Successful Primary PCI in Stanford Type A Aortic Dissection Complicated by Inferior ST-Elevation Myocardial Infarction: A Case in a Facility with No Surgical Backup

Abstract

Mortality of type A aortic dissection (TAAD) complicated with coronary malperfusion syndrome is very high even when emergency surgery is performed. Several reports suggested that primary percutaneous coronary intervention (PPCI) followed by immediate corrective surgery may reduce mortality. In many countries, immediate transfer to an aortic surgery center may not be possible. We report a case of TAAD complicated by coronary malperfusion successfully treated with PPCI followed by elective corrective surgery. A 48-year-old man was referred to emergency department with acute inferior ST-elevation myocardial infarction (STEMI) and underwent PPCI. During the procedure, we realized that the cause of STEMI was TAAD. We decided to continue because the patient experienced seizures and bradycardia. Subsequently, echocardiography and computed tomography confirmed the dissection. The patient was discharged and referred to the National Cardiovascular Center where he underwent successful elective surgery. In this patient, immediate revascularization was lifesaving and served as a bridging procedure before surgical correction.

Type A aortic dissection (TAAD) is a medical emergency with a very high mortality rate. ^{1 2} Although most deaths were caused by aortic rupture as a direct consequence of aortic dissection, some patients died from its complications such as acute heart failure or malperfusion syndrome affecting vital organs. ³ Ideally, emergency surgery is the treatment of choice to repair the underlying disease. However, in many developing countries, aortic surgery services are not widely available, resulting in a significant time delay in transferring the patient to a hospital capable of performing aortic surgery. Consequently, bridging procedures are sometimes necessary to save the patient from malperfusion syndrome that becomes more prominent.

This report presents a case of TAAD complicated with coronary malperfusion syndrome (acute inferior ST-elevation myocardial infarction [STEMI]) treated with primary percutaneous coronary intervention (PPCI). The patient survived and subsequently underwent a successful staged operation in another hospital with access to aortic surgery.

Case Illustration

A 48-year-old smoker, nondiabetic, hypertensive man was referred to the emergency department with inferoposterior STEMI. The patient complained of chest pain radiating to his back which occurred 4 hours before admission. Physical examination was unremarkable, except for an early diastolic murmur found at the patient's upper right sternal border. Electrocardiogram (ECG) showed ST-elevation in the leads II, III, aVF, and V7 to V9 ( Fig. 1A ) while cardiac troponin was elevated more than four times above normal. The patient was sent to a catheter laboratory and underwent an urgent PPCI. During the preparation, the patient had a seizure, and the ECG showed junctional rhythm; thus, a temporary pacemaker was implanted.

Fig. 1.

ECG and coronary angiogram and primary percutaneous coronary intervention. ( A ) ECG of the patient showing ST-elevation at leads II, III, aVF, and V7 to V9. ( B ) Contrast trapping during diagnostic coronary angiogram (arrow). ( C ) Selective RCA angiography showing total occlusion at the proximal site due to compression (arrow). ( D ) Stent positioning before deployment. The proximal end of the stent is positioned just before the separating line between the two aortic areas with different contrast intensity (arrow), presumably the aortic flap was separating the true and false lumens (multiple arrowheads). ( E ) Final angiogram of the RCA showing good restoration of flow (thrombolysis in myocardial infarction 3). ECG, electrocardiogram; RCA, right coronary artery.

Right radial access was chosen, from which a 5F Optitorque diagnostic catheter (Terumo, Japan) and subsequently a 6F JR Guiding catheter (Terumo) were advanced without resistance. The diagnostic angiogram showed ostial occlusion of the right coronary artery (RCA) without significant stenosis of the other arteries. However, there was contrast trapping near the RCA ostium ( Fig. 1B ), and two different contrast intensities separated by a clear line at the ascending aorta ( Fig. 1C ), raising a suspicion that the cause of the infarction was not atherothrombosis but a compression of the dissecting aortic flap. Because of the severe cardiac ischemia, stenting was continued using a 4.0- to 15-mm drug-eluting stent, which was performed without difficulty. We made sure that the proximal end of the stent was positioned just before the separating line between the two aortic areas with different contrast intensities, presumably connecting the RCA ostium and the true lumen ( Fig. 1D ). The final angiogram showed restoration of RCA flow (thrombolysis in myocardial infarction 3; Fig. 1E ). The patient was then moved to the intensive coronary care unit and underwent an echocardiogram and subsequently aortic computed tomography (CT), from which moderate aortic regurgitation and aortic dissection were confirmed ( Fig. 2 ).

Fig. 2.

Diagnostic imaging ( A ) transthoracic echocardiography showing a stent protruding into the aorta (arrow) and aortic flap (arrowhead). ( B ) Coronal view of the aortic CT; dissection is clearly visualized (multiple arrowheads). ( C ) Axial view of the aortic CT; coronary stent protrusion into the aorta maintained the patency of the RCA (arrowhead). CT, computed tomography; RCA, right coronary artery.

After almost 3 weeks of hospitalization, the patient was discharged and referred to the National Cardiovascular Center where the patient underwent successful elective corrective surgery 4 months later. The patient is currently very well and is under regular monitoring in the outpatient clinic.

Discussion

Ascending aortic dissection is associated with 50% mortality in the first 48 hours if no surgery is performed. The mortality becomes even higher when complicated by malperfusion syndrome affecting vital organs, particularly the coronary arteries. In an autopsy study of patients who died from aortic dissections, coronary ischemia accounted for 11% of the total deaths. ³ The modified Penn classification created to stratify the mortality risks of patients undergoing aortic surgery recognized the presence of preoperative coronary ischemia as a significant predictor of mortality. ⁴ Similarly, in the GERAADA (German Registry for Acute Aortic Dissection Type A) registry preoperative coronary ischemia was associated with postoperative coronary ischemia, which increased the mortality risk by nine times. ⁵

Despite open surgical repair being the definitive treatment, relieving vital organs from malperfusion syndrome may become necessary and could be more prioritized than definitive corrective intervention. Without timely revascularization, a critically ischemic organ may fall into irreversible damage that could progress to acute organ failure. Stenting or fenestration to restore flow into malperfused vital organs followed by delayed corrective surgery resulted in lower mortality than direct definitive treatment. ^{6 7 8} In a study by Uchida et al, in-hospital mortality of patients with TAAD complicated by a malperfusion syndrome who underwent surgery was five times greater than those without malperfusion syndrome. Early reperfusion before surgery was able to significantly lowered the mortality to similar levels of patients without malperfusion syndrome. ^{9 10} To note, the majority of the malperfusion cases in the study were coronary malperfusion, and the method of revascularization was PPCI. However, this success has yet to be consistently reported by other centers. Another study also reported successful revascularization followed by corrective surgery, ¹¹ but others reported no improvement in survival despite revascularization. ^{12 13} Therefore, it is still ambiguous whether coronary reperfusion should be routinely performed before corrective surgery and which patient should undergo the procedure.

Our patient was initially misdiagnosed as having only STEMI without aortic dissection and had undergone PPCI. During the procedure, the operator realized the possibility of TAAD but decided to move forward with the procedure for three reasons. First, the patient's hemodynamic was unstable; the patient experienced seizures due to bradycardic junctional rhythm and could have repeated hemodynamic instability in the absence of revascularization. Second, catheter advancement was without any resistance, suggesting the true lumen course of the device. Third, the hospital did not have an aortic surgery service; transfer to a facility with aortic surgery services would cause a significant time delay which could deteriorate the patient's condition.

Indonesia is home to more than 270 million inhabitants, and its cardiovascular services are just beginning to improve. Within the past 5 years, 250 new Cath laboratories have initiated diagnostic and interventional services throughout the country. Unfortunately, cardiac surgery services have failed to grow as fast; currently, there are only eight centers with cardiac surgery services, of which, only one regularly performs aortic surgeries. This situation is probably similar in other developing countries; therefore, such patients might have to be treated emergently without surgical backup. Two reports on successful revascularization were performed in cardiac centers with full surgical backup and the corrective surgery was performed immediately after PPCI. ^{9 10 11} In our opinion, PPCI without surgical backup in such setting remains justified knowing that the operator performs the procedure cautiously and does not further injure the aorta. The operator must be aware of the underlying cause of the STEMI and has evaluated the anatomy of the dissected aorta before commencing the procedure. This can also be facilitated by currently available technologies with integrated angiography and CT. We were fortunate that the route taken to perform the PPCI was all true lumen, although we were not aware of the dissection. Radial access was chosen, so the wire and catheter were advanced to the innominate artery and the left side of the ascending aorta, all of which were true lumen; thus, we experienced very smooth catheter advancement. In the presence of resistance, the catheter position should be evaluated, a small amount of contrast agent can be injected, and the pressure gradient should be measured to confirm the diagnosis and to decide whether to proceed with the intervention. ¹⁴

Furthermore, we suggest that the patient's individual clinical condition is critical to justify performing PPCI without surgical backup. Our patient had junctional rhythm and seizures as a consequence of the STEMI. Without revascularization, there will be a delay in the conversion of the rhythm back to normal. Thus, when severe complications as direct consequences of STEMI occur, revascularization is essential to save lives because the benefit of PPCI in preserving cardiac function exceeds the risk of tamponade or aortic rupture.

Conclusion

In summary, we presented a case of TAAD complicated by STEMI in which a PPCI was successfully performed. The patient survived and was referred to the National Cardiovascular Center, where he underwent successful elective corrective surgery. Evaluation of aortic anatomy and individual clinical condition is required to justify performing PPCI without surgical backup in such limited-resource settings.