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Canine congestive heart failure: an approach to casemanagement

Author : Mike Martin

Categories : Vets

Date : January 23, 2012

ABSTRACT

This article primarily refers to the management of the most common causes of heart failure seen ingeneral practice, such as mitral valve disease (MVD) and dilated cardiomyopathy (DCM). Theseboth lead to left-sided congestive heart failure, typically resulting in pulmonary oedema. It alsofollows on from the article on “Recognising and diagnosing heart failure in the dog” publishedin VT41.44.

It is not possible to cover every aspect of heart failure management within the word limit of thisarticle, so I have focused on what I believe is the most common presentation to practitioners: theoutpatient case. This article reflects my own personal experience and perspective.

The primary objective of heart failure medications is to relieve the clinical signs – in effect,improve the quality of life, see a resolution in any breathlessness, improve exercisetolerance, resolve ascites and reduce the coughing’s severity.

Secondary objectives are assessing improvement from diagnostic tests, such as a resolution ofpulmonary oedema on repeat chest radiographs. However, as a general rule, the old adage “treatthe patient, not the test” is useful to consider when debating uncertain findings on any diagnostictest.

Successful management involves more than just medications

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Figure 1. Successful long-term management requires three key aspects.

Long-term successful management of heart failure consists of three parts (Figure 1):

making an accurate diagnosisinitiation of appropriate medicationslong-term monitoring and fine-tuning of the medications

Successful treatment is proportional to a correct diagnosis

This might seem like an obvious statement. However, in a proportion of dogs referred to usbecause they have been poorly responsive to medications, the tentative diagnosis of heart failurehas been incorrect. For example, dogs with lung pathology and the impression of cardiomegaly onchest radiographs may be given a false-positive diagnosis of heart failure. Without a correctdiagnosis, long-term management will become frustrating and problematic.

Figures 2 and 3 are lateral chest radiographs from two middle-aged cocker spaniels. Bothpresented with a history of respiratory signs (breathlessness and coughing). Do these dogs bothhave heart failure?

In Figure 2, the radiograph is of good quality, the chest is not rotated and exposures are good.There is:

a cardiomegaly with left atrial enlargementthe cranial lobe vessels are engorged and consistent with an increased pulmonary vascularpatternan intense and diffuse increase in lung pathology (in this case, an alveolar pattern)

As discussed in the previous article (VT41.44), these features are all consistent with heart failureas the cause of the signs, and thus the lung pathology can reasonably be interpreted as pulmonaryoedema.

In Figure 3, the radiograph is rotated (note the costochondral junctions are not level with eachside) and the timing is not fully inspiratory (thus there is less air to contrast with soft tissue changesin the lungs, giving the illusion of an increase in soft tissue pathology).

Consequently, there is the impression of a cardiomegaly (because chest rotation raises the heartnearer the spine) and interpretation of the lung fields becomes unreliable (when there is under-aeration of the lungs).

Figure 4 is a radiograph of the dog in Figure 3 taken at referral. There is no cardiomegaly,although there is some lung pathology, which was found to be due to pulmonary infiltrate witheosinophils. However, the difference between Figures 3 and 4 is quite profound, and this dog wasnot responding well to heart medications. Obtaining good chest radiographs is not easy and takestime and patience, with attention to detail. The importance of good positioning and good lungaeration is highlighted by this case.

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If the diagnosis of cardiac or respiratory disease remains uncertain from chest radiographs, thenthe Cardiopet proBNP (BNP) can be useful. This blood test helps to differentiate dogs that presentwith clinical signs (if time permits waiting for the results).

Figure 2. A lateral chest radiograph from cocker spaniel A, which presented with coughing anddyspnoea.

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Figure 3. A lateral chest radiograph from cocker spaniel B, which also presented with coughingand dyspnoea.

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Figure 4. Lateral chest radiograph from cocker spaniel B (Figure 3), when repeat radiography wasperformed at the referral centre, ensuring good positioning and aeration of the lungs. The previousillusion of cardiomegaly has gone. There is good air contrast in the lung fields (inspiratory timed).This radiograph, therefore, rules out heart disease, warranting a respiratory investigation.

Heart failure medications: a brief review of the literature

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Human studies

The discovery of new heart failure drugs in the past 30 to 40 years has brought with it a flurry ofresearch and a wealth of understanding of heart disease. It has been a fantastic era for cardiology.

Angiotensin converting enzyme (ACE) inhibitors. Many thousands of peopleparticipated in double-blind, placebo-controlled trials with ACE inhibitor drugs. Theconclusions of these trials have shown that ACE inhibitors provide a benefit in reducingboth symptoms and mortality. One thought-provoking trial compared purely vasodilatingdrugs to ACE inhibitors to determine if the benefit was due to vasodilation. This showedadditional improvements over and above that of vasodilation alone, indicating theneurohormonal inhibiting actions of ACE inhibitors were important.Spironolactone. A very famous study (RALES trial) compared a low dose ofspironolactone to placebo (plus standard heart failure medications) in patients with severeheart failure. This showed a remarkable benefit in reducing mortality in patients in thespironolactone group. This was attributed to the inhibitory effects of spironolactone onaldosterone, thus reducing the degree of myocardial and vascular fibrosis and endothelialdysfunction.

Dog studies

Figure 5. The Bench study showed a benefit in survival for benazepril in dogs with heart failure dueto MVD (risk reduction 49%). Source: The BENCH study group (1999).

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Figure 6. The Quest study showed a benefit in survival with pimobendan compared to benazepril(risk reduction 32%). Source: Häggström et al (2008).

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Figure 7. Spironolactone showed a benefit in survival in dogs with early (mild) MVD (risk reductionof 55%). Source: Bernay et al (2010).

ACE inhibitors. There have been a number of studies in dogs in heart failure that havecompared ACE inhibitors to placebo, both short and long term. These, like the humanstudies, also showed a benefit in improving quality of life and prolonging survival. A trialusing benazepril (see Figure 5) showed a benefit in survival with a risk reduction of 49% indogs with mitral valve disease (MVD).Pimobendan. A number of studies on the use of pimobendan have been conducted, of

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which the QUEST study is the most recent. This was a single-blinded, positive-controlledstudy comparing pimobendan to benazepril for the treatment of heart failure due to MVD indogs. This showed a benefit in survival in the dogs receiving pimobendan with a riskreduction of 32% (Figure 6).Spironolactone. A doubleblind, placebo-controlled trial with spironolactone in dogs withmild heart failure, due to MVD, showed a risk reduction of 55% for those dogs receivingspironolactone (Figure 7). This supports the use of spironolactone as an inhibitor ofaldosterone, for treatment of dogs with MVD.Furosemide activates reninangiotensin-aldosterone system (RAAS). The effects offurosemide and pimobendan on the RAAS were examined in a small group of dogs bymeasuring urinary aldosterone excretion. This showed that either furosemide alone, orfurosemide in combination with pimobendan, resulted in activation of RAAS. The conclusionfrom this study was that when using furosemide, an inhibitor of RAAS should be usedconcurrently.Congestive heart failure (CHF) is a neuroendocrine disorder. The conclusions of all theresearch and studies over the past 30 to 40 years show a variety of neurohormones areactivated when heart failure occurs (Figure 8).

These are initially physiological responses to adapt to the failing heart, but they eventually becomemaladaptive and exacerbate the clinical signs of heart failure. The treatment goals are, therefore, toinhibit these counterproductive neuroendocrine systems.

So, how should we treat CHF in dogs?

Based on the foregoing review (evidence-based medicine) there is justification for the use of allthree categories of heart failure medications – ACE inhibitors, pimobendan and spironolactone (forthe purposes of simplifying terminology, I refer to these three drugs as the baseline medications). Itis also important to use these drugs when administering furosemide to counter the effects of RAASactivation.

Therefore, CHF treatment typically requires furosemide plus these three baseline medications. Thebaseline medications are essentially used at the manufacturers’ doses. However, use offurosemide is much more complex than it appears at face value.

The outpatient case

Furosemide: how to use it, what to expect and why monitor.

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Figure 8. Numerous neurohormones are activated by heart failure. (Click to view)

For dogs treated as outpatients, the dose of furosemide can be a lot lower than seems to be usedin many instances.

This is primarily because of the concurrent use of the baseline medications. Generally, I find a doseof 0.5mg/kg to 2mg/kg bid sufficient for the typical case. However, the dose of furosemide shouldbe proportional to the severity of pulmonary oedema, with a higher dose for severe cases and amuch lower dose for mild cases.

As a generalisation, most dogs will start to show a significant clinical response (improvement in

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respiratory rate and effort) in the first six to 12 hours. This is possibly dose dependent. Followingcorrect dosing, there should be a resolution of remaining respiratory signs within three to five days.This time point is a useful interval for a re-examination, but earlier or later reevaluation will bedictated to by the severity of each case and, possibly, telephone feedback from the owner. If therehas been a good response at the first re-assessment, then tapering the furosemide dose isindicated.

Getting the owner involved

I find it important to help the owner understand how furosemide works, why we give it and that it’simportant to finding the minimum effective dose.

I explain to owners that furosemide works on the kidneys to cause urination and get rid of retainedfluid that has accumulated in the lungs (or abdomen) because of the failing heart. Congested lungscause the dog to struggle to breathe, but as the lungs dry out, breathing becomes more relaxedand slower. I give the owners a chart and ask them to record the sleeping respiratory rate (SRR)for the first consecutive 10 days, then every week thereafter. By doing this we can establish theSRR for each individual dog for when the lungs are clear of fluid. This acts as a reference value forfuture comparison, but also a check that respiration has actually returned to near normal. This alsomakes owners aware of how furosemide works.

Tapering the dose

At the first re-examination, if respiratory rate and effort have normalised (a chest x-ray should betaken if there is any uncertainty), then continuing on the same starting dose of furosemide wouldlead to subclinical dehydration.

This causes dogs to lose their appetite and become dull, depressed and disinterested. In manycases, this leads to a prerenal azotaemia (serum urea elevated proportionally much more thancreatinine) and loss of electrolytes (decreases sodium, potassium and chloride).

I’ll often recommend the dose is reduced by 25-50% if there has been a good response, but say tothe owner he or she can re-increase the dose if there is a relapse in respiratory rate or effort.

Regular blood work is important in monitoring response

I explain to owners that in the presence of heart failure, the perfusion of the kidneys is not as goodas normal, and, additionally, the body’s organs now have to metabolise the heart medications.This puts a strain on the kidneys (pre-renal failure), can deplete electrolytes and potentially lead tosubclinical dehydration. So while we have to give furosemide to manage the fluid retention, we alsohave to be cautious not to over-use diuretics without appropriate monitoring. Therefore, routineblood work is important and, typically, I will take a blood sample one to two weeks after initiating

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heart medications, and then regularly thereafter, particularly if the dose of diuretics is increased orresults are not normal.

It is common to find at least a small increase in serum urea, but provided this does not increasefurther after using furosemide, then I’m not too worried.

Owners’ assessment of their dog

The improvements in respiratory rate and effort are often what is most noticeable to owners. Theowners should return with their SRR record. I find they begin to notice the degree of respiratoryeffort as well. I re-emphasise the importance of continuing to monitor the SRR weekly, and topreferably record this. While dogs with pulmonary oedema should be rested, as this resolves, theywill naturally begin to exercise more. Exercise is good for the dog’s circulation and well-being. Ifind it useful to record how far and how long the daily exercise routine is before developing heartfailure, and then at presentation when in heart failure, then continue to record what improvementsare apparent after treatment.

Coughing seems to be caused by a combination of airway compression of the mainstem bronchus,in addition to oedema in the airways. With treatment, the cough reduces significantly, but notalways completely because of ongoing airway compression in dogs with marked cardiomegaly.

Finally, the happiness factor. This can often be ascertained by simply asking the owners howhappy their dog is, but also by assessing its return of appetite and general demeanour.

The vet’s assessment

The priority is to listen to the owners’ history and note the improvements discussed above, as wellas making a copy of the SRR chart. Assessing respiratory effort and rate can be made in-clinic,although this will be more rapid than at rest.

A routine physical examination should also be recorded – note the mucosal colour, palpate for anyascites and palpate the femoral pulses (recording the pulse rate), along with auscultation of theheart for heart rate and rhythm (recording the heart rate), and presence of the murmur. The heartrate is likely to be higher than when rested at home, which needs to be taken into consideration.

Blood pressure is normal in many cases, but in some of the more severe cases, and in dogs thatpresent with forward failure signs (weakness, lethargy and pallor) it is important to check the bloodpressure is not too low. Above 120mmHg systolic is usually fine, less than 100mmHg is a concernand would influence my dose of drugs that result in vasodilation (such as ACE inhibitors andpimobendan), and also make me more cautious in the dose of diuretics I use.

A blood sample should be taken for haematology and biochemistry, primarily to screen for pre-

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renal azotaemia and to assess the electrolytes. Urine analysis is less useful, as the furosemidedilutes the urine, but can still be worth considering. I sometimes find taking an arterial blood sampleto assess the degree of oxygenation useful. This is a quick and inexpensive screen; if the oxygencontent is low, this suggests a chest x-ray should also be taken.

If there is uncertainty about whether pulmonary oedema has resolved, then a lateral chestradiograph is most useful. I find auscultation of lungs for assessing oedema unreliable. Pulmonarycrackles will often be heard when there is oedema in the airways (severe cases). However, I haveseen many radiographs of mild alveolar oedema or extensive interstitial oedema and heard nothingon auscultation.

On the first reassessment, lowering the dose of furosemide is usually indicated. However, ensurethe owner continues to monitor the SRR after doing this, in case oedema returns. Ideally, by trialand error, the lowest effective dose of furosemide needs to be found. This minimises the activationof RAAS and reduces any side effects, particularly on kidney function and electrolytes.

How frequently should a heart failure patient be re-examined?

There is no set frequency and each case needs to be evaluated separately, along with the degreeof severity taken into account and how quickly a patient stabilises. However, I’ll try to offer someguidelines – these should probably be viewed as some minimum recommendations. Cases thatneed hospitalisation are not covered in this article.

After initiating treatment, the first reassessment will very much depend on the case’s severity. Asevere outpatient might need reassessment the next day to ensure a satisfactory response andreassure the owner everything is going to plan, but, typically, many cases will need reassessmentin three to seven days. This is often a useful time to assess the SRR taken at home, the clinicalresponse and run some blood work – at which point, tapering the dose of furosemide is indicated.

If all goes to plan, the next revisits can slowly be stretched out from maybe seven to 10 days, thentwo to three weeks, and then maybe every one to three months, depending on how stable thecondition is. For dogs on a medium to high dose of diuretics, repeat blood work is also advisableevery one to three months. In dogs with dilated cardiomyopathy (DCM; which carries a muchpoorer prognosis), re-examinations need to remain fairly frequent. In dogs with stable MVD, lessfrequent re-examinations might be reasonable, such as every four to six months.

In less stable cases, the frequency of re-examinations and treatment readjustments increasesdepending on the individual case. As a general rule, the dose of the baseline medications remainsfairly static (until end-stage failure), whereas the dose of furosemide will be adjusted up or down,depending on clinical response and blood results, or even additional diuretics added. Wheneverthere is uncertainty about the presence or absence of oedema, then a lateral chest radiograph isvery useful (provided it is of good quality).

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Summary

Managing heart failure in dogs (Figure 1) has other aspects other than just medications (althoughfinding the lowest effective dose of diuretics is important). Based on my experience and opinion, ifwe were able to consider the population of dogs in the UK as a whole, improvements to therecognition and diagnosis of heart failure would provide the greatest difference to successfultreatment and management.

Additionally, being proactive in the aftercare, involving the owner in monitoring clinical signs (suchas SRR), as well as the results of clinical pathology, among other parameters, will provide benefitsin quality of life and survival.

Case example

Figure 9. Jerry when he initially presented.

Jerry (Figure 9) is an eight-year old male (neutered) Rhodesian ridgeback (58kg). He presentedwith a history of coughing a month prior to presenting, which did not respond to empirical treatmentwith antibiotics.

Exercise intolerance and breathlessness developed, particularly after exertion. On clinicalexamination there was pallor, a very rapid and chaotic heart rhythm (more than 200bpm). Pulseswere hard to feel and variable in strength (mostly weak), with a pulse rate much less than the heartrate (less than 100bpm) – in effect, there were pulse deficits. A soft and quiet murmur over the leftapex was suspected, but the chaotic heart rhythm made this difficult to appreciate.

From the photograph of Jerry (Figure 9), ascites appear to be present, the cephalic andsaphenous veins are prominent and, despite no-one holding his lead, he has no interest inescaping from the vet’s car park. In fact, he looks quite dull and depressed.

What’s your assessment of this case and what tests would you consider?

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The history does fit well with heart failure. A dog with MVD is likely to have a much louder murmurthan was heard here, although a chaotic heart rhythm can make it difficult to accurately assessmurmurs. Thus, if he does have heart failure, DCM or pericardial effusion might be more likely.

For a dog with pallor and ascites, it is important to rule out a haemoabdomen and performabdominal paracentesis, check the fluid’s colour and specific gravity (SG). In this case, it was astraw-coloured fluid with an SG of 1.028, which is consistent with a modified transudate and,potentially, heart failure.

The options are now to consider either a chest radiograph or echocardiography. Pros and consexist with each of these techniques. A chest radiograph will demonstrate if cardiomegaly and/orpulmonary oedema (or pleural effusion) are present. However, in such a big dog, man-handling himon to an x-ray table might be problematic and might test the limits of many x-ray machines.Therefore, it might prove difficult to obtain a good quality radiograph in this scenario.

An ultrasound examination of the chest should be able to reveal the presence of pleural effusion, ifpresent, but won’t determine if pulmonary oedema (or other respiratory diseases) is present. It willdemonstrate the presence of cardiomegaly (or pericardial effusion) and, if there is a large dilatedleft atrium, this would be supportive of the presence of heart failure. However, if there is not anobviously dilated left atrium, then the cause of the dyspnoea becomes less certain, hence,radiographs would be needed.

Figure 10. Lateral chest radiograph from Jerry. There is a cardiomegaly with left atrial enlargementand increase in pulmonary opacity, consistent with mild pulmonary oedema.

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Figure 11. This echocardiographic image shows dilation of both the left atrium (LA) and leftventricle (LV). The LV is more globoid than normal. The live (moving) image showed poor LVcontractility. All these are features of dilated cardiomyopathy (DCM).

The lateral chest radiograph (Figure 10) shows a moderate cardiomegaly with left atrial bulge. Thecranial lobe vessels are difficult to see in this photograph, but are suspiciously enlarged, as is thecaudal vena cava. There is a mild increase in pulmonary opacity, which together with thecardiomegaly and pulmonary vascular pattern, would be indicative of interstitial pulmonaryoedema. There is no other chest pathology to explain the dyspnoea (such as a thoracic mass,pleural effusion or pneumothorax).

An echocardiographic examination (Figure 11) showed a dilated and round left ventricle, and adilated left atrium. On the moving image, the left ventricle was contracting poorly. These featureswere all consistent with DCM causing the heart failure.

In conclusion, Jerry has CHF secondary to DCM. In his case, much of the signs seemed to indicatea greater forward failure component, rather than backward failure. In fact, his blood pressure was alittle low, at 110mmHg. A blood profile was unremarkable, which will also be useful for futurecomparison.

What about the arrhythmia?

An ECG was run (Figure 12) and this showed a rapid chaotic rhythm to be associated with atrialfibrillation (AF). This is a common arrhythmia in largebreed dogs with heart disease.

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Treatment

Treating CHF. The baseline medications (ACE inhibitor, pimobendan and spironolactone)were all instituted. Because his blood pressure was a little low, I was cautious aboutlowering this any further with vasodilating drugs, so opted to use a lowerend dose of thesedrugs. Based on assessment of his chest radiographs, the oedema was considered mild, soI opted for an initial dose of 60mg bid (approximately 1.0mg/kg bid). An initial injection offurosemide was given.AF treatment. I treat AF with digoxin, starting at a maintenance dose and allowing this toslowly reach serum therapeutic levels in five to seven days. In my experience, it is moreimportant to avoid over dosage (toxicity) than under dosage. This will lead to loss ofappetite, depression and, potentially, vomiting and diarrhoea, typically two to four daysfollowing its commencement. There is not a great consensus on the best way to manageAF and an extensive discussion is beyond this article, but this protocol mostly works well forme.

Figure 12. Three lead ECG taken from Jerry when he was initially presented. This shows anirregular supraventricular rhythm and absence of P waves, consistent with atrial fibrillation (AF).The heart rate in response to the AF is 220/min.

Follow-up

The owners were given an SRR chart to complete. An appointment was made with their primaryvet in five to seven days to reassess the response. The vets sent a follow-up letter and a copy of

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the blood results after that appointment. The results were unremarkable. The owners said Jerrystarted to respond within two days and his appetite returned. He was also going on short walks,and regaining some of his happiness factor. The ascites had also gone.

KEY MESSAGES

Successful canine heart failure management has three aspects:

A correct diagnosis

Good-quality radiographs are needed to avoid false positive or negative diagnoses.Serum BNP can be useful to differentiate dogs with clinical signs.If lung pathology is thought to be pulmonary oedema, there must be left atrial enlargement.

Initiate appropriate medications

Baseline medications: ACE inhibitors, pimobendan, spironolactone.Furosemide: dose appropriate to severity of congestion; taper the dose when there is aresolution of dyspnoea/tachypnoea; and monitor for side effects.

Long-term monitoring

Get the owners involved by monitoring the SRR; pro-actively plan re-examinations sufficientto stabilise the clinical sign; and continue to screen and monitor for progression of the heartfailure.

References

Bernay F et al (2010). Efficacy of spironolactone on survival in dogs with naturally occurringmitral regurgitation caused by myxomatous mitral valve disease, J Vet Intern Med 24:331-341.CONSENSUS Trial Study Group (1987). Effect of enalapril on mortality in severecongestive heart failure. Results of the Cooperative North Scandinavian Enalapril SurvivalGroup (CONSENSUS). N Eng J Med 316: 1,429-1,435.Häggström J et al (2008). Effect of pimobendan or benazepril hydrochloride on survivaltimes in dogs with congestive heart failure caused by naturally occurring myxomatous mitral

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valve disease: the QUEST study, J Vet Intern Med 22: 1,124-1,135.Lantis A C et al (2011). Effects of furosemide and the combination of furosemide and thelabeled dosage of pimobendan on the circulating renin-angiotensin-aldosterone system inclinically normal dogs, Am J Vet Res 72: 1,646-1,651.Pitt B et al (1999). The effect of spironolactone on morbidity and mortality in patients withsevere heart failure. Randomized Aldactone Evaluation Study Investigators, N Eng J Med 341: 709-717.The BENCH Study Group (1999). The effect of benazepril on survival times and clinicalsigns of dogs with congestive heart failure: results of a multicenter, prospective,randomized, double-blinded, placebocontrolled, long term clinical trial, J Vet Cardiol 1: 7-18.The COVE Study Group (1995). Controlled clinical evaluation of enalapril in dogs with heartfailure: results of the Cooperative Veterinary Enalapril Study Group, J Vet Intern Med 9:243-252.

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