Important role of mechanical circulatory support in acute myocardial infarction complicated by cardiogenic shock

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1 European Journal of Cardio-Thoracic Surgery 48 (2015) doi: /ejcts/ezu478 Advance Access publication 4 December 2014 ORIGINAL ARTICLE Cite this article as: Truby L, Naka Y, Kalesan B, Ota T, Kirtane AJ, Kodali S et al. Important role of mechanical circulatory support in acute myocardial infarction complicated by cardiogenic shock. Eur J Cardiothorac Surg 2015;48: Important role of mechanical circulatory support in acute myocardial infarction complicated by cardiogenic shock Lauren Truby a, Yoshifumi Naka a, Bindu Kalesan a, Takeyoshi Ota a, Ajay J. Kirtane b, Susheel Kodali b, Natasha Nikic a, Lily Mundy a, Paolo Colombo b, Ulrich P. Jorde b and Hiroo Takayama a, * a Department of Surgery, Columbia University Medical Center, New York, NY, USA b Department of Medicine, Columbia University Medical Center, New York, NY, USA * Corresponding author. 177 Fort Washington Ave, New York, NY 10032, USA. Tel: ; fax: ; hirofu2@hotmail.com (H. Takayama). Received 29 July 2014; received in revised form 21 October 2014; accepted 31 October 2014 Abstract OBJECTIVES: Acute myocardial infarction (AMI) complicated by cardiogenic shock (CS) remains associated with significant mortality despite the widespread application of early revascularization strategies. Recent evidence suggests that the use of intra-aortic balloon pump (IABP) counterpulsation does not improve mortality in this cohort of patients. We summarize our experience with mechanical circulatory support (MCS) therapy for AMI/CS. METHODS: This is a retrospective review of 61 patients who received MCS therapy for AMI/CS at our institution between March 2007 and March RESULTS: Mean age was 60.2 ± 10.3 years; mean ejection fraction was 24 ± 15% and 29% of patients were receiving active cardiopulmonary resuscitation at the time of support initiation. Prior to the initiation of MCS, 70.5% of patients had an IABP. Mean arterial pressure improved significantly with MCS (63 mmhg prior to MCS, 82 mmhg after MCS, P 0.01). Mean length of support was 9.5 ± 11.0 days, and overall survival to 30 days was 59.0%. Among 30-day survivors, 44.4% required device exchange to a durable MCS device. Ultimately, only 31% (52.8% of patients who survived to 30 days) achieved myocardial recovery. CONCLUSIONS: Short-term MCS therapy with subsequent aggressive use of durable MCS device may improve the unacceptably high mortality rate in AMI/CS. Rigorous prospective studies of MCS therapy in AMI/CS are warranted. Keywords: Acute myocardial infarction Mechanical circulatory support INTRODUCTION Despite decades of progress in risk factor modification and pharmacological therapy, Americans are hospitalized for new acute myocardial infarction (AMI) every year and will have a recurrent attack. Although the rates of death related to cardiovascular disease are declining, the burden of disease remains high, with coronary heart disease alone accounting for one in every six deaths in the USA [1]. Among these patients, cardiogenic shock (CS) is not uncommon, estimated to complicate 7 10% of AMIs [2]. Despite trends towards aggressive and early revascularization, mortality of AMI/CS continues to be 50 60%, approaching 80 90% in those with severe haemodynamic compromise [3]. Recently, the results of the Intra-Aortic Balloon Pump in Cardiogenic Shock II (IABP-SHOCK II) trial failed to demonstrate a mortality benefit with the use of intra-aortic balloon pump (IABP) counterpulsation a widely used adjuvant therapy in AMI/CS [4]. In light of the high mortality of AMI/CS and the failure of IABP to improve outcomes, the study of novel and innovative devices and therapies for AMI/CS is warranted [5]. Prior reported series of mechanical circulatory support (MCS) therapy for AMI/CS have been small and anecdotal [6 9]. Herein, we report our 6-year experience with MCS therapy for patients with AMI/CS. METHODS This is a retrospective, institutional review board-approved review of 61 patients who received MCS therapy for CS following AMI between March 2007 and March Due to the retrospective nature of the study, informed consent was waived. CS was defined as a state of organ hypoperfusion characterized by the following: (i) a systolic blood pressure of less than 90 mmhg for more than 30 min in the absence of hypovolaemia or pharmacological agents (e.g. vasopressors) required to achieve a systolic pressure of 90 mmhg, (ii) a decline in cardiac index The Author Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.

2 L. Truby et al. / European Journal of Cardio-Thoracic Surgery 323 (<1.8 l/min/m 2 without support or <2.2 l/min/m 2 with support) or (iii) elevated left ventricular (LV) filling pressures ( pulmonary capillary wedge pressure >18 mmhg) [10]. Our strategy for treating CS has been previously reported [11]. Patients presenting with ST-elevation AMI to our institution proceed directly to the catheterization laboratory for emergent revascularization whenever feasible. For patients with cardiopulmonary arrest or severe haemodynamic instability at any point during their hospital course, the interdisciplinary MCSD team is called to evaluate the patient. Prior to initiation of MCS, patients at our institution generally receive pharmacologic haemodynamic support and, in many cases, an IABP or other percutaneous ventricular assist device (VAD). Our devices of choice for acute circulatory support include percutaneous VADs [Impella 2.5, 5.0, CP (Abiomed, Inc., Danvers, MA, USA) and TandemHeart (CardiacAssist, Inc., Pittsburgh, PA, USA)], venoarterial extracorporeal membranous oxygenation (VA-ECMO) and a surgically placed short-term VAD [CentriMag VAD (Thoratec, Corp., Pleasanton, CA, USA)]. Only VA-ECMO and CentriMag VAD were considered to be a mechanical circulatory support device (MCSD) in the present study. We do not consider IABP and Impella 2.5 as devices of choice for severe CS due to insufficient circulatory support. In addition, our use of other percutaneous VADs is limited. Generally, biventricular support with the shortterm VAD is preferred for CS [12]. Generally, the inflow and outflow cannulation sites of the left ventricular assist device (LVAD) are the LV apex and ascending aorta, whereas those of the right ventricular assist device are the right atrium and the main pulmonary artery. The detailed insertion technique of the short-term VAD is described elsewhere [12]. In those patients with unknown mental status, severe coagulopathy, or who are too unstable to go to the operating room, VA-ECMO is utilized (Fig. 1). Whenever feasible, VA-ECMO is inserted percutaneously; the arterial cannula of Fr through the femoral artery and the venous cannula of Fr through the femoral vein. When ipsilateral pedal pulse signal is absent with Doppler examination, a 6- to 10-Fr cannula was inserted under surgical cut down into the superficial femoral artery to perfuse the limb. VA-ECMO is exchanged to a short-term VAD when prolonged support (>7 days) is expected. We do not use durable MCSDs as bridge-to-decision devices. While supported with the short-term device, patients are managed by the multidisciplinary MCSD team, and undergo evaluation for heart transplantation or implantable LVAD for destination therapy. Once a patient s general condition improves, the patient s myocardial function is evaluated by weaning the device under echocardiographic and haemodynamic monitoring. Depending on the result of these weaning studies and eligibility for heart replacement therapy, the short-term device can be explanted as a transition to one of the following destinations: durable MCSD, myocardial recovery or heart transplantation. For patients undergoing device exchange to durable MCSD, HeartMate XVE, or more recently HeartMate II and HVAD, LVADs are used for patients who need only left ventricular support. Thoratec Paracorporeal VAD, Implantable VAD or a total artificial heart are considered for those who need biventricular support. Basic demographics, past medical history and information regarding patient s hospital stay were collected. Laboratory values, haemodynamic parameters and use of inotropes and vasopressors were recorded immediately prior to and 24 h after initiation of the mechanical support. Data from the catheterization laboratory at the time of revascularization were also included. If the patient underwent right heart catheterization within 24 h prior to MCS, cardiac power output (CPO) was calculated as mean arterial pressure (MAP) CO/451. In patients who were undergoing active cardiopulmonary resuscitation (CPR), the following values were assigned: a systolic blood pressure of 60 mmhg, a diastolic blood pressure of 20 mmhg and a cardiac index of 0 l/min/m 2 [13]. These values were chosen to represent the haemodynamic effect of adequate chest compressions in accordance with the prior studies. Outcomes The primary outcome of interest was 30-day mortality. Other outcomes of interest included survival to discharge and myocardial recovery (defined as survival to 30 days or discharge from the hospital and recovery of native heart function as evidenced by ability TX & MCS Figure 1: Acute MCS decision algorithm. AMI: acute myocardial infarction; OR: operating room; VA-ECMO: venoarterial extracorporeal membranous oxygenation; LVAD: left ventricular assist device; OHT: orthotopic heart transplant.

3 324 L. Truby et al. / European Journal of Cardio-Thoracic Surgery Table 1: Patient demographics and preoperative characteristics by device Overall VA-ECMO CM P-value n =61 n =38 n =23 Age in years, mean ± SD 60.2 ± ± ± Male gender, % (n) 69 (42) 66 (25) 74 (17) 0.51 BMI (kg/m 2 ), mean ± SD 28.6 ± ± ± Hypertension, % (n) 56 (34) 53 (20) 61 (14) 0.53 Hyperlipidaemia, % (n) 46 (28) 42 (16) 52 (12) 0.44 Diabetes mellitus, % (n) 46 (28) 47 (18) 44 (10) 0.76 IABP, % (n) 71 (43) 55 (21) 96 (22) SBP (mmhg), mean ± SD 92.1 ± ± ± DBP (mmhg), mean ± SD 49.0 ± ± ± MAP (mmhg), mean ± SD 63.0 ± ± ± CVP (mmhg), mean ± SD 12.0 ± ± ± Lactate (mg/dl), median (IQR) 3.3 ( ) 3.0 ( ) 3.4 ( ) 0.55 ph, mean ± SD 7.3 ± ± ± Creatinine (mg/dl), mean ± SD 1.8 ± ± ± Active CPR, % (n) 29 (17) 37 (14) 14 (3) 0.07 VA-ECMO: venoarterial extracorporeal membranous oxygenation; CM: CentriMag; BMI: body mass index; IABP: intra-aortic balloon pump; SBP: systolic blood pressure; DBP: diastolic blood pressure; MAP: mean arterial pressure; CVP: central venous pressure; CPR: cardiopulmonary resuscitation; SD: standard deviation. to wean from mechanical support). Other outcomes included device exchange to a durable MCSD and orthotopic heart transplantation. Adverse events including infection, cerebrovascular accident and bleeding were defined according to the INTERMACS criteria. Statistical analysis Data are presented using mean values and standard deviations (SDs) for continuous variables and percentages for categorical variables. Those variables that are non-normally distributed are presented as medians and IQRs. Fisher s exact t-tests were used for comparison of means and Pearson s χ 2 test was used to compare categorical variables. Kruskal Wallis tests were used for non-parametric variables. Continuous variables were dichotomized using clinically appropriate thresholds. Because of the small number of patients reviewed and lack of sufficient power, univariate and multivariate analysis was not performed. Probit regression was used to generate predicted in-hospital mortality for varying levels of CPO. All Kaplan Meier survival estimates were created using survival days to last established contact with the patient. Stata/SE version 13 (STATA Corporation, College Station, TX, USA) was used for statistical analysis. RESULTS Patient characteristics Among over 400 patients who presented to our institution with ST-elevation AMI during the study period, a total of 61 patients received MCS therapy for AMI/CS. Initial MCSD was VA-ECMO in 38 patients and a short-term VAD in 23 patients. The average age of the patient was 60.2 ± 10.3 years and 69% were male (Table 1). Forty-eight percent of patients had triple-vessel coronary artery disease, when compared with 28% with two-vessel and 25% with Table 2: Distribution of coronary lesions and correlates of myocardial dysfunction Culprit vessel n =61 % LAD Left main Left circumflex 2 3 OM1, OM2 3 5 RCA 3 5 Coronary artery disease n =61 % Single vessel Double vessel Triple Revascularized Peak troponin ± Preop ejection fraction 24.3 ± 14.5 LAD: left anterior descending artery; OM: obtuse marginal artery; RCA: right coronary artery. single-vessel disease (Table 2). The culprit vessel was the LAD in 69% with the left main coronary artery being the second most common (16%). Seventy-five percent of patients were revascularized on the day of presentation with almost 90% undergoing primary PCI, with a median time to MCS of 1 day and mean of 4.0 ± 7.3 days. Overall, 71% of patients had an IABP placed prior to initiation of MCS therapy and 14.8% had a percutaneous VAD [Impella 2.5 LP (Abiomed, Inc.)]. Twenty-nine percent of patients were undergoing active chest compressions at the time of support initiation (37% of VA-ECMO patients). Mean peak troponin was ± µg/l with a median of 76.6 µg/l, and the mean preoperative ejection fraction of the overall cohort was 24 ± 15%. Mean length of support was 9.5 ± 11.0 days (3.8 ± 2.5 days for VA-ECMO and 18.8 ± 13.3 days for short-term VAD). Nine patients initially supported with VA-ECMO underwent device exchange to a short-term VAD for prolonged support.

4 L. Truby et al. / European Journal of Cardio-Thoracic Surgery 325 Table 3: Pre- and postoperative haemodynamics and laboratory values Table 4: Outcomes Outcomes Survival Overall VAECMO CM n Survival to discharge (%) day survival (%) Destination Myocardial recovery (%) Durable MCSD (%) MCSD: mechanical circulatory support device. Initiation of MCS resulted in significant improvements in haemodynamics (Table 3). MAP prior to MCS was 63 ± 25 mmhg, which improved to 82 ± 12 mmhg after initiation of the circulatory support (P < 0.01). BUN, creatinine and lactate tended to improve after the addition of MCS. Overall survival to 30 days was 59% (Table 4, Fig. 2). When the baseline characteristics of survivors and non-survivors to 30 days were compared, only a history of hyperlipidaemia was more likely to be found among survivors (58.3 vs 28.0%, P = 0.019) (Table 5). Among patients who survived to 30 days, 44% (n = 14) of patients were transitioned to a durable MCSD (11 to Heartmate II, 2 to Heartmate XVE and 1 to TAH). Common causes of in-hospital death included multisystem organ failure (n = 13), neurological non-recovery (n = 7) and asystole (n = 4). Eighteen patients had initial MCSD explanted for myocardial recovery during the index hospital stay with an additional 1 patient who had subsequent explant of a durable MCSD. Ultimately, 31% of the entire cohort (53% of those who survived to 30 days) achieved myocardial recovery. CPO was available in 36 of the 61 patients. Those patients who were undergoing active CPR were assigned a cardiac output of 0 l/min, and thus a CPO of 0 W as previously described [13]. Mean CPO prior to mechanical support was 0.43 ± 0.48 W. Based upon Before MCS After MCS a P-value 95% CI SBP (mmhg), mean ± SD 92.1 ± ± DBP (mmhg), mean ± SD 49.0 ± ± 2.9 < MAP (mmhg), mean ± SD 63.0 ± ± 1.9 < CVP (mmhg), mean ± SD 12.0 ± ± Mean PAP (mmhg), mean ± SD 33.6 ± ± Lactate (mg/dl), median (IQR) 4.3 ± ± ph, mean ± SD 7.3 ± ± 0.01 < Cr (mg/dl), mean ± SD 1.8 ± ± BUN (mg/dl), mean ± SD 33.1 ± ± Haemoglobin (g/dl), mean ± SD 12.0 ± ± 0.2 < AST (U/l), mean ± SD ± ± ALT (U/l), mean ± SD ± ± SBP: systolic blood pressure; DBP: diastolic blood pressure; MAP: mean arterial pressure; CVP: central venous pressure; PAP: pulmonary artery pressure; Cr: creatinine; BUN: blood urea nitrogen; AST: aspartate aminotransferase; ALT: alanine aminotransferase; SD: standard deviation. a 24 h after MCS initiation. Figure 2: Overall 30-day survival. findings from the SHOCK trial registry, a threshold of 0.53 W was utilized for bivariate analysis [14]. Lower levels of CPO were not significantly associated with an increased probability of 30-day mortality. When the probability of in-hospital mortality was generated based upon pre-mcs CPO values, the probability of in-hospital mortality was 50% for those with a CPO of 0 W decreasing to 30% at 0.69 W, which was the median of our cohort (Fig. 3). Among 30-day survivors, 17 were unable to recover native heart function. The number of vasopressors and inotropes used prior to MCS was associated with myocardial recovery without statistical significance (OR: 0.45, 95% CI: , P = 0.07). Peak troponin level was not a predictor of myocardial recovery. Adverse events INTERMACS-defined major bleeding occurred in 31%. Cerebrovascular accident occurred in 17% of the patients (3.3% haemorrhagic and 13.1% ischaemic). Among VA-ECMO patients, limb ischaemia requiring placement of a distal perfusion cannula TX & MCS

5 326 L. Truby et al. / European Journal of Cardio-Thoracic Surgery Table 5: Thirty-day survivors versus non-survivors Survivors Non-survivors P-value Age >65, n (%) 11 (44.0) 10 (27.8) 0.19 Male gender, n (%) 17 (68.0) 25 (69.4) 0.91 BMI >30, n (%) 13 (36.1) 9 (36.0) 0.99 History of hyperlipidaemia, n (%) 21 (58.3) 7 (28.0) History of diabetes mellitus, n (%) 17 (47.2) 11 (44.0) 0.80 History of hypertension, n (%) 21 (58.3) 13 (52.0) 0.62 History of COPD, n (%) 2 (5.6) 2 (8.0) 0.70 Pre-MCS IABP 27 (75.0) 16 (64.0) 0.35 Baseline mean arterial pressure <60 mmhg, n (%) 11 (39.3) 10 (47.6) 0.56 Baseline lactate >2.5 mg/dl, n (%) 9 (56.3) 5 (71.4) 0.50 Baseline ph <7.35, n (%) 13 (48.2) 7 (53.9) 0.74 Baseline creatinine >2 mg/dl, n (%) 8 (27.6) 5 (21.7) 0.63 Number of vasopressors and inotropes, mean ± SD 2.18 ± ± Revascularization prior to MCS, n (%) 30 (83.3) 18 (72.0) 0.29 Cardiac power output <0.53 W, n (%) 13 (54.2) 8 (66.7) 0.47 Pre-MCS ejection fraction 10%, n (%) 6 (28.7) 4 (23.5) 0.73 Peak troponin >227 ng/ml, n (%) 9 (32.1) 6 (28.6) 0.79 Same-day initiation of MCS, n (%) 12 (33.3) 11 (45.8) 0.33 Active CPR at MCS initiation, n (%) 9 (25.0) 8 (32.0) 0.55 BMI: body mass index; COPD: chronic obstructive pulmonary disease; IABP: intra-aortic balloon pump; MCS: mechanical circulatory support; CPR: cardiopulmonary resuscitation; SD: standard deviation. Bold values indicate significant of P values. Figure 3: Probability of in-hospital mortality based upon cardiac power output (CPO). or vascular surgery intervention occurred in 7 patients (11.5%). LV distension, requiring placement of surgical vent or decompression with a percutaneous VAD [Impella 2.5 LP (Abiomed, Inc.)], also occurred in 7 patients [15]. DISCUSSION Our analysis, one of the largest cohorts of MCS therapy in AMI/CS, demonstrated a 59% survival to 30 days among a particularly ill patient cohort. Among survivors, 53% were weaned to myocardial recovery and 44% were transitioned to a durable MCSD. Our survival is consistent with the previous studies reporting a 30-day survival ranging from 23 to 76% [7]. In 2001, Willms et al. published a series of 25 patients who received VA-ECMO for AMI/CS, demonstrating an overall survival of 23% [7]. A more recent series of 33 patients placed on VA-ECMO for AMI/CS published by Bermudez et al. demonstrated an improved 30-day survival of 64% [8]. Tang et al. reported an even better 30-day survival of 76% in 21 patients who had VA-ECMO for similar aetiology [9]. We have also summarized our experience of 27 patients who underwent CentriMag VAD insertion for various aetiologies of CS with an overall survival to discharge rate of 74% [16]. Thirteen of these patients developed CS secondary to AMI. By including all patients who received MCS therapy for AMI/CS, this study is unique in its focus on treatment strategy rather than a particular device. Comparing the outcomes of existing studies is not straightforward. Although the threshold for recognizing CS is well defined, as an entity it encompasses a broad spectrum of clinical and haemodynamic instability. As a result, variability in outcome is greatly influenced by the severity of the patients condition across studies. For instance Kagawa et al. reported their experience of combined therapy with VA-ECMO and PCI for AMI complicated by cardiac arrest, which is the most severe form of CS [17]. The 30-day survival was only 29%. Additionally, Sakamoto et al. recently published a series of 98 patients with AMI/CS complicated by CS (n = 34) or cardiac arrest (n = 64), with 32.7% surviving to discharge [18]. Based on the severity of haemodynamic instability in these cohorts, it is difficult to compare these outcomes to the aforementioned studies. The 30-day survival of 59% in our study compares favourably with the 53.3% in the SHOCK trial and the IABP-SHOCK II trial. In order to account for potential inter-study variability when comparing the present study with similar historical populations, we chose to focus on CPO: a metric found to be a significant predictor of in-hospital mortality in the SHOCK trial registry cohort [14]. Among the 406 patients with right heart catheterization data available from their registry, mean CPO was 0.62 W. In comparison, mean CPO in our cohort was 0.43 W. When the probability of in-hospital mortality was generated based on CPO, as it

6 L. Truby et al. / European Journal of Cardio-Thoracic Surgery 327 was in the SHOCK trial registry, predicted in-hospital mortality in our cohort appears satisfactory, particularly at lower levels of CPO. Interestingly, CPO was no longer a significant predictor of in-hospital mortality or 30-day mortality in our cohort. Even when patients undergoing CPR were excluded from the analysis, survival of those with the most severe degree of haemodynamic compromise approached 60% and CPO remained a nonsignificant predictor of in-hospital mortality (data not shown). Findings in the IABP-SHOCK II trial further support the need for more powerful device therapy in this patient population. While our study provides more evidence suggesting improved survival with MCS therapy in AMI/CS, no well-designed study has been conducted to definitively elucidate its role. In order to improve the unacceptably high mortality rate in AMI/CS, further investigation is warranted. It is possible that findings of such a study might lead to a paradigm shift in the current regime of AMI/CS therapy, from early revascularization to early revascularization and systemic flow restoration. Another important outcome of interest in this study was device explant to myocardial recovery. Previously published evidence suggests that the ability of MCS to unload the left ventricle may help promote myocardial recovery [19]. This is likely secondary to molecular remodelling following reduction of myocardial wall stress [20]. However, the physiology of VA-ECMO, one of the most widely used MCSDs in this cohort, exposes the damaged left ventricle to increased afterload with resultant increased wall stress [21]. The propensity for myocardial recovery has not been extensively studied in this patient cohort. Fifty-nine percent of survivors achieved this end-point in our cohort. Interestingly, variables such as culprit vessels, revascularization, peak troponin and CPO, which are associated with extent of myocardial damage and are often used clinically to predict myocardial recovery, were not found to be significant predictors of myocardial recovery in the present study. It is interesting to note, also, that despite VA-ECMO patients being more acutely ill at the time of device use, the rates of myocardial recovery are similar between VA-ECMO and Centrimag patients. While this could reflect the successful utility of the device in this acutely ill patient population, it could reflect the fact that Centrimag patients often have a longer time course of illness. Thus, while they appear more stable, they may have less ability to recover native heart function than those patients with a more acute insult. Only a history of hyperlipidaemia (OR: 2.79, 95% CI: , P = 0.07) and the number of vasopressors and inotropes used prior to MCS (OR: 0.45, 95% CI: , P = 0.07) were somewhat associated with myocardial recovery. Exchange to durable MCSD was performed in 44%, which is remarkably higher than 3.6% in the revascularization arm of the SHOCK trial. Aggressive use of heart replacement therapy might be one of the important reasons for better survival in our study. Percutaneous LVADs were not considered MCS therapy in the present study. To date, there have been three randomized trials evaluating the efficacy of percutaneous LVADs when compared with IABPs for patients with AMI/CS [22 24]. A meta-analysis of these trials included 100 patients, most with AMI/CS. Pooled survival data revealed the 45% 30-day mortality rate in LVAD patients to be non-significantly different from the 43% 30-day mortality among those treated with IABP (P = 0.80) [25]. In comparison to percutaneous VADs, VA-ECMO and surgical VADs are able to generate greater flows and can often be used for longer durations of support. However, newer generations of percutaneous LVADs that allow higher rates of flow are also likely to improve outcomes. Limitations Although these data represent one of the largest reported series of patients with AMI/CS treated with MCS, the overall power to detect independent correlates of clinical outcomes is limited. Additionally, this retrospectively conducted study does not capture the entire population (or denominator) of patients who presented to our institution with AMI/CS; as such, there is selection bias in the sample of patients who ultimately went on to require MCS. Inter-study comparisons (between our study with others previously published) are similarly difficult. CONCLUSIONS In our experience, the use of MCS was not only feasible for patients with AMI/CS, but was suggestive of improved survival compared with conventional management. Future studies to further elucidate the appropriate criteria and timing for device initiation could help to further improve outcomes. A prospective multicentre large-scale trial would aid in better evaluating the efficacy of MCS therapy in AMI/CS patients. Conflict of interest: Ulrich P. Jorde and Yoshifumi Naka receive consultant fee from Thoratec, Corp. REFERENCES [1] Go AS, Mozaffarian D, Roger VL, Benjamin EJ, Berry JD, Borden WB et al. Heart disease and stroke statistics 2013 update: a report from the American Heart Association. Circulation 2013;127:e6 e245. [2] Hochman JS, Sleeper LA, Webb JG, Sanborn TA, White HD, Talley JD et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. 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