Substrate For Complications

ABSTRACT: Acute stent thrombosis is a rare, life-threatening, and challenging complication of left main stenting. Equally challenging is treating a chronic saphenous vein graft occlusion. Though considered class III indication per ACC/AHA guidelines, the saphenous vein graft may be the only potential conduit for revascularization. Coronary perforation during chronic total occlusion revascularization after coronary artery bypass grafting is not rare but the post-coronary artery bypass grafting state itself may provide some protection against tamponade by virtue of the adhesions between pericardium and epicardium consequent to surgery. We present a case of multiple complications in one patient and a good outcome after treating each of the above complications.

J INVASIVE CARDIOL 2012;24(7):E153-E156

Key words: Left main stenosis, stent thrombosis, saphenous vein graft intervention, chronic total occlusion, coronary perforation

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Coronary artery bypass grafting (CABG) is considered the standard management strategy for patients with left main disease.^1,2 Because of significant advances in technology and techniques in the past decade, left main stenting has been recommended as an alternative to CABG under certain circumstances.³ Acute stent thrombosis is a potential catastrophic complication of percutaneous coronary intervention (PCI), especially when occurring within the left main artery.

Although saphenous vein grafts (SVG) are widely used during bypass grafting surgery, the long-term patency rate is poor. Between 40% and 50% of grafts will fail within 10 years.⁴ Due to the increased morbidity and mortality associated with repeat bypass surgery, SVG intervention has become an accepted means to revascularize patients.^5,6 However, PCI remains a class III indication (ie, not recommended) for SVG chronic total occlusion. Nevertheless, in a subgroup of patients with severe ischemia, the SVG may be the only potential conduit to revascularize the ischemic myocardium.

We present a case of left main acute stent thrombosis and a coronary perforation reached through a chronically occluded SVG during a subsequent staged intervention in the same patient resulting in hemodynamic compromise.

Case Report. A 60-year-old male with history of coronary artery disease was referred for a 4-month history of disabling dyspnea and orthopnea after suffering a myocardial infarction. Past history included prior PCI followed by CABG 12 years earlier. Six months prior, he underwent PCI to the SVG to left anterior descending artery (LAD) and posterior descending artery with drug-eluting stents during a non-ST segment elevation myocardial infarction. One month later he suffered another myocardial infarction and underwent coronary angiography, during which he developed ventricular fibrillation requiring defibrillation. After that we decided to manage the patient medically including aspirin and clopidogrel. Repeat arteriography at our facility showed 60% stenosis of the left main artery, 60% stenosis of the mid LAD (Figure 1A), 70% stenosis of the ostial left circumflex artery with total occlusions of the obtuse marginal and right coronary artery (RCA) (Figure 1B). The SVG to obtuse marginal was patent (Figure 1C). The SVGs to the LAD and RCA were occluded. Left ventriculogram showed an ejection fraction of 30% with inferior wall akinesis and anterior wall hypokinesis.

The left coronary artery was intubated with XB 3.5 guide catheter (Cordis Corporation). Bivalirudin was used for anticoagulation. A Radi PressureWire (St. Jude Medical) was used to cross the mid LAD stenosis. At this time baseline Pd/Pa was 0.85 and fractional flow reserve (FFR) was 0.53 (Figure 2A). The pressure wire was then pulled proximal to the LAD stenosis. Baseline Pd/Pa was 0.93 and FFR was 0.80. A Xience V 3.0 mm x 18 mm stent (Abbott Vascular) was deployed in mid LAD. Repeat FFR was 0.67 (Figure 2B). We claim that the left main artery was causing this value and decided to proceed with stenting of the left main stenosis. A Xience V 3.5 mm x 18 mm stent (Abbott) was deployed from distal left main artery to LAD.  The left main stent was post-dilated with a Voyager NC 4.0 mm x 12 mm balloon (Abbott). Repeat FFR was 0.89 (Figure 2C). Intravascular ultrasound (IVUS) showed a malapposed stent in the left main (Figure 2D). A 5.0 mm x 8 mm Voyager NC balloon catheter (Abbott) was used. IVUS showed better apposition of the stent in the left main artery (Figure 2E). The patient then acutely developed severe chest pain with lateral ST-segment elevation approximately 7 minutes after dilatation with 5.0-balloon catheter. Repeat angiogram showed acute stent thrombosis with partial lumen compromise with thrombus in the distal left main stent (Figure 3A). We started the patient on eptifibatide and performed aspiration thrombectomy with a Pronto aspiration catheter (Vascular Solutions) followed by balloon angioplasty, which resolved the thrombus and chest pain (Figure 3B).

Four weeks later we performed PCI to SVG to RCA as patient had angina. The SVG was intubated with a 6 Fr multipurpose guide catheter and the patient was anticoagulated with unfractionated heparin. The CTO was crossed with a Pilot-150 guidewire (Abbott) with support of an over-the-wire Apex 1.5 mm x 12 mm balloon catheter (Boston Scientific). The Pilot-150 and subsequently a Miracle Bros 4.5 gm guidewire (Asahi Medical) were unable to cross the previously stented distal segment of the graft. A Confianza Pro guidewire (Asahi) was used to cross the distal segment. Contrast injection through the over-the-wire balloon catheter showed mild stain in the inferior wall (Figure 4A). Further restoration of flow after balloon angioplasty caused extension of the stain (Figure 4B) with resultant hemodynamic compromise with blood pressure dropping to 77/42 mm Hg. Blood flow to the perforated small vessel was stopped by prolonged balloon inflation in the proximal segment of the graft along with reversal of anticoagulation (Figure 4C). Echocardiogram showed no evidence of pericardial effusion. The patient was then transferred to the coronary care unit. The patient continued to have chest pain with ST-segment depression in the inferior leads on electrocardiogram and was brought back 4 H later for repeat coronary angiogram. The SVG was occluded. We used unfractionated heparin for anticoagulation and crossed the SVG occlusion with a Pilot-50 guidewire (Abbott). We performed aspiration thrombectomy with a Pronto aspiration catheter. A Guardwire embolic protection device (Medtronic) was used. We placed 5 drug-eluting stents (XienceV 2.75 x 23; 2.75 x 28; 2.75 x 28; 2.75 x 23; and 2.5 x 12 mm from proximal to distal end) to restore graft patency with TIMI-3 flow (Figure 4D), resulting in relief of symptoms. Three months later, the patient was completely symptom free and was able to participate in a graded exercise program. 

Discussion and Review. Data show left main stenting as safe and comparable to CABG surgery.⁷ Left main stent thrombosis is a very rare complication of PCI.⁸ Many risk factors have been shown to predict acute stent thrombosis including the procedure itself with resultant stent malapposition and/or underexpansion, number of implanted stents, stent length, persistent slow coronary blood flow and dissections, patient and lesion characteristics, stent design, and premature cessation of antiplatelet drugs.^9,10 In our patient, we performed IVUS imaging after the stent deployment and malapposition of left main stent was present and addressed with post dilation with confirmation of expansion with repeat IVUS. Patient was adequately anticoagulated with bivalirudin and previous stent deployed in the LAD was patent. Based on known risk factors, it is unclear as to why the patient developed acute stent thrombosis. However, one can speculate that overexpansion of left main stented segment or left main/LAD diameter mismatch resulted in non-laminar flow leading to stent thrombosis. Sukavaneshvar and colleagues performed in vitro studies looking at predictors of stent thrombosis. They reported that residual stenosis within or just outside of the stent can cause alterations in flow dynamics leading to increased thrombi accumulation.¹¹ Hyun et al found that regions that are susceptible to thrombi formation are near the expansion wall and reattachment points within stents because of non-uniform hemodynamic indicators, which are near-zero wall shear stress and elevated wall shear stress gradients.¹² These could be the factors that lead to stent thrombosis in our case.

Historically, interventions of chronically occluded saphenous vein grafts have been difficult with reportedly low success rates.¹³ Alternatively, the risk of procedural complications has been reported as higher than other types of PCI.¹⁴ As such, even with improvements in equipment, pharmacology, and technique, PCI of an SVG CTO still remains a Class III indication.¹⁵ Acute graft closures have a better outcome regarding flow restoration, but still remain rather high-risk as many of these occlusions have a large thrombus burden.¹⁶ When deciding whether or not to intervene on native arteries or vein grafts, the majority of operators would choose the native artery. In this case we decided to proceed with SVG intervention because this was considered a “comparatively recent occlusion” (estimated to be 5 months in duration) and it had a favorable characteristic of  “a beak.” During the initial procedure, a small inferior wall contrast stain was noted that was likely from a wire perforation. The stain propagated after establishing flow in the graft, resulting in hemodynamic compromise. Previous CABG surgery could protect against progression to tamponade in a coronary perforation due to the fact that there are pericardial adhesions. Sometimes following surgery, the pericardium is repaired with the notion that it will reduce the formation of adhesions. However, pericardium is not repaired routinely. In cases of unrepaired pericardium, there is a pseudo space between the chambers and pericardium laterally, and posterior and chest wall anteriorly. In this scenario, it is possible that extravasated blood may cause a compression of the cardiac chambers leading to tamponade physiology.¹⁷ Graft occlusion with balloon inflation prevented further deterioration by stopping the inflow of the leak. Patient continued to have chest discomfort that was initially thought to be secondary to pericardial irritation. Since the discomfort had typical angina characteristics with electrographic changes, patient was brought back for repeat angiography in 4 H. SVG intervention was successful with restoration of TIMI-3 flow and resolution of discomfort and electrocardiographic changes. The perforation was sealed.

Our patient continued to have angina with electrographic changes and was brought back to the laboratory. Recrossing was comparatively easy. Aspiration thrombectomy followed by distal protection and revascularization with stent placement resulted in restoration of blood flow and perforation stayed sealed.

In conclusion, FFR results in tandem lesions should be interpreted with caution and FFR can worsen in second lesion after PCI to first lesion. A normal FFR post-stenting may occur in malapposition, emphasizing the need for IVUS to assure complete apposition. The presence of previous CABG does not guarantee that a perforation will be contained.

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From the Central Arkansas Veterans Healthcare System and University of Arkansas for Medical Sciences, Little Rock, Arkansas.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Sachdeva is on the Speaker’s Bureaus of St Jude Medical and Volcano Corporation. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted January 30, 2012, provisional acceptance given March 21, 2012, final version accepted March 30, 2012.
Address for correspondence: Rajesh Sachdeva, MD, 4300 W 7th Street, Little Rock, Arkansas, 72205, USA. Email: rrsachdeva@gmail.com