³ While it is impossible to compare the two populations, one difference identified is that none of the dogs in the previous study received pimobendan, whereas all hospitalized dogs in this study and 9 of 10 dogs received pimobendan therapy chronically. Studies have shown improved survival times in dogs with myxomatous mitral valve disease and dilated cardiomyopathy receiving pimobendan.^10–12 As pimobendan is an inodilator, it improves contractility and promotes arteriolar vasodilation which has been suggested to increased left ventricular forward stroke volume and reduce left ventricular and atrial size.^13–15 Pimobendan has also been shown to reduce left atrial pressure in dogs with experimentally induced mitral valve regurgitation as well.¹⁶ The role of pimobendan in the emergent management of LAR secondary to myxomatous mitral valve disease requires further evaluation.

Previous studies on LAR in dogs reported a male predisposition as well as a possible breed predisposition for dachshunds and cocker spaniels.^1–3 However, our study identified a relatively equal distribution between male and female dogs and none of the dogs in our study were dachshunds or cocker spaniels. This difference in signalment and breeds identified may be related to the small sample size of our study as well as case selection criteria.

Despite the presence of significant cardiac disease as well as a LAR, none of the dogs in the study were treated with anticoagulant therapy. A previous study reported dogs with CHF secondary to myxomatous mitral valve disease or dilated cardiomyopathy are hypercoagulable compared with normal dogs.¹⁷ However, there was no clinical suspicion of thromboembolic disease in any of the 10 dogs with long term follow-up. As such there is no clinical evidence that antithrombotic therapy is indicated in the long-term management of dogs with LAR.

Limitations to the study are inherent in its retrospective design as well as the relatively small sample size. As previously mentioned, the criteria of a full echocardiogram being required for inclusion biased the study population toward a more stable population of dogs with LAR that likely contributed to the improved survival to discharge rates. Management for LAR tended to be similar between cases typically involving the use of loop diuretics and pimobendan in the emergent setting and, therefore, it is impossible to evaluate if one treatment significantly improved survival time over other therapeutic protocols. As our hospital computer system does not track frequency of presentation of different canine breeds, the authors were unable to evaluate if one breed is at higher risk for LAR than others.

Conclusion

In conclusion, the long term survival of dogs with LAR provided they survive the immediate period was more favorable in this study than previously reported. Dogs diagnosed with LAR with no previous history of CHF have a significantly longer survival time than dogs with a previous history of CHF.