Aortic Dissection Caused by Percutaneous Coronary Intervention: 2 New Case Reports and Detailed Analysis of 86 Previous Cases

Abstract

Aortic dissection, a rare sequela of percutaneous coronary intervention, can be fatal when it is not recognized and treated promptly. Treatment varies from conservative management to invasive aortic repair and revascularization. We report the cases of 2 patients whose aortic dissection was caused by percutaneous coronary intervention. In addition, we present detailed analyses of 86 previously reported cases. Aortic dissection was most often seen during intervention to the right coronary artery (in 76.7% of instances). The 2 most frequently reported causes were catheter trauma (in 54% of cases) and balloon inflation (in 23.8%). The overall mortality rate was 7.1%. We conclude that most patients can be treated conservatively or by means of stenting alone, with no need for surgical intervention.

Aortic dissection is a rare and potentially fatal sequela of percutaneous coronary intervention (PCI). The exact prevalence of aortic dissection after PCI is unknown, because occurrences might be unreported. The first case was reported in 1992.¹ We found 86 published instances^1–62 and have categorized these in detail. In addition, we present 2 new cases of aortic dissection consequent to PCI, and we discuss their specific treatment.

Case Reports

Patient 1

A 52-year-old hypertensive man presented with acute inferior ST-segment-elevation MI (STEMI). He had a distant history of inferior myocardial infarction (MI) that had been treated with placement of a drug-eluting stent. At the current presentation, he was immediately taken for cardiac catheterization. Initial views of the left coronary system with use of a 6F Judkins left (JL)4 diagnostic catheter revealed no significant lesions. Views of the right coronary artery (RCA), examined with use of a 6F Judkins right (JR)4 diagnostic catheter, showed occlusion of the original proximal RCA stent. The diagnostic catheter was immediately removed, and a 6F JR4 guide catheter was used without difficulty to engage the RCA. A 180-cm Asahi Prowater Flex guidewire (Abbott Vascular, part of Abbott Laboratories; Abbott Park, Ill) was inserted into the RCA but could not cross the culprit lesion. This wire was exchanged for a 190-cm Hi-Torque Whisper guidewire (Abbott Vascular), and the lesion was successfully crossed with support from a 1.5 × 15-mm Maverick^™ Over-the-Wire Balloon Catheter (Boston Scientific Corporation; Natick, Mass). Two brief inflations were done at pressures of 12 atm within the stent for 10 s each. The wire was upgraded to a 300-cm Asahi Prowater Flex wire while the Maverick balloon was still inside the artery. The patient reported chest pain, and his systolic blood pressure (SBP) fell to 78 mmHg. The balloon was removed. An angiogram showed dissection of the proximal RCA, extending retrograde into the right aortic cusp and ascending aorta (Fig. 1). In addition, slow flow and evidence of thrombus were noted in the RCA. A Pronto V3 extraction catheter (UDG Healthcare plc; Dublin, Ireland) was immediately inserted, and manual-aspiration thrombectomy was performed. Then, a 3.5 × 28-mm Vision^® bare-metal stent (Abbott Vascular), deployed in the proximal RCA at a pressure of 12 atm, was extended into the ostium to seal the dissection flap (Fig. 2).

Fig. 1.

Patient 1. Coronary angiogram (left anterior oblique view) reveals stent thrombosis and shows dissection of the proximal right coronary artery with retrograde extension into the aorta.

Supplemental motion image ^{(3.3MB, mp4)} is available for Figure 1.

Fig. 2.

Patient 1. Coronary angiogram (left anterior oblique view) after ostial-proximal right coronary artery stenting shows obliteration of the dissection flap and restoration of coronary flow.

Supplemental motion image ^{(3.3MB, mp4)} is available for Figure 2.

The patient was started on a dopamine infusion. Within minutes, his hemodynamic status improved and chest pain resolved, so the dopamine was discontinued. A post-stenting angiogram showed significant stenosis distal to the stent, but we did not believe the stenosis to be the cause; given the acute STEMI and eventful course, we instead suspected a role of spasm and distal embolization. We intended to obtain another angiogram in a few weeks, to reevaluate that lesion.

The patient was transferred to the coronary care unit for monitoring. The next day, a transesophageal echocardiogram showed no dissection or hematoma. The patient was discharged from the hospital 4 days later in stable condition and was lost to follow-up thereafter.

Patient 2

A 68-year-old man with a history of hypertension presented for coronary angiography because of chest pain and abnormal results of a stress test. A diagnostic angiogram with use of a 6F JL4 catheter revealed significant stenosis of the mid left circumflex coronary artery (LCx). We used a 6F Extra Back-Up 4.0 guide catheter to engage the left main coronary artery (LMCA), crossed the lesion with a 0.014-in Hi-torque Whisper wire, and performed angioplasty with a 2 × 15-mm Mini trek Coronary Dilatation Catheter (Abbott Vascular). Subsequently, we deployed a 2.5 × 15-mm Xience V^® everolimus-eluting stent (Abbott Vascular) across the lesion at a pressure of 16 atm and postdilated it with use of a 3 × 15-mm noncompliant Quantum^™ balloon (Boston Scientific).

During the final postinterventional angiography, the patient reported severe chest pain, and his SBP fell to 60 mmHg. At that moment, the angiogram revealed dissection of the LMCA, starting from the point of contact of the guide catheter with antegrade extension into the LCx and retrograde into the aortic root (Fig. 3). This was followed by no-flow phenomenon. We attributed the dissection to roofing of the tip of the guide catheter combined with a forceful contrast injection. The wire had come out of the LCx at that point; therefore, to avoid its entry into the false lumen, we placed it in the left anterior descending coronary artery (LAD). We immediately deployed a 3 × 33-mm Xience drug-eluting stent in the LMCA (this long stent extended to the LAD) to seal the origin of the dissection flap, and Thrombolysis In Myocardial Infarction-3 blood flow was restored in the coronary arteries (Fig. 4). We then inserted an intra-aortic balloon pump; however, the patient's hemodynamic status and vital signs had already begun to improve.

Fig. 3.

Patient 2. Coronary angiogram (left anterior oblique caudal view) shows left main dissection with antegrade extension into the aortic cusp and retrograde into the left circumflex coronary artery.

Supplemental motion image ^{(3MB, mp4)} is available for Figure 3.

Fig. 4.

Patient 2. Coronary angiogram (left anterior oblique caudal view) after left main stenting shows obliteration of the dissection flap and restoration of coronary flow.

Supplemental motion image ^{(3MB, mp4)} is available for Figure 4.

After discussion between the cardiologists and the patient's family, the patient was sent for coronary artery bypass grafting (CABG). This solution was proposed because of uncertainty about the progression of the dissection, despite the patient's hemodynamically stable status after stenting. After a 2-week hospitalization, he was discharged in stable condition.

Discussion

During PCI, iatrogenic aortic dissection occurs in 0.02% to 0.07% of cases.¹⁰ We searched the English-language medical literature for relevant reports. Our PubMed search terms were “aortic dissection,” “iatrogenic dissection of aorta,” “coronary angiography,” “percutaneous coronary intervention,” and “angioplasty.” We found 86 cases of aortic dissection caused by percutaneous coronary angiography or PCI (Table I).^1–46 Ten of those occurred during attempted intervention on chronic total occlusion (Table II),^36,47–55 and 7 were in patients who had histories of CABG (Table III).^56–62 Of the 86 cases, 26 (30.2%) occurred during emergency catheterization. The extent of dissection was mentioned in 85 instances. The dissection was limited to the aortic root in 33 (38.8%), the ascending aorta in 35 patients (41.1%), the aortic arch in 11 (12.9%), and the descending aorta in 6 (7.1%).

TABLE I.

Reports of Aortic Dissection Caused by Percutaneous Coronary Intervention

TABLE II.

Reports of Aortic Dissection during Percutaneous Coronary Intervention of Chronic Total Occlusion

TABLE III.

Reports of Aortic Dissection during Percutaneous Coronary Intervention in Prior CABG Patients ^*

TABLE I continued.

Reports of Aortic Dissection Caused by Percutaneous Coronary Intervention

TABLE I continued.

Reports of Aortic Dissection Caused by Percutaneous Coronary Intervention

Of the outcomes reported in 85 occurrences, 6 patients died—3 who were treated conservatively and 3 who underwent surgery (7.1%). In those 6 patients, the dissection extended to the ascending aorta in 4, the aortic arch in one, and the descending aorta in one. As for the 3 deaths in the conservatively treated patients, the cause was unknown in one.¹ The second refused surgery after a failed attempt to stent the origin of the dissection, and he died of refractory ventricular tachycardia and fibrillation from reinfarction.¹² The third had renal failure due to extension of the dissection to the descending aorta; surgery was deemed too risky, and he died 4 months later of cardiogenic shock.¹⁷ The deaths of 2 of the 3 surgically treated patients were attributed to postoperative multiorgan failure,^6,10 and the third died in the operating room when weaning from cardiopulmonary bypass failed.¹⁰

Iatrogenic aortic dissections occurred during interventions to the RCA in 66 patients (76.7%), the LAD in 10 (11.6%), the LCx in 6 (7%), the LMCA in 3 (3.6%), and the obtuse marginal branch in 1 (1.2%). The probable cause of dissection was reported in 63 instances: catheter trauma in 34 patients (54%), balloon inflation in 15 (23.8%), and contrast injection in 13 (20.6%). Of note, wire trauma was the reported cause of dissection in only 7 patients (11.1%).

Among the 34 reports of guide-catheter trauma, the sizes and types of catheters were specified in 23 and 27 instances, respectively. Eighteen of the 23 occurrences involved sizes larger than 6F (8F=6 and 7F=12), and the remaining 5 occurred in association with the 6F size. The catheter types reported most often as causes of dissection were the Amplatz left (in 11 cases) and the JR (in 9).

Stenting as sole treatment for aortic dissection was performed in 46 patients (53.5%). Aortic repair, CABG, or both followed stenting in another 9 cases (10.5%). Seventeen patients (19.8%) underwent aortic repair and CABG. A conservative approach was adopted in 19 patients (22.1%), and CABG alone was performed in 3 patients (3.5%).

There are no guidelines for treating aortic dissection caused by PCI. Dunning and colleagues¹⁰ proposed surgical intervention if a dissection extended more than 4 cm into the ascending aorta. However, patients whose dissections extended even to the aortic arch have been successfully treated conservatively, or nonsurgically by means of stenting. The most important factors that guide treatment are the patient's hemodynamic stability and the practitioner's rapidity in stenting the origin of the dissection, to prevent the dissection from expanding.