Introduction
Aortic dissection is associated with cardiac tamponade, aortic regurgitation, and ischemia in various branches, depending on the progress of dissection. Coronary malperfusion is one of the fatal complications of acute type A aortic dissection (AAAD). The in-hospital mortality rate in AAAD patients without any complications ranges from 8 to 19%, whereas that in AAAD patients with coronary malperfusion ranges from 20 to 30% [
1‐
3]. Malperfusion in the left main coronary artery (LMCA) is particularly associated with catastrophic outcomes, because it can cause cardiogenic shock or cardiac arrest [
3,
4]. Immediate revascularization is necessary for AAAD patients with LMCA malperfusion to treat myocardial ischemia and provide hemodynamic stability.
The current guidelines suggest surgical resection and thoracic aorta replacement as the gold standard for the treatment of AAAD [
5,
6]. According to previous research, any delay in the door-to-balloon time in patients with ST elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI) is associated with higher in-hospital mortality [
7], and preoperative PCI is effective for coronary malperfusion caused by AAAD [
4,
8‐
12]. However, regarding LMCA malperfusion in AAAD, its analytical treatment data are scarce because of its low incidence, and, therefore, which treatment should take priority, surgical correction or reperfusion therapy, remains controversial.
Here we present a case series of patients undergoing PCI for LMCA malperfusion caused by AAAD, describe their in-hospital and long-term outcomes, and discuss the optimal treatment strategy.
Methods
This retrospective, single-center, observational study was based on an initial cohort of 10,530 consecutive patients with acute coronary syndrome undergoing emergent PCI between January 1995 and January 2020. In this cohort, we included patients with LMCA malperfusion caused by AAAD. Patients with right coronary artery malperfusion were not included. The study was done in accordance with the provision of the Declaration of Helsinki and the guidelines for epidemiological studies issued by the Ministry of Health, Labour, and Welfare of Japan. All the patients provided informed consent for the procedure and subsequent data collection, and the patients included in this case series provided consent for publication.
PCI procedures
When a patient was diagnosed with AAAD after coronary angiography, we immediately referred the patient to cardiovascular surgeons, and emergent surgery was prepared. Then, both reperfusion therapy for the LMCA in the catheterization laboratory to stabilize the hemodynamics and emergent surgery were prepared simultaneously. The final decision was made by the heart team consisting of interventional cardiologists, cardiovascular surgeons, and other medical staff. All PCI procedures were performed in the cardiac catheterization laboratory. Heparin was given to all patients as a bolus intravenously to achieve an activated clotting time of > 250 s. The guidewires were carefully inserted into the left anterior descending artery and left circumflex artery to avoid false lumen insertion. Plain old balloon angioplasty was performed before stenting as needed. Bare metal stents or drug-eluting stents were deployed under angiography or intravascular ultrasound guidance to completely cover the dissection. Intra-aortic balloon pumping (IABP) or a percutaneous left ventricular support device was used in patients with cardiogenic shock, which was defined as systolic blood pressure < 80 mm Hg or the need for parenteral inotropic or vasoactive medication to maintain systolic blood pressure ≥ 80 mm Hg. Venoarterial extracorporeal membrane oxygenation (VA-ECMO) was inserted to patients without return of spontaneous circulation after cardiopulmonary arrest or those with hemodynamic collapse.
Surgical procedures
Patients were transferred to the operating room after PCI and underwent central repair, except for those with poor cardiac function even after PCI or those with neurological manifestations. After the initiation of extracorporeal circulation and the transection of the ascending aorta, blood cardioplegia was infused from the coronary ostium. In patients with localized aortic dissection at the aortic root, direct repair was performed by closing the false channel with surgical glue. In patients with aortic dissection extending to the ascending aorta, ascending aorta replacement, hemiarch replacement, or total arch replacement was performed. In patients, where complete coronary revascularization was not achieved, coronary artery bypass grafting to the left anterior descending artery and/or the left circumflex artery was performed using saphenous vein grafts.
Follow-up
We evaluated in-hospital and 5 year outcomes of patients with LMCA malperfusion caused by AAAD by reviewing the hospital charts and contacting the patients.
Statistical analysis
Data are expressed as mean ± standard deviation for continuous variables. Categorical variables are reported as numbers with relative percentages. SPSS version 25 (International Business Machines, Armonk, NY, USA) was used for all statistical calculations. The data were not analyzed for statistical difference due to the small size of the study population, however.
Discussion
This case series is the first report to systematically investigate the clinical characteristics, procedures, and outcomes in patients undergoing PCI for LMCA malperfusion caused by AAAD. The main findings of this study were as follows: first, AAAD was difficult to diagnose accurately in the emergency room; second, the in-hospital mortality rate in AAAD patients with LMCA malperfusion undergoing PCI was 44%; and third, patients with poor prognosis (non-survivors) tended to have cardiopulmonary arrest requiring VA-ECMO, higher D-dimer levels, and severe metabolic acidosis.
Clinical presentation of AAAD is similar to that of acute coronary syndrome, which frequently results in misdiagnosis [
13]. In this study, seven (78%) of the nine patients were diagnosed with acute coronary syndrome in the emergency room and were transferred to the cardiac catheterization laboratory. All patients underwent bedside transthoracic echocardiography; however, a mobile flap was found in the ascending aorta of only one patient (Case 7). According to previous research, three important findings of transthoracic echocardiography indicating AAAD are aortic root dilation, aortic eccentric regurgitation, and pericardial effusion [
14]. Because both two patients who were diagnosed with AAAD before coronary angiography survived to discharge, early diagnosis of AAAD may contribute to raise the survival rate. However, diagnosing AAAD in patients with hemodynamic instability is difficult in emergency situations. In this study, although seven of the nine patients were diagnosed with AAAD after coronary angiography, reperfusion therapy in the LMCA was performed without any delay. Because hemodynamic stabilization has to be the top priority, the initial treatment strategy for this condition is similar to that for acute coronary syndrome with cardiogenic shock. In patients with right coronary artery malperfusion who have less hemodynamic instability and lower mortality, surgical aortic repair should be selected as an initial treatment strategy [
3]. If AAAD is diagnosed prior to coronary angiography, the patient may benefit from being transported to a hybrid operating room immediately and undergoing reperfusion therapy for the LMCA and subsequent surgical aortic repair.
In this study, both the in-hospital and 5 year follow-up survival rates were 56% (5/9 patients), without either hospitalization for heart failure or target vessel revascularization, which were better than those of previous studies on patients with acute myocardial infarction due to LMCA disease (in-hospital: approximately 50%; 6 month follow-up: 41%) [
15‐
17]. Comorbid aortic dissection may not affect the in-hospital and long-term outcomes, and early reperfusion therapy may contribute to preserve left ventricular function and prevent heart failure. In addition, the etiology of myocardial ischemia in our study population was not atherosclerotic disease, which may have led to the favorable long-term outcomes.
The presence of myocardial ischemia, cardiopulmonary arrest on arrival, and LMCA ischemia have been reported to be risk factors for operative death and postoperative low cardiac output syndrome in AAAD patients [
3]. In this study, eight (89%) of the nine patients had cardiogenic shock, which indicates that our study population suffered severe hemodynamic instability. Fatal myocardial ischemia tends to occur before surgical reconstruction of coronary blood flow. According to previous research, the shorter door-to-balloon time decreases the mortality rate in STEMI patients by reducing myocardial damages [
7,
18,
19]. In this study, because all patients with severe metabolic acidosis and hemodynamic deterioration requiring VA-ECMO could not be saved, preoperative PCI may be an effective approach to reduce myocardial damages and stabilize hemodynamics in patients with LMCA malperfusion caused by AAAD. IABP as circulatory support is considered a contraindication for AAAD patients because of the concerns over flap extension and aortic rupture. In this study, the four patients were supported by IABP to maintain hemodynamic stability and had no adverse events associated with IABP, and the three patients supported by IABP alone were successfully treated by PCI and subsequent surgery and survived to discharge. Using IABP may be one of the strategies to prevent prolonged cardiogenic shock and subsequent progressive acidosis.
The current study has several limitations. First, this is a retrospective, single-center, observational study with a small study population. Larger prospective studies are warranted to confirm the findings of this study. Second, surgical strategies for AAAD patients with LMCA malperfusion were not assessed. Third, AAAD patients with LMCA malperfusion who had been directly transferred from the emergency room to the operating room were not included. Fourth, the differences in the clinical characteristics between AAAD patients with LMCA malperfusion and acute coronary syndrome patients with LMCA atherosclerosis were not evaluated in this case series. Finally, accurate drug information on perioperative antithrombotic therapy could not be collected.
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