Perforation of the Ramus Intermedius and Fistula Formation with the Great Cardiac Vein

From the *Division of Cardiovascular Medicine, Winthrop-University Hospital and SUNY Stony Brook School of Medicine, 259 First Street, Mineola, New York, and the §Division of Cardiovascular Medicine, NYU Langone Medical Center, New York, New York. The authors report no conflicts of interest regarding the content herein. Address for correspondence: Adam Davis, DO, Winthrop University Hospital, Division of Cardiology, 259 First Street, Mineola, NY 11501. E-mail:ad0531dr@yahoo.com

_________________________________________________ ABSTRACT: Type III coronary perforations are a lethal complication of percutaneous intervention. While most involve “cavity-spilling”, or extravasation of contrast into the pericardial space, a few flow into an anatomic chamber. A case of balloon angioplasty-induced Type III perforation of the ramus intermedius (RI) with iatrogenic fistula formation to the great cardiac vein is presented and, to our knowledge, is the first report involving a perforated RI with a resultant fistula to the great cardiac vein.

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J INVASIVE CARDIOL 2009;21:E57–E59 Percutaneous intervention (PCI)-induced Type III coronary artery perforations can result in tamponade, myocardial infarction and the need for emergent surgery. Originally described angiographically by Ellis et al, the majority of Type III perforations involve extravasation of blood into the pericardial space, though a few communicate with surrounding circulatory chambers. Fistula formation by perforation has been reported between a coronary artery and the left ventricle, right ventricle or directly with the coronary sinus, but not, to our knowledge, between the ramus intermedius (RI) and the great cardiac vein (GCV). Here we describe a case of a Type III coronary perforation from balloon angioplasty causing RI dissection with extravasation and fistula formation between the RI and GCV. Case Report. A 70-year-old Caucasian female presented to our institution with episodic angina pectoris. She had a history of hypothyroidism, gastric esophageal reflux disease and coronary artery disease (CAD) with prior PCI and placement of a drug-eluting stent (DES) to the mid-RI. Elective cardiac catheterization was performed for the evaluation of in-stent restenosis and progression of her coronary artery disease. Coronary angiography revealed a right-dominant anatomy and normal left main and left anterior descending arteries. A 30% nonobstructive distal lesion of the right coronary artery and a diffusely diseased left circumflex artery were also observed. The RI branch had moderate stenosis in the mid-segment of the previously implanted Taxus® drug-eluting stent (Boston Scientific Corp., Natick, Massachusetts). The left ventriculogram showed mild hypokinesia of the mid-inferior wall of the left ventricle, with an estimated ejection fraction of 54%. An initial 6 Fr EBU guiding catheter (Medtronic, Inc., Minneapolis, Minnesota) was first used to assess the left coronary anatomy. Eagle Eye intravascular ultrasound (IVUS) (Volcano Therapeutics, Rancho Cordova, California) confirmed significant in-stent restenosis of the Taxus stent, with underdeployment and a a minimal luminal diameter estimated at 3.5 mm. Angiography further revealed a diseased RI with thrombus in the previously underdeployed Taxus stent (Figure 1). A 0.014 x 190 cm Cougar guidewire (Medtronic) was then advanced to the mid-RI, and the restenotic lesion was dilated with a 3.5 x 6 mm Stormer Zipper balloon (Medtronic). Following balloon deflation, there was aneurysm formation just distal to the stent without obvious perforation (Figure 2). A 3.0 x 24 mm Taxus stent was then deployed at 18 atm for 54 seconds. Immediately after deflation of the balloon, angiography confirmed a large perforation of the RI branch, with extravasation of contrast into the GCV (Figure 3) of the coronary sinus. The patient remained hemodynamically stable, with no evidence of active ischemia. Anticoagulation was not reversed. Emergent 2-dimensional echocardiography excluded hemopericardium, effusion or tamponade physiology. Two 3.0 x 16 mm JoStent polytetrafluoroethylene (PFTE) covered stents (JoMed International AB, Helsingborg, Sweden) were deployed in the RI at the perforation site (Figure 4). Post JoStent deployment angiography showed no evidence of active perforation. The patient was conservatively managed, her physical examination was unchanged, her echocardiography remained normal and her cardiac biomarkers were not elevated. She remained asymptomatic and was discharged from the hospital 2 days later. Discussion. Coronary artery perforation is a rare but serious complication of PCI that may lead to tamponade, myocardial infarction, emergency surgical intervention or death. The reported incidence is l

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