23: Coronary Perforation

Published on 02/03/2015 by admin

Filed under Internal Medicine

Last modified 22/04/2025

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CASE 23 Coronary Perforation

Case presentation

A remarkably healthy and independent 89-year-old woman, with a prior history of hypertension and carotid atherosclerosis treated with lisinopril, hydrochlorothiazide, and aspirin, reported a 6-month history of progressive fatigue and dyspnea. Previously able to regularly walk several miles at a time, her symptoms caused a marked restriction in her exercise capacity and, at the time of presentation, she was no longer able to walk more than a block without having to stop to rest. Additionally, over the preceding 3 weeks, she developed chest tightness with minimal exertion. This symptom prompted her to seek medical attention. Her physician scheduled a stress test but she developed rest chest pain along with severe dyspnea and diaphoresis before this test could be performed and was admitted to the hospital.

Upon presentation in the emergency department, she was symptom-free and a 12-lead electrocardiogram showed Q waves inferiorly without acute ischemic changes. Serum cardiac biomarkers were not elevated. Her physical examination was notable for systolic hypertension with a blood pressure of 214/77 mmHg in both arms, a heart rate of 73 beats per minute, bilateral carotid bruits, and a systolic murmur of aortic sclerosis. The routine admission laboratory studies were normal, including renal function.

Given her advanced age, negative cardiac isoenzymes, and marked systolic hypertension on presentation without a trial of adequate medical therapy, a beta-blocker, statin, and long-acting nitrates were added to her medical regimen. A pharmacologic stress perfusion scan was performed the next day. During the test she developed severe chest pain associated with diffuse ST-segment depression and reversible ischemia in the anterior wall. The patient agreed to undergo catheterization.

Cardiac catheterization

Coronary angiography revealed multivessel coronary disease with severe disease in the proximal segment of the right coronary artery and severe disease of the midportion of the left anterior descending coronary artery (Figures 23-1, 23-2 and Video 23-1). The operator judged the right coronary artery suitable for percutaneous coronary intervention; however, the left anterior descending artery provided several challenges. Not only did the vessel appear small in caliber, there was also marked tortuosity with diffuse disease surrounding the severely stenosed segment. Prior to the catheterization, the patient dismissed the option of bypass surgery and agreed only to percutaneous revascularization. The patient confirmed this after she was presented with the catheterization results, and the operator proceeded with a multivessel intervention on the right coronary artery and left anterior descending artery.

Following administration of a bolus and infusion of the direct thrombin inhibitor bivalirudin, the operator began with the right coronary artery. This lesion was first dilated with a 3.0 mm diameter by 15 mm long compliant balloon and a 3.5 mm diameter by 28 mm long sirolimus-eluting stent was deployed successfully with an acceptable angiographic result (Figure 23-3). The operator then turned to the left anterior descending artery. A 6 French, 45 C-curve guide catheter was engaged and a 0.014 inch floppy-tipped guidewire advanced to the distal portion of the vessel. The 3.0 mm by 15 mm compliant balloon used to predilate the right coronary lesion was advanced to the lesion and inflated to 8 atmospheres for 30 seconds (Figure 23-4). The operator deflated the balloon and observed contrast extravasation at the balloon angioplasty site (Figure 23-5 and Video 23-2). The vessel was immediately tamponaded using the same balloon inflated to 6 atmospheres and the infusion of bivalirudin was discontinued. The patient developed transient hypotension and bradycardia. This corrected quickly with 1 mg of atropine and a 500 cc bolus of fluid. An urgent echocardiogram revealed a small pericardial effusion. The balloon remained inflated for 15 minutes and repeat angiography confirmed successful sealing of the perforation. The operator noted some difficulty advancing the previously-inflated balloon to the lesion because of vessel angulation. Subsequently, two short bare-metal stents (2.5 mm diameter by 13 mm long distally and a 2.5 mm diameter by 12 mm long proximally) were deployed to 12 atmospheres and covered the diseased segment of the mid-LAD. Postdeployment, the stents appeared well-deployed with no further evidence of contrast extravasation (Figure 23-6 and Video 23-3). The patient left the catheterization laboratory hemodynamically stable with minimal chest discomfort.

Discussion

The perforation in this case was likely caused by employing an oversized balloon in an angulated artery in an elderly woman. In an effort to economize resources in a patient undergoing a multivessel intervention, the operator chose to predilate the left anterior descending artery with the balloon used earlier to predilate the right coronary artery. In addition, vessel rigidity required higher inflation pressures causing further growth in diameter of the compliant balloon. The end result was an oversized balloon creating an extensive and deep dissection, resulting in the observed perforation.

The ultimately favorable outcome in this case emphasizes several important concepts in the management of a patient with a coronary perforation. Based on the classification system described by Ellis and colleague the Type II perforation present in this case would be expected to result in tamponade in 10% to 15% of cases.1,2 Rapid recognition and management by the operator prevented this. The operator acted quickly, rapidly repositioning and inflating the balloon at the site of the perforation while simultaneously discontinuing the infusion of bivalirudin. This quick response allowed only a small amount of blood to enter the pericardium, thus preventing tamponade. Even a small delay might have caused enough blood to accumulate in the pericardial space to cause dramatic hemodynamic deterioration requiring patient resuscitation and a potentially less favorable outcome. Note that the brief period of hypotension and bradycardia occurring immediately after the perforation likely represented a vagal reaction, a common sequelae of an acute perforation. In this case, the brief period of hypotension and bradycardia responded immediately to atropine and fluid bolus.

Reversal of anticoagulation and prolonged balloon inflation successfully sealed the perforation in this case. In the event of ongoing bleeding despite these measures, a polytetrafluoroethylene (PTFE)-covered stent is indicated; however, this might have been very difficult or impossible to deliver based on the small caliber and marked tortuosity of the artery. Surgical correction, necessary in 10% to 30% of perforations, is another option should these measures fail to control bleeding, but would not have been desirable given the patient’s advanced age.