Abstract
Coronary artery perforation (CAP) is an infrequent yet a very dangerous complication of percutaneous coronary intervention. We describe the successful treatment of a guidewire-induced distal coronary branch vessel perforation using localized distal injection of intracoronary thrombin with a microcatheter. This technique appears to be safe and effective for the treatment of life-threatening distal guidewire perforations, even in the smallest tertiary coronary branches.
1
Introduction
Coronary artery perforation (CAP) is an infrequent yet a very dangerous complication of percutaneous coronary intervention (PCI) . We have previously reported the successful use of localized intracoronary thrombin injection via the wire lumen of a very small diameter over-the-wire balloon catheter in order to seal coronary artery perforation or rupture .
The incidence of coronary perforation during PCI ranges from 0.1% to 3% and seems to occur more frequently with the use of cardiac devices such as atheroablative devices and hydrophilic wires . The use of glycoprotein IIb/IIIa inhibitors in PCI makes the management of small guidewire-induced perforations more problematic .
In the current case study, we have modified the technique of injecting thrombin via the end-hole of a small (inflated) balloon catheter. In this very challenging case, we successfully used a very small and very flexible microcatheter to inject thrombin into a tiny tortuous side branch after a guidewire-induced perforation. This case report and discussion helps to review the percutaneous options to deal with this life-threatening complication.
2
Case report
A 67-year-old man with no history of coronary artery disease was transferred emergently to our medical center for management of ST-elevation myocardial infarction. Cardiac catheterization via a transfemoral approach revealed a 100% occlusion of proximal left anterior descending (LAD) artery at the diagonal branch ( Fig. 1 A). He was treated with weight-based intravenous heparin combined with intravenous abciximab bolus and infusion.
A 6-Fr XB 3.5 guide catheter (Cordis, Miami, FL) was used to engage the left main coronary artery. A 0.014-in. hydrophilic wire (PT Graphix, Boston Scientific/Scimed, Maple Grove, MN) was used to cross the total occlusion. The lesion was predilated using Sprinter 2.5×15-mm balloon (Medtronic, Minneapolis, MN), which established Thrombolysis in Myocardial Infarction (TIMI) 3 flow beyond the lesion ( Fig. 1 B). The patient was given intracoronary nicardipine and nitroglycerin. The lesion was then treated with a Xience 3.0×28-mm drug-eluting stent (Abbott Vascular, Santa Clara, CA). The stent was postdilated with a noncompliant balloon, yielding minimal residual stenosis with TIMI 3 flow.
During the final angiogram, with the hydrophilic wire residing distally in a very small diagonal branch, the final contrast injection caused a forceful distal movement of the hydrophilic wire into the tertiary aspect of a small diagonal branch ( Fig. 1 C, D). The initial angiogram performed after removing the wire did not immediately demonstrate evidence of perforation.
A 7.5-Fr intra-aortic balloon pump (Datascope, Fairfield, NJ) was placed because of ongoing hypotension. The patient received a loading dose of clopidogrel and was transferred to the intensive care unit (ICU) with intravenous phenylephrine, heparin and abciximab drips.
Several hours later, in the ICU, the patient developed chest discomfort and progressive hypotension. Tamponade was suspected, so a limited echocardiogram was performed, and an anterior pericardial effusion without tamponade physiology was demonstrated. Coronary angiography was repeated and demonstrated excellent stent patency in the proximal LAD. However, it was recognized that there was active extravasation of contrast into the pericardial space from the distal portion of a very small (<1 mm diameter) distal diagonal branch. This extravasation of contrast was consistent with a small, but potentially life-threatening perforation ( Fig. 2 A), which was presumably caused by the forceful distal movement of the hydrophilic coronary guidewire.
Although there was no definite pericardial tamponade, there was concern that this active coronary leak would lead to tamponade, particularly considering the anticoagulation and antiplatelet therapy that the patient had received. A 2.5-mm Sprinter balloon was immediately advanced into the distal LAD at the site of the diagonal branch. It was inflated at 8 atm. Angiography confirmed that this obstructed the diagonal branch flow. Abciximab and heparin drips were discontinued. Protamine was given to reverse the heparin. A platelet transfusion was ordered.
In an attempt to seal the perforation, the balloon was initially inflated for 15 min. Interestingly, the patient’s hypotension appeared to resolve during the balloon inflation and worsen following balloon deflation. After this prolonged balloon inflation, angiography demonstrated a persistent contrast leak. The balloon was reinflated for another 30 min, which also failed to affect the coronary leak. The placement of a “covered” (Jomed) stent to cover and occlude the origin of this small side branch was not felt to be a viable option given the small diameter of the distal LAD artery (∼2.1 mm). The deliverability challenges, and the high incidence of stent thrombosis with covered stents in smaller vessels, would make this a poor option.
At this point, we decided to inject thrombin locally into the distal portion of the small diagonal branch to try to “seal” the leak. The diagonal branch came off at a nearly 100° angle from the distal LAD and was very small. The smallest 1.5 mm over-the-wire balloon catheter was too large and stiff to track into this ∼0.5- to 0.75-mm-diameter diagonal branch. It was therefore elected to try a unique variation of the distal thrombin injection technique in an attempt to avoid open-heart surgery and/or pericardiocentesis and to seal this leak.
A 1.9-Fr EV3 microcatheter (Microtherapeutics, Irvine, CA) was advanced over an ATW 0.014-in. wire (Cordis, Miami, FL) into the diagonal branch ( Fig. 2 B). A test injection through the lumen of the microcatheter was performed with diluted contrast to confirm no “back-leak” into the distal LAD artery.
A thrombin solution (100 IU/ml) was prepared from lyophilized powder (5000 IU per bottle). The powder was dissolved in normal saline to achieve the desired concentration of 100 IU/ml. The 0.014-in. guidewire was withdrawn ( Fig. 2 C), and 250 U of thrombin solution was then injected slowly through the microcatheter, using a 3-ml syringe, over 5 min. A very small (<0.5 ml) bolus of air was intentionally injected through the microcatheter to further diminish retrograde movement of thrombin or anterograde blood flow into the diagonal branch.
Angiography demonstrated minimal but persistent leak. The wire was readvanced into the diagonal and an additional 300 U of thrombin was injected over a 5- to 6-min period, yielding a total delivered thrombin dose of 550 IU into the distal diagonal perforation site.
The microcatheter was then flushed with 2 ml of normal saline to clear any residual air and/or thrombin from the lumen. The microcatheter was then withdrawn quickly into the guiding catheter. Repeat angiography demonstrated that the diagonal branch was now completely occluded just past the microcatheter tip with obliteration of the leak from guidewire perforation ( Fig. 2 D, arrow). Final angiography after removal of the microcatheter revealed the LAD flow to be TIMI 3 with no evidence of thrombin back flow into the LAD. The patient tolerated the procedure very well and returned in a stable condition to the ICU.
He was easily weaned off of the phenylephrine drip and the intra-aortic balloon pump. A repeat echocardiogram, the next day, revealed no increase in the amount of pericardial effusion. He had an uneventful hospital course and was discharged to home in a stable condition 4 days after admission.
2
Case report
A 67-year-old man with no history of coronary artery disease was transferred emergently to our medical center for management of ST-elevation myocardial infarction. Cardiac catheterization via a transfemoral approach revealed a 100% occlusion of proximal left anterior descending (LAD) artery at the diagonal branch ( Fig. 1 A). He was treated with weight-based intravenous heparin combined with intravenous abciximab bolus and infusion.
