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Case Report
Left Anterior Descending Artery-to-Right Ventricle Fistula and Left Ventricular Free Wall Perforation after Rotational Atherecto
August 2005
Coronary artery perforation is a rare but serious complication of percutaneous coronary intervention (PCI). The incidence is 0.1% with lesions treated by balloon angioplasty and 0.5–3.0% with lesions treated by atheroablative devices.1 It can result in hemopericardium and cardiac tamponade,2–5 fistulae to the left or right ventricle,2,5–8 or coronary arteriovenous fistulae1,2,5 and a high incidence of death, myocardial infarction, and emergency surgery. We describe a case of perforation of the left descending artery (LAD) after rotational atherectomy and stent implantation, leading to both cardiac tamponade and a fistula to the right ventricle with a fatal outcome despite surgery.
Case Report. A 75-year-old man presented with stable angina for 6 months and anterior wall ischemia on thallium scintigraphy. He received stent implantation to the left circumflex (LCx) and right coronary arteries (RCA) 2 years before. Coronary angiography demonstrated diffuse calcified 80% stenosis in the proximal to mid-LAD (Figure 1A), with a reference diameter of 3.45 mm and a lesion length of 36.09 mm by quantitative angiography. The LCx and RCA were free of significant disease, with no restenosis in previously stented sites. After administering unfractionated heparin at 70 U/kg for procedural anticoagulation, the LAD lesion was treated with rotational atherectomy using a 1.75 mm burr (Boston Scientific, Maple Grove, Minnesota), followed by implantation of overlapping 3.5 x 32 mm and 3.5 x 8 mm Express™ II stents (Boston Scientific) from proximal to mid LAD. The patient developed severe chest pain immediately after dilating the stents with the stent balloon at 15 atmospheres.
Angiography revealed staining in the myocardium, contrast extravasation to the pericardium, and contrast leakage from the mid-LAD via a fistula to the right ventricle (RV; Figure 1B and C). Protamine was given intravenously to reverse the heparin effect. Pericardiocentesis was performed to relieve the cardiac tamponade. The perforation persisted after prolonged balloon inflation and was finally sealed by implanting a 2.5–5.0 x 19 mm covered stent (JoMed), which was mounted on a 3.0 x 20 mm Maverick™ balloon (Boston Scientific). Although angiography did not reveal contrast extravasation from the LAD, the patient was in persistent hypotension with continuous drainage of blood from the pericardial drain, and was therefore taken to the operating room. There was a large amount of fresh blood and clots in the pericardial space with tamponade effect. A large hematoma was present in the left ventricle (LV) over the proximal and mid-LAD territory, with arterial bleeding from two free wall perforations. The tissues were friable and attempted repair of the bleeding sites resulted in further tear at the adjacent sites. New perforations appeared after applying sutures to control the initial bleeding sites. Bleeding could not be stopped despite almost complete covering of the anterior LV wall by Teflon strips. The patient succumbed shortly after weaning off cardiopulmonary bypass. Postmortem examination showed a fistula from a small perforation in the posterior wall of the mid-LAD to the RV 3 cm below the pulmonic annulus (Figures 2, 3, and 4). The anterior LV wall could not be assessed because of multiple patches and sutures. Histologic section revealed portions of the fistula as a ragged tract containing scanty polymorphs and disrupted myocytes with contraction band necrosis (Figure 5).
Discussion. Coronary artery perforation is an uncommon complication of PCI with an increased incidence in the new device era.2–5 A majority (> 75%) of the perforations belong to types II (pericardial or myocardial blush without contrast jet extravasation) and III (extravasation through ? 1 mm perforation).2 The incidence of type IV perforations (contrast extravasation into a cardiac chamber or cavity) is low, and accounts for 2.1% to 3.2% of all perforations.2,5 Our case is unique in that it has both the characteristics of type III and type IV perforations. There were multiple risk factors for perforation in this case, namely, elderly, calcified artery, lesion length, lesion eccentricity, and use of rotational atherectomy. The altered integrity of the vessel wall by rotational atherectomy, together with the barotrauma of high-pressure dilatation using the semi-compliant stent balloon, may be the more important factors contributing to the perforation.
Prolonged balloon inflation is a recommended management of type II and III perforations and may obviate the need for surgery in 60–70% of the cases.1 There are recent reports demonstrating good results after using covered stents to seal coronary perforations.9–11 Although the perforation in our case was apparently sealed on angiography after implanting a covered stent, there was ongoing severe bleeding into the pericardial space, as evidenced by the continued drainage of blood from the pericardial drain and persistent hemodynamics of cardiac tamponade. It was only noted in the operating room that the source of bleeding was from perforations of the LV free wall, but not from the artery, which was not suspected pre-operatively. The free wall perforations may have resulted from ischemia, leading to myocardial infarction from prolonged balloon inflation. But this case is unusual in that the ventricular wall integrity was so severely damaged that sutures could not be taken for repairing the perforations, leading to the fatal outcome despite surgical intervention.
Email: whchen@hku.hk
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