Case presentation

A 43-year-old woman with untreated hypertension and ongoing tobacco use presented with 2 hours of chest pain occurring at rest and associated with diaphoresis and nausea. An electrocardiogram revealed inferior Q waves and nonspecific inferolateral ST-segment changes. Initially normal, her serum troponin I rose to 0.11 ng/mL. After treatment with aspirin, metoprolol, topical nitrates, atorvastatin, and 1 mg/kg of enoxaparin subcutaneously twice a day, she remained pain-free and was referred for cardiac catheterization.

Cardiac catheterization

Catheterization was performed during the hospital admission. Left ventricular function appeared normal and there was no significant disease noted in the left coronary artery (Figure 27-1); however, collateral filling of the distal right coronary artery was noted. The right coronary artery arose aberrantly high and anterior in the right coronary sinus. Heavy calcification along with severe atherosclerotic narrowing affected the midportion of the right coronary artery, and atherosclerotic disease also narrowed the ostium of the posterolateral side branch (Figures 27-2, 27-3 and Videos 27-1, 27-2).

FIGURE 27-1 This is a representative left coronary angiogram. There is no significant obstructive disease noted.

FIGURE 27-2 This is a left anterior oblique (LAO) image of the right coronary artery. There is severe disease of the mid portion of the right coronary artery with heavy calcification noted as well as narrowing of the ostium of the posterolateral branch (arrow).

FIGURE 27-3 This right anterior oblique (RAO) projection with caudal angulation shows the severely diseased segment of the right coronary artery.

Her physician decided to proceed with percutaneous coronary intervention of the right coronary artery. Adequate backup for intervention required a left Amplatz 2.0 guide catheter. Procedural anticoagulation included intravenous bolus of heparin (50 U/kg) and double bolus plus infusion of eptifibatide using standard doses. The operator predilated the stenotic segment with a 2.5 mm diameter by 30 mm long compliant balloon, and chose bare-metal stents because of concern about the patient’s compliance with long-term clopidogrel. Two stents successfully treated the diseased segment with a 2.5 mm diameter by 18 mm long stent placed distally and a 3.0 mm diameter by 28 mm long stent deployed proximally (Figure 27-4 and Video 27-3). At this point, the ostium of the posterolateral branch appeared narrowed but remained patent. Noncompliant balloons (2.5 mm diameter by 20 mm long distally and 3.5 mm diameter by 15 mm long proximally) inflated to high pressure were used to postdilate the stented segment. Angiography after high-pressure balloon inflations demonstrated improved appearance of the stented segment but occlusion of the posterolateral side branch (Figures 27-5, 27-6 and Videos 27-4, 27-5). Although the operator was able to pass a hydrophilic guidewire into the side branch, it was not possible to pass a 2.0 mm diameter by 15 mm long compliant balloon and the side branch remained closed. The patient left the cardiac catheterization laboratory with ongoing mild chest pain, but her rhythm and blood pressure remained stable and she was transferred to a telemetry unit for monitoring.

FIGURE 27-4 Right coronary angiogram (LAO projection) after placement of stents. Note continued patency of the posterolateral branch (arrow).

FIGURE 27-5 After postdilatation with a high-pressure balloon, loss of the posterolateral branch was noted on this LAO angiogram (arrow).

FIGURE 27-6 RAO angiogram post high-pressure balloon showing loss of posterolateral side branch.

Postprocedural course

Postprocedure electrocardiogram remained unchanged and chest pain resolved 1 hour after the procedure. She ambulated without any further symptoms. Serial creatine phosphokinase assays rose from a normal baseline (86 U/L with MB fraction of 2.5 ng/mL) to a peak of 253 U/L with MB fraction 21.8 ng/mL 18 hours after the procedure. She was discharged the second day postprocedure on 325 mg aspirin, 75 mg of clopidogrel, metoprolol, and atorvastatin. She remained well with no further chest pain at follow-up 6 months later.

Discussion

Percutaneous management of lesions involving the bifurcation of a side branch can prove challenging. The chief concern relates to the potential loss of the side branch; this event may cause a periprocedural myocardial infarction and result in significant morbidity if the side branch is large. The risk of side branch closure depends on the location of the atheroma. The highest risk of closure occurs when atheroma surrounds and also involves the ostium of the side branch; in such cases, almost 70% of side branches will close following stenting of the main vessel.¹ The risk is lowest when the side branch ostium is free of involvement; closure complicates only about 6% of such cases.¹ As shown in the case presented here, most side branches occlude after post-stent dilatation with a high-pressure balloon. However, closure may also occur after pre-stent balloon inflation or after initial stent deployment.

The wide variety of methods proposed over the years to preserve the side branch is a testimony to the ineffectiveness of most of them. Placing a guidewire into the side branch before stenting the main branch might help maintain patency in some cases but, in the event of closure after stenting, this wire cannot be used for balloon angioplasty or stenting of the side branch because it lies trapped behind the stent in the main artery. At a minimum, this wire will help guide the operator to the location of the side branch ostium and may facilitate recrossing with a new guidewire. In the author’s experience, pretreatment of the side branch with either balloon angioplasty or rotational atherectomy before deploying the stent in the main artery is not a guaranteed method of preserving the side branch. Again, closure of the side branch most commonly occurs after the stent is placed or after high-pressure balloon inflation of the stent has been performed, due to the plaque shifts occurring with these events; pre-stent treatment of the side branch (particularly with a balloon) is unlikely to influence this.

Different treatment strategies to treat bifurcation lesions have been proposed, but it appears that optimal outcomes are obtained using a simple strategy of stenting only the main vessel with provisional stenting of the side branch performed only if an unacceptable result is obtained in the side branch.² In the author’s experience, the “crush” stent technique is the most reliable method of preserving large side branches, but is associated with a high rate of restenosis and stent thrombosis particularly if a final “kissing” balloon cannot be performed.³

In the event of side branch closure, a guidewire can often be successfully negotiated through the stent struts and passed distally into the side branch, particularly if there is some residual patency of the side branch. Hydrophilic wires may be successful if a floppy-tipped guidewire fails. Once a guidewire is positioned, low-pressure balloon angioplasty of the ostium can improve the lumen and restore patency. A satisfactory result is defined by restoration of patency without dissection or significant luminal narrowing. It is usually not necessary to strive for a “perfect” angiographic result. Aggressive attempts to enlarge the lumen may dissect the artery and lead to a more complex repair than otherwise necessary. In the case shown here, complete occlusion of the side branch was present and, although a guidewire successfully crossed into the side branch, a low-profile, compliant balloon failed to pass the stent struts and the side branch remained closed. When this occurs, the operator may try removing and repositioning the side branch guidewire in the hope that it passes by a different set of struts, thus allowing passage of the balloon.