Clinical Signs And Prognosis Between Dogs With Left Atrial Rupture Secondary To Myxomatous Mitral Valve Disease And Neoplastic Cardiac Tamponade | VETgirl Veterinary Continuing Education Podcasts
March 2024
In today’s VETgirl online veterinary CE podcast, we review the clinical signs, clinical course and prognosis for dogs diagnosed with pericardial effusion secondary to either left atrial rupture from myxomatous mitral valve disease versus those with neoplastic cardiac tamponade. This is based off a recent study by Sugiura et al entitled “Retrospective evaluation of clinical signs, clinical course, and prognosis between dogs with left atrial rupture secondary to myxomatous mitral valve disease and those with neoplastic cardiac tamponade (2015-2019): 70 cases.”
Now, as a criticalist, I love seeing pericardial effusion, as it’s fun to diagnose and treat… but that’s because I love performing a pericardiocentesis. That said, I personally never make the call on FAST ultrasound if the pericardial effusion is from a right atrial mass versus other causes, as I’ve seen the rare case where necropsy has revealed a “blood clot” versus a right atrial mass. I leave the echocardiogram to pros like cardiologists or radiologists.
One thing this VETgirl can diagnose? Cardiac tamponade. So what exactly is cardiac tamponade and what causes it. Cardiac tamponade occurs when there is compression of the cardiac chambers (secondary to accumulation of pericardial effusion), leading to secondary hemodynamic collapse and shock. Cardiac tamponade secondary is a life-threatening condition that can occur depending on volume and/or rate of accumulation of pericardial effusion. While neoplasia represents the most common etiology of pericardial effusion in dogs, other causes do occur, including rupture of the left atrium (LAR) in association with myxomatous mitral valve disease (what we’ll call MMVD from now on). When VETgirl sees this? Small dogs with loud heart murmurs (V/IV) that present in congestive heart failure that don’t “classically” get idiopathic or neoplastic pericardial effusion… like Chihuahuas or Yorkies. That’s because left atrial rupture can be seen secondary to MMVD secondary to chronic atrial dilation/thinning due to progressive mitral regurgitation in conjunction with direct trauma to the left atrial endocardium by the regurgitant jet itself. If the wall ruptures in the septal region of the left atrium, an acquired atrial septal defect occurs, which is not acutely life-threatening. It is in cases of caudal wall rupture that hemopericardium, and potentially tamponade, results.
So, Sugiura et al wanted to evaluate this in a retrospective study entitled “Retrospective evaluation of clinical signs, clinical course, and prognosis between dogs with left atrial rupture secondary to myxomatous mitral valve disease and those with neoplastic cardiac tamponade (2015-2019): 70 cases” to better classify the clinical findings and prognosis associated with left atrial rupture in comparison with neoplastic cardiac tamponade, which has been more thoroughly described in the existing literature.
Before we begin, remember that in cases of neoplastic cardiac tamponade, pericardiocentesis is almost always indicated to stabilize the patient. However, in cases of pericardial effusion secondary to left atrial rupture, the appropriate treatment path is not entirely clear. In left atrial rupture, direct communication of the left atrial chamber with the pericardial space exists, which creates the potential for immediate recurrent hemopericardium (and eventual exsanguination) if pericardiocentesis is performed/repeated. We’ll discuss this more in detail a bit later – for now, let’s keep our eyes open to see if this study sheds any light on whether a particular treatment strategy is most appropriate with left atrial rupture.
In this study, cases were selected from the time frame of 2015-2019. Cardiac tamponade was defined as physical examination findings consistent with hemodynamic shock in conjunction with echocardiographic evidence of collapse of the right atrium during diastole, and presence of tamponade served as the primary criteria for inclusion. As expected, clinical history, examination, lab work, imaging findings, and survival were recorded. Causes other than neoplasia or left atrial rupture were excluded. Dogs were classified in the left atrial rupture group if they had evidence of mitral valve thickening, severe mitral regurgitation, and left atrial enlargement [defined as left atrial-to-aortic root ratio (LA:Ao) 1.5:1] in the absence of a readily identifiable neoplastic lesion originating from the myocardium.
A total of 70 dogs ultimately qualified for inclusion in the study. 23 dogs were assigned to the left atrial rupture group compared with 47 in the neoplasia group. The most common tumor location in the neoplasia group was the right atrium, occurring in 91% of cases. This location is typically predictive of hemangiosarcoma in dogs. No differences in age or sex were identified between groups. Dogs with left atrial rupture were significantly smaller than those with neoplasia, which is not surprising given the demographic of dogs known to be affected by mitral valve disease (e.g., small dogs!) versus cardiac neoplasia (think Golden retriever, German shepherd or Labrador retriever!). Interestingly, though, the most common breed represented in the neoplasia group was still a small breed, the miniature dachshund (34%)! (Personally, this VETgirl hasn’t seen a Dachshund with pericardial effusion EVER!?!). I would speculate this may be a local geographic/demographic finding given that this study is exclusively from a single site in Japan, where smaller breed dogs may be more popular due to an urban setting. (In Minnesota, I only see Labradors, Goldens, and GSPs!).
In this study, the left atrial-to-aortic root ratio (LA:Ao) was significantly larger in the left atrial rupture group, and a large proportion of dogs in this group were receiving one or multiple cardiac therapies at the time of presentation. No surprises here, folks. These dogs have severe mitral valve disease and big atriums!
In this study, the clinical presentation of dogs in BOTH groups shared signs of hemodynamic shock such as collapse, altered mentation, pale mucous membranes, and hyperlactatemia. Presence of a heart murmur was more common in the left atrial rupture group, as expected, but so was tachypnea or dyspnea. No difference in basic vital signs (such as temperature, pulse and respiratory rate) was observed. Dogs with left atrial rupture had higher blood glucose but lower total protein, albumin and cholesterol. Dogs with left atrial rupture had a significantly higher incidence of detectable intrapericardial thrombus material (n=16) than dogs in the neoplasia group (n=3). Pericardial thrombus was defined as a homogenous structure in the pericardial space that was hyperechoic relative to the adjacent pericardium on ultrasound. In my experience, these pericardial thrombi are also usually crescent-shaped – conforming to the shape of the pericardium- and highly mobile within the effusion compared with neoplastic lesions that are anchored to the myocardium.
So, what’d they find in this study? Let’s look at their reported findings with regards to treatment. Interestingly (I’ll explain why I find it interesting later…), pericardiocentesis was attempted in 83% of dogs in the left atrial rupture group, but in 58% of the cases where it was attempted (11/19) it was entirely unsuccessful as the pericardial thrombus material impeded aspiration of fluid. This is in stark contrast to the neoplasia group in which pericardiocentesis was effective in 98% of the cases in which it was attempted (which was 89% of neoplasia cases overall). This difference in effectiveness of the procedure was highly significant between groups (P < 0.001).
43% percent of dogs in the left atrial rupture group had radiographic evidence of concurrent cardiogenic pulmonary edema at time of presentation, and 74% of dogs in this group received furosemide at some point during treatment. Cardiogenic pulmonary edema and use of furosemide was not documented in the neoplasia group. Over one-third of dogs in the left atrial rupture group received pimobendan and/or dobutamine for cardiovascular support, which also did not occur in the neoplasia group. A significantly greater number of dogs in the neoplasia group received intravenous crystalloid fluid therapy compared with the left atrial rupture group, but it is worth noting that 65% of dogs in the left atrial rupture group did receive some form of fluid therapy.
So, how did these dogs with cardiac tamponade fare, and did their underlying etiology affect this outcome? Well it appeared so in this study, at least initially. 35% of dogs within the left atrial rupture group died within 48 hours of visiting a hospital, compared with only 9% of dogs with underlying neoplasia. However, no difference in overall survival time was observed between groups, and was not lengthy in either group (26 days with left atrial rupture versus 44 days for neoplasia).
There are some key takeaways from this study, and discussion of this topic, for VETgirl listeners across the globe. The pathophysiology, clinical presentation, ultrasonographic findings and treatment for dogs with cardiac tamponade due to cardiac neoplasia are historically well-described and quite clear. Pericardiocentesis is successful at stabilizing such patients, saves lives (well, buys some time), and is indicated in nearly all cases. Concurrent intravenous fluid therapy to increase intracardiac pressures (thus resisting the effects of cardiac tamponade) is also appropriate, and use of diuretics such as furosemide is widely accepted to be contraindicated in such cases as it can reduce intracardiac pressures and exacerbate shock. Pretty straightforward, right?
Well, cardiac tamponade secondary to left atrial rupture is a whole other hemodynamic “ballgame”, if you will. The jist is, this population has significant heart disease and often is in congestive heart failure and doesn’t want to see ANY fluids! Yes, these dogs present with cardiac tamponade, but they have a direct intracardiac to pericardial communication through the left atrial wall and can theoretically hemorrhage indefinitely if pericardiocentesis is performed because, ironically, the rising intrapericardial pressure also serves as an opposing force to continued effusion while the atrial wall attempts to spontaneously seal. Added to this theoretical concern that the procedure itself is more likely than not to be technically ineffective because of catheter obstruction by pericardial thrombus material, and the clinician needs to think long and hard about the risk versus reward of pericardiocentesis in these dogs.
Intravenous fluid therapy may temporarily improve the effects of tamponade, but may also promote cardiogenic pulmonary edema formation in dogs with severe, chronic mitral valve disease. These dogs have chronically elevated left atrial pressures to begin with, and as this study indicated, many have concurrent pulmonary edema at the time of presentation with left atrial rupture anyway, probably because they are decompensating to congestive heart failure just prior to atrial rupture itself. So should they receive fluid therapy? Keep listening. And in case you fall asleep, NO, they shouldn’t, in this VETgirl’s opinion.
Finally, what about diuretics? Yes, the typical concerns exist for exacerbating tamponade, but as noted earlier, these dogs likely have chronically elevated left atrial pressures from their severe mitral valve disease and often have concurrent cardiogenic pulmonary edema at time of presentation, it seems. What’s a clinician to do?
The short answer is to some of these questions is, we don’t know for certain yet, and designing a prospective study that is ethically palatable is likely going to be difficult. The survival time for dogs with cardiac tamponade secondary to left atrial rupture in this study was quite poor (26 days) which correlates with one prior study (Reineke et al) cited by the authors in which 64% of dogs did not even survive to discharge. However, another study cited by the authors (Nakamura et al) reported a median survival time of 203 days, and a recent abstract presented at the 2023 European Society of Veterinary Internal Medicine (ECVIM) Congress (Wong, et al), which was after the time of publication of the present study, reported a median survival time of 238 days in 33 dogs with left atrial rupture. Only 12 of those dogs were determined to have overt cardiac tamponade, and pericardiocentesis was attempted in only 4. This also highlights that not all dogs with left atrial rupture necessarily have cardiac tamponade, which would be an important distinction to make in determining course of action, as well.
In my personal, non-randomized or controlled clinical experience, I have usually been remiss to attempt pericardiocentesis in these patients, and equally reluctant to pursue fluid therapy beyond perhaps an initial bolus(es) to improve hypotension in a few cases. I generally lean heavily on pimobendan and pressor therapies (e.g. dobutamine) in addition to oxygen support. I will administer (or continue if already receiving) diuretic therapy if concurrent cardiogenic pulmonary edema is present, but likely tread much more lightly with dosing than for a typical congestive heart failure patient (in other words, don’t reach for the 4 mg/kg, frequent blousing!). If concurrent pulmonary edema is not present, I will generally avoid administering diuretics until 1) there is clear evidence that the left atrial rupture is sealing via identification of resolving effusion and thrombus on echocardiogram and/or 2) the patient develops respiratory signs attributable to development of radiographic pulmonary edema. I have observed some dogs with left atrial rupture develop acute kidney injury and severe azotemia from the initial hypotension associated with the rupture event, which further complicates decision-making around diuretic therapy in the first 24-48 hours.
Based solely on my experiences, in dogs with left atrial rupture, I generally prepare owners that if their dog survives the first 6-12 hours, there is a reasonable chance they will make it home. I also advise them that there are absolutely cases where such dogs can still go on to live a relatively “typical” survival time for chronic congestive heart failure, an assertion that appears supported by the Nakamura and Wong studies.
Realistically, the size of the atrial tear likely plays the biggest role in prognosis, which is not a piece of information that can be readily ascertained on echocardiogram. Large tears won’t seal spontaneously, whereas small tears or pinpoint rupture sites can seal with pericardial adherence – this is readily observed on post-mortem in these patients. Surgical correction would be optimal for larger tears, and has actually been reported in three dogs in a recent case series by Yoshida and colleagues!
So, what do we take away from this VETgirl podcast? Dogs with left atrial rupture secondary to mitral valve disease truly represent a population where the “art” of emergency medicine and patient-specific treatment decisions by the attending clinician are paramount to a chance at survival!
When in doubt, if the dog is small, smells like a myxomatous mitral valve disease dog, and has pulmonary edema, this VETgirl would NOT reach for IV fluids or a pericardiocentesis catheter and would be very judicious with furosemide therapy. When in doubt, dial your local cardiologist for help!
References:
1. Sugiura H, Suzuki T, Mimura S et al. Retrospective evaluation of clinical signs, clinical course, and prognosis between dogs with left atrial rupture secondary to myxomatous mitral valve disease and those with neoplastic cardiac tamponade (2015-2019): 70 cases. J Vet Emerg Crit Care 2022;32:784-790.
2. Reineke EL, Burkett DE, Drobatz KJ. Left atrial rupture in dogs: 14 cases (1990-2005). J Vet Emerg Crit Care 2008;18(2):158-164.
3. Nakamura RK, Tompkins E, Russell NJ, et al. Left atrial rupture secondary to myxomatous mitral valve disease in 11 dogs. J Am Anim Hosp Assoc 2014;50(6):405-408.
4. Wong S, Siess S, Kramer G. Left atrial rupture secondary to myxomatous mitral valve disease in 33 dogs (2017-2022). Proceedings, ECVIM-CA Congress , September 2023, Barcelona, Spain.
5. Yoshida T, Matsuura K, Chieh-Yen C, et al. Surgical treatment for left atrial rupture due to myxomatous mitral valve disease in three dogs: A case report. Vet Med Sci 2022;8:2261–2267.
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