Clinical Outcomes Following Emergent Percutaneous Coronary Intervention for Acute Total/Subtotal Occlusion of the Left Main Coronary Artery

Abstract

Background: Data regarding the clinical features, outcomes and prognostic factors in patients presenting with acute total/subtotal occlusion of the unprotected left main coronary artery (LMCA) remain limited.

Methods and Results: From a multi-center registry, 134 patients due to acute total/subtotal occlusion of the unprotected LMCA were reviewed. Emergency room (ER) status classification was defined according to the presence of cardiogenic shock and cardiopulmonary arrest (CPA) in the ER (class 1=no cardiogenic shock; class 2= cardiogenic shock but not CPA; and class 3=CPA). In-hospital mortality and cerebral performance category (CPC) as the endpoints were evaluated. One-half (67/134) of the enrolled patients presented with total occlusion of the unprotected LMCA. Regarding ER status classification, class 1, 2, and 3 were observed in 30.6%, 45.5%, and 23.9% of the patients, respectively. In-hospital mortality occurred in 73 (54.5%) patients; of the remaining patients, 52 (85.3%) could be discharged with a CPC 1 or 2. ER status classification (odds ratio 4.4 [95% confidence interval: 2.33–10.67]; P<0.001) and total occlusion of the unprotected LMCA (odds ratio 8.29 [95% confidence interval 2.93–23.46]; P<0.001) were strong predictors of in-hospital mortality.

Conclusions: Acute total/subtotal occlusion involving the unprotected LMCA appeared to be associated with high in-hospital mortality. ER status classification and initial flow in the unprotected LMCA were significant predictive factors of in-hospital mortality.

Acute myocardial infarction (AMI) remains one of the leading causes of mortality all over the world.^1,2 The efficacy of the emergent percutaneous coronary intervention (PCI) has been well documented in patients with AMI.^3–5 AMI responsible for unprotected left main coronary artery (LMCA) as a culprit lesion is relatively rare, accounting for only 0.2–2.4% of all AMI cases treated using emergency PCI.^6–8 Moreover, some acute coronary syndrome (ACS) patients who had an unprotected LMCA may have a sudden death because of a large risk area in the myocardium before being transferring to medical centers for treatment.^9,10 Therefore, detailed data including patient characteristics, clinical presentation, and prognosis in LMCA-ACS patients have not been fully elucidated. Furthermore, most studies have reported outcomes of the entire cohort of patients with LMCA-ACS,^8,11–14 whereas few have focused on acute total/subtotal occlusion involving the unprotected LMCA, which represents more critical situations. Therefore, the aim of this study was to investigate detailed clinical features and outcomes of patients from a multicenter registry, including brain damage, to explore the factors related to in-hospital mortality, following emergent PCI in patients with acute total/subtotal occlusion involving the unprotected LMCA.

Methods

Study Population and Evaluation

N-Registry is an ongoing, physician-directed, non-company-sponsored, retrospective multicenter registry, investigating clinical issues of patients with cardiovascular disease.¹⁵ Among emergent PCI cases between January 2006 and November 2017, patients with acute total/subtotal occlusion of the unprotected LMCA identified on emergent angiography were included. Total occlusion was defined as 100% occlusion with Thrombolysis in Myocardial Infarction (TIMI) flow 0, and subtotal occlusion as 99% stenosis with TIMI flow 1 or 2.¹⁶ Patients who had experienced out-of-hospital cardiopulmonary arrest (CPA) were not excluded, whereas patients in whom the culprit lesion did not involve the unprotected LMCA, or when an initial angiography revealed TIMI flow 3, were excluded. Collected data included clinical, angiographic and procedural characteristics, and adverse clinical events. The collateral circulation information from the right coronary artery (RCA) was evaluated using criteria proposed by Rentrop et al.¹⁷ To represent the severity, emergency room (ER) status was classified into 3 groups according to ER vital status at first clinical examination in the ER: class 1=no cardiogenic shock; class 2=cardiogenic shock (systolic blood pressure <90 mmHg) but not CPA experience; and class 3=CPA experience (patients both with CPA on ER arrival and who experienced CPA before ER but recovered before first clinical examination in the ER were classified as class 3).

This study adhered to the guidelines of the Declaration of Helsinki and was approved by the institutional review boards of the participating institutions.

PCI Procedure

Percutaneous coronary intervention was performed by well-trained interventional cardiologists according to standard practices used in the participating centers. The use of stenting, thrombus aspiration, distal protection, and other devices were at the discretion of the operators. According to antiplatelet therapy, the combination of aspirin 200 mg plus clopidogrel 300 mg, or aspirin 200 mg plus prasugrel 20 mg as a loading dose, followed by aspirin 100 mg plus clopidogrel 75 mg, or aspirin 100 mg plus prasugrel 3.75 mg as a maintenance dose was used. The use of mechanical support, such as intratracheal intubation, intra-aortic balloon pump (IABP) and veno-arterial extracorporeal membrane oxygenation (VA-ECMO), and a targeted temperature management were left to clinical decision, including use and timing (i.e., before, during, or after PCI).

Study Endpoint

The primary endpoint was in-hospital mortality. Furthermore, to evaluate brain damage from anoxic injury in the patients who survived to discharge, the cerebral performance category (CPC) was used: CPC 1, good cerebral performance (patient is alert and exhibits normal cerebral function); CPC 2, moderate disability (patient is alert and has sufficient cerebral function to live independently and work part-time); CPC 3, severe cerebral disability (patient is conscious but dependent on others for daily support due to impaired brain function); and CPC 4, a vegetative state.^18–20 This neurologic outcome was obtained from the clinical chart review and evaluated by ≥2 physicians.

Statistical Analysis

All patient data were pooled in a single prespecified structured dataset for analysis. Continuous variables are expressed as mean±standard deviation (SD) or median (interquartile range), and compared using a Student’s t-test or the Wilcoxon rank-sum test. Categorical variables are expressed as proportions and percentages, and were compared using Fisher’s exact test. Multivariate logistic regression analysis was used to estimate the odds ratio (OR) and corresponding 95% confidence interval (CI) for in-hospital mortality. Variables with P<0.10 in the univariate analysis and judged to be of clinical significance were selected for the multivariate model. Sequential univariate models were used for biologically and clinically relevant covariates; P<0.05 was considered to be statistically significant. All statistical analyses were performed using SPSS version 21.0 (IBM Corporation, Armonk, NY, USA).

Results

Study Population, Procedural Characteristics, and Clinical Outcome

Among 11,977 cases undergoing emergency PCI, 134 (1.1%) were treated with emergent PCI due to acute total/subtotal occlusion of the unprotected LMCA. Patient background data are presented in Table 1. The mean age of the patients was 69.9±11.3 years, 103 (76.9%) were male, and 46 (34.3%) had diabetes mellitus. The majority of patients presented with Killip 4 at the first clinical examination in the ER (67.9%). Regarding ER status classification, classes 1, 2, and 3 were observed in 30.6%, 45.5% and 23.9%, respectively.

Table 1. Baseline Patient Characteristics

	All patients (n=134)	In-hospital mortality group (n=73)	Surviving discharge group (n=61)	P value
Age (years)	69.9±11.3	70.4±10.7	69.2±12.0	0.55
Males	103 (76.9)	59 (80.8)	44 (72.1)	0.24
BMI	23.2±3.4	23.4±3.6	22.9±3.2	0.36
Hypertension	81 (60.4)	43 (58.9)	38 (62.3)	0.69
Diabetes mellitus	46 (34.3)	23 (31.5)	23 (37.7)	0.45
Insulin	7 (5.2)	2 (2.7)	5 (8.2)	0.16
Oral hypoglycemic agent	25 (18.7)	10 (13.7)	15 (24.6)	0.11
Dyslipidemia	74 (55.2)	36 (49.3)	38 (62.3)	0.13
Current smoker	44 (32.8)	23 (31.5)	21 (34.4)	0.72
eGFR <60 mL/min/1.73 m2	84 (62.7)	54 (74)	30 (49.2)	0.003
Dialysis	7 (5.2)	3 (4.2)	4 (6.5)	0.55
Prior MI	13 (9.7)	8 (11)	5 (8.2)	0.59
Prior PCI	21 (15.7)	10 (13.7)	11 (18)	0.49
Prior CABG	2 (1.5)	1 (1.4)	1 (1.6)	0.9
Prior Stroke/TIA	11 (8.2)	7 (9.6)	4 (6.6)	0.52
Serum albumin (g/dL)	3.7±0.7	3.5±0.7	3.9±056	0.001
Hemoglobin (g/dL)	13.4±2.2	13.1±2.3	13.7±2.1	0.09
Systolic blood pressure (mmHg)	88 (67–123)	74 (60–89)	118 (84–144)	<0.001
Heart rate (beats/min)	85 (65–102)	90 (65–101)	83 (64–104)	0.92
Killip class				<0.001
1	13 (9.7)	1 (1.4)	12 (19.7)
2	13 (9.7)	3 (4.1)	10 (16.4)
3	17 (12.7)	5 (6.8)	12 (19.7)
4	91 (67.9)	64 (87.7)	27 (44.2)
CPA	71 (63.4)	51 (69.9)	20 (32.8)	<0.001
CPA on ER arrival	20 (14.9)	16 (21.9)	4 (6.6)
Experienced CPA but recovered before ER arrival	12 (9)	7 (9.6)	5 (8.2)
CPA after ER arrival	39 (29.1)	28 (38.4)	11 (18)
ER status classification				<0.001
1	41 (30.6)	8 (11)	33 (54.1)
2	61 (45.5)	42 (57.5)	19 (31.1)
3	32 (23.9)	23 (31.5)	9 (14.8)

Data are presented as absolute numbers (n) and percentages, means±standard deviation, or median (lower quartiles–upper quartiles), unless otherwise specified. BMI, body mass index; CABG, coronary artery bypass graft; CPA, cardiopulmonary arrest; eGFR, estimated glomerular filtration rate; ER, emergency room; MI, myocardial infarction; PCI, percutaneous coronary intervention; TIA, transient ischemic attack.

Angiographic and procedural characteristics of the study cohort are summarized in Table 2. Initial LMCA flow was TIMI 0 (total occlusion) in 50% and TIMI 1 or 2 (subtotal occlusion) in 50%. The majority of access sites were femoral (n=112 [83.6%]). Intravascular ultrasound was used in 99 (73.9%) patients. Almost all patients required IABP (n=128 [95.5%]); furthermore, VA-ECMO was needed in approximately one-half of the patients (n=63 [47%]). The median maximum creatine kinase level after PCI was 8,492 (3,639–12,800) IU/L.

Table 2. Angiographic, Procedural, and Clinical Outcome Characteristics

	All patients (n=134)	In-hospital mortality group (n=73)	Surviving discharge group (n=61)	P value
LMCA stenosis				0.003
99% (subtotal)	67 (50)	28 (38.4)	39 (63.9)
100% (total)	67 (50)	45 (61.6)	22 (36.1)
RCA disease	33 (24.6)	16 (21.9)	17 (27.9)	0.43
Rentrop criteria				0.006
0	61 (47.7)	39 (56.5)	22 (37.3)
1	34 (26.6)	20 (29)	14 (23.7)
2	16 (12.5)	7 (10.1)	9 (15.3)
3	17 (13.3)	3 (4.3)	14 (23.7)
Single stent	96 (71.6)	50 (68.5)	46 (75.4)	0.38
2-stent	20 (14.9)	9 (12.2)	11 (18)	0.36
Stent less	18 (13.4)	14 (19.2)	4 (6.6)	0.03
DES use	75 (56)	39 (53.4)	36 (59)	0.52
Stent number	1.2±0.8	1.1±0.8	1.4±0.8	0.03
LMCA stent diameter (mm)	3.4±0.4	3.3±0.4	3.4±0.3	0.24
Total stent length (mm)	24.1±16.8	21.7±16.8	27.0±16.4	0.07
Pre dilatation	97 (72.4)	54 (74)	43 (70.5)	0.65
Post dilatation	90 (67.2)	44 (60.3)	46 (75.4)	0.06
Final TIMI flow†				0.001
0	2 (1.7)	2 (3)	0
1	5 (4.1)	5 (7.5)	0
2	34 (28.1)	26 (38.8)	8 (14.8)
3	80 (66.1)	34 (50.7)	46 (85.2)
Access site				0.35
Radial	14 (10.4)	6 (8.2)	8 (13.1)
Brachial	8 (6)	6 (8.2)	2 (3.3)
Femoral	112 (83.6)	61 (83.6)	51 (83.6)
IVUS	99 (73.9)	49 (67.1)	50 (82.0)	0.051
OCT	0	0	0
Rotational atherectomy	2 (1.5)	0	2 (3.3)	0.12
Aspiration	83 (61.9)	50 (68.5)	33 (54.1)	0.09
Distal protection	11 (8.2)	6 (8.2)	5 (8.2)	0.96
ELCA	3 (2.2)	1 (1.4)	2 (3.3)	0.46
IABP	128 (95.5)	72 (98.6)	56 (91.8)	0.057
VA-ECMO	63 (47.0)	53 (72.6)	10 (16.4)	<0.001
Targeted temperature management	19 (14.2)	14 (19.2)	5 (8.2)	0.07
Intratracheal intubation	94 (69.9)	66 (90.4)	28 (45.9)	<0.001
Maximum CK after PCI (IU/L)	8,492 (3,639–12,800)	11,075 (7,174–17,036)	5,514 (1,442–9,100)	<0.001
Onset to balloon time (min)	160 (116–252)	150 (117–202)	171 (114–315)	0.13

Data are presented as absolute numbers (n) and percentages and means±standard deviation, or median (lower quartiles–upper quartiles), unless otherwise specified. ^†Data were not available for 13 patients. CK, creatine kinase; DES, drug-eluting stent; ELCA, excimer laser coronary atherectomy; IABP, intra-aortic balloon pump; IVUS, intravenous ultrasound; LMCA, left main coronary artery; OCT, optical coherence tomography; PCI, percutaneous coronary intervention; RCA, right coronary artery; TIMI, thrombolysis in myocardial infarction; VA-ECMO, veno-arterial extracorporeal membrane oxygenation.

In-hospital mortality occurred in 73 (54.5%) patients. In terms of the cause of death, most were due to ACS-related death (n=64 [87.7%]) such as circulatory failure, heart failure, lethal arrhythmia, and multiple organ failure. Septic shock due to infection (n=4), acute limb ischemia (n=1), aortic dissection (n=1), rhabdomyolysis (n=1), tracheorrhagia (n=1), and lung cancer (n=1) were observed occasionally. Data regarding CPC are shown in Figure 1. Among surviving discharged patients, 40 (65.6%) patients and 12 (19.7%) patients were discharged from hospital with CPC 1 and CPC 2, respectively. In contrast, CPC 3 and 4 were identified in 8 (13.1%) patients and 1 (1.6%) patient, respectively.

Figure 1.

Result of in-hospital mortality and CPC (cerebral performance category) at patient discharge.

Analysis According to In-Hospital Mortality

The patients who experienced in-hospital mortality were compared with in-hospital survivors (Tables 1 and 2). In the in-hospital mortality group, the presence of estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m² at admission was observed more frequently, and serum albumin levels at admission were lower compared with those who survived at discharge. In addition, Killip classification was more severe, and resuscitation for cardiac arrest was more frequently required in the in-hospital mortality group (87.7% vs. 44.2%, P<0.001, 69.9% vs. 32.8%, P<0.001, respectively). The use of VA-ECMO and the intubation rate were significantly higher in the in-hospital mortality group. The peak creatine kinase level was significantly higher in the in-hospital mortality group than in the surviving discharge group (11,075 IU/L vs. 5,514 IU/L; P<0.001).

Results of the logistic regression analysis are summarized in Table 3. Multiple logistic regression analysis revealed that the presence of eGFR <60 mL/min/1.73 m² on admission, collateral circulation from the RCA, total of the LMCA, and ER status classification were identified as independent predictors of in-hospital mortality.

Table 3. Univariate and Multivariate Logistic Analysis for In-Hospital Mortality

Variables	Univariate analysis		Multivariate analysis
	OR (95% CI)	P value	OR (95% CI)	P value
Age	1.01 (0.98–1.04)	0.55	1.01 (0.96–1.06)	0.69
Male	1.63 (0.73–3.65)	0.24
BMI	1.05 (0.94–1.18)	0.36
Hypertension	0.87 (0.43–1.74)	0.69
Diabetes mellitus	0.76 (0.37–1.55)	0.45
Dyslipidemia	0.59 (0.30–1.18)	0.13
Renal dysfunction	2.94 (1.42–6.06)	0.004	4.43 (1.47–13.32)	0.008
Hemoglobin	0.87 (0.74–1.02)	0.09	0.96 (0.73–1.27)	0.78
Serum albumin	0.38 (0.20–0.71)	0.003	0.44 (0.16–1.22)	0.12
Collateral from RCA	0.55 (0.39–0.79)	0.001	0.50 (0.31–0.79)	0.003
Total occlusion of LMCA	2.85 (1.41–5.76)	0.004	8.29 (2.93–23.46)	<0.001
ER status classification†	3.51 (2.01–6.12)	<0.001	4.4 (2.33–10.67)	<0.001

^†ER status classification was treated as a continuous variable. CI, confidence interval; ER, emergency room; LMCA, left main coronary artery; OR, odds ratio; RCA, right coronary artery.

In-hospital mortality rates according to ER status classification and initial LMCA flow are shown in Figure 2 (A and B, respectively). From the perspective of ER status classification, the in-hospital mortality rate was 19.5% in class 1, 68.9% in class 2, and 71.9% in class 3 (P<0.001). Furthermore, patients with total occlusion of the unprotected LMCA exhibited a significantly higher mortality rate compared to those with subtotal occlusion (67.2% vs. 41.8%; P=0.003).

Figure 2.

In-hospital mortality rates according to ER status classification and total/subtotal LMCA. (A) In-hospital mortality according to ER status classification. (B) In-hospital mortality according to initial flow of LMCA. ER, emergency room; CPA, cardiopulmonary arrest; LMCA, left main coronary artery.

Discussion

Based on registry data, we evaluated clinical outcomes following emergent PCI for acute total/subtotal occlusion in the unprotected LMCA. The main findings are as follows:

(1) The in-hospital mortality rate was extremely high (54%). In evaluating brain damage from anoxic injury, approximately 85% of remaining patients could be discharged with CPC 1 or 2.

(2) The in-hospital mortality rate was significantly elevated as ER status classification became progressively worse. In other words, ER status classification may be a strong predictor of in-hospital mortality.

(3) Total occlusion of unprotected LMCA (initial TIMI flow 0) was associated with significantly poorer outcome compared with subtotal occlusion (initial TIMI flow 1 or 2).

LMCA-ACS is uncommonly encountered in clinical practice, and the literature addressing LMCA-ACS is relatively limited.^7,21–24 From these reports, IABP was required in 20–80% of patients and VA-ECMO in 6–22%, and the resultant in-hospital mortality rate was 33–57%. Compared with previous reports, we focused only on acute total/subtotal occlusion with flow-limited stenosis of LMCA-ACS, with detailed data for patient background, clinical presentation, and prognosis from this multicenter registry. In our study, two-thirds of the patients had cardiogenic shock and experienced cardiac arrest requiring resuscitation before emergent PCI, practically all patients required IABP, and approximately one-half required VA-ECMO to maintain hemodynamic status, though the patient demographic profile was consistent with previous studies. This implies a greater severity of illness in the present study population compared with previous studies focusing on the entire population with LMCA-ACS;²⁵ as a result, our study revealed a very high in-hospital mortality rate (54.5%). In addition, a large proportion of in-hospital deaths were attributed to ACS-related factors, such as heart failure, lethal arrhythmia and multiple organ failure due to the large area of myocardial infarction, which is a consequence of pump failure. Our study offers novel information and new insights of LMCA-ACS, as our study investigated real-world data consisting of the most critically ill patients.

In this population type, neurological status should be important because significant neurological injury dying after cardiac arrest has a large effect on prognosis.²⁶ CPC is the gold standard to assess neurological recovery after cardiac arrest,²⁷ and is useful to assess the effectiveness of resuscitation care,¹¹ and moreover, corresponds to functional status and quality of life.^28–30 To achieve a better result for neurological function in patients with cardiogenic shock or for those resuscitated after CPA, intensive systemic management is crucial, and may include antithrombotic therapy, pharmacological inotropes, anesthetic support and infection control, as well as stabilizing hemodynamics with immediate restoration and use of hemodynamic support devices.³¹ Thus, future studies should investigate if these aspects can improve the clinical outcomes of patients with LMCA-ACS whose in-hospital mortality remains extremely high.

Our study suggests that ER status classification is a strong predictive factor of in-hospital mortality. To classify cardiovascular disease, Killip class is one of the well-known classifications to understand a patient’s hemodynamic status; however, due to the specificity of our patients, the majority of Killip class classifications cannot distinguish the presence of CPA requiring resuscitation. It has been established that cardiac arrest and/or cardiogenic shock are both strong predictors of in-hospital mortality for ACS patients;^1,6–8,12 however, there is a large difference between the presence or absence of CPA because it may not only force us to weigh the option of implementation of mechanical support, such as intubation and VA-ECMO in the ER, which may lead to the delay of PCI, but also complications related to resuscitation, such as pneumothorax and sternal fracture. A previous study revealed that the requirement of cardiopulmonary resuscitation in patients with unprotected LMCA occlusion leads to poor outcomes and is strongly correlated with in-hospital mortality.⁶ Furthermore, new detailed classification of cardiogenic shock has been proposed to guide the treatment and predict outcome because the prognosis of cardiogenic shock may vary widely based on etiology and comorbidities.³² Our study suggested ER status classification might be much easier to judge because it required only the presence or absence of CPA and blood pressure, without any blood tests or detailed physical information. It may be useful not only to understand the patient’s situation in the ER and to judge intubation or VA-ECMO insertion in the ER immediately, but also to predict in-hospital outcomes. Our study showed that eGFR <60 mL/min/1.73 m² was one of the strong predictors of in-hospital mortality. Renal dysfunction on admission has been shown to be associated with development of acute kidney injury³³ and poor prognosis in patients with AMI.³⁴ Further, renal dysfunction on admission might represent not only patient baseline renal function, but also the severity of circulation status, including cardiogenic shock or CPA, especially in this population type.³⁵ We also demonstrated that the better collateral circulation from the RCA was associated with lower in-hospital mortality in our study population. Collateral circulation is well known to be related to the clinical outcome in AMI patients,^36,37 and we confirmed that in the specific population of this study as well.

Our study suggests that the rate of in-hospital mortality is significantly higher in patients with total occlusion of the unprotected LMCA compared to those with subtotal occlusion. It is well known that initial TIMI flow is associated with myocardial damage and is an independent predictor of myocardial infarction size;^38,39 however, only a few studies have focused on differences in initial TIMI flow 0 vs. TIMI 1 and 2.²⁴ Our study determined that in-hospital mortality was significantly higher in patients with total occlusion (initial TIMI flow 0) than subtotal occlusion (initial TIMI flow 1 or 2). This result may be useful for estimating in-hospital mortality in clinical practice, and also may be a benchmark for future studies investigating LMCA-ACS.

Study Limitations

Several limitations should be acknowledged. First, this was a retrospective observational study with a relatively small sample size. Due to the study design, some detailed data were not available, including the timing and doses of antithrombotic medications. Those factors might affect the results. Second, because this study only included patients undergoing PCI, we did not evaluate patients who died before undergoing PCI or proceeded directly to coronary artery bypass surgery; therefore, the true incidence and prognosis may be underestimated. Third, due to the critical status of our study population, some cases required urgent VA-ECMO implementation just after ER department arrival, which might affect the obtained data. Fourth, whereas the use of IABP remains controversial, it was used in almost all patients in our study. Moreover, Impella^®, as a percutaneous ventricular-assist device, may provide better left ventricular and circulatory support compared with IABP in theory. During the study period, however, the Impella^® device was not available in Japan. Notwithstanding these limitations, as limited data are available regarding acute total/subtotal occlusion of LMCA-ACS, our data are of importance in clinical practice.

Conclusions

This study evaluated clinical setting, morbidity, and mortality in patients with acute total/subtotal occlusion of the unprotected LMCA from a multi-center registry. The in-hospital mortality rate was extremely high, >50%, and approximately 85% of remaining patients were discharged with CPC 1 or 2. ER status classification may be a useful and convenient metric to predict in-hospital mortality, as well as initial flow in the LMCA.

Disclosures

T. Murohara and H. Ishii are members of Circulation Journal’s Editorial Team.

H. Ishii received lecture fees from Astellas Pharma Inc., Astrazeneca Inc., Daiichi-Sankyo Pharma Inc., and MSD K.K. Y. Uemura received lecture fees from Otsuka Pharma Ltd. I. Morishima received lecture fees from Daiichi-Sankyo Co., Ltd., Nippon Boehringer Ingelheim Co., Ltd., Abbott Japan. T. Murohara received lecture fees from Bayel Pharmaceutical Co., Ltd., Daiichi-Sankyo Co., Ltd., Dainippon Sumitomo Pharma Co., Ltd., Kowa Co., Ltd., MSD K.K., Mitsubishi Tanabe Pharma Co., Nippon Boehringer Ingelheim Co., Ltd., Novartis Pharma K.K., Pfizer Japan Inc., Sanofi-aventis K.K., and Takeda Pharmaceutical Co., Ltd. T. Murohara received an unrestricted research grant for the Department of Cardiology, Nagoya University Graduate School of Medicine from Astellas Pharma Inc., Daiichi-Sankyo Co., Ltd., Dainippon Sumitomo Pharma Co., Ltd., Kowa Co., Ltd., MSD K.K., Mitsubishi Tanabe Pharma Co., Nippon Boehringer Ingelheim Co., Ltd., Novartis Pharma K.K., Otsuka Pharma Ltd., Pfizer Japan Inc., Sanofi-aventis K.K., Takeda Pharmaceutical Co., Ltd., and Teijin Pharma Ltd. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

IRB Information

This study protocol was approved by the Ethics Committee of Nagoya University Hospital (approval number 2017-0466).

Data Availability

The deidentified participant data will not be shared.

References

• 1.   Pedrazzini GB, Radovanovic D, Vassalli G, Surder D, Moccetti T, Eberli F, et al. Primary percutaneous coronary intervention for unprotected left main disease in patients with acute ST-segment elevation myocardial infarction the AMIS (Acute Myocardial Infarction in Switzerland) plus registry experience. JACC Cardiovasc Interv 2011; 4: 627–633.
• 2.   Montalescot G, Brieger D, Eagle KA, Anderson FA Jr, FitzGerald G, Lee MS, et al. Unprotected left main revascularization in patients with acute coronary syndromes. Eur Heart J 2009; 30: 2308–2317.
• 3.   Steg PG, James SK, Atar D, Badano LP, Blomstrom-Lundqvist C, Borger MA, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J 2012; 33: 2569–2619.
• 4.   Kimura K, Kimura T, Ishihara M, Nakagawa Y, Nakao K, Miyauchi K, et al. JCS 2018 guideline on diagnosis and treatment of acute coronary syndrome. Circ J 2019; 83: 1085–1196.
• 5.   Vahdatpour C, Collins D, Goldberg S. Cardiogenic shock. J Am Heart Assoc 2019; 8: e011991.
• 6.   Edes IF, Ruzsa Z, Lux A, Geller L, Molnar L, Nowotta F, et al. Acute, total occlusion of the left main stem: Coronary intervention options, outcomes, and recommendations. Postepy Kardiol Interwencyjnej 2018; 14: 233–239.
• 7.   Patel N, De Maria GL, Kassimis G, Rahimi K, Bennett D, Ludman P, et al. Outcomes after emergency percutaneous coronary intervention in patients with unprotected left main stem occlusion: The BCIS national audit of percutaneous coronary intervention 6-year experience. JACC Cardiovasc Interv 2014; 7: 969–980.
• 8.   Gharacholou SM, Ijioma NN, Lennon RJ, Rihal CS, Bell MR, Brenes-Salazar JA, et al. Characteristics and long term outcomes of patients with acute coronary syndromes due to culprit left main coronary artery disease treated with percutaneous coronary intervention. Am Heart J 2018; 199: 156–162.
• 9.   Alabas OA, Brogan RA, Hall M, Almudarra S, Rutherford MJ, Dondo TB, et al. Determinants of excess mortality following unprotected left main stem percutaneous coronary intervention. Heart 2016; 102: 1287–1295.
• 10.   Puricel S, Adorjan P, Oberhansli M, Stauffer JC, Moschovitis A, Vogel R, et al. Clinical outcomes after PCI for acute coronary syndrome in unprotected left main coronary artery disease: Insights from the Swiss Acute Left Main Coronary Vessel Percutaneous Management (SALVage) study. EuroIntervention 2011; 7: 697–704.
• 11.   Yap J, Singh GD, Kim JS, Soni K, Chua K, Neo A, et al. Outcomes of primary percutaneous coronary intervention in acute myocardial infarction due to unprotected left main thrombosis: The Asia-Pacific Left Main ST-Elevation Registry (ASTER). J Interv Cardiol 2018; 31: 129–135.
• 12.   Liu HW, Han YL, Jin QM, Wang XZ, Ma YY, Wang G, et al. One-year outcomes in patients with ST-segment elevation myocardial infarction caused by unprotected left main coronary artery occlusion treated by primary percutaneous coronary intervention. Chin Med J (Engl) 2018; 131: 1412–1419.
• 13.   Pepe M, Napodano M, Tarantini G, Fraccaro C, Cutolo A, Peluso D, et al. Percutaneous coronary intervention for unprotected left main disease in very high risk patients: Safety of drug-eluting stents. Heart Vessels 2011; 26: 17–24.
• 14.   Hurtado J, Pinar Bermudez E, Redondo B, Lacunza Ruiz J, Gimeno Blanes JR, Garcia de Lara J, et al. Emergency percutaneous coronary intervention in unprotected left main coronary arteries: Predictors of mortality and impact of cardiogenic shock. Rev Esp Cardiol 2009; 62: 1118–1124.
• 15.   Negishi Y, Tanaka A, Ishii H, Takagi K, Inoue Y, Uemura Y, et al. Contrast-induced nephropathy and long-term clinical outcomes following percutaneous coronary intervention in patients with advanced renal dysfunction (estimated glomerular filtration rate <30 ml/min/1.73 m(2)). Am J Cardiol 2019; 123: 361–367.
• 16.   TIMI Study Group. The Thrombolysis in Myocardial Infarction (TIMI) trial: Phase I findings. N Engl J Med 1985; 312: 932–936.
• 17.   Rentrop KP, Cohen M, Blanke H, Phillips RA. Changes in collateral channel filling immediately after controlled coronary artery occlusion by an angioplasty balloon in human subjects. J Am Coll Cardiol 1985; 5: 587–592.
• 18.   Jennett B, Bond M. Assessment of outcome after severe brain damage. Lancet 1975; 1: 480–484.
• 19.   Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002; 346: 549–556.
• 20.   Becker LB, Aufderheide TP, Geocadin RG, Callaway CW, Lazar RM, Donnino MW, et al. Primary outcomes for resuscitation science studies: A consensus statement from the American Heart Association. Circulation 2011; 124: 2158–2177.
• 21.   De Luca G, Suryapranata H, Thomas K, van’t Hof AW, de Boer MJ, Hoorntje JC, et al. Outcome in patients treated with primary angioplasty for acute myocardial infarction due to left main coronary artery occlusion. Am J Cardiol 2003; 91: 235–238.
• 22.   Chia PL, Khoo BC, Ng CK, Lim JT. Primary percutaneous coronary intervention for acute myocardial infarction secondary to acute left main coronary occlusion in an institution without on-site cardiothoracic surgical support. EuroIntervention 2009; 4: 617–619.
• 23.   Valeur N, Gaster AL, Saunamaki K. Percutaneous revascularization in acute myocardial infarction due to left main stem occlusion. Scand Cardiovasc J 2005; 39: 24–29.
• 24.   Sakai K, Nakagawa Y, Kimura T, Ando K, Yokoi H, Iwabuchi M, et al. Primary angioplasty of unprotected left main coronary artery for acute anterolateral myocardial infarction. J Invasive Cardiol 2004; 16: 621–625.
• 25.   Higami H, Toyofuku M, Morimoto T, Ohya M, Fuku Y, Yamaji K, et al. Acute coronary syndrome with unprotected left main coronary artery culprit: An observation from the AOI-LMCA Registry. Circ J 2018; 83: 198–208.
• 26.   Laver S, Farrow C, Turner D, Nolan J. Mode of death after admission to an intensive care unit following cardiac arrest. Intensive Care Med 2004; 30: 2126–2128.
• 27.   Brain Resuscitation Clinical Trial I Study Group. Randomized clinical study of thiopental loading in comatose survivors of cardiac arrest. N Engl J Med 1986; 314: 397–403.
• 28.   Raina KD, Callaway C, Rittenberger JC, Holm MB. Neurological and functional status following cardiac arrest: Method and tool utility. Resuscitation 2008; 79: 249–256.
• 29.   Stiell IG, Nesbitt LP, Nichol G, Maloney J, Dreyer J, Beaudoin T, et al. Comparison of the Cerebral Performance Category score and the Health Utilities Index for survivors of cardiac arrest. Ann Emerg Med 2009; 53: 241–248.
• 30.   Longstreth WT Jr, Dikmen SS. Outcomes after cardiac arrest. Ann Emerg Med 1993; 22: 64–69.
• 31.   Komeyama S, Takagi K, Tsuboi H, Tsuboi S, Morita Y, Yoshida R, et al. The early initiation of extracorporeal life support may improve the neurological outcome in adults with cardiac arrest due to cardiac events. Intern Med 2019; 58: 1391–1397.
• 32.   Baran DA, Grines CL, Bailey S, Burkhoff D, Hall SA, Henry TD, et al. SCAI clinical expert consensus statement on the classification of cardiogenic shock: This document was endorsed by the American College of Cardiology (ACC), the American Heart Association (AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019. Catheter Cardiovasc Interv 2019; 94: 29–37.
• 33.   Fox CS, Muntner P, Chen AY, Alexander KP, Roe MT, Wiviott SD. Short-term outcomes of acute myocardial infarction in patients with acute kidney injury: A report from the National Cardiovascular Data Registry. Circulation 2012; 125: 497–504.
• 34.   Yamaguchi J, Kasanuki H, Ishii Y, Yagi M, Nagashima M, Fujii S, et al. Serum creatinine on admission predicts long-term mortality in acute myocardial infarction patients undergoing successful primary angioplasty: Data from the Heart Institute of Japan Acute Myocardial Infarction (HIJAMI) Registry. Circ J 2007; 71: 1354–1359.
• 35.   Tarvasmäki T, Haapio M, Mebazaa A, Sionis A, Silva-Cardoso J, Tolppanen H, et al. Acute kidney injury in cardiogenic shock: Definitions, incidence, haemodynamic alterations, and mortality. Eur J Heart Fail 2018; 20: 572–581.
• 36.   Wang B, Han YL, Li Y, Jing QM, Wang SL, Ma YY, et al. Coronary collateral circulation: Effects on outcomes of acute anterior myocardial infarction after primary percutaneous coronary intervention. J Geriatr Cardiol 2011; 8: 93–98.
• 37.   Berry C, Balachandran KP, L’Allier PL, Lespérance J, Bonan R, Oldroyd KG. Importance of collateral circulation in coronary heart disease. Eur Heart J 2007; 28: 278–291.
• 38.   Joost A, Stiermaier T, Eitel C, Fuernau G, de Waha S, Desch S, et al. Impact of initial culprit vessel flow on infarct size, microvascular obstruction, and myocardial salvage in acute reperfused ST-elevation myocardial infarction. Am J Cardiol 2016; 118: 1316–1322.
• 39.   Rakowski T, Dudek D, Dziewierz A, Yu J, Witzenbichler B, Guagliumi G, et al. Impact of infarct-related artery patency before primary PCI on outcome in patients with ST-segment elevation myocardial infarction: The HORIZONS-AMI trial. EuroIntervention 2013; 8: 1307–1314.