brintellex
  • Users Online: 171
  • Print this page
  • Email this page


 
 
Table of Contents
CASE REPORT
Year : 2020  |  Volume : 10  |  Issue : 2  |  Page : 92-96

Multivessel percutaneous coronary intervention in midterm anastomotic failure of all grafts post CABG: An unpredictable enigma?


Department of Cardiology, Aayush Hospital, Vijayawada, Andhra Pradesh, India

Date of Submission05-Feb-2020
Date of Decision11-Apr-2020
Date of Acceptance19-Apr-2020
Date of Web Publication25-Sep-2020

Correspondence Address:
Dr. Raghuram Palaparti
Department of Cardiology, Aayush Hospitals, Ramachandra Nagar, Vijayawada - 520 008, Andhra Pradesh
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JICC.JICC_5_20

Rights and Permissions
  Abstract 


Coronary bypass graft failure can be divided into three temporal categories: Early (0–30 days), midterm (30 days to 1 year), or late (after 1 year). Early to midterm graft failure is still a significant problem in the clinical practice and often under reported. Here, we report a case of midterm failure of all grafts post CABG. A 56-year-old male presented to us with unstable angina and found to have triple vessel disease. He underwent CABG with left internal mammary artery (LIMA) to left anterior descending, venous grafts to diagonal and obtuse marginal. As ostial right coronary artery disease was moderate, it was not grafted. Three months later, he presented with acute coronary syndrome, acute heart failure, and moderate left ventricular (LV) dysfunction. Coronary and graft angiogram revealed critical anastomotic lesions of LIMA and both the venous grafts. Rapid progression of native vessel disease was also observed. He underwent successful multivessel percutaneous coronary intervention (PCI) with improvement in LV function. Midterm saphenous venous graft failure is mainly caused by neointimal hyperplasia leading to occlusive stenosis. Midterm failure of coronary artery bypass grafts is not a uniformly predictable response and has been the focus of extensive clinical research. Various mechanical strategies involving improvement of surgical techniques and various pharmacological strategies have been studied but did not address the problem adequately. PCI is the preferred strategy in these high-risk patients as it is less invasive and gives excellent results. Graft surveillance, early recognition of the problem and aggressive management has shown to improve the graft patency rates and decrease recurrent cardiovascular events in these patients.

Keywords: Midterm anastomotic failure of grafts, multivessel percutaneous coronary intervention, neointimal hyperplasia, post CABG


How to cite this article:
Palaparti R, Koduru GK, Palaparthi S, S. Chowdary P S, Kondru PR, Ghanta S. Multivessel percutaneous coronary intervention in midterm anastomotic failure of all grafts post CABG: An unpredictable enigma?. J Indian coll cardiol 2020;10:92-6

How to cite this URL:
Palaparti R, Koduru GK, Palaparthi S, S. Chowdary P S, Kondru PR, Ghanta S. Multivessel percutaneous coronary intervention in midterm anastomotic failure of all grafts post CABG: An unpredictable enigma?. J Indian coll cardiol [serial online] 2020 [cited 2020 Oct 21];10:92-6. Available from: https://www.joicc.org/text.asp?2020/10/2/92/296124




  Introduction Top


Coronary bypass graft failure can be divided into three temporal categories: Early (0–30 days), midterm (30 days to 1 year), or late (after 1 year). Early to midterm graft failure is still a significant problem in the clinical practice and often under reported and under diagnosed. Here, we report a case of midterm failure of all grafts post coronary artery bypass graft surgery (CABGs) who underwent successful multi-vessel percutaneous coronary intervention (MV PCI) for revascularization. Although the PCI itself is not very challenging, the disease process is intriguing and raises concerns about the ideal preventive and management strategies in these patients.


  Case Report Top


A 56-year-old male, diabetic, hypertensive, and a chronic smoker presented with anginal chest pain on exertion for 2 weeks. On evaluation, he was found to have normal resting electrocardiogram (ECG), negative cardiac troponins, preserved left ventricular (LV) function on echocardiography, and positive stress ECG testing. His coronary angiogram on March 24, 2017, revealed critical mid left anterior descending artery (LAD) disease, significant diagonal disease, occlusion of major obtuse marginal (OM), diffuse distal left circumflex artery (LCx) disease, and moderate ostial right coronary artery (RCA) disease. He underwent CABG on March 27, 2017 with left internal mammary artery (LIMA) graft to LAD, saphenous venous grafts (SVG) to diagonal and OM. As ostial RCA disease was moderate, it was not grafted. His early postoperative course was uneventful and discharged on day 8. He was doing well until 3 months after surgery, when he presented with crescendo angina, New York Heart Association Class III dyspnea and easy fatigability for 1 week to emergency. His ECG showed nonspecific ST-T changes, troponins were positive-0.12 ng/ml (0.00–0.05), brain natriuretic peptide was elevated, 2D echocardiography showed moderate LV dysfunction (ejection fraction-0.38) with moderate ischemic mitral regurgitation (MR) [Videos 1-3]. After stabilization, a coronary and graft angiography showed critical lesions in SVGs to diagonal and OM at anastomotic sites. Critical LIMA to LAD distal anastomotic site lesion, occlusion of native LAD and LCx with progression of ostial RCA disease was also noted [Videos 4-9]; [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6].
Figure 1: Right anterior oblique caudal view shows occluded mid left anterior descending, diffusely diseased proximal left anterior descending and occluded major obtuse marginal

Click here to view
Figure 2: Anterior-posterior cranial view shows long segment left anterior descending disease and occlusion

Click here to view
Figure 3: This image shows critical calcific ostial right coronary artery disease. Significant pressure damping was noted

Click here to view
Figure 4: This image shows critical lesion of the anastomotic site of saphenous venous graft to obtuse marginal

Click here to view
Figure 5: This image shows the critical lesion of the anastomotic site of saphenous venous graft to diagonal

Click here to view
Figure 6: This image shows the left internal mammary artery to left anterior descending injection with critical lesion at the anastomotic site

Click here to view


Treatment options considered were a Re-do CABG (in view of occluded LIMA, pan-graft failure, global ischemia) or MV PCI. A heart team discussion favored MV PCI as he was deemed to be at higher risk for Re-do CABG. The patient also preferred and underwent MV PCI. He was planned for native LAD, LCX and RCA intervention and graft intervention for SVG to diagonal.

The left coronary artery was cannulated with 3.5 Extra-Back-Up guiding catheter. LAD was wired with Sion blue 0.014-inch wire using microcatheter (Corsair, ASAHI) support. Long segment LAD disease was predilated with 2.5 mm × 20 mm NC Trek balloon at 20 atm. A 2.5 × 38 XIENCE Alpine everolimus-eluting stent (EES) stent deployed distally and a 3.0 mm × 48 mm XIENCE Xpedition EES proximally. Stents were post dilated with 2.5 mm × 18 mm NC Trek balloon distally and proximal optimization done with 3.25 mm × 8 mm NC Trek at 20 atm with good result [Videos 10-12]; [Figure 7], [Figure 8], [Figure 9]. As native diagonal is stent jailed and a large vessel, PCI was done for SVG to D1. As the lesion is at the anastomotic site, PCI was done without embolic protection. Lesion predilated with 1.5 mm × 15 mm NC balloon, stented with 2.25 mm × 15 mm XIENCE V at 10 atm followed by optimization with 2.75 mm NC balloon at 16 atm with good result [Video 13]; [Figure 10]. Native LCx chronic total occlusion was attempted however could not be wired. Hence, we opted for SVG PCI to OM. It was also an anastomotic site critical lesion; hence PCI was done without embolic protection. Lesion predilated with 1.5 mm × 15 mm NC balloon at14 atm and stented with 2.5 mm × 15 mm XIENCE V at 12 atm. Post dilated with 2.75 × 8 NC balloon at 16 atm with good result [Video 14]; [Figure 11]. He underwent staged PCI after 4 weeks to critical ostial RCA lesion. RCA cannulated with JR 4.0 guide catheter. RCA wired with Sion blue 0.014-inch wire. Ostial RCA lesion dilated using Angiosculpt 3 mm × 10 mm balloon at 12 atm. Ostial RCA stented using 3 mm × 18 mm XIENCE V stent at 12 atm with good result [Video 15]; [Figure 12]. Significant improvement in LV function and complete resolution of MR was noted in follow-up [Video 16]. He was started on Aspirin + Ticagrelor, high-dose statin (atorvastatin 80 mg), antidiabetic medication and optimal doses of beta blockers and angiotensin-converting enzyme inhibition. After 1 year of follow-up he was continued on the duration of dual antiplatelet therapy (Aspirin + Clopidogrel), as he was considered to be at high risk for recurrent events. He is in our follow-up for the last 30 months and is asymptomatic.
Figure 7: Left anterior descending wired with the help of corsair, ASAHI microcatheter support and sion blue wire

Click here to view
Figure 8: This image shows final result after left anterior descending angioplasty-AP cranial view

Click here to view
Figure 9: This image shows final result after left anterior descending angioplasty-AP caudal view

Click here to view
Figure 10: Final result-saphenous venous graft to diagonal

Click here to view
Figure 11: Final result saphenous venous graft to obtuse marginal

Click here to view
Figure 12: Right coronary artery final result after angioplasty

Click here to view



  Discussion Top


Early SVG graft failure due to thrombotic complications is mainly attributable to technical errors during harvesting, anastomosis, or comprised anatomic runoff.[1],[2],[3],[4] Midterm SVG failure is mainly caused by fibro intimal hyperplasia leading to occlusive stenosis. Neointimal hyperplasia (NIH) in coronary artery bypass grafts is not a uniformly predictable response and has been the focus of extensive clinical research. Various mechanical strategies involving surgical techniques and various pharmacological strategies have been studied but did not address the problem adequately. The release of a variety of mediators, growth factors, and cytokines by the injured endothelium, platelets and activated macrophages will cause migration and proliferation of smooth muscle cells (SMC). Diminished production of endothelial nitric oxide, prostaglandins and adenosine will further contribute to enhanced SMC proliferation, leading to development of NIH.[1],[4],[5],[6],[7],[8] Changes in the flow pattern within the vessel (shear stress) and ischemic insults may contribute to changes in the SVG at this stage. SVGs are exposed to much higher mechanical pressure than that they were adapted to which can potentially stimulate SMC proliferation. Moreover, after encountering arterial flow patterns increased levels of intracellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemotactic protein-1 will facilitate leukocyte-endothelial interactions so that leukocyte infiltration of the lesions will ensue.[9] Finally, the adaptive response to hemodynamic factors, i.e., wall shear stress, may affect the distal site of the anastomosis leading to SVG failure.[10],[11] Midterm SVG failure accounts for an additional 15%–30%.[12],[13] In SVG there is no focal compensatory enlargement in the stenotic segments which is in contrast to native atherosclerotic arteries in which the development of an atherosclerotic plaque is associated with enlargement of the vessel and preservation of the lumen area until plaque progression exceeds the compensatory mechanism of the vessel.[14] Several studies show that SVG patency at 10 years is no more than 50%–60%.[1],[15],[16] Finally, several studies have suggested a role of immune cells in neointimal formation as macrophages are found in the intima, while T-lymphocytes are present in the adventitia of neointimal lesions with a predominance of CD4+ cells.[17],[18],[19] The extended benefit achieved by anti-inflammatory agents like colchicine in patients after myocardial infarction supports this theory.[20] Our patient had midterm failure (at 3 months) of all grafts at the anastomotic sites most probably due to NIH. The involvement of all anastomotic sites at a time temporally and rapid progression of native disease in our patient also raises a strong suspicion for a diffuse inflammatory/immune response. Intravascular imaging either by intravascular ultrasound or optical coherence tomography could not be done in our patient due to financial constraints. It would have shed more light in to the pathophysiology of graft stenosis.

When internal mammary artery (IMA) graft failure occurs, technical error is the most common cause in the early postoperative period. In the subsequent weeks to months, localized NIH may occur at the cleft between the native artery and the IMA graft at the anastomotic suture site, on the hood and on the floor of the native LAD, which can result in a localized stenosis.[21] The cellular mechanisms involved are similar to venous grafts. Performing an IMA bypass on a low-grade LAD stenosis or supplying an infarcted LAD territory leads to competitive flow and low flow, respectively, and adversely affects IMA graft patency (“disuse atrophy”). Causes for late (and rare) IMA failure include progressive fibro intimal proliferation and/or atherosclerosis either in the IMA graft or in the native LAD vessel.[22] The IMA graft failure in our patient is also likely to be due to the same pathophysiologic process as venous grafts. All the graft lesions including LIMA anastomotic site in our patient are soft and yielded with low pressure predilatation suggesting that they originated by cellular hyperplasia of recent onset.

The atypical presentations of chest pain post CABG patients may also delay the diagnosis of early and midterm graft failure. Routine adoption of high sensitivity troponins in clinical practice and a lower threshold for evaluation in high risk patients help us to identify the graft occlusions earlier. Graft surveillance, mechanical interventions such as PCI and aggressive medical management with antiplatelets and high-dose statins have been shown to improve the graft patency rates.[23],[24],[25]


  Key Message/conclusion Top


Intermediate/midterm graft failure (30 days to 1 year) post CABG is still a significant problem in clinical practice. NIH has been proposed as the reason for graft failure at that stage. It is neither uniformly predictable nor completely preventable. No major trials have looked in to this problem specifically. PCI being less invasive is the preferred strategy in these high-risk patients and gives excellent results as shown in various small studies. Careful follow-up for early identification and aggressive management is required to prevent recurrent cardiovascular events in these patients.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Motwani JG, Topol EJ. Aortocoronary saphenous vein graft disease: Pathogenesis, predisposition, and prevention. Circulation 1998;97:916-31.  Back to cited text no. 1
    
2.
Barboriak JJ, Pintar K, Van Horn DL, Batayias GE, Korns ME. Pathologic findings in the aortocoronary vein grafts. A scanning electron microscope study. Atherosclerosis 1978;29:69-80.  Back to cited text no. 2
    
3.
Vlodaver Z, Edwards JE. Pathologic changes in aortic-coronary arterial saphenous vein grafts. Circulation 1971;44:719-28.  Back to cited text no. 3
    
4.
Waller BF, Roberts WC. Remnant saphenous veins after aortocoronary bypass grafting: Analysis of 3,394 centimeters of unused vein from 402 patients. Am J Cardiol 1985;55:65-71.  Back to cited text no. 4
    
5.
Rao GN, Berk BC. Active oxygen species stimulate vascular smooth muscle cell growth and proto-oncogene expression. Circ Res 1992;70:593-9.  Back to cited text no. 5
    
6.
Nwasokwa ON. Coronary artery bypass graft disease. Ann Intern Med 1995;123:528-45.  Back to cited text no. 6
    
7.
Schwartz SM, deBlois D, O'Brien ER. The intima. Soil for atherosclerosis and restenosis. Circ Res 1995;77:445-65.  Back to cited text no. 7
    
8.
Zhang L, Peppel K, Brian L, Chien L, Freedman NJ. Vein graft neointimal hyperplasia is exacerbated by tumor necrosis factor receptor-1 signaling in graft-intrinsic cells. Arterioscler Thromb Vasc Biol 2004;24:2277-83.  Back to cited text no. 8
    
9.
Zou Y, Dietrich H, Hu Y, Metzler B, Wick G, Xu Q. Mouse model of venous bypass graft arteriosclerosis. Am J Pathol 1998;153:1301-10.  Back to cited text no. 9
    
10.
Leask RL, Butany J, Johnston KW, Ethier CR, Ojha M. Human saphenous vein coronary artery bypass graft morphology, geometry and hemodynamics. Ann Biomed Eng 2005;33:301-9.  Back to cited text no. 10
    
11.
Butany JW, David TE, Ojha M. Histological and morphometric analyses of early and late aortocoronary vein grafts and distal anastomoses. Can J Cardiol 1998;14:671-7.  Back to cited text no. 11
    
12.
Domanski MJ, Borkowf CB, Campeau L, Knatterud GL, White C, Hoogwerf B, et al. Prognostic factors for atherosclerosis progression in saphenous vein grafts: The postcoronary artery bypass graft (Post-CABG) trial. Post-CABG Trial Investigators. J Am Coll Cardiol 2000;36:1877-83.  Back to cited text no. 12
    
13.
Mehta D, Izzat MB, Bryan AJ, Angelini GD. Towards the prevention of vein graft failure. Int J Cardiol 1997;62 Suppl 1:S55-63.  Back to cited text no. 13
    
14.
Hermiller JB, Tenaglia AN, Kisslo KB, Phillips HR, Bashore TM, Stack RS, et al.In vivo validation of compensatory enlargement of atherosclerotic coronary arteries. Am J Cardiol 1993;71:665-8.  Back to cited text no. 14
    
15.
Atkinson JB, Forman MB, Vaughn WK, Robinowitz M, McAllister HA, Virmani R. Morphologic changes in long-term saphenous vein bypass grafts. Chest 1985;88:341-8.  Back to cited text no. 15
    
16.
Lie JT, Lawrie GM, Morris GC Jr. Aortocoronary bypass saphenous vein graft atherosclerosis. Anatomic study of 99 vein grafts from normal and hyperlipoproteinemic patients up to 75 months postoperatively. Am J Cardiol 1977;40:906-14.  Back to cited text no. 16
    
17.
Amano J, Suzuki A, Sunamori M, Tsukada T, Numano F. Cytokinetic study of aortocoronary bypass vein grafts in place for less than six months. Am J Cardiol 1991;67:1234-6.  Back to cited text no. 17
    
18.
Dietrich H, Hu Y, Zou Y, Huemer U, Metzler B, Li C, et al. Rapid development of vein graft atheroma in ApoE-deficient mice. Am J Pathol 2000;157:659-69.  Back to cited text no. 18
    
19.
Kockx MM, Cambier BA, Bortier HE, De Meyer GR, Declercq SC, van Cauwelaert PA, et al. Foam cell replication and smooth muscle cell apoptosis in human saphenous vein grafts. Histopathology 1994;25:365-71.  Back to cited text no. 19
    
20.
Tardif JC, Kouz S, Waters DD, Bertrand OF, Diaz R, Maggioni AP, et al. Efficacy and Safety of Low-Dose Colchicine after Myocardial Infarction. N Engl J Med 2019;381:2497-505.  Back to cited text no. 20
    
21.
Shelton ME, Forman MB, Virmani R, Bajaj A, Stoney WS, Atkinson JB. A comparison of morphologic and angiographic findings in long-term internal mammary artery and saphenous vein bypass grafts. J Am Coll Cardiol 1988;11:297-307.  Back to cited text no. 21
    
22.
Otsuka F, Yahagi K, Sakakura K, Virmani R. Why is the mammary artery so special and what protects it from atherosclerosis? Ann Cardiothorac Surg 2013;2:519-526.  Back to cited text no. 22
    
23.
Collins MJ, Li X, Lv W, Yang C, Protack CD, Muto A, et al. Therapeutic strategies to combat neointimal hyperplasia in vascular grafts. Expert Rev Cardiovasc Ther 2012;10:635-47.  Back to cited text no. 23
    
24.
McKavanagh P, Yanagawa B, Zawadowski G, Cheema A. Management and prevention of saphenous vein graft failure: A review. Cardiol Ther 2017;6:203-23.  Back to cited text no. 24
    
25.
Harskamp RE, Alexander JH, Ferguson TB Jr., Hager R, Mack MJ, Englum B, et al. Frequency and predictors of internal mammary artery graft failure and subsequent clinical outcomes: Insights from the project of ex-vivo vein graft engineering via transfection (PREVENT) IV trial. Circulation 2016;133:131-8.  Back to cited text no. 25
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
Abstract
Introduction
Case Report
Discussion
Key Message/conc...
References
Article Figures

 Article Access Statistics
    Viewed42    
    Printed0    
    Emailed0    
    PDF Downloaded8    
    Comments [Add]    

Recommend this journal