Left Anterior Descending Coronary Artery to Right Ventricular Fistula Complicating Coronary Stenting

Denes Korpas, MD, Celso Acevedo, MD, Richard L. Lindsey, MD, Alan H. Gradman, MD
Denes Korpas, MD, Celso Acevedo, MD, Richard L. Lindsey, MD, Alan H. Gradman, MD
Coronary artery perforation is a rare complication of percutaneous transluminal coronary angioplasty (PTCA) and coronary stenting. This complication most commonly results in a communication between the coronary artery lumen and the pericardial space; tamponade may ensue. Fistulization to the left or *right ventricle has been described during PTCA; however, it has never been reported as a complication of coronary stenting. We report a case where vessel rupture following stent placement led to the development of a fistula between the left anterior descending artery (LAD) and the right ventricle (RV). Case Report.A 75-year-old male was admitted for cardiac catheterization because of worsening chest pain. A perfusion myocardial scan suggested apical ischemia and inferior scar. The patient had a past medical history of hypertension, hypercholesterolemia and type-2 diabetes mellitus. Six years ago, he underwent coronary artery bypass grafting with a left internal mammary graft to the third diagonal branch of the LAD and a saphenous vein graft to the left circumflex artery. Coronary and bypass graft angiography revealed a patent saphenous vein graft to the left circumflex artery. The internal mammary artery graft to the third diagonal branch was also patent. The LAD was occluded after the second diagonal branch. Since the patient was symptomatic, with apical ischemia on the perfusion scan suggesting distal LAD distribution, recanalization of the chronically occluded LAD was attempted (Figure 1). Prior to the procedure, 6,000 IU of intravenous heparin was given. A Crosswire was manipulated across the obstruction with some difficulty. A 0.25 mg/kg bolus of intravenous abciximab was then administered, followed by 0.125 mcg/kg/minute continuous infusion. A 1.5 mm Ranger angioplasty balloon was advanced across the lesion. The intraluminal position was confirmed by dye injection through the balloon catheter lumen. Coronary angioplasty was then performed with the 1.5 mm balloon catheter. After several balloon inflations, a small linear dissection was present without any evidence for contrast extravasation or flow limitation (Figure 2). Intravascular ultrasound was performed; measurements demonstrated a vessel size of 4.2 mm proximal to the lesion and a vessel size of 2.7 mm distal to the lesion. Because of vessel size disparity, it was decided to deploy a 3.0 x 30 mm AVE S 670 stent at low pressure (6 atm) to under-expand the distal stent within the 2.7 mm lumen and further expand the proximal stent at higher pressure (12 atm) in the larger lumen. After balloon deflation, the stented vessel was noted to have perforated and extravasation of contrast was observed through a relatively long defect into the right ventricular outflow tract without staining of the myocardium or the pericardial space (Figure 3). The patient remained hemodynamically stable without any symptoms. A 3.0 x 20 mm perfusion balloon was inflated to 4 atm and left in place for 10 minutes to try to seal off the perforation. After balloon deflation, however, the contrast extravasation persisted without any further evidence of pericardial leak. Since the patient remained asymptomatic, the heparin was not reversed and platelets were not given. Echocardiogram did not demonstrate any pericardial fluid. The location of the shunt between the LAD and RV was confirmed from multiple views; therefore, oxymetry was not performed. The clinical situation was monitored closely and surgical consult was obtained. Given the stable clinical condition, the patient was treated conservatively with close observation in the Coronary Care Unit. There was no evidence of myocardial infarction by ECG or enzyme criteria. He developed a holosystolic murmur over the left parasternal border consistent with the intracardiac shunt. Follow-up coronary angiogram in 48 hours confirmed the fistula between the LAD and the RV (Figure 4). Again, no contrast extravasation was seen into the pericardial space. The patient remained asymptomatic and was discharged from the hospital two days later. He continued to do well at a 6-week follow-up visit. Three months later he remained asymptomatic, with his initial holosystolic murmur having regressed to early systolic. Follow-up cardiac catheterization was performed at 6 months; it demonstrated diffuse in-stent restenosis and disappearance of the fistula (Figure 5). Discussion. One of the most serious complications of percutaneous coronary intervention is coronary perforation. This complication occurs relatively rarely, but can be associated with serious morbidity and mortality. The reported incidence in the literature is about 0.1–2.1%, with the lower rates being described with conventional balloon angioplasty and directional atherectomy, while the incidence is higher with rotational (RA), laser (ELCA) and transluminal extraction (TEC) atherectomy. Other risk factors for coronary perforation and rupture include a balloon/artery ratio > 1.3 during PTCA, a device/artery ratio > 0.8 with TEC, ELCA and complex lesion morphology (B2 or C).1,2 Women and elderly patients are also at higher risk. The exact incidence of coronary perforation with stenting is unknown, but high-pressure deployment might be a contributing factor. Perforation of a coronary artery into a cavity chamber is the rarest form of perforation. In the literature, there have been three cases when PTCA of the LAD resulted in coronary perforation and the development of a LAD-RV fistula. In the first report, a false aneurysm developed at the site of the previous PTCA, which later ruptured.3 In the two other cases, the perforation and fistula formation occurred during the angioplasty.4,5 To our knowledge, no case of LAD-RV fistula during stent placement has been reported. Treatment of coronary perforation with limited or frank contrast extravasation includes prolonged balloon inflation with conventional or perfusion balloon catheter, and, in cases of contrast spill, reversal of heparin anticoagulation with protamine. When large molecule platelet glycoprotein IIb/IIIa inhibitor (abciximab) is administered, platelet transfusion is recommended with persistent pericardial leak. A relatively new treatment option is the deployment of a stent-graft or a stent covered with autologous vein or artery at the site of the perforation.6 Most patients with brisk pericardial extravasation, however, require surgical intervention. Perforation into an anatomic cavity chamber, on the other hand, carries a more favorable prognosis. Ellis et al. reviewed two cases of coronary perforation with cavity spilling (CS); both cases had a benign clinical course.1 In another review, patients in whom congenital coronary artery fistulas were found during diagnostic coronary angiography had no major hemodynamic abnormalities with a low pulmonary to systemic flow ratio.7 Our present case underscores the potential benign course of this type of coronary rupture. The same benign course was described in a similar case during PTCA. These patients, if hemodynamically stable, can be managed medically without the need for surgical intervention. The best treatment for coronary perforation, however, is prevention. In our patient, the cause of rupture was probably an oversized stent as well as the chronic total occlusion. It is important to avoid oversized balloons/stents with high-pressure inflations and rather choose a smaller balloon/stent with which high-pressure deployment is safer. We also might have created a channel between the LAD and RV with the guidewire during crossing and the administration of abciximab may have facilitated the fistula formation. In cases of total occlusion, it seems reasonable to withhold administration of glycoprotein IIb/IIIa inhibitors until intraluminal position has been confirmed with contrast injection through a balloon catheter. It is plausible that in our patient the reason for the absence of pericardial leak was the intramyocardial location of this distal LAD segment or the previous bypass surgery resulting in epicardial adhesions and preventing hemorrhaging into the pericardial space. The fistula was sealed by the subsequent in-stent restenosis.
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