Case presentation

A 58-year-old man, with a history of documented coronary artery disease found by catheterization 4 years earlier, remained asymptomatic on medical therapy until he presented to his cardiologist with a 6-week history of dyspnea and chest tightness occurring with minimal exertion. Medical therapy consisted of simvastatin, niacin, aspirin, metoprolol, and long-acting nitrates. His past history is also remarkable for diet-controlled diabetes mellitus, hypertension, dyslipidemia, and hypothyroidism. He actively smokes tobacco. The physical exam, electrocardiogram, and routine laboratory evaluations were all normal. Diagnosed with crescendo angina pectoris, he was referred for cardiac catheterization.

Cardiac catheterization

Ventriculography revealed normal left ventricular function. Coronary angiographic findings included a codominant circulation, with a diffusely diseased but small right coronary artery (Figure 5-1) and moderate distal disease in the left circumflex and obtuse marginal branches (Figures 5-2, 5-3). The proximal segment of the left anterior descending artery contained moderate disease (Figure 5-2 and Video 5-1) that in some views appeared nonobstructive (Figures 5-2, 5-3) but in other views appeared more concerning (Figure 5-4 and Video 5-2). Much of the disease present on this study appeared similar to the appearance on angiography 4 years earlier, leaving the operator at a loss for the dramatic change in symptoms.

FIGURE 5-1 A small, diffusely-diseased right coronary artery is present but is unchanged from a prior angiogram.

FIGURE 5-2 This view shows the moderate distal disease in the left circumflex and obtuse marginal artery (arrows); there is also moderate disease in the left anterior descending artery (double arrow).

FIGURE 5-3 In this left anterior oblique view of the left coronary artery with cranial angulation, the disease in the left anterior descending artery does not appear significant.

FIGURE 5-4 This left anterior oblique view with caudal angulation suggests a significant lesion in the left anterior descending artery (arrow).

The concerning symptoms, along with an ambiguous lesion in the proximal left anterior descending artery, prompted the operator to measure fractional flow reserve of this vessel (Figure 5-5). After a 6 French guide catheter was inserted, a pressure wire was advanced past the lesion and hyperemia induced with 100 μg of intracoronary adenosine; fractional flow reserve measured 0.69. Thus, the angiographically-moderate disease represented a flow-limiting lesion, and the operator decided to treat the lesion percutaneously. Following the administration of intravenous heparin and eptifibatide, the procedure began with balloon predilatation, using a 2.5 mm by 20 mm long compliant balloon. At nominal inflation pressure, a significant waist remained in the compliant balloon (Figure 5-6 and Video 5-3). Switching to a 2.5 mm by 10 mm noncompliant balloon inflated to 18 atmospheres failed to fully expand the balloon (Figure 5-7). Although these balloon inflations did not improve the luminal appearance, there was no evidence of dissection or perforation (Figure 5-8 and Video 5-4).

FIGURE 5-5 Pressure wire measurement of the left anterior descending artery. The arrow depicts the location of the transducer.

FIGURE 5-6 A compliant balloon failed to fully expand in the lesion.

FIGURE 5-7 A noncompliant balloon inflated to high pressures failed to fully expand in the lesion.

FIGURE 5-8 Angiographic appearance after high pressure balloon inflation.

Faced with a rigid and undilatable lesion, the operator chose to perform rotational atherectomy with a 1.5 mm burr. Three 30-second runs at 160,000 rpm successfully allowed the burr to pass the diseased area without deceleration (Video 5-5). Following this, a 2.5 mm by 20 mm long compliant balloon fully inflated at nominal pressure (Figure 5-9). Two, everolimus-eluting stents (2.5 mm diameter by 23 mm long and 2.5 mm by 18 mm long) easily crossed and expanded fully at 16 atmospheres of pressure, resulting in an excellent final angiographic appearance (Figure 5-10 and Videos 5-6, 5-7).

FIGURE 5-9 After rotational atherectomy, a compliant balloon could be fully expanded at nominal inflation pressures.

FIGURE 5-10 Final angiographic result after successful stenting.

Postprocedural course

After an uneventful overnight period of observation, he was discharged the next morning on his usual medications, along with clopidogrel for at least 1 year. He remained free of angina at follow-up 1 year later.

Discussion

This case provides two valuable lessons to a budding interventional cardiologist. First, it is an excellent example of one of the important limitations of coronary angiography. The hemodynamic significance of many lesions of only moderate severity may be very difficult to assess by angiography alone, potentially leading to a wrong decision.¹ Although the patient presented with a convincing history of crescendo angina pectoris, on first glance, the angiogram did not reveal an obvious culprit lesion. In fact, the angiogram appeared very similar to one he had 4 years earlier. Despite careful review of the angiogram and multiple angiographic views, the operator was unable to decide if the disease in the left anterior descending artery represented a significant lesion. This is the ideal time to consider further assessment of the artery by either intravascular ultrasound or fractional flow reserve. In this case, fractional flow reserve confirmed the hemodynamic significance of the disease and led to a revascularization decision that successfully eliminated the patient’s symptoms.

Once percutaneous intervention was chosen, the rigid nature of the lesion surprised the operator, as this was not expected given the minimal extent of calcium noted by fluoroscopy. When a compliant balloon fails to fully expand at nominal inflation pressures, the operator risks coronary dissection by further increasing inflation pressure. This is due to the fact that a compliant balloon will grow significantly both in diameter and length under increasing pressure. The increasing pressure and enlarging balloon diameter is not transmitted to the offending site, but instead to the softer adjacent sites, often resulting in dissection or perforation. In this case, the operator wisely chose to try a noncompliant balloon, capable of exerting high pressures without significantly changing the balloon size. However, this strategy also failed, with continued underexpansion of the balloon despite very high pressures.

At this point, a decision was made to use rotational atherectomy. It is important to carefully review the angiogram after balloon dilatation in such cases, as the presence of a significant dissection precludes the use of rotational atherectomy. If present, the dissection should be allowed to heal for a few weeks before attempting this strategy. As shown in this case, even minimal debulking with rotational atherectomy led to success; more aggressive debulking was not necessary. Likely, a small area of luminal calcium prevented balloon expansion. Removal of this component of the plaque allowed full balloon inflation and successful intervention.

This case also provides an example of a potential risk of direct stenting (i.e., without balloon predilatation). Some operators choose this tactic in an effort to save time and reduce equipment cost. However, in this case, this approach would have resulted in an underexpanded and poorly-deployed stent. When this occurs, options are limited, which might have led to aggressive balloon inflations at very high pressures in a desperate effort to expand the stent, potentially causing a perforation or dissection in adjacent segments. Failure to fully expand the stent, in spite of these measures, often leads to an adverse outcome, including stent thrombosis or restenosis.^2,3