Case presentation

An otherwise healthy and active 65-year-old man, with a past history notable for coronary artery bypass surgery 14 years earlier consisting of a right internal mammary artery graft to the right coronary artery, presents for cardiac catheterization. Five years earlier, he presented with an acute inferolateral wall myocardial infarction and underwent bare-metal stent placement to the first obtuse marginal artery and to his first diagonal artery; a long occluded segment of the distal circumflex artery was noted and deemed not treatable percutaneously. He remained free of cardiac symptoms until 3 months prior to his presentation, when he developed effort angina. Anginal symptoms progressed and began limiting his ability to work in his yard or to engage in hunting and fishing. Medical therapy, consisting of metoprolol, long-acting nitrates, aspirin, clopidogrel, and simvastatin, failed to improve his symptoms and he was referred for cardiac catheterization. Physical examination and routine laboratory evaluations were unremarkable. His baseline electrocardiogram revealed a prior inferolateral infarction and an incomplete right bundle branch block.

Cardiac catheterization

Left ventricular systolic function was preserved, with an estimated ejection fraction of 60% and only mild inferior wall hypokinesis. A widely patent right internal mammary artery graft provided an excellent distal blood supply to a severely diseased right coronary artery (Figure 16-1). Stents placed in the diagonal and obtuse marginal arteries were widely patent and the previously-noted long occluded segment of the distal circumflex remained unchanged (Figure 16-2). A long, tubular stenosis of moderate severity was apparent in the midportion of the left anterior descending artery (Figure 16-3 and Videos 16-1, 16-2). Given the uncertainty of the stenosis severity, the operator measured fractional flow reserve using a pressure wire and intracoronary adenosine to achieve maximal hyperemia. With classic anginal symptoms despite maximal medical therapy and a fractional flow reserve measuring 0.78, the physician decided to revascularize the left anterior descending artery percutaneously. Following administration of intravenous heparin and eptifibatide, the operator directly stented the diseased segment using a 6 French left coronary guide catheter with a 3.0 mm diameter by 32 mm long sirolimus-eluting stent inflated to 12 atmospheres (Figure 16-4).

FIGURE 16-1 Patent right internal mammary artery graft to the severely diseased right coronary artery.

FIGURE 16-2 A large first obtuse marginal artery is free of disease; there is occlusion of a long segment of the distal circumflex artery (arrow).

FIGURE 16-3 Long, tubular stenosis in the midportion of the left anterior descending artery (arrow).

FIGURE 16-4 Position of the stent at the site of the lesion in the left anterior descending artery.

Immediately following stent deployment, the angiogram demonstrated free extravasation of contrast emanating from the midportion of the stented segment consistent with a coronary artery perforation (Figure 16-5 and Video 16-3). The patient reported substernal chest and left shoulder pain; ST-segment elevation was apparent on the monitored leads. Central aortic pressure fell to a systolic pressure of 70 mmHg and the heart rate increased to 110 beats per minute. A 3.0 mm diameter by 20 mm long compliant balloon was immediately advanced over the 0.014 inch guidewire and inflated at the site of contrast extravasation (Figure 16-6). This maneuver, along with simultaneous infusion of saline and initiation of intravenous dopamine, led to immediate stabilization of blood pressure.

FIGURE 16-5 Free extravasation of contrast (arrow) is noted from the midportion of the stent, consistent with perforation of the coronary artery.

FIGURE 16-6 Balloon inflated at the site of the perforation temporarily halted further hemorrhage into the pericardial space.

At this point, the operator stopped the eptifibatide infusion and performed an emergent echocardiogram. This revealed a small, loculated effusion over the anterior wall. The patient remained hemodynamically stable with the balloon inflated for 10 minutes. Repeat angiography following this prolonged balloon inflation showed continued, free-flowing contrast extravasation (Video 16-4), and the balloon was reinflated at the site.

Working quickly, the operator deflated the balloon, removed the guidewire, and replaced the 6 French sheath and guide catheter with an 8 French system. After repositioning an exchange-length, 0.014 inch guidewire in the left anterior descending artery, the physician centered a 3.0 mm diameter by 19 mm long polytetrafluoroethylene-covered (PTFE) stent (Jostent Graftmaster) centered on the site of contrast extravasation (Figure 16-7), successfully sealing the perforation (Video 16-5). The dopamine infusion was stopped with no further hypotension and he was observed in the cardiac catheterization laboratory for an additional 15 minutes; a final angiogram revealed no further evidence of contrast extravasation.

FIGURE 16-7 Position of the PFTE-covered stent at the site of the perforation. Note the contrast staining at the site of the perforation (arrow).

Postprocedural course

Following the procedure, the patient was admitted to the coronary care unit for observation. He remained hemodynamically stable, but noted pleuritic chest and shoulder pain for 24 hours following the procedure that responded to nonsteroidal antiinflammatory agents. Echocardiography performed the day after the procedure showed a small effusion. The postprocedure troponin level peaked at 34 ng/mL. He was discharged the second day postprocedure and returned for follow-up 2 months later feeling well and without angina.

Discussion

Coronary artery perforation complicates less than 0.5% of coronary interventions¹ but is potentially lethal, particularly in the event of free extravasation into the pericardial space as exemplified in this case. More commonly seen with ablative techniques such as rotational or directional atherectomy, coronary perforation may be caused by vessel disruption from barotrauma (the likely cause in this case) or from deep dissection extending through the adventitia. Guidewire perforations may occur at the site of the lesion during attempts at crossing a stenosis or may occur distally from migration of the wire tip into a small vessel, with subsequent perforation.

Freely extravasating contrast, as seen in this case, is a true emergency. Once identified, the operator must work rapidly to control the hemorrhage into the pericardial space. Immediate balloon expansion proximal to or directly at the perforation site effectively halts the hemorrhage, allowing time to plan subsequent management. At this point, anticoagulation should be stopped or reversed. Platelet transfusion is necessary if abciximab was used and protamine administration may be considered if unfractionated heparin was given and the activated clotting time is excessive. Pericardiocentesis should be performed if there is ongoing hemodynamic instability despite fluid and pressor support. While all this activity is taking place, it is a good idea to notify a cardiothoracic surgeon; this will limit delays if attempts to seal the perforation fail and the patient requires emergency surgery. In the case presented here, the history of prior bypass surgery may have helped maintain stability by limiting the extent of tamponade due to the presence of pericardial adhesions.

Small perforations may seal with reversal of anticoagulation and prolonged balloon inflation at the perforation site. Large, free-flowing rents in the artery, like the one shown in this case, usually require sealing with a PTFE-covered stent.^2,3 These devices consist of a thin layer of PTFE sandwiched between two stents. They are fairly bulky and may be difficult to position and are not available in sizes smaller than 2.5 mm diameter. Importantly, they require large-bore guides, usually necessitating a change in the sheath and guide during an emergency. If the patient cannot tolerate release of the inflated balloon used to temporarily staunch the bleeding, then access should be obtained in the contralateral femoral artery and the appropriately sized sheath and guide catheter placed while the balloon remains inflated.

Major perforations are fairly morbid events with a high rate of periprocedural infarction of about 10% to 15% of patients. Infarction is often caused by the prolonged balloon inflation needed to stabilize a patient, but may also be due to the presence of external compression by a subepicardial hematoma. Death occurs in about 10% to 15% of major perforations, and about 10% require surgery to repair them. Pericarditis, arrhythmia, and need for blood transfusion are additional consequences. The PFTE-covered stents have a high restenosis rate, particularly at the edges.