Management of Distal Coronary Perforations
- Volume 20 - Issue 6 - June, 2008
- Posted on: 8/1/08
- 0 Comments
- 11195 reads
Coronary artery perforation (CAP) is an uncommon, yet potentially devastating, complication of percutaneous coronary interventions (PCI).1 Early reports of this catastrophic complication date back to the early 1980s.2 In a recent review of 6,245 patients undergoing coronary intervention, the incidence of CAP was 0.77%.3 Coronary perforations appear to be increasing in frequency. The aggressive use of glycoprotein IIb/IIIa inhibitors and pretreatment of patients with clopidogrel and ticlopidine have rendered it difficult for previously benign distal guidewire-related microperforations to seal themselves. The increased use of hydrophilic guidewires whose distal tips are difficult to control have also led to an increased incidence of guidewire-related perforations.
Another mechanism of coronary perforation results from rupture of the coronary artery. These are usually large perforations associated with hemodynamic collapse and occur in proximal coronary segments. These perforations carry a high mortality risk and their management revolves around prompt restoration of hemodynamics and definitive treatment with a polytetrafluoroethylene (PTFE)-covered stent. The incidence of perforations is higher in the elderly, women, patients in whom aggressive balloon sizing is used and with the adjunctive use of atheroablative devices.4–6
Management modalities for CAP have evolved from surgical to less invasive percutaneous techniques. Reported treatment modalities have included open surgical repair, covered stent/grafts, transcatheter injection of polyvinyl alcohol, autologous blood seal, gel foam embolization, transcatheter subcutaneous tissue delivery and coil embolization.7–10 All reported treatment strategies are preceded by reversal of anticoagulation and balloon inflation at the site of the perforation or just proximal to the perforation to prevent continued extravasation and tamponade.
This case report describes the nonsurgical management of a distal left anterior descending artery (LAD) perforation and is accompanied by a brief review of the different techniques available for sealing off a persistent leak in a perforated distal vessel. This case is clinically relevant because most interventional cardiologists are experienced with using covered stents when confronted with perforations. These are life-saving devices for proximal perforations and in large vessels where they can be safely delivered, but are of little to no value in distal perforations and in small vessels. Most cardiac catheterization laboratories are not equipped with the different coils, embolic glues and delivery catheters necessary to manage distal perforations. This case report attempts to familiarize the cardiac interventionalist with the different options available in managing this increasingly frequent emergency.
Case Report. An 80-year-old diabetic female underwent elective left-heart catheterization for refractory angina and abnormal myocardial perfusion imaging 6 months following PCI of the distal LAD. Angiography revealed flow-limiting in-stent restenosis of the distal LAD (Figure 1). After 2 drug-eluting stents were deployed in the distal LAD, a Type III coronary perforation was noted in the distal LAD with brisk extravasation of contrast media into the pericardial sac (Figure 2). Anticoagulation with bivalirudin was stopped and a 2.5 mm Maverick balloon (Boston Scientific Corp., Natick, Massachusetts) was inflated to 12 atm just proximal to the site of perforation.
Pericardiocentesis was performed to relieve cardiac tamponade, and 200 cc of fresh blood was drained from the pericardial space. A pigtail catheter was left in place in the pericardium. The balloon was then deflated and repeat angiography showed persistent extravasation of contrast media. At this point, the options were referral for open repair of the distal vessel without any option of revascularization distal to the perforation, continued balloon inflation, or embolization. It was felt that loss of the apical LAD territory would be reasonably well tolerated in a patient with normal left ventricular function, thus the option of embolizing the distal vessel was pursued.
A 3 Fr Renegade® STC 18 microcatheter (Boston Scientific) was advanced to the distal LAD and coil embolization was performed with deployment of 2 overlapping VortX®Diamond Interlock fibered coils (2/3 mm x 2.3 cm and 2/4 mm x 4.1 cm, Boston Scientific). A post-coil LAD arteriogram demonstrated good angiographic result with total occlusion of the distal LAD and no further extravasation (Figure 3). A postprocedure echocardiogram on the following day revealed an ejection fraction of 60% with preserved apical wall motion and trivial pericardial effusion. The peak infarct size, as measured by serum biomarkers, was a troponin of 0.13 μg/L and a creatine phosphokinase of 67 mg/dL. The patient had an uneventful course in the coronary care unit and was discharged home 3 days later in stable condition. At 3-month follow up, she remains stable with no clinical signs of angina or heart failure.