Perforation of saphenous vein graft with mediastinal haemorrhage leading to near closure of distal graft segment

Introduction

Saphenous venous graft (SVG) perforations during percutaneous coronary interventions (PCI) are rare, potentially lethal complications.^1,2 Overestimating of angioplasty balloon diameter, severely calcified and degenerated vessels are main risk factors of a graft rupture. Depending of perforation type, treatment with a prolonged balloon inflation and/or conventional/covered stent implantation should be performed.^3,4

Case report

We present a case of 76-year-old woman with history of hypertension and hyperlipidemia who underwent coronary artery bypass grafting 3 months prior to admission, which consisted of left internal mammary artery (LIMA) to left anterior descendant artery (LAD) graft and SVGs to obtuse marginal (OM) and right coronary artery (RCA). Patient presented with acute, typical chest pain. Initial 12-lead electrocardiogram (ECG) revealed ST-segment depression in leads II, III, aVF, V5 and V6. Serum troponin T levels rise was diagnostic for non-ST elevation myocardial infarction. Coronary angiogram (CA) showed 20% stenosis in left main (LM), relevant lesions in LAD with indirect features of LIMA patency, occlusion of circumflex artery (CX) and RCA at implantation site. Among grafts, there were two critical lesions in SVG-RCA (Figure 1a), three relevant stenoses in SVG-Cx and also one in LIMA-LAD, with lesions present in all implantation sites. PCI with drug-eluting stent (DES; Biotronik Orsiro) placement was performed in both lesions of SVG-RCA: first one in near-anastomosis area (2.75 × 15 mm/14 bar), followed with the procedure in proximal area (4.0 × 30 mm/14 bar). Then, a rupture and heavy extravasation of contrast at proximal lesion was noted (Figure 1b), qualified as Ellis Type III, with subsequent deployment of polyurethane-covered stent (Biotronik Papyrus 3.5 mm/18 atm) and successful sealing of vascular wall (Figure 1c). Patient was hemodynamically stable; echocardiography revealed no signs of hemopericardium. Prompt ECG-guided chest computed tomography (CT) displayed mediastinal haematoma near the heart base, surrounding large vessels and right heart margin, sparing pleura and pericardium (Figure 1d) No extra contrast during CT imaging was administered. After 3 h, patient presented with pain recurrence with ST-segment elevation in inferior wall leads. Another immediate CA revealed near occlusion of SVG-RCA distally to covered stent (Figure 1e), which required DES implantation (3.5 × 26 mm/14 atm) (Figure 1f). Antimicrobial treatment was started. Patient was free of chest pain during in-hospital follow-up. CT scan performed after 10 days revealed regression of non-contrasting haematoma, and was treated conservatively.

OPEN IN VIEWER

Figure 1.

(a) Baseline view of saphenous vein graft to right coronary artery, with two critical lesions (broad arrows), in proximal and distal, implantation part. (b) Massive extravasation of arterial blood into mediastinum after perforation in proximal segment (c) repaired with polyureathane-covered stent with no contrast leak observed. (d) Chest CT scan presenting spread of contrasting blood into mediastinal space (dotted circle); covered stent’s section pointed with dotted arrow. € External pressure from extravasated blood to distal SVG part resulting in near closure of the vessel; (f) treated with PCI with final result depicted.

Discussion

In this case, an intrathoracic bleeding with further external compression on SVG, resulting in ST-segment elevation, is of particular interest. Absence of hemopericardium, as presented in transthoracic echocardiography and CT scan, was probable due to several reasons: extrapericardial course of affected SVG or pericardial adhesions limiting spreading of blood with possible patent pericardiotomial gap. ⁵ On the contrary, mediastinal space lying posteriorly and superiorly, in the absence of natural boundaries, acts as area of lowest resistance. Nevertheless, high-volumed extravasation embraced also further part of the graft itself.

Another relevant issue concerns early failure of bypass grafts. Despite a well-known fact that saphenous grafts are prone to degeneration due to arterial flow pressure and neointimal proliferation, in this clinical scenario, the manifestation of accelerated graft dysfunction contributed in acute myocardial infarction and subsequent, life-threatening complication.