Coronary artery perforation during interventional procedures

Coronary artery perforation complicating percutaneous coronary intervention occurs in 0.1–0.6% of cases [1–4]. When ablation devices are used, the frequency is substantially higher than with balloon angioplasty or stents [5,6]. Rapid recognition is essential to employ potentially life saving management techniques in a timely manner. A case illustrating the occurrence and management of this complication in contemporary practice is presented. An 84-year-old woman presented to the emergency room in cardiogenic shock. She had been in her usual state of health until the previous evening when she began to experience recurrent episodes of severe chest tightness and squeezing. On arrival, her blood pressure was 80/40 mm Hg, pulse 120 bpm, and respirations 25/min. The chest was filled with crackles and there was a loud summation gallop at the apex. The ECG showed ST-segment elevations of 6 mm amplitude in leads V1-6 with reciprocal changes in the limb leads. Intravenous dopamine and dobutamine, abciximab, heparin, and oxygen by mask were instituted immediately and 325 mg of aspirin and 300 mg of clopidogrel were administered orally. She was electively intubated and transferred to the cath lab where an IABP was inserted. Diagnostic coronary angiography demonstrated severe three-vessel disease and an acutely occluded proximal LAD with TIMI grade 1 flow (Fig. 1). The lesion was easily crossed by a guidewire and inflation with a 3.0 3 20 mm balloon initiated. Postinflation coronary angiography demonstrated a huge thrombus distal to the bifurcation with a large diagonal branch (Fig. 2). Numerous downstream thromboemboli developed. Over the course of the next 15 min, multiple balloon inflations at various sites of thrombosis were undertaken; however, recurrent thrombosis continued. The ACT was 275 sec and more heparin was administered. Finally, the LAD appeared moderately clear of clot and TIMI grade II flow was present. The blood pressure was 100/60 mm Hg with 10 lg kg/min of dopamine. A 3.5 3 18 mm bare metal stent was placed at the site of the initial lesion. The guidewire was withdrawn to check for wall thrombosis. After 10 min, repeat angiography showed no change in vessel status, but then angiographically evident recurrent thromboembolism appeared. The heart rate exceeded 125/ min and the blood pressure fell rapidly. Ventricular tachycardia was treated with IV amiodarone and lidocaine. The guidewire was re-inserted using the initial angiogram as a roadmap; however, the image intensifier was now in a more angulated projection. The balloon was inflated at the site of a thrombus during which the blood pressure rose, but with deflation, it decreased to a systolic pressure of 40 mm Hg. Angiography showed a type III B coronary artery perforation near a large septal perforator (Fig. 3). The balloon was re-inflated proximal to the site of perforation, with a modest rise in blood pressure. An echocardiogram showed a small to moderate sized pericardial effusion without signs of cardiac tamponade. A PTFE covered stent over a second guidewire could not be safely positioned as even a few seconds of balloon deflation led to hemodynamic collapse. The patient was taken for