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    Figure 1

    Transesophageal echocardiographic images obtained during an LAD procedure in a dog. A—In the still frame, tenting of the IAS can be seen in orthogonal imaging planes simultaneously. B—Fluoroscopic image of the same patient during tenting of the IAS.

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    Figure 2

    Images obtained during necropsy of dogs that had previously undergone LAD. The right atrial aspect of the IAS is shown. A—The iASD was created in the fossa ovalis of this dog. Notice the healed margins. B—The iASD was created cranial to the intervenous tubercle of this dog. Notice the smaller size of the iASD and more muscular rim, compared with the iASD of the dog of panel A. CS = Coronary sinus. FO = Fossa ovalis. IVT = Intervenous tubercle. TV = Tricuspid valve.

  • 1.

    Borgarelli M, Buchanan JW. Historical review, epidemiology and natural history of degenerative mitral valve disease. J Vet Cardiol 2012;14:93101.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2.

    Sisson D, Kvart C, Darke PGG. Acquired valvular heart disease in dogs and cats. In: Fox PR, Sisson D, Moise NS, eds. Textbook of canine and feline cardiology. 2nd ed. Philadelphia: Saunders, 1999;536565.

    • Search Google Scholar
    • Export Citation
  • 3.

    Atkins CE, Häggström J. Pharmacologic management of myxomatous mitral valve disease in dogs. J Vet Cardiol 2012;14:165184.

  • 4.

    Mizuno T, Mizukoshi T, Uechi M. Long term outcome in dogs undergoing mitral valve repair with suture annuloplasty and chordae tendinae replacement. J Small Anim Pract 2013;54:104107.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Uechi M, Mizukoshi T, Mizuno T, et al. Mitral valve repair under cardiopulmonary bypass in small breed dogs: 48 cases (2006–2009). J Am Vet Med Assoc 2012;240:11941201.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Uechi M. Mitral valve repair in dogs. J Vet Cardiol 2012;14:185192.

  • 7.

    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;33:11271140.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8.

    Orvalho JS, Cowgill LD. Cardiorenal syndrome. Vet Clin North Am Small Anim Pract 2017;47:10831102.

  • 9.

    Martinelli E, Locatelli C, Bassis S, et al. Preliminary investigation of cardiovascular-renal disorders in dogs with chronic mitral valve disease. J Vet Intern Med 2016;30:16121618.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10.

    Pouchelon JL, Atkins CE, Bussadori C, et al. Cardiovascular-renal axis disorders in the domestic dog and cat: a veterinary consensus statement. J Small Anim Pract 2015;56:537552.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11.

    Keene BW, Bonagura JD. Management of heart failure in dogs. In: Kirk's current veterinary therapy XV. St Louis: Elsevier, 2014;77284.

    • Search Google Scholar
    • Export Citation
  • 12.

    Shah SR, Waxman S, Gaasch WH. The impact of an atrial septal defect on hemodynamics in patients with congestive heart failure. US Cardiol Rev 2017;11:7274.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Masutani S, Senzaki H. Left ventricular function in adult patients with atrial septal defect: implication for development of heart failure after transcatheter closure. J Card Fail 2011;17:957963.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Peddle GD, Buchanan JW. Acquired atrial septal defects secondary to rupture of the atrial septum in dogs with degenerative mitral valve disease. J Vet Cardiol 2010;12:129134.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    Buchanan JW. Spontaneous left atrial rupture in dogs. Adv Exp Med Biol 1972;22:315334.

  • 16.

    Hung Y, Kim H, Hun C. Rupture of atrial septum in a Pomeranian dog secondary to advanced degenerative mitral valve disease. J Biomed Res 2014;15:151155.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 17.

    Lake-Bakaar GA, Mok YM, Kittleson MD. Fossa ovalis tear causing right to left shunting in a Cavalier King Charles Spaniel. J Vet Cardiol 2012;14:541545.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 18.

    Veldtman GR, Norgard G, Wahlander H, et al. Creation and enlargement of atrial defects in congenital heart disease. Pediatr Cardiol 2005;26:162168.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    Bauer A, Khalil M, Lüdemann M, et al. Creation of a restrictive atrial communication in heart failure with preserved and mid-range ejection fraction: effective palliation of left atrial hypertension and pulmonary congestion. Clin Res Cardiol 2018;107:845857.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    De Rosa R, Schranz D. Creation of a restrictive atrial left-to-right shunt: a novel treatment for heart failure. Heart Fail Rev 2018;23:841847.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 21.

    Rogers JH, Armstrong EJ, Bolling SF. Percutaneous approaches for treating mitral regurgitation. In: Lasala JM, Rogers JH, eds. Interventional procedures for adult structural heart disease. St Louis: Elsevier, 2014;143153.

    • Search Google Scholar
    • Export Citation
  • 22.

    O'Brien B, Zafar H, De Freitas S, et al. Transseptal puncture—review of anatomy, techniques, complications and challenges. Int J Cardiol 2017;233:1222.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23.

    Yeo KK, Rogers JH, Low RI. Transseptal heart catheterization. In: Lasala JM, Rogers JH, eds. Interventional procedures for adult structural heart disease. St Louis: Elsevier, 2014;3649.

    • Search Google Scholar
    • Export Citation
  • 24.

    Rajeshkumar R, Pavithran S, Sivakumar K, et al. Atrial septostomy with a predefined diameter using a novel occlutech atrial flow regulator improves symptoms and cardiac index in patients with severe pulmonary arterial hypertension. Catheter Cardiovasc Interv 2017;90:11451153.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25.

    Del Trigo M, Bergeron S, Bernier M, et al. Unidirectional left-to-right interatrial shunting for treatment of patients with heart failure with reduced ejection fraction: a safety and proof-of-principle cohort study. Lancet 2016;387:12901297.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 26.

    Søndergaard L, Reddy V, Kaye D, et al. Transcatheter treatment of heart failure with preserved or mildly reduced ejection fraction using a novel interatrial implant to lower left atrial pressure. Eur J Heart Fail 2014;16:796801.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 27.

    Amat-Santos IJ, Del Trigo M, Bergeron S, et al. Left atrial decompression using unidirectional left-to-right interatrial shunt: initial experience in treating symptomatic heart failure with preserved ejection fraction with the V-wave device. JACC Cardiovasc Interv 2015;8:870872.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28.

    Hasenfuß G, Hayward C, Burkhoff D, et al. A transcatheter intracardiac shunt device for heart failure with preserved ejection fraction (REDUCE LAP-HF): a multicentre, open-label, single arm, phase 1 trial. Lancet 2016;387:12981304.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29.

    Kaye DM, Hasenfuß G, Neuzil P, et al. One-year outcomes after transcatheter insertion of an interatrial shunt device for the management of heart failure with preserved ejection fraction. Circ Heart Fail 2016;9:e003662.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 30.

    Feldman T, Mauri L, Kahwash R, et al. A transcatheter interatrial shunt device for the treatment of heart failure with preserved ejection fraction (REDUCE LAP-HF I): a phase 2, randomized, sham-controlled trial. Circulation 2018;137:364375.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 31.

    Kaye DM, Petrie MC, McKenzie S, et al. Impact of an interatrial shunt device on survival and heart failure hospitalization in patients with preserved ejection fraction. ESC Heart Fail 2019;6:6269.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 32.

    Hoffmann R, Altiok E, Reith S, et al. Functional effect of new atrial septal defect after percutaneous mitral valve repair using the Mitraclip device. Am J Cardiol 2014;113:12281233.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 33.

    Boon J. Acquired valvular disease. In: Veterinary echocardiography. 2nd ed. Ames, Iowa: Blackwell-Wiley, 2011;267302.

  • 34.

    Martinez CA, Moscucci M. Percutaneous approach, including transseptal and apical puncture. In: Moscucci M, ed. Grossman and Baim's cardiac catheterization, angiography, and intervention. 8th ed. Philadelphia: Lippincott Williams & Wilkins, 2014;139169.

    • Search Google Scholar
    • Export Citation
  • 35.

    Mitchell SE, Anderson JH, Swindle MM, et al. Atrial septostomy: stationary angioplasty balloon technique—experimental work and preliminary clinical applications. Pediatr Cardiol 1994;15:17.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 36.

    Cequier A, Bonan R, Serra A, et al. Left to right atrial shunting after percutaneous mitral valvuloplasty. Circulation 1990;81:11901197.

  • 37.

    Hart EA, Zwart K, Teske AJ, et al. Haemodynamic and functional consequences of the iatrogenic atrial septal defect following Mitraclip therapy. Neth Heart J 2017;25:137142.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 38.

    Hanslik A, Pospisil U, Salzer-Muhar U, et al. Predictors of spontaneous closure of isolated secundum atrial septal defect in children: a longitudinal study. Pediatrics 2006;118:15601565.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 39.

    Scollan KF, Sisson DD. Pathophysiology of heart failure. In: Ettinger SJ, Feldman EC, Côté E, eds. Textbook of veterinary internal medicine. 8th ed. St Louis: Elsevier, 2017;11531163.

    • Search Google Scholar
    • Export Citation
  • 40.

    Chandraprakasam S, Satpathy R. When to close iatrogenic atrial septal defect after percutaneous edge to edge repair of mitral valve regurgitation. Cardiovasc Revasc Med 2016;17:421423.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 41.

    Kaye D, Shah SJ, Borlaug BA, et al. Effects of an interatrial shunt on rest and exercise hemodynamics: results of a computer simulation in heart failure. J Card Fail 2014;20:212221.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 42.

    Yousuf MA, Haq S, O'Donnell RE, et al. Hemodynamically significant atrial septal defect after atrial fibrillation ablation: a hole to remember. Heart Rhythm 2015;12:19871989.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 43.

    Guglielmini C, Diana A, Pietra M, et al. Atrial septal defect in five dogs. J Small Anim Pract 2002;43:317322.

  • 44.

    Klimek-Piotrowska W, Holda MK, Koziej M, et al. Anatomy of the true interatrial septum for transseptal access to the left atrium. Ann Anat 2016;205:6064.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 45.

    Sánchez-Quintana D, Doblado-Calatrava M, Cabrera JA, et al. Anatomical basis for the cardiac interventional electrophysiologist. Biomed Res Int 2015;2015:547364.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 46.

    Tzeis S, Andrikopoulos G, Deisenhofer I, et al. Transseptal catheterization: considerations and caveats. Pacing Clin Electrophysiol 2010;33:231242.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 47.

    Anderson RH, Brown NA. The anatomy of the heart revisited. Anat Rec 1996;246:17.

  • 48.

    Anderson RH, Brown NA, Webb S. Development and structure of the atrial septum. Heart 2002;88:104110.

  • 49.

    Howard SA, Quallich SG, Benscoter MA, et al. Tissue properties of the fossa ovalis as they relate to transseptal punctures: a translational approach. J Interv Cardiol 2015;28:98108.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 50.

    MacDonald ST, Arcidiacono C, Butera G. Fenestrated Amplatzer atrial septal defect occlude in an elderly patient with restrictive left ventricular physiology. Heart 2011;97:438.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 51.

    Mainzer G, Goreczny S, Morgan GJ, et al. Stenting of the inter-atrial septum in infants and small children: indications, techniques and outcomes. Catheter Cardiovasc Interv 2018;91:12941300.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 52.

    Gupta A, Bailey SR. Update on devices for diastolic dysfunction: options for a no option condition? Curr Cardiol Rep 2018;20:85.

  • 53.

    Hascoët S, Baruteau A, Jalal Z, et al. Stents in paediatric and adult congenital interventional cardiac catheterization. Arch Cardiovasc Dis 2014;107:462475.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 54.

    Meadows J, Moore P. Atrial septal defect creation. In: Lasala JM, Rogers JH, eds. Interventional procedures for adult structural heart disease. St Louis: Elsevier, 2014;277286.

    • Search Google Scholar
    • Export Citation
  • 55.

    Bauer A, Esmacili A, DeRosa R, et al. Restrictive atrial communication in right and left heart failure. Transl Pediatr 2019;8:133139.

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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)

Justin W. AllenDepartment of Cardiology, VCA West Los Angeles Animal Hospital, Los Angeles, CA 90025.

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Kevin L. PhippsDepartment of Cardiology, VCA West Los Angeles Animal Hospital, Los Angeles, CA 90025.

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Anthony A. LlamasDepartment of Cardiology, VCA West Los Angeles Animal Hospital, Los Angeles, CA 90025.

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Kirstie A. BarrettDepartment of Cardiology, VCA West Los Angeles Animal Hospital, Los Angeles, CA 90025.

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Abstract

OBJECTIVE

To determine whether left atrial decompression (LAD) would reduce left atrial pressure (LAP) in dogs with advanced myxomatous mitral valve disease (MMVD) and left-sided congestive heart failure (CHF) and to describe the LAD procedure and hemodynamic alterations and complications.

ANIMALS

17 dogs with advanced MMVD and left-sided CHF that underwent LAD.

PROCEDURES

The medical record database was retrospectively reviewed for all LAD procedures attempted in dogs with MMVD and left-sided CHF between October 2018 and June 2019. Data were collected regarding signalment (age, breed, weight, and sex), clinical signs, treatment, physical examination findings, and diagnostic testing before and after LAD. Procedural data were also collected including approach, technique, hemodynamic data, complications, and outcome.

RESULTS

18 LAD procedures performed in 17 patients were identified. Dogs ranged in age from 7.5 to 16 years old (median, 11 years) and ranged in body weight from 2.9 to 11.6 kg (6.4 to 25.5 lb) with a median body weight of 7.0 kg (15.4 lb). Minimally invasive creation of an atrial septal defect for the purpose of LAD was successful in all dogs without any intraoperative deaths. Before LAD, mean LAP was elevated and ranged from 8 to 32 mm Hg with a median value of 14 mm Hg (reference value, < 10 mm Hg). Following LAD, there was a significant decrease in mean LAP (median decrease of 6 mm Hg [range, 1 to 15 mm Hg]). Survival time following LAD ranged from 0 to 478 days (median, 195 days).

CONCLUSIONS AND CLINICAL RELEVANCE

For dogs with advanced MMVD and left-sided CHF, LAD resulted in an immediate and substantial reduction in LAP.

Abstract

OBJECTIVE

To determine whether left atrial decompression (LAD) would reduce left atrial pressure (LAP) in dogs with advanced myxomatous mitral valve disease (MMVD) and left-sided congestive heart failure (CHF) and to describe the LAD procedure and hemodynamic alterations and complications.

ANIMALS

17 dogs with advanced MMVD and left-sided CHF that underwent LAD.

PROCEDURES

The medical record database was retrospectively reviewed for all LAD procedures attempted in dogs with MMVD and left-sided CHF between October 2018 and June 2019. Data were collected regarding signalment (age, breed, weight, and sex), clinical signs, treatment, physical examination findings, and diagnostic testing before and after LAD. Procedural data were also collected including approach, technique, hemodynamic data, complications, and outcome.

RESULTS

18 LAD procedures performed in 17 patients were identified. Dogs ranged in age from 7.5 to 16 years old (median, 11 years) and ranged in body weight from 2.9 to 11.6 kg (6.4 to 25.5 lb) with a median body weight of 7.0 kg (15.4 lb). Minimally invasive creation of an atrial septal defect for the purpose of LAD was successful in all dogs without any intraoperative deaths. Before LAD, mean LAP was elevated and ranged from 8 to 32 mm Hg with a median value of 14 mm Hg (reference value, < 10 mm Hg). Following LAD, there was a significant decrease in mean LAP (median decrease of 6 mm Hg [range, 1 to 15 mm Hg]). Survival time following LAD ranged from 0 to 478 days (median, 195 days).

CONCLUSIONS AND CLINICAL RELEVANCE

For dogs with advanced MMVD and left-sided CHF, LAD resulted in an immediate and substantial reduction in LAP.

Introduction

Left-sided CHF is a common clinical syndrome in dogs and is most frequently the result of MMVD.1,2 Progressive worsening of mitral regurgitation in patients with MMVD results in an increase in LAP.2 If the regurgitation continues to worsen, pulmonary capillary wedge pressure rises, resulting in extravasation of fluid and pulmonary edema.2 Signs of CHF impact both quality and duration of life and demand treatment. Medical treatment of CHF is effective at alleviating clinical signs in most dogs for some time. The underlying valve disease is progressive, however, and most patients will die of recurrent CHF or complications of medical treatment within 2 years.3 Surgical treatment for patients with symptomatic MMVD is the standard of care in humans and has been performed in dogs with a high success rate and low complication rate in single center reports4,5,6; however, the high cost of the procedure and complicated nature of cardiac bypass in dogs render it unavailable, unaffordable, or both for most patients to which it may be recommended. There may then be a large unmet need for a lower cost, more accessible option that improves quality of life and extends survival time in patients with MMVD and left-sided CHF, particularly in patients with CHF that is difficult to control with standard medical care.

Dogs with advanced heart failure from MMVD can be difficult to manage without clearly defined or well-tolerated treatment options.7 Additionally, in the authors' experience there is a subset of dogs with less advanced or less chronic heart failure that nevertheless do poorly on standard medical care. This is most commonly the result of cardiorenal syndrome (which includes azotemia and electrolyte deficiencies),8,9,10 but can also be the result of a wide range of other clinical problems. These can include compliance issues (inability or unwillingness to administer adequate doses of diuretics), inappetence, activity intolerance, or other quality-of-life concerns that lead to an inability to administer doses of medications necessary to alleviate clinical signs of CHF.11 These patients may benefit from a nonpharmacologic approach to heart failure treatment.

Atrial septal defects, whether congenital or acquired, may provide some protection against acute and severe exacerbations in left atrial hypertension.11 This has been observed in humans with Lutembacher syndrome (ie, ASD and concurrent mitral stenosis) and humans with ASD closure with concurrent subclinical diastolic dysfunction12,13 and has been proposed in dogs with atrial septal rupture in the setting of MMVD.14 Atrial septal rupture in dogs with MMVD is a rare clinical entity that has been recognized for decades, with numerous case descriptions.14,15,16 Although not all acquired ASDs are considered beneficial,17 most of the clinical effects have been salutary, suggesting the possibility of resolution of left-sided CHF signs and development of right-sided CHF resulting from the acquired ASD.

Left atrial decompression is a minimally invasive procedure that reduces LAP in human patients with left atrial hypertension and heart failure from a variety of causes.18,19,20 It could provide an alternative to more definitive interventional21 or surgical mitral repair options in dogs, which are currently limited by expense, availability, and device size. Left atrial decompression is performed percutaneously; venous access is achieved, followed by routine transseptal puncture.22,23 Balloon dilatation (with or without a cutting balloon or high-pressure balloon) of the septum is then performed, with the intention of creating a persistent iASD. Stents or specifically designed devices20,24 can also be implanted in the septum in an attempt to maintain long-term patency and control the size of the iASD. There are currently 2 interatrial shunt devices that are undergoing enrollment in pivotal heart failure trials in humans to investigate the usefulness of iASD creation in patients with heart failure and preserved ejection fraction.20 These devices have already been shown to improve quality of life and reduce clinical signs of heart failure in patients with elevated LAP.25,26,27,28,29,30,31 Additionally, there is some postulated hemodynamic benefit to iASD creation in patients undergoing implantation of a clip that is attached to the mitral valve for interventional treatment of mitral valve disease.32 On the basis of these reports and experience with dogs with acquired ASD, we hypothesized that LAD performed in dogs with advanced MMVD would reduce LAP without serious adverse effects. We sought to describe the procedural technique, hemodynamic alterations, and complications that occurred in all dogs that underwent this procedure over the initial 8-month period.

Materials and Methods

Case selection criteria

The medical record database at a single tertiary care center (VCA West Los Angeles Animal Hospital) was retrospectively reviewed for all LAD procedures attempted in dogs with MMVD and left-sided CHF between October 2018 and June 2019. Owners provided informed consent for diagnostic testing and treatment in all patients in accordance with hospital policies. Owners were informed of the potential risks, potential benefits, and novel nature of the procedure when providing consent for LAD.

Medical records review

Data were collected regarding signalment (age, breed, weight, and sex), clinical signs, treatment, physical examination findings, and diagnostic testing before and after LAD. Procedural data were also collected including approach, technique, hemodynamic data, complications, and outcome. Eighteen procedures performed in 17 patients were identified.

Procedures

Echocardiography and thoracic ultrasonography were performed without sedation before and after LAD in all patients by a board-certified veterinary cardiologist (JWA and KAB) or a resident in training (KLP and AAL). Echocardiographic images were reviewed by 1 observer (JWA), and routine data and measurements were obtained by use of standard techniques.33

Procedural techniques were modified throughout the study period because of the novel nature of the procedure and continual technique refinement and are summarized as follows. Dogs were anesthetized and placed in left lateral recumbency. Anesthetic protocols were also variable and modified throughout the study period.

Transesophageal echocardiography with 4-D capabilitya was performed throughout the procedure by a board-certified veterinary cardiologist (KAB) or a resident in training (KLP). Percutaneous access to the right jugular vein was attempted in all procedures by use of the modified Seldinger technique.34 When percutaneous access was not successfully achieved, a vascular cutdown was performed and the right jugular vein was surgically isolated and approached via venotomy. A 5F or 6F introducer sheathb–d was placed in the right jugular vein. Right heart catheterization was performed in all procedures with standard catheter equipment. Right atrial pressure, right ventricular pressure, and pulmonary artery pressure (with or without pulmonary capillary wedge pressure) were obtained. Nonselective angiography was then performed through the jugular introducer with iohexol (300 mOsm/mL; 0.3 to 1 mL/kg [0.14 to 0.45 mL/lb]) by manual injection, with recording of dextrophase and levophase in lateral projection. Fluoroscopic images were reviewed to outline the approximate location of the fossa ovalis, caudodorsal to the aortic root on the lateral projection (Supplementary Video S1, available at: avmajournals.avma.org/doi/suppl/10.2460/javma.258.6.638).

A guidewiree was then used to access the caudal vena cava. The guidewire frequently encountered resistance because of the atrial septal convexity, whereupon a diagnostic catheter was placed over the guidewire and used to steer it safely into the caudal vena cava. The guidewire was then exchanged for a stiffer 0.035-inch (outer diameter) guidewire.f The catheter and introducer were exchanged for an introducer sheathg–i large enough to accommodate the transseptal needle selected for the procedure, which was determined on the basis of dog size. In patients with a body weight ≤ 7 kg (15.4 lb), pediatric Brockenbrough transseptal needlesj were used; these needles fit through the 0.038-inch dilator of the smaller, more pliable sheaths.g If the patient body weight was > 7 kg, adult needlesk,l were used, which required larger and stiffer transseptal dilators and sheaths.h,i The chosen sheath and dilator were passed into the caudal vena cava over the guidewire. The needle was then advanced through the dilator while allowing for free rotation of the needle but maintaining a generally dorsally directed needle tip. Caution was taken not to extrude the needle or stylet during needle advancement. The stylet was removed when the needle approached the dilator tip, and the assembly (comprised of the needle, dilator, and sheath) was then retracted into the RA. As the tip of the dilator entered the RA, ventromedial rotation (clockwise) of the assembly was performed to engage the IAS. This method, however, frequently resulted in difficulty engaging the fossa ovalis; thus, manual reshaping of the needle angle was performed in the remainder of the procedures. The needle was manually reshaped by passing it through the dilator, prior to insertion into the sheath and external to the patient, then bending the needle and dilator to better engage the fossa ovalis. The angle of the needle bend increased with time and was ultimately approximately 90° in most patients. Once the needle was reshaped, it was retracted from the tip of the dilator and the stylet was removed. The needle was then flushed. The needle and dilator were then introduced into the sheath (which remained in the caudal vena cava), allowing relatively free rotation while maintaining a generally dorsally directed angle on fluoroscopy. Once the dilator approached the tip of the sheath, the dilator was held in place and the sheath was retracted over the dilator to reduce the risk of inadvertent caudal vena caval puncture by the stiff dilator tip. The assembly was then retracted into the RA and rotated medially and ventrally during retraction in an attempt to engage the fossa ovalis as visualized on fluoroscopy and biplane TEE.

When tenting of the IAS with the dilator was visualized on biplane TEE at the level of the fossa ovalis (Figure 1), the needle was extruded. After puncture was performed, the needle was flushed with 0.5 mL of saline (0.9% NaCl) solution to confirm position in the LA on TEE; alternatively, 0.5 mL of iohexol–saline solution was injected through the needle during fluoroscopy to confirm position within the LA. If position was deemed appropriate, the dilator and sheath were passed over the needle into the body of the LA. Care was taken not to pass the dilator to the caudal border of the LA to reduce the risk of puncture. Once the dilator was within the LA, the sheath was advanced over the dilator into the LA and the dilator and needle were removed. Heparin (100 U/kg [45.5 U/lb], IV) was administered following access to the LA in procedures that were not complicated by inadvertent puncture of the RA or LA and pericardial effusion.

Figure 1
Figure 1

Transesophageal echocardiographic images obtained during an LAD procedure in a dog. A—In the still frame, tenting of the IAS can be seen in orthogonal imaging planes simultaneously. B—Fluoroscopic image of the same patient during tenting of the IAS.

Citation: Journal of the American Veterinary Medical Association 258, 6; 10.2460/javma.258.6.638

Balloon dilatation of the IAS was performed with a cutting balloonm following passage of the appropriately sized guidewire into the body of the LA or caudal pulmonary veins. A 3.5- or 4-mm-diameter cutting balloon was initially used, then pressures were measured. Upsizing of the balloon by 2-mm increments was performed if LAP reduction was not evident or if LAP to RAP gradient was < 2 mm Hg. The initial goal was the inflation of a balloon with a minimum diameter of 8 mm; this number was chosen to minimize the risk of closure over time and was derived from previous studies in animals,35 studies in human patients with ASD,18,19,20,36,37,38 and prior clinical experience with management of acquired ASD and atrial septostomies. Following an 8-mm-diameter balloon inflation, further balloon upsizing was determined on the basis of LAP reduction and RAP to LAP gradients. Evaluation of LAP and RAP were performed after a minimum of 3 minutes following removal of each balloon and prior to an increase in balloon size. Access to the LA was maintained by a guidewire or catheter remaining in the LA following retraction of the sheath into the RA. Passage of a 6F pigtail cathetern into the LA was performed to obtain an LAP measurement if a distinct left atrial waveform was not visualized when performed through the sheath. The sheath and catheters were removed following LAP and RAP measurements. Images were obtained through TEE for offline analysis of iASD size and location when possible.

Complications

Information on complications was extracted from the medical records. Major intraprocedural complications were defined as death or procedural complications sufficient to necessitate discontinuation (eg, pericardial effusion or tamponade, arrhythmias, or inability to access the LA safely). Minor procedural complications were defined as any arrhythmias or hypotension that required treatment or self-limiting pericardial effusions. Major postoperative complications were defined as death or euthanasia that was potentially related to the procedure.

Statistical analysis

Commercially available softwareo,p was used to generate descriptive statistics, including median and range values. All statistical analyses used appropriate nonparametric testing because of a low sample size. Significance was set at a value of P ≤ 0.05. Spearman and Kendall correlation analyses were performed to examine correlations between the various continuous variables. Wilcoxon signed rank analysis was used to examine differences between paired continuous variables.

Results

Patient population

Eighteen LAD procedures performed in 17 patients were identified within the 8-month period. One patient had a second LAD performed after the initial iASD closed; the second LAD was included for descriptive purposes but data were excluded from statistical analysis. There were 9 females and 8 males. Multiple breeds and types of dogs were identified, including Cavalier King Charles Spaniel (n = 3), Maltese (3), mixed breed (5), and other (7; 1 each). Age range was 7.5 to 16 years (median, 11 years), and body weight range was 2.9 to 11.6 kg (6.4 to 25.5 lb; median, 7.0 kg [15.4 lb]; Supplementary Table S1, available at: avmajournals.avma.org/doi/suppl/10.2460/javma.258.6.638).

An iASD was successfully created in all patients for which it was attempted, with no intraoperative deaths (procedural data are provided in Supplementary Table S2, available at: avmajournals.avma.org/doi/suppl/10.2460/javma.258.6.638). Left atrial decompression was performed in patients for which alternative options were considered limited by the attending clinician.

The most common reason for performing LAD was chronic CHF that required more intensive medical treatment to control clinical signs, but patients or owners were intolerant of attempts at intensification (n = 11 procedures). This usually consisted of anorexia (with or without worsened azotemia) following increases in diuretic dose (procedures 8, 11, 12, 13, and 17), vasodilator treatment (procedure 2), or both (procedure 1). There were 4 dogs (procedures 3, 9, 15, and 18) for which LAD was offered because of the owner's inability to administer treatment at an adequate dosage or frequency to alleviate CHF signs, which resulted in repeat hospitalizations for CHF.

Alternatively, 5 LAD procedures (Nos. 5, 6, 10, 14, and 16) were offered as a treatment for acute and severe pulmonary edema. Four dogs were refractory to nitroprusside discontinuation and transition to alternative injectable and orally administered medication. Left atrial decompression was offered for 1 dog as an alternative to ventilator treatment (procedure 6).

Two LAD procedures (Nos. 4 and 7) were performed in patients with CHF following closure of a preexisting ASD (1 acquired and 1 iatrogenic). The decompensation was thought to be partly the result of closure of the ASD, and the owners elected to perform an LAD to reestablish an ASD.

The range of time since initial diagnosis of CHF (defined time since initiation of diuretic therapy) in all dogs was 1 to 887 days, with a median of 397 days (patient management data are supplied in Supplementary Table S3, available at: avmajournals.avma.org/doi/suppl/10.2460/javma.258.6.638).

Dogs had active CHF (defined as clinical and diagnostic findings consistent with pulmonary edema, including cough, dyspnea, tachypnea, and ultrasonographic pulmonary B-lines or radiographic pulmonary infiltrates consistent with cardiogenic edema) on the day of 11 of 18 LAD procedures and within 14 days prior to another 5 procedures. A flail mitral leaflet, chordal rupture, or both were identified in all patients on TEE. Seven patients received nitroprusside to treat severe pulmonary congestion within 24 hours prior to LAD; of these, 6 dogs could not be successfully weaned off nitroprusside prior to LAD because of progressive dyspnea and pulmonary congestion during attempts at dose reduction. These patients were defined as hemodynamically unstable.

Procedural details

For all but the first LAD, total IV anesthetic techniques were used, thereby avoiding inhalant anesthetics. Premedications most commonly included hydromorphone (4 procedures; 0.1 mg/kg [0.045 mg/lb], IM), butorphanol (7 procedures; 0.3 to 0.5 mg/kg [0.14 to 0.23 mg/lb], IM), and maropitant (9 procedures, 1 mg/kg [0.45 mg/lb], SC). Two patients were given atropine (0.2 to 0.4 mg/kg [0.09 to 0.18 mg/lb], IM) and 1 each were administered midazolam (0.2 mg/kg, IM), ketamine (2 mg/kg [0.9 mg/lb], IM), and fentanyl (3 mg/kg [1.36 mg/lb], IV). For 10 of 18 LAD procedures, induction of anesthesia was performed with a combination of fentanyl (2 to 3 mg/kg, IV); a benzodiazepine, either midazolam (0.5 mg/kg, IV) or diazepam (0.3 to 0.4 mg/kg, IV); and etomidate (0.4 to 1.1 mg/kg [0.18 to 0.5 mg/lb], IV). For the remaining 8 procedures, midazolam (0.2 to 0.5 mg/kg, IV) or diazepam (0.3 to 0.4 mg/kg, IV) and alfaxalone (0.6 to 3 mg/kg [0.27 to 1.4 mg/lb], IV) were administered. Maintenance of anesthesia was accomplished with continuous IV infusions of fentanyl (10 procedures, 3 to 30 μg/kg/h [1.4 to 13.6 μg/lb/h]) or butorphanol (8 procedures, 0.1 to 0.5 mg/kg/h), midazolam (13 procedures, 0.1 to 0.6 mg/kg/h), alfaxalone (12 procedures, 0.5 to 8 mg/kg/h [0.23 to 3.6 mg/lb/h]), and ketamine (4 procedures, 5 to 33 μg/kg/min [2.3 to 15 μg/lb/min]). Six patients received at least 1 bolus of atracurium (2 mg/kg, IV).

Surgical cutdown was performed during 2 LAD procedures following unsuccessful attempts at percutaneous access. Right heart catheterization was completed in 14 of 18 procedures. In the 4 remaining procedures, attempts at passage of the catheter into the pulmonary artery were discontinued because of increased perceived risk of arrhythmias or trauma. In those patients, right atrial and ventricular pressures were measured and recorded. The needle was then passed through the dilator to the tip in the first 3 LAD procedures and the 4 procedures in which a TSX transseptal needle was used. Manual reshaping of the needle to achieve the necessary angle to engage the fossa ovalis was performed in 11 of 18 procedures. Following needle puncture, heparin was administered during 15 procedures. In 4 LAD procedures, a cutting balloon was the only balloon used. In 12 procedures, cutting balloon inflation was followed by inflation of a low-pressure balloon catheter. In 2 procedures, a low-pressure balloon catheter was the only balloon used.

A pediatric Brockenbrough transseptal needle was used in 12 LAD procedures, an adult needle was used in 1 procedure, and a TSX transseptal needle (86°) was used in the remaining 5 procedures (Supplementary Table S2). A 3.5- or 4 mm-diameter cutting balloon was used in 11 LAD procedures, and an 8-mm cutting balloon was used in 4 procedures. Left atrial decompression was discontinued following cutting balloon inflation if the left atrial V-wave pressure measurement, mean LAP, or both decreased by > 50% or if the difference in mean LAP and mean RAP was < 2 mm Hg. If this was not observed, a larger low-pressure balloon was used. An 8-mm-diameter low-pressure balloon was used in 2 LAD procedures, a 10-mm-diameter low-pressure balloon was used in 9 procedures, and a 12-mm-diameter low-pressure balloon was used in 2 procedures.

Left atrial V-wave pressure measurements before LAD ranged from 18 to 93 mm Hg (median, 30 mm Hg; Supplementary Table S2). Before LAD, mean LAP was elevated and ranged from 8 to 32 mm Hg with a median value of 14 mm Hg (reference, < 10 mm Hg).39 Following LAD, there were significant (P < 0.001) decreases in left atrial V-wave pressure measurements (median reduction of 14 mm Hg [range, 5 to 38 mm Hg]) and mean LAP (median decrease of 6 mm Hg [range, 1 to 15 mm Hg]). There was a significant (P < 0.001) increase in mean RAP following LAD (median increase of 1 mm Hg [range, −1 to 9 mm Hg]).

For 9 of 17 dogs, an iASD was created in a location considered ideal, which was defined as the fossa ovalis or caudoventral rim (craniodorsal to the coronary sinus ostium) and identified on TEE and fluoroscopy; all of these iASDs remained patent during the follow-up period (range, 144 to 307 days). For 3 dogs, iASDs were created cranial to the fossa ovalis (Figure 2; Supplementary Video S2, available at: avmajournals.avma.org/doi/suppl/10.2460/javma.258.6.638). Of these 3 dogs with iASDs created cranial to the fossa ovalis, the first had an iASD that spontaneously closed at day 87, the patient with the second died at day 144 with a patent 3-mm-diameter iASD, and the patient with the third was still alive at 478 days postoperatively, with a patent iASD detected on echocardiography. There were 5 of 17 dogs with iASDs created caudal to the fossa ovalis; 2 patients with caudally created iASDs had closure of the iASD during the study period at postoperative days 151 and 152. The remaining 3 patients were alive with patent iASDs at the time of last recheck (267 to 385 days after the LAD procedure).

Figure 2
Figure 2

Images obtained during necropsy of dogs that had previously undergone LAD. The right atrial aspect of the IAS is shown. A—The iASD was created in the fossa ovalis of this dog. Notice the healed margins. B—The iASD was created cranial to the intervenous tubercle of this dog. Notice the smaller size of the iASD and more muscular rim, compared with the iASD of the dog of panel A. CS = Coronary sinus. FO = Fossa ovalis. IVT = Intervenous tubercle. TV = Tricuspid valve.

Citation: Journal of the American Veterinary Medical Association 258, 6; 10.2460/javma.258.6.638

Complications

There were no major procedural complications. Minor procedural complications occurred in 9 of 18 procedures. Major postoperative complications occurred in 3 of 18 procedures. Pericardial effusion was observed in 3 patients, presumably secondary to inadvertent atrial wall puncture. This was self-limiting in each case and did not require centesis. In 1 patient, this occurred while attempting to pass a guidewire into the caudal vena cava across the atrial septal convexity and was recognized when the guidewire followed an extravascular path (within the pericardial space). In subsequent procedures, a guide catheter was used to aid crossing the septal convexity to avoid that complication. In another patient, the transseptal needle assembly was thought to have punctured the dorsomedial aspect of the RA as a result of insufficient contact with the fossa ovalis (the needle was felt to slide caudodorsally during the initial attempted puncture); the error was recognized because of the lack of contrast agent within the LA after puncture was palpable. In subsequent procedures, the angle of the needle was shaped to reduce the risk of that complication. The final instance of pericardial effusion was thought to be caused by puncture of the caudal aspect of the left atrial wall after crossing the IAS too forcefully. This was the first use of the TSX transseptal needle and sheath, which has different handling properties, compared with the Brockenbrough transseptal needles and sheaths previously used. All 3 procedures were temporarily suspended to monitor for continued accumulation of effusion. When this did not occur, the procedure was successfully completed in each patient. Arrhythmias occurred in all patients and did not generally require treatment. They included atrial (18/18 procedures) and ventricular (13/18 procedures) premature complexes (associated with guidewire or catheter manipulation, or both), accelerated idioventricular rhythm (2 procedures), transient sinus bradycardia and atrioventricular block (second degree, 2 procedures; third degree, 1 procedure), and atrial flutter (1 procedure). Treatment for sinus bradycardia, atrioventricular block, and accelerated idioventricular rhythm consisted of reductions in anesthetic depth and administration of atropine (0.02 mg/kg [0.009 mg/lb], IV administration of boluses until resolution of atrioventricular block and sinus bradycardia). The patient with atrial flutter underwent successful transcutaneous electric cardioversion following the procedure and prior to anesthetic recovery. The patient with transient third-degree atrioventricular block and sinus bradycardia developed the arrhythmia during catheter manipulation across the IAS; desaturation and hypotension were coincident with the arrhythmia. This occurred prior to final balloon inflation and did not appear to be directly a result of septal puncture or balloon inflation; the episode was managed by anesthetic discontinuation, IV administration of fluid boluses, and accelerated termination of the procedure following final balloon inflation (no pressure measurements obtained). Recovery was prolonged in this patient, and the patient remained weak after discharge the following day; recovery was complete within 2 weeks, and the patient remained alive without CHF signs 154 days after the LAD procedure. Jugular or cranial caval thrombosis occurred in 1 patient after the procedure.

Follow-up and outcome

There were 12 deaths during the study period, occurring 8 hours to 371 days after the procedure. There were 2 deaths within the immediate postoperative period. The first death occurred 8 hours after the procedure and was consistent with airway obstruction caused by brachycephalic airway syndrome. The second occurred 6 hours after the procedure while the patient was in the intensive care unit following substantial improvement in the degree of dyspnea; the cause of death was not determined and necropsy was not allowed. One patient was euthanized at 36 hours after remaining on the ventilator after the LAD procedure. One death occurred 14 days following the procedure; necropsy revealed pheochromocytoma, pulmonary hemorrhage, and pneumonia. The iASD in this dog was ellipsoid, with a major axis diameter of 11 mm and a minor axis diameter of 5 mm (Supplementary Video S3, available at: avmajournals.avma.org/doi/suppl/10.2460/javma.258.6.638). The patient with caval thrombosis developed chylous pleural and pericardial effusion, and euthanasia was performed on postoperative day 19. Necropsy revealed a pulmonary neuroendocrine (carcinoid) tumor. One patient (procedure 2) died 144 days after the procedure; necropsy did not reveal a cause. The iASD was patent with a 3 mm diameter. There was trace pleural and abdominal effusion without pulmonary edema; no signs of dyspnea or tachypnea were observed by the owner prior to death. The remaining 6 patient deaths resulted from euthanasia (166 to 371 days after the LAD procedure). Reasons for euthanasia included recurrent decompensated CHF (n = 3), progressive renal failure (2), and cardiac tamponade resulting from a left atrial tear (1). The remaining 5 patients were alive and free of CHF signs at the time of final follow up (range, 273 to 478 days after the LAD procedure). Twelve of 17 patients died during the study period. Death was most common in patients with decompensated and hemodynamically unstable CHF at the time of LAD (2/6 affected dogs).

Five dogs developed recurrent left-sided CHF during the follow-up period. Three of these patients developed signs of left-sided CHF following identification of spontaneous iASD closure (procedures 1, 12, and 13). The first dog underwent a second LAD procedure and was discharged the following day with iASD patency until the time of euthanasia for progressive renal failure (284 days after the second LAD procedure). The second dog presented for acute onset dyspnea as result of pulmonary edema 166 days after surgery and was euthanized for financial reasons. Closure of the iASD was confirmed on necropsy. In the third dog, iASD closure was identified on postoperative day 153 after development of a cough and tachypnea necessitating escalation of medical treatment. The patient was euthanized 62 days later for acute collapse resulting from left atrial rupture; necropsy confirmed closure of the iASD. The fourth dog developed pulmonary edema on postoperative day 19 (procedure 9), which was thought to be partly caused by administration of a β-adrenoreceptor blocking agent. Left-sided CHF was responsive to gradual discontinuation of the β-adrenoreceptor blocking agent and a 30% increase in daily diuretic dosage; the dog remained alive on the same diuretic dosage 391 days after the procedure. The fifth dog (procedure 18) developed left-sided CHF after inadvertent medication discontinuation and was euthanized 195 days postoperatively. No other dogs required postoperative diuretic escalation or had documented iASD closure during the study period. No dogs developed persistent right heart failure (defined as ascites or pleural effusion) during the study period.

Discussion

The current investigation provided evidence that LAD is feasible in patients that are refractory to or intolerant of standard medical treatment for CHF resulting from MMVD. In these patients, LAD resulted in a substantial and clinically relevant drop in LAP in all dogs that underwent the procedure. The decrease in left atrial V-wave pressure measurement and mean LAP was generally similar, with some individual variation. This was accomplished at the cost of RAP elevation, which was expected. The rise in RAP was deemed clinically acceptable, as no patients have thus far required abdominocentesis (only 1 patient developed transient ascites after LAD) or have shown signs of worsened pulmonary hypertension. Vigilance is recommended, however, as these are potential complications arising from the elevation in right-sided heart filling pressures and increase in pulmonary blood flow.36,40,41

The complications of LAD were predictable and treatable (or preventable) in most dogs of the present study. Left atrial decompression was performed most frequently in patients that required additional treatment to alleviate clinical signs of CHF but was poorly tolerated by the patients or owners (because of compliance or scheduling issues or medication effects on the patients' quality of life). This is a well-recognized and nearly inevitable7 clinical problem in patients with advanced MMVD and has direct clinical application. These patients tolerated the LAD procedure well, with all patients discharged from the hospital on the same or the following day. In contrast, the procedure had a higher mortality rate in patients with decompensated and hemodynamically unstable CHF. This was expected, as these patients had an anticipated mortality rate approaching 100% (ie, CHF could not be managed outside the intensive care unit).

The intention when performing LAD was to create an iASD large enough to reduce the likelihood of spontaneous closure and improve left heart filling pressure via a reduction in preload, while simultaneously avoiding pulmonary overcirculation resulting in acute right ventricular failure, severe pulmonary hypertension, or both.41,42,43 More accurate measurement of pulmonary-to-systemic flow ratio (Qp:Qs; aiming for a ratio of 1.3 to 1.4)41 would potentially be preferable to minimize the risk and maximize the benefit of the procedure, but was not deemed feasible because of practical constraints and attempts to minimize procedural time, complications, and complexity.

Creating the iASD in a location considered ideal also proved challenging. The ideal location of the iASD was thought to be the fossa ovalis on the basis of IAS anatomy and extrapolation from experience in human medicine.22,44,45 In people, septal puncture in any location outside the fossa ovalis and its associated structures (eg, limbus and anteroinferior rim) passes through the exterior surface of the heart, potentially resulting in pericardial effusion.44,46,47,48,49,50,51,52,53,54 This did not appear to be the case for the dogs of the present report. Creation of iASDs in other areas of the septum in these patients was well tolerated; in fact, iASDs were created in the location considered ideal in all dogs of the present report that died within 21 days of the LAD procedure, confirmed by necropsy in all but 1 dog (which was confirmed through 3D TEE). However, we believe the fossa ovalis is still the ideal location to create an iASD in dogs from the perspective of both patient safety and iASD persistence. The fossa ovalis is the least muscular and vascularized portion of the IAS.44,48,49 It is therefore easier to cross, less likely to result in thrombosis following LAD, and less likely to spontaneously close postoperatively. Additionally, if closure of the iASD is necessary (via a transcatheter or surgical approach), an iASD in the fossa ovalis would be simpler and easier to close. A staged interventional approach is theoretically possible with a fenestrated occluder device.50 This could be followed by device closure of the residual iASD if it remained poorly tolerated.13 The fossa ovalis is not easy to reach from a cranial approach, and we attempted to overcome this limitation via manually reshaping the needle in 11 procedures and by use of a preformed TSX transseptal needle with an 86° curve in 4 procedures. There was a learning curve with the use of the preformed TSX needle; the initial 3 iASDs created with this needle were caudal to the intended location. Although this was apparently well tolerated in these patients, the risk involved in puncture and dilatation of that portion of the IAS would be expected to be higher.

Spontaneous closure of the iASD occurred in 3 patients of the present study, all of which subsequently developed left-sided CHF. Spontaneous closure is a known complication of ASD creation in people, which spurred the development of stent placement51 and device development52 to maintain patency. Stent placement was considered as a component of LAD in the patient population of the present report but was not performed because of the increased cost and potential complications (eg, thrombosis, erosion, infection, or migration are possible52,53,54). It was also deemed likely that the elevated LAP in these patients would increase the likelihood of long-term iASD patency, which has been postulated in human patients with residual mitral regurgitation following mitral clip implantation.32 Additionally, the LAD procedure is repeatable if closure occurs. Follow-up to document iASD patency over time is required to determine whether stent placement would be beneficial in these patients to maintain patency of the iASD.

Appropriate timing of the intervention is unknown. It was performed in the present study in patients with few, if any, alternative options. This included patients with medication intolerance, those not responding to advanced medical treatments, and patients with uncontrolled (or medically uncontrollable) pulmonary congestion. It may be more appropriate and safer to perform this procedure at an earlier time point,19,55 but it was deemed unethical to perform an investigational procedure in patients of the present study prior to knowing the risk profile and tolerability unless there were no other valid options. Following our initial experiences, our belief is that the procedure may be beneficial at an earlier time point in the disease process. Future studies should be performed to help evaluate appropriate timing, optimal iASD location and size, and postoperative management.

Left atrial decompression is an attractive option for dogs with advanced MMVD for a number of reasons. It can be performed percutaneously with equipment that is already available in most catheterization laboratories and is potentially reversible if poorly tolerated (either immediately or at a future date). It is less expensive and invasive than procedures requiring bypass surgery (mitral repair or replacement) or those requiring device implantation. It provides a nonpharmacological option to reduce LAP in patients at risk of pulmonary edema. It is repeatable if necessary. In the present study, the LAP procedures also resulted in a great deal of previously difficult to obtain imaging and invasive hemodynamic data from our patient population, which may prove useful in directing future treatment efforts.

There were many limitations of the present study, primarily as a result of its retrospective nature. Accordingly, there was not a standardization of equipment, technique, diagnostic, and follow-up protocols. Several animals had missing data. Although missing data resulted from patient safety considerations, the gaps in data were an issue in interpretation. All procedures were performed at a single center by a single operator (JWA); thus, results may not be generalizable. Procedural technique was variable, which was a result of the investigational nature of the procedure but renders interpretation of outcome more difficult. Outcome data, although interesting, can only be regarded as hypothesis-generating because of the nonstandardized follow-up, treatment protocols, and lack of a control group. All of the dogs in the present study were on an intensive medical management strategy, and it is not possible to separate the effects of LAD from the effects of medication in these patients.

In conclusion, LAD was a feasible procedure in patients of the present study with advanced MMVD and left-sided CHF and resulted in a substantial and clinically important reduction in LAP. In affected dogs, the LAD procedure may translate into improved patient quality of life and survival time, though this remains unknown. Complications were frequent but were manageable or preventable in most cases. Left atrial decompression can be performed in most catheterization laboratories with standard equipment, although a learning curve exists regarding location of the iASD and in minimizing complications. On the basis of findings of the present report, procedural success can be expected to improve with experience.

Acknowledgments

No external funding was used in this study. The authors declare that there were no conflicts of interest.

Presented in abstract form at the American College of Veterinary Internal Medicine Forum, Phoenix, Arizona, June 2019.

The authors thank Janell Tran for technical assistance, Dr. Etienne Côté for assistance in manuscript preparation, Dr. Philip Bergman for assistance with statistical analysis, and Dr. Michael Geist for support during the study period.

Abbreviations

ASD

Atrial septal defect

CHF

Congestive heart failure

IAS

Interatrial septum

iASD

Iatrogenic atrial septal defect

LA

Left atrium

LAD

Left atrial decompression

LAP

Left atrial pressure

MMVD

Myxomatous mitral valve disease

RA

Right atrium

RAP

Right atrial pressure

TEE

Transesophageal echocardiography

Footnotes

a.

Vivid E95 echocardiographic system and 6VT-D TEE transducer, GE Healthcare, Milwaukee, Wis.

b.

Check-Flo Performer introducer set, Cook Inc, Bloomington, Ind.

c.

Glidesheath Slender, Terumo Medical Corp, Elkton, Md.

d.

Infiniti introducer kit, Infiniti Medical, Redwood City, Calif.

e.

VETBG-007 Weasel wire (0.035 inch), Infiniti Medical, Menlo Park, Calif.

f.

Safe T-J curved (0.035 inch), Cook Medical, Bloomington, Ind.

g.

Flexor Check-Flo introducer (6 to 7F), Ansel-1 Modification (45 cm), Cook Inc, Bloomington, Ind.

h.

Mullins transseptal adult sheath (8F), Medtronic Inc, Minneapolis, Minn.

i.

TSX 55° fixed curve transseptal sheath, Boston Scientific, Marlborough, Mass.

j.

Pediatric Brockenbrough needle (56 cm), Medtronic Inc, Minneapolis, Minn.

k.

Adult Brockenbrough needle (71 cm), Medtronic Inc, Minneapolis, Minn.

l.

TSX 86° transseptal needle (71 cm), Boston Scientific, Marlborough, Mass.

m.

Small peripheral cutting balloon (3.5, 4 or 8 mm), Boston Scientific, Marlborough, Mass.

n.

Torcon NB Advantage catheter (6F), Cook Inc, Bloomington, Ind.

o.

StatView, version 5.0, SAS Institute Inc, Cary, NC.

p.

Excel, Microsoft Office 2013: Microsoft Corp, Redmond, Wash.

References

  • 1.

    Borgarelli M, Buchanan JW. Historical review, epidemiology and natural history of degenerative mitral valve disease. J Vet Cardiol 2012;14:93101.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2.

    Sisson D, Kvart C, Darke PGG. Acquired valvular heart disease in dogs and cats. In: Fox PR, Sisson D, Moise NS, eds. Textbook of canine and feline cardiology. 2nd ed. Philadelphia: Saunders, 1999;536565.

    • Search Google Scholar
    • Export Citation
  • 3.

    Atkins CE, Häggström J. Pharmacologic management of myxomatous mitral valve disease in dogs. J Vet Cardiol 2012;14:165184.

  • 4.

    Mizuno T, Mizukoshi T, Uechi M. Long term outcome in dogs undergoing mitral valve repair with suture annuloplasty and chordae tendinae replacement. J Small Anim Pract 2013;54:104107.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Uechi M, Mizukoshi T, Mizuno T, et al. Mitral valve repair under cardiopulmonary bypass in small breed dogs: 48 cases (2006–2009). J Am Vet Med Assoc 2012;240:11941201.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Uechi M. Mitral valve repair in dogs. J Vet Cardiol 2012;14:185192.

  • 7.

    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;33:11271140.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8.

    Orvalho JS, Cowgill LD. Cardiorenal syndrome. Vet Clin North Am Small Anim Pract 2017;47:10831102.

  • 9.

    Martinelli E, Locatelli C, Bassis S, et al. Preliminary investigation of cardiovascular-renal disorders in dogs with chronic mitral valve disease. J Vet Intern Med 2016;30:16121618.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10.

    Pouchelon JL, Atkins CE, Bussadori C, et al. Cardiovascular-renal axis disorders in the domestic dog and cat: a veterinary consensus statement. J Small Anim Pract 2015;56:537552.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11.

    Keene BW, Bonagura JD. Management of heart failure in dogs. In: Kirk's current veterinary therapy XV. St Louis: Elsevier, 2014;77284.

    • Search Google Scholar
    • Export Citation
  • 12.

    Shah SR, Waxman S, Gaasch WH. The impact of an atrial septal defect on hemodynamics in patients with congestive heart failure. US Cardiol Rev 2017;11:7274.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Masutani S, Senzaki H. Left ventricular function in adult patients with atrial septal defect: implication for development of heart failure after transcatheter closure. J Card Fail 2011;17:957963.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Peddle GD, Buchanan JW. Acquired atrial septal defects secondary to rupture of the atrial septum in dogs with degenerative mitral valve disease. J Vet Cardiol 2010;12:129134.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    Buchanan JW. Spontaneous left atrial rupture in dogs. Adv Exp Med Biol 1972;22:315334.

  • 16.

    Hung Y, Kim H, Hun C. Rupture of atrial septum in a Pomeranian dog secondary to advanced degenerative mitral valve disease. J Biomed Res 2014;15:151155.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 17.

    Lake-Bakaar GA, Mok YM, Kittleson MD. Fossa ovalis tear causing right to left shunting in a Cavalier King Charles Spaniel. J Vet Cardiol 2012;14:541545.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 18.

    Veldtman GR, Norgard G, Wahlander H, et al. Creation and enlargement of atrial defects in congenital heart disease. Pediatr Cardiol 2005;26:162168.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    Bauer A, Khalil M, Lüdemann M, et al. Creation of a restrictive atrial communication in heart failure with preserved and mid-range ejection fraction: effective palliation of left atrial hypertension and pulmonary congestion. Clin Res Cardiol 2018;107:845857.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    De Rosa R, Schranz D. Creation of a restrictive atrial left-to-right shunt: a novel treatment for heart failure. Heart Fail Rev 2018;23:841847.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 21.

    Rogers JH, Armstrong EJ, Bolling SF. Percutaneous approaches for treating mitral regurgitation. In: Lasala JM, Rogers JH, eds. Interventional procedures for adult structural heart disease. St Louis: Elsevier, 2014;143153.

    • Search Google Scholar
    • Export Citation
  • 22.

    O'Brien B, Zafar H, De Freitas S, et al. Transseptal puncture—review of anatomy, techniques, complications and challenges. Int J Cardiol 2017;233:1222.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23.

    Yeo KK, Rogers JH, Low RI. Transseptal heart catheterization. In: Lasala JM, Rogers JH, eds. Interventional procedures for adult structural heart disease. St Louis: Elsevier, 2014;3649.

    • Search Google Scholar
    • Export Citation
  • 24.

    Rajeshkumar R, Pavithran S, Sivakumar K, et al. Atrial septostomy with a predefined diameter using a novel occlutech atrial flow regulator improves symptoms and cardiac index in patients with severe pulmonary arterial hypertension. Catheter Cardiovasc Interv 2017;90:11451153.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25.

    Del Trigo M, Bergeron S, Bernier M, et al. Unidirectional left-to-right interatrial shunting for treatment of patients with heart failure with reduced ejection fraction: a safety and proof-of-principle cohort study. Lancet 2016;387:12901297.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 26.

    Søndergaard L, Reddy V, Kaye D, et al. Transcatheter treatment of heart failure with preserved or mildly reduced ejection fraction using a novel interatrial implant to lower left atrial pressure. Eur J Heart Fail 2014;16:796801.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 27.

    Amat-Santos IJ, Del Trigo M, Bergeron S, et al. Left atrial decompression using unidirectional left-to-right interatrial shunt: initial experience in treating symptomatic heart failure with preserved ejection fraction with the V-wave device. JACC Cardiovasc Interv 2015;8:870872.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28.

    Hasenfuß G, Hayward C, Burkhoff D, et al. A transcatheter intracardiac shunt device for heart failure with preserved ejection fraction (REDUCE LAP-HF): a multicentre, open-label, single arm, phase 1 trial. Lancet 2016;387:12981304.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29.

    Kaye DM, Hasenfuß G, Neuzil P, et al. One-year outcomes after transcatheter insertion of an interatrial shunt device for the management of heart failure with preserved ejection fraction. Circ Heart Fail 2016;9:e003662.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 30.

    Feldman T, Mauri L, Kahwash R, et al. A transcatheter interatrial shunt device for the treatment of heart failure with preserved ejection fraction (REDUCE LAP-HF I): a phase 2, randomized, sham-controlled trial. Circulation 2018;137:364375.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 31.

    Kaye DM, Petrie MC, McKenzie S, et al. Impact of an interatrial shunt device on survival and heart failure hospitalization in patients with preserved ejection fraction. ESC Heart Fail 2019;6:6269.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 32.

    Hoffmann R, Altiok E, Reith S, et al. Functional effect of new atrial septal defect after percutaneous mitral valve repair using the Mitraclip device. Am J Cardiol 2014;113:12281233.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 33.

    Boon J. Acquired valvular disease. In: Veterinary echocardiography. 2nd ed. Ames, Iowa: Blackwell-Wiley, 2011;267302.

  • 34.

    Martinez CA, Moscucci M. Percutaneous approach, including transseptal and apical puncture. In: Moscucci M, ed. Grossman and Baim's cardiac catheterization, angiography, and intervention. 8th ed. Philadelphia: Lippincott Williams & Wilkins, 2014;139169.

    • Search Google Scholar
    • Export Citation
  • 35.

    Mitchell SE, Anderson JH, Swindle MM, et al. Atrial septostomy: stationary angioplasty balloon technique—experimental work and preliminary clinical applications. Pediatr Cardiol 1994;15:17.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 36.

    Cequier A, Bonan R, Serra A, et al. Left to right atrial shunting after percutaneous mitral valvuloplasty. Circulation 1990;81:11901197.

  • 37.

    Hart EA, Zwart K, Teske AJ, et al. Haemodynamic and functional consequences of the iatrogenic atrial septal defect following Mitraclip therapy. Neth Heart J 2017;25:137142.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 38.

    Hanslik A, Pospisil U, Salzer-Muhar U, et al. Predictors of spontaneous closure of isolated secundum atrial septal defect in children: a longitudinal study. Pediatrics 2006;118:15601565.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 39.

    Scollan KF, Sisson DD. Pathophysiology of heart failure. In: Ettinger SJ, Feldman EC, Côté E, eds. Textbook of veterinary internal medicine. 8th ed. St Louis: Elsevier, 2017;11531163.

    • Search Google Scholar
    • Export Citation
  • 40.

    Chandraprakasam S, Satpathy R. When to close iatrogenic atrial septal defect after percutaneous edge to edge repair of mitral valve regurgitation. Cardiovasc Revasc Med 2016;17:421423.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 41.

    Kaye D, Shah SJ, Borlaug BA, et al. Effects of an interatrial shunt on rest and exercise hemodynamics: results of a computer simulation in heart failure. J Card Fail 2014;20:212221.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 42.

    Yousuf MA, Haq S, O'Donnell RE, et al. Hemodynamically significant atrial septal defect after atrial fibrillation ablation: a hole to remember. Heart Rhythm 2015;12:19871989.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 43.

    Guglielmini C, Diana A, Pietra M, et al. Atrial septal defect in five dogs. J Small Anim Pract 2002;43:317322.

  • 44.

    Klimek-Piotrowska W, Holda MK, Koziej M, et al. Anatomy of the true interatrial septum for transseptal access to the left atrium. Ann Anat 2016;205:6064.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 45.

    Sánchez-Quintana D, Doblado-Calatrava M, Cabrera JA, et al. Anatomical basis for the cardiac interventional electrophysiologist. Biomed Res Int 2015;2015:547364.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 46.

    Tzeis S, Andrikopoulos G, Deisenhofer I, et al. Transseptal catheterization: considerations and caveats. Pacing Clin Electrophysiol 2010;33:231242.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 47.

    Anderson RH, Brown NA. The anatomy of the heart revisited. Anat Rec 1996;246:17.

  • 48.

    Anderson RH, Brown NA, Webb S. Development and structure of the atrial septum. Heart 2002;88:104110.

  • 49.

    Howard SA, Quallich SG, Benscoter MA, et al. Tissue properties of the fossa ovalis as they relate to transseptal punctures: a translational approach. J Interv Cardiol 2015;28:98108.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 50.

    MacDonald ST, Arcidiacono C, Butera G. Fenestrated Amplatzer atrial septal defect occlude in an elderly patient with restrictive left ventricular physiology. Heart 2011;97:438.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 51.

    Mainzer G, Goreczny S, Morgan GJ, et al. Stenting of the inter-atrial septum in infants and small children: indications, techniques and outcomes. Catheter Cardiovasc Interv 2018;91:12941300.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 52.

    Gupta A, Bailey SR. Update on devices for diastolic dysfunction: options for a no option condition? Curr Cardiol Rep 2018;20:85.

  • 53.

    Hascoët S, Baruteau A, Jalal Z, et al. Stents in paediatric and adult congenital interventional cardiac catheterization. Arch Cardiovasc Dis 2014;107:462475.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 54.

    Meadows J, Moore P. Atrial septal defect creation. In: Lasala JM, Rogers JH, eds. Interventional procedures for adult structural heart disease. St Louis: Elsevier, 2014;277286.

    • Search Google Scholar
    • Export Citation
  • 55.

    Bauer A, Esmacili A, DeRosa R, et al. Restrictive atrial communication in right and left heart failure. Transl Pediatr 2019;8:133139.

Contributor Notes

Address correspondence to Dr. Allen (justin.allen@vca.com).