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Case Study
Dealing with a left ventricular pseudoaneurysm during assist device implant
Asian Cardiovascular & Thoracic Annals 0(0) 1–3 ß The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492315579555 aan.sagepub.com
Richard V Ha1, Peter Chiu1, Dipanjan Banerjee2 and Ahmad Y Sheikh1
Abstract Despite increasing use of left ventricular devices for the surgical treatment of heart failure, there is limited experience with implantation of devices in the setting of challenging left apical anatomy. We report the case of a 68-year-old man with a chronic post-infarction calcified apical pseudoaneurysm, who underwent pseudoaneurysmectomy, ventricular myoplasty, and left ventricular assist device implantation. A review of the literature and operative strategies are presented.
Keywords Aneurysm, false, calcinosis, heart failure, heart-assist devices, prosthesis implantation
Introduction Alongside heart transplantation, left ventricular assist device (LVAD) implantation is the mainstay for patients with endstage heart failure.1 In the present era, LVAD implantation is being offered to progressively more complex patients with numerous medical and anatomical challenges that must be overcome. A calcified left ventricular (LV) apical pseudoaneurysm may be an obstacle to successful inflow cannula positioning, with the possible complications of bleeding and suction events.2 Literature describing approaches to LVAD implantation in the setting of LV apical aneurysms is scarce.3,4 We describe a patient with a chronic calcific pseudoaneurysm following myocardial infarction. Our operative approach of pseudoaneurysmectomy, LV myoplasty, and implantation of a continuous-flow HeartMate II LVAD (Thoratec Corportation, Pleasanton, CA, USA) is described.
Case report A 68-year-old man suffered a myocardial infarction complicated by LV free-wall rupture at age 55. At that time, he was admitted, stabilized, and managed expectantly. He also underwent automatic implantable
cardiac defibrillator implantation during his initial presentation. He subsequently developed worsening heart failure and dysrhythmias with increasing frequency of medical admissions for management of his heart failure symptoms. Significant comorbidities included poorly controlled diabetes mellitus (hemoglobin A1c 7.5%), severe chronic obstructive pulmonary disease (forced expiratory volume in 1 s 56% of predicted, and ratio of forced expiratory volume in 1 s to forced vital capacity 47% of predicted), stage 3 A chronic kidney disease (serum creatinine of 1.3 mgdL1; estimated glomerular filtration rate 56 mL/min/1.73 m2), atrial fibrillation, and hypertension. The patient was on an optimal medical regimen including warfarin, amiodarone, digoxin, metoprolol, torsemide, spironolactone, losartan, aspirin, and insulin. He was referred to our center for definitive 1 Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA, USA 2 Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA
Corresponding author: Ahmad Y Sheikh, MD, Department of Cardiothoracic Surgery, 300 Pasteur Drive, Stanford, CA 94305, USA. Email: [email protected]
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Asian Cardiovascular & Thoracic Annals 0(0)
Figure 1. Preoperative imaging demonstrating an enlarged heart with a calcified apical pseudoaneurysm. (A) Plain chest radiograph and (B) computed tomography revealing the calcified apical cap of the aneurysm (red arrows). (C) Three-dimensional reconstruction of the thorax demonstrates the relationship of the calcified apex to the chest wall and the relative size of the aneurysmal segment of the left ventricle.
surgical management. On presentation, he had severe congestive heart failure symptoms despite optimal medical therapy (New York Heart Association class IV). He was designated as Interagency Registry for Mechanically Assisted Circulatory Support level 5. His LV ejection fraction on echocardiography was 20%, with relatively preserved right ventricular function. Right heart catheterization revealed: mean pulmonary artery pressure 25 mm Hg, cardiac index 1.83 Lmin1m2, and pulmonary capillary wedge pressure was 12 mm Hg. Pulmonary vascular resistance was calculated to be 3.5 Woods units. Imaging demonstrated a 7-cm calcified aneurysmal dilation of the LV apex containing a thrombus (Figure 1). Given the patient’s history of contained LV rupture and the ‘‘neck-like’’ appearance of the apex on multimodality imaging, a presumptive diagnosis of post-infarction pseudoaneurysm was made. The patient was discussed at our multidisciplinary heart failure conference and considered to be unsuitable for heart transplantation given his severe diabetes and chronic obstructive lung disease. In spite of these comorbidities, he was deemed an appropriate candidate for pseudoaneurysm resection and LVAD implantation as destination therapy. Sternotomy and creation of the LVAD pocket were performed in the usual fashion. After systemic heparinization, a side-biting clamp was used to exclude a portion of the aorta for anastomosis of the LVAD outflow cannula. Standard ascending aortic and venous cannulation were carried out. On cardiopulmonary bypass, extensive adhesiolysis of the apex was undertaken and the pseudoaneurysm was excised with evacuation of the calcific organized thrombus (Figure 2A, Figure 2B). This resulted in a 4 4-cm defect in the LV apex. A circular felt patch was trimmed to an appropriate size, and a central defect was made to create a ring shape designed to lie outside the ventricle. This was secured in place with 4 separate 2/0 Ethibond sutures. Everting stitches were then placed through the felt ring and passed through the LVAD inflow cannula
sewing ring. A 2/0 monofilament cerclage stitch was woven in and out of the apical myocardium and tightened to cinch down the rim of myocardium around the inflow cannula (Figure 2C). The pump was connected to the inflow cannula and positioned (Figure 2D). The patient was weaned from cardiopulmonary bypass with moderate inotropic support (epinephrine 0.07 mg kg1 min1 and dopamine 5 mgkg1 min1). Inhaled nitric oxide was employed throughout for right ventricular support. The patient’s postoperative course was notable for aspiration pneumonia treated with a 10-day course of intravenous vancomycin and piperacillin/tazobactam. The rest of his postoperative course was uncomplicated. He was discharged home on the 27th postoperative day. At follow-up 15 months postoperatively, he was doing well.
Discussion This patient posed a high operative risk given his unusual anatomy, and he was not a candidate for heart transplantation due to his diabetes and severe chronic obstructive pulmonary disease. As experience with LVAD implantation grows, practitioners are likely to encounter patients with increasingly complex anatomical obstacles previously thought to preclude successful surgical intervention. In previous iterations of approaching a hostile LV apex, prosthetic material has been used to reconstruct the inflow tract in a manner similar to the Dor endoventricular circular patch plasty procedure.2–5 However, the calcified pseudoaneurysm in our patient represented a unique anatomical challenge. We employed similar principles to reduce the LV end-diastolic volume but opted not to perform endoventricular circular patch plasty, thereby simplifying the procedure. The presence of a neck in the aneurysmal segment, not commonly found in true apical aneurysms, allowed for myoplasty, thus creating an adequate inflow conduit (avoiding the need to fashion an outflow tract with prosthetic material).
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Figure 2. Intraoperative images detailing the procedure. (A) Resection of the calcified apex. (B) The excised apical segment with an arrow demonstrating the thrombus (scale bar ¼ 2 cm). (C) The reconstructed left ventricular apex with the left ventricular assist device inflow cannula in place. (D) The completed implantation of the assist device demonstrates the spatial relationship between the reconstructed left ventricular apex, the inflow cannula, and the left ventricular assist device pump. (E) Postoperative contrastenhanced computed tomography showing the remodeled neo-ventricle (red arrow) and the position of the outflow cannula (red circle).
In patients with significant comorbid conditions and LV apical pseudoaneurysm who are not eligible for orthotopic heart transplantation, LVAD implantation with concomitant pseudoaneurysm excision is a viable solution. Given the excellent intermediate result achieved in this patient, it may be reasonable to expand this technique for use as a bridge to transplantation or in patients with complications of myocardial infarction requiring LVAD implantation including post-myocardial infarction ventricular septal defect, free wall rupture, and cardiogenic shock. Funding This research received no specific grant from any funding agency in the public, commerical, or not-for-profit sectors.
2. Atluri P, Dymond DJ and Woo YJ. Continuous-flow left ventricular assist device implantation in the presence of a hostile ventricular apex. J Thorac Cardiovasc Surg 2013; 146: 981–982. 3. Chernyavskiy AM, Marchenko AV, Lomivorotov VV, Doronin D, Alsov SA and Nesmachnyy A. Left ventricular assist device implantation combined with surgical ventricular reconstruction. Tex Heart Inst J 2012; 39: 627–629. 4. Garbade J, Bittner HB, Barten MJ, et al. Combined surgical left ventricular reconstruction and left ventricular assist device implantation for destination therapy in endstage heart failure. Circ Heart Fail 2011; 4: e14–e15. 5. Dor V, Civaia F, Alexandrescu C, Sabatier M and Montiglio F. Favorable effects of left ventricular reconstruction in patients excluded from the Surgical Treatments for Ischemic Heart Failure (STICH) trial. J Thorac Cardiovasc Surg 2011; 141: 905–916.
Conflict of interest statement None declared.
References 1. Slaughter MS, Rogers JG, Milano CA, et al. Advanced heart failure treated with continuous-flow left ventricular assist device. N Engl J Med 2009; 361: 2241–2251.
Downloaded from aan.sagepub.com at WASHINGTON UNIV SCHL OF MED on November 16, 2015
(AAN)
[1–3] [PREPRINTER stage]
Case Study
Dealing with a left ventricular pseudoaneurysm during assist device implant
Asian Cardiovascular & Thoracic Annals 0(0) 1–3 ß The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492315579555 aan.sagepub.com
Richard V Ha1, Peter Chiu1, Dipanjan Banerjee2 and Ahmad Y Sheikh1
Abstract Despite increasing use of left ventricular devices for the surgical treatment of heart failure, there is limited experience with implantation of devices in the setting of challenging left apical anatomy. We report the case of a 68-year-old man with a chronic post-infarction calcified apical pseudoaneurysm, who underwent pseudoaneurysmectomy, ventricular myoplasty, and left ventricular assist device implantation. A review of the literature and operative strategies are presented.
Keywords Aneurysm, false, calcinosis, heart failure, heart-assist devices, prosthesis implantation
Introduction Alongside heart transplantation, left ventricular assist device (LVAD) implantation is the mainstay for patients with endstage heart failure.1 In the present era, LVAD implantation is being offered to progressively more complex patients with numerous medical and anatomical challenges that must be overcome. A calcified left ventricular (LV) apical pseudoaneurysm may be an obstacle to successful inflow cannula positioning, with the possible complications of bleeding and suction events.2 Literature describing approaches to LVAD implantation in the setting of LV apical aneurysms is scarce.3,4 We describe a patient with a chronic calcific pseudoaneurysm following myocardial infarction. Our operative approach of pseudoaneurysmectomy, LV myoplasty, and implantation of a continuous-flow HeartMate II LVAD (Thoratec Corportation, Pleasanton, CA, USA) is described.
Case report A 68-year-old man suffered a myocardial infarction complicated by LV free-wall rupture at age 55. At that time, he was admitted, stabilized, and managed expectantly. He also underwent automatic implantable
cardiac defibrillator implantation during his initial presentation. He subsequently developed worsening heart failure and dysrhythmias with increasing frequency of medical admissions for management of his heart failure symptoms. Significant comorbidities included poorly controlled diabetes mellitus (hemoglobin A1c 7.5%), severe chronic obstructive pulmonary disease (forced expiratory volume in 1 s 56% of predicted, and ratio of forced expiratory volume in 1 s to forced vital capacity 47% of predicted), stage 3 A chronic kidney disease (serum creatinine of 1.3 mgdL1; estimated glomerular filtration rate 56 mL/min/1.73 m2), atrial fibrillation, and hypertension. The patient was on an optimal medical regimen including warfarin, amiodarone, digoxin, metoprolol, torsemide, spironolactone, losartan, aspirin, and insulin. He was referred to our center for definitive 1 Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA, USA 2 Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA
Corresponding author: Ahmad Y Sheikh, MD, Department of Cardiothoracic Surgery, 300 Pasteur Drive, Stanford, CA 94305, USA. Email: [email protected]
Downloaded from aan.sagepub.com at WASHINGTON UNIV SCHL OF MED on November 16, 2015
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(AAN)
[1–3] [PREPRINTER stage]
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Asian Cardiovascular & Thoracic Annals 0(0)
Figure 1. Preoperative imaging demonstrating an enlarged heart with a calcified apical pseudoaneurysm. (A) Plain chest radiograph and (B) computed tomography revealing the calcified apical cap of the aneurysm (red arrows). (C) Three-dimensional reconstruction of the thorax demonstrates the relationship of the calcified apex to the chest wall and the relative size of the aneurysmal segment of the left ventricle.
surgical management. On presentation, he had severe congestive heart failure symptoms despite optimal medical therapy (New York Heart Association class IV). He was designated as Interagency Registry for Mechanically Assisted Circulatory Support level 5. His LV ejection fraction on echocardiography was 20%, with relatively preserved right ventricular function. Right heart catheterization revealed: mean pulmonary artery pressure 25 mm Hg, cardiac index 1.83 Lmin1m2, and pulmonary capillary wedge pressure was 12 mm Hg. Pulmonary vascular resistance was calculated to be 3.5 Woods units. Imaging demonstrated a 7-cm calcified aneurysmal dilation of the LV apex containing a thrombus (Figure 1). Given the patient’s history of contained LV rupture and the ‘‘neck-like’’ appearance of the apex on multimodality imaging, a presumptive diagnosis of post-infarction pseudoaneurysm was made. The patient was discussed at our multidisciplinary heart failure conference and considered to be unsuitable for heart transplantation given his severe diabetes and chronic obstructive lung disease. In spite of these comorbidities, he was deemed an appropriate candidate for pseudoaneurysm resection and LVAD implantation as destination therapy. Sternotomy and creation of the LVAD pocket were performed in the usual fashion. After systemic heparinization, a side-biting clamp was used to exclude a portion of the aorta for anastomosis of the LVAD outflow cannula. Standard ascending aortic and venous cannulation were carried out. On cardiopulmonary bypass, extensive adhesiolysis of the apex was undertaken and the pseudoaneurysm was excised with evacuation of the calcific organized thrombus (Figure 2A, Figure 2B). This resulted in a 4 4-cm defect in the LV apex. A circular felt patch was trimmed to an appropriate size, and a central defect was made to create a ring shape designed to lie outside the ventricle. This was secured in place with 4 separate 2/0 Ethibond sutures. Everting stitches were then placed through the felt ring and passed through the LVAD inflow cannula
sewing ring. A 2/0 monofilament cerclage stitch was woven in and out of the apical myocardium and tightened to cinch down the rim of myocardium around the inflow cannula (Figure 2C). The pump was connected to the inflow cannula and positioned (Figure 2D). The patient was weaned from cardiopulmonary bypass with moderate inotropic support (epinephrine 0.07 mg kg1 min1 and dopamine 5 mgkg1 min1). Inhaled nitric oxide was employed throughout for right ventricular support. The patient’s postoperative course was notable for aspiration pneumonia treated with a 10-day course of intravenous vancomycin and piperacillin/tazobactam. The rest of his postoperative course was uncomplicated. He was discharged home on the 27th postoperative day. At follow-up 15 months postoperatively, he was doing well.
Discussion This patient posed a high operative risk given his unusual anatomy, and he was not a candidate for heart transplantation due to his diabetes and severe chronic obstructive pulmonary disease. As experience with LVAD implantation grows, practitioners are likely to encounter patients with increasingly complex anatomical obstacles previously thought to preclude successful surgical intervention. In previous iterations of approaching a hostile LV apex, prosthetic material has been used to reconstruct the inflow tract in a manner similar to the Dor endoventricular circular patch plasty procedure.2–5 However, the calcified pseudoaneurysm in our patient represented a unique anatomical challenge. We employed similar principles to reduce the LV end-diastolic volume but opted not to perform endoventricular circular patch plasty, thereby simplifying the procedure. The presence of a neck in the aneurysmal segment, not commonly found in true apical aneurysms, allowed for myoplasty, thus creating an adequate inflow conduit (avoiding the need to fashion an outflow tract with prosthetic material).
Downloaded from aan.sagepub.com at WASHINGTON UNIV SCHL OF MED on November 16, 2015
XML Template (2015) [24.3.2015–8:33am] //blrnas3.glyph.com/cenpro/ApplicationFiles/Journals/SAGE/3B2/AANJ/Vol00000/150039/APPFile/SG-AANJ150039.3d
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[1–3] [PREPRINTER stage]
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3
Figure 2. Intraoperative images detailing the procedure. (A) Resection of the calcified apex. (B) The excised apical segment with an arrow demonstrating the thrombus (scale bar ¼ 2 cm). (C) The reconstructed left ventricular apex with the left ventricular assist device inflow cannula in place. (D) The completed implantation of the assist device demonstrates the spatial relationship between the reconstructed left ventricular apex, the inflow cannula, and the left ventricular assist device pump. (E) Postoperative contrastenhanced computed tomography showing the remodeled neo-ventricle (red arrow) and the position of the outflow cannula (red circle).
In patients with significant comorbid conditions and LV apical pseudoaneurysm who are not eligible for orthotopic heart transplantation, LVAD implantation with concomitant pseudoaneurysm excision is a viable solution. Given the excellent intermediate result achieved in this patient, it may be reasonable to expand this technique for use as a bridge to transplantation or in patients with complications of myocardial infarction requiring LVAD implantation including post-myocardial infarction ventricular septal defect, free wall rupture, and cardiogenic shock. Funding This research received no specific grant from any funding agency in the public, commerical, or not-for-profit sectors.
2. Atluri P, Dymond DJ and Woo YJ. Continuous-flow left ventricular assist device implantation in the presence of a hostile ventricular apex. J Thorac Cardiovasc Surg 2013; 146: 981–982. 3. Chernyavskiy AM, Marchenko AV, Lomivorotov VV, Doronin D, Alsov SA and Nesmachnyy A. Left ventricular assist device implantation combined with surgical ventricular reconstruction. Tex Heart Inst J 2012; 39: 627–629. 4. Garbade J, Bittner HB, Barten MJ, et al. Combined surgical left ventricular reconstruction and left ventricular assist device implantation for destination therapy in endstage heart failure. Circ Heart Fail 2011; 4: e14–e15. 5. Dor V, Civaia F, Alexandrescu C, Sabatier M and Montiglio F. Favorable effects of left ventricular reconstruction in patients excluded from the Surgical Treatments for Ischemic Heart Failure (STICH) trial. J Thorac Cardiovasc Surg 2011; 141: 905–916.
Conflict of interest statement None declared.
References 1. Slaughter MS, Rogers JG, Milano CA, et al. Advanced heart failure treated with continuous-flow left ventricular assist device. N Engl J Med 2009; 361: 2241–2251.
Downloaded from aan.sagepub.com at WASHINGTON UNIV SCHL OF MED on November 16, 2015
