Cardiogenic shock is the severest form of acute heart failure, with mortality rates reaching 50% when complicating acute myocardial infarctions.1 Venoarterial extracorporeal membrane oxygenation (VA-ECMO) has been used as an acute therapy for cardiogenic shock, because of its significant cardiopulmonary support and rapid deploy times.1–4 However, VA-ECMO is linked to adverse events such as bleeding, limb ischemia, and infection. In addition, retrograde aortic VA-ECMO flow can increase afterload to the left ventricle and lead to left ventricular distension—an under-recognized and under-reported complication on VA-ECMO with clinical consequences including pulmonary edema, ventricular arrhythmia, and myocardial ischemia.5 Several strategies for left ventricular decompression have been suggested, including intra-aortic balloon pump, balloon artrial septostomy, and additional cannulations into the pulmonary artery, left atrium, or left ventricle.6–9 However, such strategies may insufficiently unload the left ventricle or complicate acute mechanical circulatory support.10 , 11
In this context, the use of the Impella (Abiomed, Denvers, MA) percutaneous left ventricular assist device (pLVAD) has recently been proposed as a feasible, alternative approach to left ventricular decompression on VA-ECMO.10–13 This percutaneous microaxial flow pump sits across the aortic valve pulling blood from the left ventricle and expelling it into the aorta. Via this mechanism, this pLVAD has been shown to decrease left ventricular afterload, as evidenced by decreases in pulmonary capillary wedge pressures, pulmonary edema, and left ventricular end diastolic diameters.11 , 12 However, studies of left ventricular decompression with percutaneous left ventricular assist devices while on VA-ECMO have been limited to case reports and small case studies with mixed results.10–14 As more of such devices are used in the catheterization laboratory, addition of VA-ECMO to ongoing pLVAD support is becoming an increasing therapeutic modality; however, studies of combinatorial therapy in this context are absent. Such a strategy may improve hypoxia, right heart failure, and systemic blood flow.15
This study therefore examined our experience with concomitant use of VA-ECMO and Impella percutaneous left ventricular assist device (EC-VAD) for left ventricular unloading (by adding the Impella pump to VA-ECMO) as well as for management of insufficient systemic blood flow and hypoxia (by adding VA-ECMO to the Impella pump) in the context of refractory cardiogenic shock (RCS).
Materials and Methods
Patient Population, Data Abstraction, and Outcomes of Interest
The Columbia University Institutional Review Board approved this study with a waiver of consent from subjects. This study was a retrospective review of 29 patients who underwent concurrent VA-ECMO and Impella axial blood pump for RCS between the periods of January 2010 and October 2014. Subjects were divided into groups based on whether they first received VA-ECMO (group E→EC-VAD, n = 14) or the Impella pump (group I→EC-VAD, n = 15) for cardiogenic shock. Either Impella model CP (n = 8) or model LP 2.5 (n = 21) was used. Retrospective data extracted include the following: patient demographics, etiology of cardiogenic shock, hemodynamics and other clinical variables (e.g., complete blood counts, electrolytes), adverse events, and survival. Available records of the variables were collected at baseline, immediately postinitiation of mechanical circulatory support device monotherapy with the first device (VA-ECMO or Impella axial blood pump), and immediately before, immediately after, and 24 hours after initiation of combined device therapy (EC-VAD). Patients who received VA-ECMO alone for RCS in this time period (group ECMO-only, n = 196) served as a control group. The outcomes of interest were hemodynamic change with EC-VAD, 30-day survival, and adverse events.
The definition of cardiogenic shock has varied across the literature. This study used a previously reported definition of RCS: 1) a systolic blood pressure less than 90 mm Hg, a cardiac index less than 2.0 L/(min·m2), pulmonary capillary wedge pressure over 16 mm Hg (or evidence of pulmonary edema in the absence of a pulmonary artery catheter), and evidence of end-organ failure, or 2) the inability to be weaned off cardiopulmonary bypass for postcardiotomy shock despite maximal pharmacologic interventions and/or intra aortic balloon pump.4 For patients undergoing chest compressions at the time of VA-ECMO/Impella pump implant (1 I→EC-VAD and 40 ECMO-only patients), a systolic blood pressure of 60 mm Hg and a diastolic blood pressure of 20 mm Hg (mean arterial pressure, 33 mm Hg) were assigned. These values were chosen to represent the hemodynamic effect of adequate chest compressions in accordance with the prior studies.16
The etiology of RCS was categorized as postcardiotomy shock, acute myocardial infarction, graft dysfunction after an orthotopic heart transplant, acute decompensated heart failure, or other. Vasoactive-inotropic score was utilized to assess pharmacologic use (vasoactive-inotropic score = dopamine + dobutamine + milrinone × 10 + epinephrine × 100 + norepinephrine × 100 (all in µg/kg/min) + vasopressin (units/kg/min) × 10000).17 Myocardial recovery was defined as the ability to be weaned off mechanical circulatory support device therapy and survival to hospital discharge or 30 days after explant. Adverse events were defined in accordance with the Interagency Registry for Mechanically Assisted Circulatory Support definitions whenever appropriate.18 In this study, the definition of hemolysis was modified from the Interagency Registry for Mechanically Assisted Circulatory Support definition of minor hemolysis: a serum lactate dehydrogenase (LDH) greater than two and one-half times the upper limits of the normal range at the implanting center (normal LDH range at our center: 115–221 u/l) postdevice implant.18 To rule out elevated LDH secondary to liver dysfunction, this definition also requires an absence of elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels over three times their normal ranges (AST normal range, 12–38; ALT normal range, 7–41).
Algorithm for MCS Therapy in Cardiogenic Shock
The institution’s algorithm for evaluation and management of RCS has been reported elsewhere.4 In brief, when a patient with cardiogenic shock is identified, a Shock Team is activated to rapidly evaluate the patient’s condition.19 When indicated, a short-term ventricular assist device with CentriMag pump (Thoratec, Corp., Pleasanton, CA) or VA-ECMO is promptly inserted as a bridge to a more durable device or myocardial recovery.20
Venoarterial extracorporeal membrane oxygenation is usually used for patients with RCS that are too unstable to send to the operating room, have an unknown neurological status, or have severe coagulopathy.3 Depending on the clinical status of the patient and the emergency of the procedure, VA-ECMO is placed at bedside, in the catheterization laboratory, or in the operating room. The VA-ECMO circuit consists of Quadrox iD oxygenator (Maquet, Wayne, NJ), the Rotaflow centrifugal pump (Maquet,Wayne, NJ), and SMART-coating tubing (Sorin, Italy). Peripheral cannulation of VA-ECMO via femoral access with a small arterial cannula (15Fr-17Fr) is preferred whenever feasible.21
Occasionally, depending on the patient’s status in the catheterization lab, Impella LP 2.5 or CP System (Abiomed, Denvers, MA) is utilized instead of CentriMag or VA-ECMO as a bridge-to-decision at the operator’s discretion. The device is most commonly implanted percutaneously via femoral access, under fluoroscopic guidance. Further details regarding combined VA-ECMO and Impella axial blood pump implantation are reported elsewhere.12
Continuous variables were presented as mean ± 1 standard deviation. Categorical variables were expressed as proportions and absolute numbers. Nonnormally distributed variables were presented as medians and interquartile ranges (IQRs). Differences were detected using Fischer’s exact test for categorical variables. Wilcoxon signed-rank tests and Wilcoxon rank-sum tests were used for intragroup and intergroup analysis of nonparametric variables, respectively. To address missing data, pairwise exclusion of patients for individual analyses was incorporated. A p value < 0.05 was considered as statistically significant. All p values were results of two-tailed tests. StataSE version 13 (StataCorp, LP College Station, TX) was utilized for analysis.
Addition of Impella pLVAD to VA-ECMO (E→EC-VAD)
Among 29 EC-VAD runs, addition of the Impella pump to 14 individuals receiving ongoing VA-ECMO therapy occurred with a median interval of 12 hours (IQR, 4–26) for the following indications: pulmonary edema and/or hypoxia (n = 7), blood stagnation within the left ventricle (n = 5), and refractory ventricular arrhythmia (n = 2). Patient preoperative characteristics are summarized in Table 1. Summarizing all patients in the study, the median age was 57 (IQR, 46–67), and 69.3% of patients were male; these variables did not differ significantly among groups. Coronary artery disease was significantly more prevalent in group E→EC-VAD (n = 10, 71.43%) compared with group ECMO-only (n = 81, 41.33%, p = 0.047). Prevalence of diabetes mellitus was also greater in group E→EC-VAD (n = 8, 57.14%) than in group ECMO-only (n = 51, 26.02%, p = 0.026). Incidence of RCS secondary to acute decompensated heart failure was also higher in group E→EC-VAD (n = 5, 35.71%) than in group ECMO-only (n = 22, 11.22%, p = 0.017).
E→ EC-VAD intragroup analysis of differences in hemodynamics and laboratory values immediately before and 24 hours after initiation of EC-VAD are summarized in Table 2. By 24 hours after EC-VAD implant, E→EC-VAD patients demonstrated significant decreases in systolic (pre, 36.00 ± 16.84 mm Hg versus 24-hour, 30.63 ± 12.13 mm Hg, p = 0.049) and diastolic (pre, 24.25 ± 13.45 mm Hg versus 24-hour, 17.25 ± 7.96 mm Hg, p = 0.049) pulmonary arterial pressures. E→EC-VAD patients also demonstrated high vasoactive-inotropic scores before EC-VAD therapy, which decreased by 24 hours (pre, 27.67 ± 19.11 mm Hg versus post, 22.57 ± 15.57 mm Hg, p = 0.173).
Addition of VA-ECMO to Impella pLVAD
Addition of VA-ECMO to 15 patients receiving ongoing Impella axial blood pump therapy was performed with a median of 7 hours (IQR, 3–31) for more cardiac output (10) and cardiac arrest (5). I→EC-VAD preoperative characteristics were compared with that of ECMO-only patients (Table 1). Whereas post cardiotomy shock was the most common etiology of RCS within group ECMO-only (n = 80, 40.82%), no I→EC-VAD patients developed RCS from postcardiotomy shock (p = 0.001). Instead, there was a higher incidence of RCS developing secondary to acute myocardial infarction in group I→EC-VAD (n = 11, 73.33%) compared with group ECMO-only (n = 42, 21.43%, p < 0.001).
Intragroup analysis of I→EC-VAD hemodynamics before and after EC-VAD implant also demonstrated decreases in systolic (pre, 41.80 ± 17.46 mm Hg versus 24-hour, 23.20 ± 6.46 mm Hg, p = 0.043) and diastolic (pre, 20.60 ± 7.13 mm Hg versus 24-hour, 15.00 ± 4.58 mm Hg, p = 0.056) pulmonary arterial pressures (Table 3). Likewise, group I→EC-VAD demonstrated a reduction in vasoactive-inotropic scores following initiation of EC-VAD therapy (pre, 48.00 ± 29.11 mm Hg versus 24-hour, 15.27 ± 9.78 mm Hg, p = 0.080). Furthermore, the ratio of partial pressure arterial oxygen to fraction of inspired oxygen (PaO2/FiO2) significantly improved by 24 hours in group I→EC-VAD (pre, 148.55 ± 67.69 mm Hg versus 24-hour, 374.51 ± 170.97 mm Hg; p = 0.043). I→EC-VAD patients also demonstrated a significant increase in mixed venous oxygen saturation (SvO2) by 24 hours after EC-VAD implant (pre, 43.14 ± 16.75% versus 24-hour, 75.18 ± 13.88%, p = 0.043), and a significant reduction in lactate (pre, 5.57 ± 4.44 mg/dL versus 24-hour, 2.03 ± 0.64 mg/dL, p = 0.046).
Comparison of EC-VAD and ECMO-Only Hemodynamics
Intergroup analysis of all EC-VAD patient hemodynamics at baseline before any device insertion and 24 hours EC-VAD initiation were compared with that of group ECMO-only in Tables 4 and 5. At baseline, ECMO-only patients had a lower average mean arterial pressure compared with EC-VAD patients (EC-VAD, 71.70 ± 16.39 mm Hg versus ECMO-only, 60.11 ± 22.80 mm Hg, p = 0.012) (Table 4). Other baseline hemodynamics between EC-VAD and ECMO-only patients were not statistically significant (Table 4). Similarly, no statistically significant differences in hemodynamics, including pulmonary pressures, and PaO2/FiO2, were observed between EC-VAD patients and ECMO-only patients at 24 hours postinitiation of EC-VAD or ECMO therapy, respectively (Table 5). SvO2 was excluded from this analysis due to severely limited SvO2 data available for ECMO-only patients both at baseline and 24 hours post-ECMO insertion (7 of 196 patients).
Outcomes of EC-VAD Therapy
Overall outcomes comparing the EC-VAD subgroups with group ECMO-only are summarized in Table 6. Thirty-day survival was 49% in group ECMO-only, 47% in group I→EC-VAD, and 43% in group E→EC-VAD (p = 0.913). Survival to discharge was similar among the groups (36% in E→EC-VAD, 40% in I→EC-VAD, and 42% in ECMO-only, p = 0.911). In a Kaplan-Meier survival analysis, E→EC-VAD patients appeared to have earlier deaths (Figure 1); however, 30-day survival rates were similar between the three groups (p = 0.746).
Myocardial recovery was less frequent in EC-VAD patients (29% in E→EC-VAD, 27% in I→EC-VAD, and 39% in ECMO-only, p = 0.555). Transition to VAD was more common in group I→EC-VAD (n = 10, 67%) compared with group ECMO-only (n = 48, 24.49%, p = 0.001).
Regardless of group, most patients had a length of device support of 3 or 4 days, and a median hospital stay of about 29 days. Median ICU stay was longer in group I→EC-VAD (27 days; IQR, 8–34) compared with ECMO-only (16 days; IQR, 6–32), but this was not statistically significant (p = 0.931). No statistical difference in ICU stay was observed between ECMO-only and E→EC-VAD.
Adverse events are summarized in Table 7 comparing all EC-VAD patients to ECMO-only patients. Hemolysis was more common in EC-VAD patients (44.83% versus 17.35%, p = 0.002) though 4 EC-VAD and 17 ECMO-only patients were excluded from the analysis due to elevated transaminases. No EC-VAD patients developed infection post-EC-VAD implant, whereas 14% of ECMO-only runs were complicated by infection (p = 0.030). Differences in rates of other adverse events, including bleeding, limb ischemia, arrhythmia, or need for renal-replacement therapy, were not found to be statistically different between ECMO-only and EC-VAD patients.
This study evaluates concomitant use of VA-ECMO and a percutaneous left ventricular assist device for patients with RCS. It contributes to the growing, yet limited literature on this topic by describing this strategy in a relatively large number of patients. The study uniquely subcategorizes this therapy based on indications for addition of VA-ECMO to the Impella pump, and vice-versa. Among the primary findings of this study are that addition of Impella axial blood pump to VA-ECMO demonstrated reduction of pulmonary artery pressure and that addition of VA-ECMO to the Impella pump demonstrated reduction of pulmonary artery pressure and improvement in SvO2. Survival rates between EC-VAD and ECMO-only patients were also comparable in the study, and EC-VAD therapy did not significantly increase adverse events except for hemolysis.
Although there has been extensive research toward mechanical circulatory support device monotherapy for RCS, research involving combined device therapy is scarce. Furthermore, case reports and series on combined ECMO-Impella pump therapy have focused on evaluating the addition of the Impella pump to VA-ECMO for left ventricular venting.6–9 , 12 However, establishment of EC-VAD support in a reverse order of the device insertion is increasingly observed with the rising use of the Impella pump in the catheterization laboratory to support percutaneous coronary interventions in the presence of unstable hemodynamics and/or high risk, complicated coronary anatomy. These two cohorts have significant differences in demographics and response to the EC-VAD therapy as shown in this study.
Adding Impella to VA-ECMO
We have recently published the incidence and clinical implications of left ventricular distension during VA-ECMO support.22 Previous research has looked at using the Impella axial blood pump as a viable, percutaneous option for managing left ventricular distention secondary to ECMO-induced increased afterload in cardiogenic shock patients.10–13 Other options for treating left ventricular distension exist, such as percutaneous atrial septostomy, or central VA-ECMO cannulations with additional left atrial or left ventricular cannulas. These strategies are not without disadvantages. Surgical left-heart decompression through the insertion of a left atrial or left ventricular venting cannula carries a high risk of bleeding. Simple balloon septostomy may vent the left atrium adequately initially, but the defect is prone to spontaneously close. Atrial stenting may help circumvent this, but at an increased risk of malpositioning due to a thin, unstable atrial septum and potential impingement of adjacent structures.5
This study shows a similar result to a previous report of one of the first successful cases of percutaneous insertion of Impella model LP 2.5 for effective left ventricular decompression of an adult VA-ECMO patient.12 Similarly, analysis of E→EC-VAD patients immediately before and after EC-VAD implant demonstrated decreases in pulmonary pressures by 24 hours, suggesting effective left ventricular unloading by Impella pLVAD in VA-ECMO physiology (Table 2). The comparable survival rates between E→EC-VAD and ECMO-only patients, despite the former group developing significant complications such as left ventricular blood stagnation and pulmonary edema while on VA-ECMO alone, supports the hypothesis that EC-VAD therapy may preserve survival in otherwise challenging cases of RCS.
Adding VA-ECMO to Impella
It has been previously reported that addition of the Impella pump to VA-ECMO could not only reduce left ventricular distension, but also increase cardiac output and tissue perfusion.10 , 23 However, whether such improvements are a direct result of circulatory augmentation provided by the Impella pump is unclear. One hypothesis is that increased tissue improvements following the addition of Impella axial blood pump to VA-ECMO may reflect delayed perfusion improvements driven primarily by VA-ECMO.8 In group I→EC-VAD, EC-VAD support resulted in significantly better hemodynamics and oxygenation. Such a finding suggests that these pLVADs (Impella model LP 2.5 or model CP) alone may not provide adequate blood flow to patients in profound cardiogenic shock and/or that the cardiogenic shock in the present cohort had a greater component of right ventricular failure that could not be well supported by the Impella pLVAD. Having said that, given the fact that 11 of 15 patients who had received the Impella pump first had cardiogenic shock complicating acute myocardial infarction, the latter explanation is less likely (left heart failure was evidenced in each of the acute myocardial infarction cases with severe occlusion of the left main or left anterior descending coronary arteries).
EC-VAD Versus ECMO-Only Hemodynamics
It is important to note that except for a difference in baseline mean arterial pressure, no statistically significant hemodynamic differences were observed between EC-VAD patients and ECMO-only patients at baseline and after starting their respective devices therapies. The cohort size was too small to perform propensity score matching, but the results suggest that merely combining VA-ECMO with a percutaneous ventricular assist device may not be of benefit in patients already on ECMO monotherapy without clinically significant left ventricular distension and/or its sequela.
EC-VAD as a Therapy
The present study demonstrated comparable 30-day mortality, hospital stay, and ICU stay between EC-VAD and ECMO-only patients. However, the number of EC-VAD patients remains too small for making more rigorous outcome analyses.
A concern disfavoring this combined circulatory support device approach for left ventricular decompression is that the risk of adverse events common to such devices (bleeding, infection, hemolysis, and so on) may increase with multiple, concomitantly operating devices in a patient. Particularly, the risk of mechanical failure with multiple devices is of concern, since they are perceived to complicate a patient’s circulatory framework. In this case series, however, rates of many adverse events between EC-VAD and ECMO-only patients were similar. An important exception was increased hemolysis with EC-VAD. This makes theoretical sense in that simultaneous use of two devices that can individually cause hemolysis would exacerbate the event. Nevertheless, we did not observe a significant increase in need for continuous veno-venous hemodialysis in the EC-VAD cohort. Together, these findings characterize EC-VAD as a feasible device therapy in RCS.
There are several limitations in this study. Most conspicuous is the statistical power of the analyses, given the study’s cohort of 29 EC-VAD patients. Certain hemodynamic and laboratory results were especially underappreciated as they only reflect a subpopulation of our EC-VAD patients. Analysis of left ventricular distension was particularly limited by a lack of routinely collected pulmonary wedge pressures, as well as echocardiographic data, such as changes in left ventricular end diastolic dimensions following addition of pLVAD.
The clinical significance of hemolysis in this study remains unclear as clinical manifestations of hemolysis, such as urine discoloration and hemolysis-induced renal dysfunction, could not be investigated due to the retrospective nature of the data collection. An absence of routine plasma free hemoglobin or haptoglobin testing further limited the study’s analysis on the severity of hemolysis in this cohort. Routine baseline LDH testing was also not captured in this cohort, potentially leading to an overestimate of patients categorized as having hemolysis attributable to their device therapy.
This study was also limited in assessing Impella axial blood pump migration and malposition—known complications of Impella pump therapy—because these incidences were not reliably recorded. A lack of an Impella-only cohort prevented a more thorough analysis on the efficacy of isolated Impella pump therapy in RCS for this cohort. Importantly, cost analyses were not performed for this study, and such a combined therapy would certainly be under criticism for its high expense. Lastly, the study was limited by selection bias and other limitations intrinsic to retrospective analysis.
Combination of VA-ECMO with a percutaneous left ventricular assist device is a feasible treatment option. Furthermore, addition of ECMO to patients on the Impella pump may provide a viable means for immediate tissue perfusion and cardiac output augmentation as well as for improving oxygenation while also circumventing left ventricular distention associated with ECMO monotherapy. Rates of adverse events do not appear to be significantly increased while on this combined therapy; however, the risk minor hemolysis could be a concern. The present study suggests the feasibility, safety, and efficacy of the combined therapy. A further study in a large scale with a prospective fashion is warranted in order to confirm these findings and establish a therapeutic role of the EC-VAD therapy.
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Keywords:Copyright © 2019 by the American Society for Artificial Internal Organs
mechanical circulatory support; heart failure