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New Innovations in Circulatory Support With Ventricular Assist Device and Extracorporeal Membrane Oxygenation Therapy

Sladen, Robert N. MBChB, FCCM

doi: 10.1213/ANE.0000000000001629
Cardiovascular Anesthesiology

The past decade has seen an exponential increase in the application and development of durable long-term as well as nondurable short-term mechanical circulatory support for cardiogenic shock and acute or chronic heart failure. Support has evolved from bridge-to-transplant to destination therapy, bridge to rescue, bridge to decision making, and bridge to a bridge. Notable trends include device miniaturization, minimally invasive and/or percutaneous insertion, and efforts to superimpose pulsatility on continuous flow. We can certainly anticipate that innovation will accelerate in the months and years to come. However, despite—or perhaps because of—the enhanced equipment now available, mechanical circulatory support is an expensive, complex, resource-intensive modality. It requires considerable expertise that should preferably be centralized to highly specialized centers. Formidable challenges remain: systemic inflammatory response syndromes and vasoplegia after device insertion; postoperative sepsis; optimal anticoagulation regimens to prevent device-induced thrombosis and cerebral thromboembolism; wound site, intracranial, and gastrointestinal bleeding; multisystem injury and failure; patient dissatisfaction (even when providers consider the procedure a “success”); and ethical decision making in conditions of futility.

Published ahead of print December 15, 2016.

From the Department of Anesthesiology, Columbia University Medical Center, New York, New York.

Published ahead of print December 15, 2016.

Accepted for publication August 24, 2016.

Funding: None.

The author declares no conflicts of interest.

Reprints will not be available from the author.

Address correspondence to Robert N. Sladen, MBChB, FCCM, Department of Anesthesiology, Columbia University Medical Center, College of Physicians & Surgeons of Columbia University, 630 West 168th St, PH 527-B, New York, NY 10032. Address e-mail to

Table 1.

Table 1.

Figure 1.

Figure 1.

The medical and economic effect of heart disease in the United States is enormous. Today, an estimated 5.8 million Americans suffer from heart failure, representing 650,000 new cases annually with more than 1 million hospital admissions, more than 300,000 deaths, and a health care cost approaching $40 million per year.1 The latter part of the twentieth century saw steady development of mechanical circulatory support (MCS) for end-stage heart disease or circulatory shock. However, in the past decade, its utilization and applications have exponentially increased (Figure 1 and Table 1).2 This progress has been driven by the quarter million patients with advanced heart failure (New York Heart Association [NYHA] class IIIb or IV), of which a substantial proportion become refractory to medical management (American Heart Association stage D).

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Development of the Total Artificial Heart

In the 1960s, Congress approved the goal of developing a total artificial heart (TAH) for advanced heart failure. In 1967, the world’s attention focused on what was thought to be an exciting future for orthotopic heart transplantation (OHT), and, in 1969, Cooley et al5 used the first TAH, the Liotta-Heart, as a 3-day bridge to transplant (BTT). The obstacle of acute rejection stunted the application of OHT for the next decade, but with the introduction of cyclosporine in the early 1980s, transplantation reemerged as a viable therapeutic option. However, the supply of donor hearts was far less than the demand, to the extent that more than half of potential recipients died while awaiting a transplant. This drove the development of durable MCS to sustain recipients as a BTT. In 1982, the Jarvik-7 TAH kept a 61-year-old patient alive for 112 days,6 and, in 1985, Copeland et al7 achieved the first successful BTT with this device. The Jarvik-7 TAH underwent considerable modification before being approved as the Syncardia TAH for BTT in 2004.

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Development of the Left Ventricular Assist Device

The early 1990s saw the introduction of the “first-generation” left ventricular assist device (LVAD), the HeartMate XVE, which provided pulsatile circulatory support in series with the left ventricle (LV). A major watershed was the publication of the REMATCH study in 2001, which demonstrated that pulsatile LVAD support achieved a 1-year survival twice that of optimal medical management (OMM), approximately 50% vs 25%.8 However, the pulsatile LVAD was limited by its large size, extensive subdiaphragmatic pocket, loud noise, potential for bleeding and pocket infection, and unidirectional inflow and outflow porcine valves that deteriorated after about 12 months. It is no longer in use.

In 2007, the “second-generation” and first continuous flow LVAD (CF-LVAD) was introduced as the HeartMate II. This valveless impeller device provides axial flow from the LV apex to the ascending aorta, usually in parallel with the native circulation flowing through the aortic valve. It has a much smaller (although still subdiaphragmatic) profile than the XVE, and a dramatic improvement in durability. In a pivotal study that established the superiority of a continuous versus pulsatile LVAD, the HeartMate II provided significantly greater 2-year survival (58% vs 24%) and freedom from disabling stroke or device malfunction (46% vs 11%) than the XVE.9 This opened the door for durable LVAD support as destination therapy (DT) for patients who were not candidates for OHT.

The “third-generation” CF-LVADs introduced a miniaturized centrifugal device implanted intrapericardially into the apex of the LV. Examples include the HeartWare HVAD, which achieved a 180-day survival of 91% as BTT,10 and the HeartMate III, currently undergoing trials for BTT and DT. A comparison between axial flow and centrifugal flow devices is summarized in Table 2 and Figure 2. A “fourth-generation” CF-VAD is represented by a further miniaturized intrapericardial device, the MVAD, that combines both axial and centrifugal flow; and a so-called fifth-generation supradiaphragmatic impeller device, the HeartAssist 5, provides remote wireless monitoring via an integrated cell phone. By 2015, more than 15,000 durable implantable devices had been placed, with a current 1-year survival rate of more than 80%.4 The current status of durable CF-VADs is summarized in Table 3.

Table 2.

Table 2.

Table 3.

Table 3.

Figure 2.

Figure 2.

Some patients qualifying for a durable long-term device still have potential for myocardial recovery. Ventricular chamber volume unloading may promote reverse myocardial remodeling with a shift of the end-diastolic pressure–volume relationship back toward normal. Recovery may be further enhanced by neurohormonal blockade with angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and α-β antagonist therapy.1

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Unresolved Challenges of LVAD Implantation

Notwithstanding the dramatic advances in CF-LVAD therapy, formidable challenges remain. These include acute surgical bleeding, vasoplegic shock and systemic inflammatory response syndrome, acute right heart failure, device thrombosis, thromboembolic stroke, platelet dysfunction from acquired von Willebrand syndrome11, and recurrent gastrointestinal bleeding from the development of arteriovenous malformations.12 Although gastrointestinal bleeding is seldom fatal, it is responsible for frequent hospital readmissions and impaired quality of life (QOL). Stroke is the most devastating complication of MCS, especially when it occurs in young patients who are doing well as candidates for heart transplantation.

As a consequence of these complications, a certain proportion of patients will have a disproportionally prolonged intensive care unit (ICU) and hospital length of stay; recurrent readmissions to the hospital and ICU; and impaired QOL after hospital discharge. These are discussed in more detail in the section on The Continuous Flow Left Ventricular Assist Device.

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Development of Short-term, Nondurable Devices

In recent years, there has also been exponential development of short-term, nondurable devices for rescue therapy in cardiogenic shock, or to temporarily decompress the ventricles and enhance their recovery in acute heart failure. They may thereby serve as a bridge to recovery, or bridge to a decision regarding viability, transplantation, or a long-term VAD.

Short-term, nondurable MCS includes extracorporeal membrane oxygenation (ECMO); surgically implanted external centrifugal devices such as the CentriMag; and an increasing number of percutaneous devices (Table 4). Placement of these devices is currently transitioning from invasive sternotomy or minimally invasive thoracotomy performed by surgeons, to peripheral percutaneous placement increasingly done by cardiologists in the cardiac catheterization laboratory or at the bedside.

Table 4.

Table 4.

Prioritization for long-term device placement is based upon a consensus functional risk assessment profile called INTERMACS (International Registry of Mechanical Assistance of Circulatory Support), first established in 2007,3 and since updated annually (Table 5).4 By 2015, more than 15,000 patients were on the registry as having received durable long-term VADs.

Table 5.

Table 5.

Patients in cardiogenic shock (INTERMACS 1) or cardiogenic shock with intractable ventricular arrhythmias (INTERMACS 1A) may undergo percutaneous institution of ECMO with or without a short-term nondurable device as a bridge to recovery or decision. Currently accepted indications for a durable LVAD placement include patients at INTERMACS level 1 to 3, but, as device safety and longevity improve, there is an increasing hope that earlier placement (INTERMACS 4 or even higher) may become justified.

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Long-Term Durable Devices

The Total Artificial Heart

Syncardia TAH.

The first TAH, the Jarvik-7, was implanted in 1982. Subsequently, the device was enhanced and marketed as CardioWest, and currently as the Syncardia TAH. It comprises 2 pneumatically driven ventricles with 2 mechanical valves sewn into the atria and is capable of generating cardiac outputs of up to 9 L/min. It is primarily indicated for patients who are not candidates for an LVAD because of complications such as intractable ventricular tachyarrhythmias, an ischemic ventricular septal defect (VSD), intracardiac thrombus, congenital heart disease, or severe right heart failure (RHF). The TAH obviously cannot be used as a bridge to recovery.

In 2004, the Syncardia TAH was approved by the Food and Drug Administration (FDA) for BTT, and trials for DT are underway. The limitations of the Syncardia TAH have been its large volume displacement, which makes it largely unsuitable for female and small patients, and its massive console. A small portable console was introduced in 2012, and an option for smaller chambers (50 mL vs 70 mL) is in progress.

In 2012 Copeland et al14 published the results achieved at the University of Arizona in 101 patients who received the Syncardia TAH as BTT. Despite the fact that 90% of the patients were at INTERMACS 1 or 1A, the total group had n almost 70% survival to transplant and a less than 10% incidence of stroke, although there was a 25% incidence of take-back for bleeding. The authors concluded that the TAH provides a “real alternative” for patients who are not candidates for an LVAD, and who otherwise would be assigned to terminal hospice care. Nonetheless, implantation of the Syncardia TAH is largely confined to 3 major centers, 2 in Europe and 1 in the United States. About 1300 of these devices have been implanted over the last 3 decades, which represents less than 10% of all durable MCS.

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Development of the CARMAT TAH was initiated by Carpentier as long ago as 1993, and since 2008 has been developed by CARMAT SAS as a “second-generation” TAH.15 It consists of two 65-mL chambers covered by a flexible compliance bag with actuating fluid. Enhancements over the Syncardia TAH include noiseless electrohydraulic pumps that produce pulsatile flow; biocompatible processed bovine pericardial tissue membranes to decrease contact activation, thrombosis, and bleeding; and ventricular pressure sensors that govern a sophisticated control algorithm responding to changes in preload and afterload with a variable cardiac output (CO) range of 2 to 9 L/min.

Limitations of the CARMAT TAH are its large (750 mL) displacement, suitable for only 15% of female candidates; and its unknown long-term durability. If the sensors fail, the entire device must be replaced. By January 2016, a 3-year feasibility study had been completed on 4 patients, who survived between 2 and 8 months, and a pivotal study is underway.16

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The Continuous Flow Left Ventricular Assist Device

Advances in Hemodynamic Management.

The CF-VAD provides assisted flow that is in parallel to the native circulation, such that a variable proportion of the LV stroke volume is ejected via the native aorta. As a consequence, aortic valve function must be preserved, and the valve repaired or replaced if there is significant aortic stenosis or regurgitation. Continuous or intermittent opening of the aortic valve is an important safeguard against valve thrombosis, which may be exacerbated by inadvertently excessive oversewing of an incompetent valve. Conversely, if there is a known aortic valve thrombus (not uncommon in chronic advanced heart failure), it may be prudent to keep pump speed (rpm) at a level low enough to avoid aortic valve opening.

The proportion of ventricular ejection that flows through the device versus the aortic valve is dependent on the pump speed (rpm), and the pressure differential between the device inflow at the LV apex, and the device outflow into the aorta. Thus, the CF-VAD is both preload and afterload dependent. VAD preload (ie, LV filling) is determined by intravascular volume, right ventricular (RV) function, and pump speed.

An important hemodynamic variable monitored by most devices is the pulsatility index (PI), a unitless measure of systolic pump flow created by contraction of the native LV. The PI is the averaged magnitude of flow pulses over a defined time period, for example, 15 seconds. An increase in pump speed increases LV unloading and PI decreases; conversely, a decrease in pump speed decreases LV unloading and PI increases. Other displayed parameters include set pump speed in rpm, pump power (watts), and pump flow, which may be calculated from rpm and power (HeartWare II)—and therefore unreliable—or directly measured with centrifugal pumps (HeartWare HVAD and HeartMate III).

A “suction event” is a potentially devastating consequence of inadequate LV filling that results in acute obstruction of the VAD inflow by inward septal shift that in turn compromises RV outflow, triggers ventricular arrhythmias, and potentially results in circulatory collapse.17 It may or may not be heralded by sudden loss of power and PI. An urgent immediate intervention is to decrease pump speed and LV unloading, facilitating septal return and RV recovery. The most effective means of anticipating or diagnosing a suction event is by transthoracic or transesophageal echocardiography (TTE or TEE), which reveals conversion of the short-axis round LV to a “D”-shape induced by the flattened or convex intraventricular septum.18

Suction events are more likely to occur with axial than centrifugal flow devices (Table 2). The pressure differential between inflow and outflow at low flow states increases much more with axial pumps, so that they pull harder with a greater risk of ventricular suck down.19 The HeartMate II (an axial pump) has internal device algorithms that detect suction events when they occur, automatically decrease the pump speed, and allow time for providers to address the underlying cause. In contrast, because centrifugal pumps have greater accuracy in flow estimation, they can detect low-flow states and alarm before an actual suction event occurs.19

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Advances in the Management of Elevated Pulmonary Vascular Resistance and Right Heart Failure.

Cardiac modeling has demonstrated that the RV free wall comprises transverse fibers that contract with a bellows action and contribute only about 20% of the RV stroke volume.20 In contrast, the RV septum comprises oblique fibers shared with the LV septum, whose contraction contributes 80% of the RV stroke volume (systolic ventricular interaction). Using TEE, RV contractility can be quantitated by calculating the distance the tricuspid annulus moves toward the RV apex with systolic LV septal contraction, known as tricuspid annular plane systolic excursion (TAPSE). A TAPSE of <1.6 cm is indicative of RV systolic dysfunction.

Progressive LV failure increases left atrial pressure, which is indirectly measured by pulmonary artery occlusion pressure. This in turn increases pulmonary artery pressure and RV afterload, further increasing RV dependence on the interventricular septum for its ejection. Impaired LV septal contraction increases the effect of the increased pulmonary vascular resistance (PVR) in diminishing RV ejection fraction, leading to a vicious cycle of progressive RHF.

LV septal contraction is inevitably compromised in patients requiring a durable LVAD, so that RV output is highly dependent on the maintenance of low RV afterload, that is, a low PVR. Elevated PVR contributes to the acute RHF and impairs LVAD filling and output. Perioperative factors causing acute increases in PVR include hypoxemia, hypercarbia, endogenous or exogenous catecholamines, inflammatory responses to cardiopulmonary bypass (CPB), transfusion or protamine reactions, or acute respiratory distress syndrome induced by transfusion-associated circulatory overload or immunologic-mediated transfusion-related acute lung injury.

Maintenance of effective RV function is essential to achieve a good outcome after LVAD placement.18 Acute RHF may occur in up to 40% of patients receiving an LVAD21 and is associated with an increased risk of reoperation for bleeding and postoperative acute kidney injury, increased ICU length of stay, impaired LVAD success as BTT, and early mortality. About a third of the patients with RHF ultimately require a right ventricular assist device (RVAD).

The principles of the management of RV function include maintenance of RV coronary perfusion pressure by appropriate vasopressor therapy; prevention of RV volume overload by controlling right atrial pressure; avoidance of excessive RV afterload induced by iatrogenic pulmonary vasoconstriction; timely administration of inhaled pulmonary vasodilators such as nitric oxide and prostacyclins; and combined inodilator therapy with milrinone and dobutamine.18

There is as yet no long-term RVAD, and the primary long-term option for intractable right heart or biventricular failure remains the TAH. A more recent but as yet uncertain innovation is the combination of 2 miniaturized devices such as the HVAD simultaneously implanted into the left and right ventricle (Figure 5B).22

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Advances in Anticoagulation and Prevention and Diagnosis of Pump Thrombosis.

Pump thrombosis is an uncommon but potentially devastating complication of a durable LVAD, especially within the first 2 years of implantation. Predisposing factors may be related to the pump itself—nonpulsatile flow and sheer stress are inherently prothrombotic—or there may be inflow cannula malposition or kinking, or low pump flow. They may be exacerbated by inadequate anticoagulation and/or antiplatelet therapy because of patient noncompliance, genetic resistance, or suboptimal dosing. Intracardiac thrombosis may be induced by preexisting stasis or atrial fibrillation. Hypercoagulable states may be genetic (low levels of endogenous anticoagulant factors) or triggered by surgical stress, shock, or sepsis.

Early diagnosis hinges on looking for signs of hemolysis heralded by increasing lactate dehydrogenase levels above 500 IU/L, and progressive or intermittent increases in LVAD pump power. When the diagnosis is missed or delayed, patients may present with rapidly progressive LV failure or even cardiogenic shock.23 A definitive diagnosis can be achieved with a ramp study, where the pump speed is ramped up to its maximum with simultaneous echocardiographic and hemodynamic monitoring.24 Normally ramped pump speed results in progressive LV emptying and decrease in LV end-diastolic diameter, decrease in central venous and pulmonary artery occlusion pressure, and loss of aortic valve opening. Attenuation of these responses to speed ramping is highly suggestive of pump thrombosis.

Certain risk factors have been defined for pump thrombosis, including younger age, large body mass index, severe RHF, and noncompliance with medications.25 Once it occurs, there is a high likelihood of recurrence. The risk of pump thrombosis is decreased by strict compliance to a preventative protocol.26 There should be assiduous attention to pump pocket size and device placement, with careful positioning of the inflow cannula and outflow graft. Strict anticoagulation protocols should be followed, including heparin titrated to achieve a therapeutic partial thromboplastin time within 48 hours of surgery; early antiplatelet therapy with aspirin (plus dipyridamole in younger patients); and warfarin therapy titrated to an international normalized ratio of 2 to 3, depending on the device. Slow pump speeds, for example, <8600 rpm for the HeartMate II, should be avoided. Strict maintenance of mean arterial pressure <90 mm Hg has been shown to be especially important to prevent stroke induced by the HeartWare HVAD. Despite all this, on the basis of an individual patient, the yin and yang between bleeding and thrombosis remains unsolved.

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Innovations in the Continuous Flow Left Ventricular Device Development

HeartMate II.

The HeartMate II is a valveless pencil-like impeller pump that rotates at 8000 to 10,000 rpm and creates axial flow (Figure 3A). Although it is implanted in a subdiaphragmatic preperitoneal pocket, it is less than a quarter of the size of the pulsatile HeartMate XVE. It is FDA approved for both BTT and DT and is currently the most widely used LVAD with some DT recipients surviving 7 years or more.

Figure 3.

Figure 3.

In operating the HeartMate II, there is no built-in variability of pump speed, so rpm must be adjusted to allow some aortic valve opening to prevent thrombus formation. Ideally, the PI should be kept between 4.0 and 6.0. Pump flow is calculated, not measured, and is based on the power (watt) and rpm. At the extremes of flow, this calculation is subjected to error and may indicate “normal” flow in low-flow states such as cardiac tamponade.18

Between 2010 and 2013, a higher incidence of pump thrombosis (8.4% vs 2.2%) and earlier onset (3 vs 18 months) was noted with the HeartMate II in 3 major implantation centers.27 Medical management alone with aggressive heparin anticoagulation and/or thrombolysis with tissue plasminogen activator was associated with a 50% mortality rate in the ensuing 6 months, and improved survival required urgent OHT or VAD replacement. However, by 2014, this trend had started to reverse, perhaps reflecting earlier diagnosis.25 Subsequently, preliminary findings of the PREVENT study demonstrated a substantial reduction in the 3-month incidence of VAD thrombosis, using a protocol that paid careful attention to inflow cannula and outflow graft positioning, anticoagulation, adequacy of pump speed (>8600 rpm), and tight blood pressure control.26

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Jarvik 2000.

The Jarvik 2000 is a unique miniaturized titanium axial flow device with an integrated inflow placed directly into the apex of the LV, with an efferent conduit placed either into the ascending or descending aorta.28 The latter facilitates placement via a left minithoracotomy, sparing sternotomy. The driveline is threaded within the thoracic cavity to emerge at an occipital retroauricular skull-mounted pedestal, which substantially decreases the risk of VAD pocket infection and increases the patient mobility.29

The Jarvik 2000 controller is extremely simple, consisting of a watt meter and a “five gear” rpm setting adjustable by the patient between 1 and 5 (8000 to 12,000 rpm). Every minute the device decreases its output for 8 seconds to allow aortic ejection, maintain aortic valve function, and minimize thrombus formation. One limitation of the Jarvik 2000 is that its peak outflow is about 7 L/min, so it is suited for smaller patients or those with greater intrinsic LV function.

A nonrandomized pivotal clinical trial on 150 patients in the United States was completed in 2012 ( NCT00591799), and the prospective, controlled RELIVE trial comparing with to the HeartMate II in 350 patients for DT is currently in progress ( NCT01627821).

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HeartWare HVAD.

The HeartWare HVAD is a miniaturized centrifugal device in which the inflow cannula is cored directly into the LV apex so that the device is intrapericardial and entirely above the diaphragm (Figure 3B).30 It has a driveline that is exteriorized and attached to small portable battery packs. A major advance is that through magnetic or hydrodynamic levitation, there is no contact between the impeller and the drive mechanism, with minimal blood contact. The impeller rotates centrifugally more slowly than the rotary devices, at 2750 to 3000 rpm. The advantages claimed are decreased hemolysis and thrombogenesis and greater mechanical durability.

The HVAD was FDA-approved for BTT in 2012, and its use has been associated with a 91% 6-month survival and 84% 1-year survival.10 However, the ENDURANCE trial,31 which compared the HVAD with the HeartMate II for DT approval, demonstrated a 3-fold higher incidence of ischemic and hemorrhagic stroke, 28.7% vs 12.1% (data presented at the 35th ISHLT Meeting in 2015). The major risk factor identified was a mean arterial pressure >90 mm Hg. Other factors associated with an increased risk of stroke included the use of low-dose aspirin ≤81 mg/day and an international normalized ratio <2. In the original HVAD, the inflow cannula is made of a highly polished titanium alloy that promotes tissue ingrowth that may be prothrombogenic. Subsequently, titanium microspheres were sintered (heated and coalesced without liquefaction) onto the external surface, and markedly impede the tissue ingrowth.32 A follow-up study, the ENDURANCE Supplemental Trial ( NCT01966458) is currently investigating the effect of tight blood pressure control on stroke incidence with the HVAD.

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HeartMate III.

The HeartMate III is a third-generation centrifugal-flow pump seated in an intrapericardial pocket and is essentially an enhanced, miniaturized CentriMag pump (Figures 3C and 4). Its major advantage is its fully magnetically levitated rotor with wider blood flow gaps that theoretically minimize red blood cell damage, thrombus formation, and von Willebrand syndrome.33 Rotor speeds that alternate every 2 seconds promote pulsatile flow that contributes to these benefits. Sintered titanium microspheres on surfaces making contact with blood promote endothelial ingrowth to diminish the probability of contact-activated thrombus formation, much like the HeartMate XVE. The controller display is identical to the HeartMate II, except that pump speed is typically kept 3000 to 5000 rpm; pump flow is directly measured and therefore reliable, and the PI goal is lower, between 3.0 and 5.0.

Figure 4.

Figure 4.

The U.S. MOMENTUM 3 study ( NCT02224755) is actively randomly assigning more than 1000 patients to HeartMate III or HeartMate II to study its efficacy and safety as for BTT and DT.

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HeartWare MVAD.

The MVAD is an innovative, miniaturized (22-mL volume displacement) VAD device that combines centrifugal and axial flow into a tiny longitudinal pump implanted via a minithoracotomy into the LV apex without requiring CPB, and with an outflow cannula that passes through the aortic valve to just proximal to the innominate artery. As such it provides antegrade ejection alongside the native flow that can be varied from full to partial assist by virtue of a pump speed between 12,000 and 22,000 rpm.34 The platinum alloy impeller is suspended in a ceramic tube by passive magnetic and hydrodynamic forces. A gimbal sewing ring allows modification of device direction and pump depth, with the potential for RV placement and biventricular assist device (BiVAD) support. Introduction of the MVAD has been somewhat beset by technical problems, including pump thrombosis. The nonrandomized MVAdvantage Trial ( NCT01831544) was designed to study MVAD safety and performance in 70 subjects with NYHA IIIB or IV heart failure over 24 months, with a primary end point of survival at 6 months. It is currently on hold.

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HeartAssist 5.

The HeartAssist 5 (for “fifth generation”) is an axial flow impeller device modified from the MicroMed DeBakey Noon VAD developed as long ago as 1988. It was first implanted in Berlin in 1998 for BTT, and in the United States in 2002.35 Since then it has undergone numerous technical modifications to attempt to decrease thrombus formation. It is an external device similar in configuration to the HeartMate II, but considerably smaller (92 vs 282 g) and is placed in an extrapericardial supradiaphragmatic pocket. The most sophisticated aspect of HeartAssist 5 technology is that it incorporates a wireless transmitter that provides continuous data acquisition that can be captured by a computer or smartphone, with a patient home support system called HeartAttendant that can transmit alarm alerts to a support center ( A randomized prospective study on just under 200 patients is active, comparing 180-day success among the HeartAssist 5, HeartMate II, and HVAD ( NCT02205411).

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Challenges and Further Innovations in the Continuous Flow Left Ventricular Device Support

Biventricular Assist Device (BiVAD) Support.

Refractory RHF is estimated to occur in as many as 30% of patients who have a durable CF-LVAD.36 Short-term RV support can be provided by an increasing array of surgically placed or percutaneous devices (see below), but until very recently, the primary option for durable RV support has been the placement of a TAH.14

There have been isolated case reports of BiVAD application of the Jarvik LVAD. The first, in 2004, utilized a previous version, the Jarvik Flowmaker, to provide support with an apical LVAD coupled with a right atrial device, but the patient succumbed after 12 days (Figure 5A).37 In 2014, a Japanese group reported a successful BiVAD with the Jarvik 2000 placed in the left and right ventricles.38 After a 2-year course, the RVAD started to fail, but the patient was able to undergo life-saving OHT. Most recently, Brenner et al39 reported a case series of 3 severely ill patients who received biventricular Jarvik support. Two patients died of other causes at 3 and 50 days postoperatively, and 1 died a year later after RVAD pump shutdown.

Figure 5.

Figure 5.

The most successful experience thus far is that of the group at the Berlin Heart Center, using 2 HVAD devices, with the RVAD implanted into the RV free wall (Figure 5B).22 In 2011, they reported on their experience with 17 patients, who had an 82% 30-day survival, and 59% were discharged from hospital. Two key technical innovations were to avoid excessive pulmonary blood flow and pulmonary edema by reducing the graft outflow diameter to increase RVAD afterload, and 2 silicon suture rings were used to shorten the length of the inflow cannula. The RVAD speed was adjusted between 2400 and 3800 rpm based on central venous pressure, with the LVAD adjusted to provide maximal flow. In 1 patient, who had a compressed RV, the RVAD was successfully repositioned in the right atrium. Two patients had delayed RV recovery and underwent successful RVAD decannulation. In a case report from Germany, a patient with cardiogenic shock secondary to a massive ischemic ventricular septal defect was successfully bridged to transplant 14 weeks after BiVAD implantation of 2 HVAD.40

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Maintenance of Arterial Pulsatility.

Nonpulsatile continuous flow appears to promote the development of arteriovenous malformations throughout the gastrointestinal tract that predispose to recurrent gastrointestinal bleeding.1 Bleeding is exacerbated by acquired Von Willebrand syndrome, which appears to be because of the sheer stress–induced activation of a metaloprotease, ADAMTS-13 that cleaves off the high-molecular-weight multimers essential for platelet activation by von Willebrand factor.41

Continuous flow with the absence of aortic valve opening predisposes to valve thrombosis. Over time, the aortic valve commissure starts to fuse, and about 30% of all long-term VAD patients develop some degree of aortic regurgitation that may require surgical intervention.

A number of strategies have been developed to enhance pulsatility and intermittent aortic valve opening, which may prevent valve or chamber thrombus formation by inhibiting stasis or recirculation zones. These include periodic rpm slowing (Jarvik 2000) or pump speed modulation that generates intrinsic pulsatile flow from the LVAD (HeartMate III). Pump speed manipulation may be asynchronous or synchronous, that is, independent of or consistent with the native heart rate.1 Synchronous pump speed manipulation can maximize LVAD flow during LV systole (copulsation) or diastole (counterpulsation). The latter favors LV unloading, diminished LV pressure work, and the potential for remodeling and recovery.

In the near future, devices will incorporate speed modulation algorithms that adjust device output during exercise, fluctuations in blood pressure, and arrhythmias.

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Transcutaneous Energy Transfer.

The development of a safe, effective transcutaneous energy transfer (TET) system for durable ventricular support devices has been in progress for more than 3 decades.42 The TET system uses electromagnetic induction to transfer power from a transmitter coil belt worn by the patient to a small power system implanted alongside the VAD. By eliminating the driveline and its potential for infection, the TET system could provide total device implantability and markedly improve patient acceptance and QOL. A number of challenges remain, including the potential for electrical burns, infection of implanted material, and component durability. Although many devices have been patented, at this stage, investigations remain confined to animal studies.43

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Nondurable devices are placed for emergent short-term rescue of acute heart failure or cardiogenic shock; as bridge to recovery, for example, for postcardiotomy shock, acute myocarditis, or acute myocardial infarction; or as a bridge to decision if recovery is not immediate (Table 4). Surgical implantation is rapidly being supervened by percutaneous placement in the cardiac catheterization laboratory. Decision making is often complex because these devices are inserted urgently or emergently, but consideration must be taken of advance directives (do not resuscitate, do not intubate), terminal illness, rescue after protracted cardiopulmonary resuscitation, severe neurologic injury, or severe sepsis.

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Intraaortic Balloon Pump

The intraaortic balloon pump (IABP) is a short-term counterpulsation device introduced a half-century ago. It augments cardiac output by not more than 0.5 L/min, and its primary function is to enhance myocardial oxygen balance during acute myocardial ischemia. Placed percutaneously via the femoral artery into the descending aorta, balloon inflation provides diastolic pressure augmentation that increases coronary perfusion pressure (CPP) and myocardial oxygen supply, whereas subsequent deflation decreases LV afterload and myocardial oxygen supply. Major limitations include the requirement for a competent aortic valve and stable heart rate and rhythm; inability to mobilize the patient; and complications related to leg ischemia, bleeding, or thrombosis.

Although the IABP is often a successful first line of support for post-CPB shock because of the short-lived ischemia reperfusion injury, cardiologists still frequently place an IABP as primary support for cardiogenic shock. However, the large (600 patient) Shock II trial demonstrated no difference in 1-year survival whether or not an IABP was placed in patients with cardiogenic shock complicating acute myocardial infarction where early percutaneous or surgical coronary revascularization was planned.44

Femoral veno-arterial (VA) ECMO increases LV afterload because its arterial output is retrograde to native aortic outflow. Counterpulsation by IABP placement could be an important means of decreasing LV afterload. Although there is evidence that the combination of IABP with ECMO enhances coronary graft flow,45 and decreases pulmonary artery pressures and LV dimensions, no improvements in microcirculation46 or outcome47 have been demonstrated.

Another innovation is the placement of the IABP via the subclavian or axillary artery, which allows full patient mobilization, and may provide a much longer-term support as a bridge to recovery, VAD, or transplant.47,48

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Thoratec CentriMag

The Thoratec CentriMag, introduced in 2007, is an external, short-term device, whose magnetically levitated centrifugal pump was the forerunner for that incorporated into the HeartMate III. Separate circuits and pumps may be utilized as an isolated LVAD (inflow from left atrium, outflow to aorta), or RVAD (inflow from right atrium, outflow to pulmonary artery) or BiVAD.49 The small cannulas (7 mm) facilitate surgical rapid placement during cardiac surgery or via a new sternotomy. A bedside console displays rpm and ultrasound-sensed flow rate. A membrane oxygenator is easily placed in the RVAD circuit to support acute lung injury.50

Cannula vibration or “chatter” may reveal hypovolemia or excessive ventricular emptying, although it may also be induced by return of ventricular contractility. The CentriMag LVAD is FDA approved for 6 hours only, but in clinical practice, it is left in place for considerably longer—days to weeks.51 The CentriMag RVAD is FDA approved for up to 30 days for acute RHF.

Since its introduction in 2003, the CentriMag has become established as the predominant medium-term device for pre- and postcardiotomy cardiogenic shock; posttransplant graft rejection or failure; and acute RHF after LVAD placement, with survival rates between 60% and 80%. The CentriMag may serve as a bridge to recovery, or a bridge to decision, that is, whether the patient is a candidate for a long-term LVAD as BTT or DT. In about 25% of cases, it is placed as a part of an ECMO circuit (see Veno-Arterial Extracorporeal Membrane Oxygenation).

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Veno-Arterial Extracorporeal Membrane Oxygenation

In the half-decade between 2006 and 2011, application of adult ECMO has increased more than 4-fold in the United States.52 VA-ECMO is analogous to CPB, in which the function of the heart is replaced or supplemented by the ECMO pump, with or without lung replacement. VA-ECMO is primarily instituted as rescue therapy in cardiogenic shock; as a bridge to recovery; or, more often, as a bridge to a decision. It supports circulatory resuscitation and stabilization, allows assessment of neurologic status, facilitates myocardial recovery, and evaluation of patient candidacy for VAD or transplant.53,54 There is an increasing application of VA-ECMO for refractory cardiac arrest, so-called extracorporeal cardiopulmonary resuscitation or E-CPR. When combined with mechanical CPR, therapeutic hypothermia, and, when indicated, primary percutaneous coronary intervention (PCI), good neurologic outcomes and survival rates as high as 54% were reported in the CHEER Trial.55 However, best outcomes are predicated on initiation of VA-ECMO within 30 minutes of cardiac arrest.

For many years, the provision of postoperative VA-ECMO essentially required a CPB machine at the bedside, staffed full-time by a perfusionist. However, in the past decade, there has been remarkable miniaturization and improvement in safety. The development of a polymethylpentene (PMP) membrane oxygenator (Quadrox-D)56 driven by a small centrifugal pump reduces the footprint of the device to one that can be mounted on an IV stand. The PMP membrane avoids the plasma leakage associated with conventional hollow-fiber oxygenators and decreases—but does not eliminate—the risk of thrombogenesis. Indeed, thrombocytopenia, coagulopathy, disseminated intravascular coagulation, bleeding, blood and blood product transfusion, stroke, sepsis, and dialysis-dependent acute renal failure continue to be formidable risks in these very sick patients. Depending on the circumstances, overall in-hospital mortality with VA-ECMO varies between 35% and 80%.57,58

Central VA-ECMO is provided for intractable cardiac failure in the operating room (OR) and is essentially a continuation of the CPB circuit, that is, venous cannulation of the atria or superior vena cava with arterial cannulation of the aorta. The latter provides high anterograde flow of oxygenated blood to the heart and brain, with LV afterload reduction. However, the sternum has to be left open, so within 24 to 48 hours, the patient either has to recover sufficiently to be weaned off central ECMO or transitioned to another modality such as peripheral ECMO or CentriMag.

Peripheral VA-ECMO can be placed relatively quickly via femoral venous and arterial cannulas in the cardiac catheterization laboratory, OR, ICU, or emergency department. However, there are a number of potentially adverse effects, not the least of which is the inability to mobilize the patient. ECMO flow is limited by the arterial cannula diameter, but the greater the size relative to the native femoral artery, the greater the risk of arterial occlusion and limb ischemia. In the worst case, this may result in muscle edema, a fascial compartment syndrome, severe rhabdomyolysis, and acute renal failure. Prevention requires the placement of a reperfusion catheter adjacent to the arterial cannula or in the posterior popliteal artery.59

Retrograde oxygenated arterial inflow via a femoral cannula may not reach the heart and brain, especially via the right carotid artery, because it competes with the native aortic output. Arterial oxygenation (Spo2) should always be monitored by a pulse oximeter on the right hand, to better reflect the Spo2 of blood reaching the brain. In an extreme case, the patient’s head may appear blue, whereas the legs appear red, the so-called Harlequin syndrome.13 This situation becomes dire with acute hypoxemic respiratory failure, necessitating additional venovenous circuits (VAV-ECMO) to the upper vasculature to ameliorate this situation.60

Retrograde femoral arterial ECMO flow increases LV afterload, LV end-diastolic volume (LVEDV), and LV end-diastolic pressure (LVEDP). It may thereby induce pulmonary congestion and edema, adversely affect myocardial oxygen balance, and decrease the potential for LV recovery. This effect is exaggerated when LV function is severely impaired and the chamber is distended.13 Increased LV afterload may be ameliorated by decreasing ECMO flow, but this compromises circulatory support. Inotropic support with drugs such as dobutamine and/or milrinone may improve intrinsic LV contractility but increases the risk of ventricular tachyarrhythmias. Concomitant use of an IABP or ventricular decompression by an Impella device (Abiomed, Danvers, MA) may decrease LV afterload and chamber distension but can impede blood flow and oxygenation to the head. The most expeditious solution is to decompress the LV by an apical vent that is then spliced into the ECMO circuit.61

Figure 6.

Figure 6.

Innovative circuitry systems provide useful alternative approaches to VA-ECMO.62,63 As illustrated in Figure 6A, the arterial inflow cannula can be grafted percutaneously into the right axillary and subclavian artery. This ensures superior oxygenation of the head and brain, as well as anterograde flow into the aortic arch. Care must be taken not to “flood” the arm with blood, but this can be ameliorated by placing a snare on the cannula. The venous cannula drains deoxygenated blood from the inferior vena cava, as per standard VA-ECMO, and then returns it to the arterial circulation via a pump and oxygenator. A major innovation is placing an arterial outflow cannula as an LV vent into the ventricular apex via a minithoracotomy and splicing it into the VA-ECMO circuit just before the pump. With the aid of the oxygenator, the patient can be weaned from mechanical ventilatory support and proceed to tracheal extubation. When lung function improves, the femoral venous cannula and oxygenator are removed, leaving what is essentially a peripheral CentriMag LVAD circuit in place (Figure 6B). This facilitates early mobilization and ambulation and minimizes the potential for ICU-related complications such as ventilator-associated lung injury, delirium, muscle weakness, and bedsores. The circuit may serve as a bridge to recovery or to a long-term VAD. If the latter is required, the percutaneous minithoracotomy approach decreases the bleeding and inflammatory response associated with reopening a previous median sternotomy to place a durable LVAD.

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The TandemHeart is a versatile percutaneous VAD (pVAD) that utilizes an external centrifugal pump. It can be placed percutaneously or by open surgical cannulation and can support the LV, RV, or both.64 For LVAD support, a femoral vein cannula is passed into the right atrium and thence across the intraatrial septum into the left atrium, from which it withdraws oxygenated blood and pumps it into a femoral artery cannula. Support of the RV may be provided by a surgically placed right atrial cannula that drains venous blood and pumps it via an oxygenator into a surgically placed pulmonary artery cannula. Alternatively, using imaging, a specialized triple lumen cannula can be passed percutaneously into the pulmonary artery. Right atrial blood is drawn into the cannula via 2 orifices and then pumped via an oxygenator through a channel that terminates in the pulmonary artery.

The TandemHeart provides several advantages. It decompresses the left atrium and LV, and decreases LVEDV, LVEDP and myocardial oxygen demand, but this may be offset by its retrograde aortic flow. Compared with the IABP in cardiogenic shock, the TandemHeart provides enhanced end-organ perfusion with decreased lactate levels, but no difference in 30-day mortality (45% vs 43%). Although introduced as a short-term rescue device, the TandemHeart has met with some success as bridge to a durable VAD or transplantation.65,66

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The Impella System

The Impella system comprises a family of short-term, nondurable multiport pigtail axial devices to provide LV rescue in cardiogenic shock, support hemodynamically unstable patients in the cardiac catheterization laboratory during PCIs, or to decompress a distended LV during VA-ECMO.13 The catheter is placed via the femoral artery across the aortic valve and pumps in series with the LV outflow. Unlike the IABP or Tandem Heart, the Impella decreases LV preload without increasing afterload, thereby enhancing myocardial oxygen balance.

A series of increasingly large devices named for the maximal flow augmentation in liters per min (Impella 2.5, 4.0/CP, 5.0) have been designed to provide increasingly greater flow and LV support. The device has also been placed via the axillary artery to facilitate patient mobilization.67 A right-sided device (Impella RP) has been introduced that is advanced up the femoral vein and across the pulmonary valve to enhance RV flow in acute RHF.

A number of studies support the Impella’s ability to decrease mortality in acute myocardial infarction with cardiogenic shock68 and to enhance the completeness of revascularization, mapping, or arrhythmia ablation during PCI.69 In a small case series of Impella RP placement in 30 patients with acute RHF complicating LVAD implantation, cardiotomy, or acute myocardial infarction, hemodynamic improvement was immediate, and overall 30-day survival rate was 73.3%.70

As with all percutaneous arterial devices, there is a risk of bleeding and limb ischemia. Management of the Impella requires close attention and considerable skill. Although the monitor provides continuous information about ventricular pressure, power, and flow, frequent echocardiography is required to ensure proper central positioning of the axial pump across the aortic valve, as well as ventricular chamber filling, thrombus formation, and ventricular recovery.71 Impella flow may be acutely impaired or completely obstructed by catheter migration, malposition, kinking, or thrombus. As with a durable LVAD, mural pump inflow obstruction and complete cessation of flow (a “suckdown” or suction event) may be precipitated by acute LV emptying caused excessive pump speed, hypovolemia or acute pulmonary hypertension, or RHF.

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HeartMate Percutaneous Heart Pump

The HeartMate percutaneous heart pump (PHP) is a new percutaneous axial flow pump that appears analogous to the Impella. However, it has a distal collapsible elastomeric impeller that passes through a relatively small 14F introducer; once through the aortic valve, the impeller expands to 24F, capable of generating a flow of 4 to 5 L/min at approximately 20,000 rpm. The HeartMate PHP is approved for PCI support in the European Union, and, in the United States, it is currently undergoing a large randomized open-label noninferiority trial versus the Impella 2.5 for support during PCI (SHIELD II, NCT02468778).

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Aortix System

The Aortix system is a miniaturized axial flow pump that represents a radical departure from current percutaneous devices in that it is intended to provide partial circulatory assist in less-sick patients (NYHA III). Passed through the femoral artery, it deploys expandable side anchors that secure the pump in the supradiaphragmatic descending aorta above the renal arteries. It has entraining jets that entrain blood to augment flow (“jet pumping”) in series with the circulation, thus decreasing LV afterload while minimizing central thromboembolic risk. In an ischemic heart failure sheep model, the Aortix system not only decreased myocardial oxygen consumption and improved LV ejection fraction and CO, but also increased renal blood flow and urine output.72 Clinical studies are planned in 2016 and 2017.

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Figure 7 illustrates some generic clinical pathways for mechanical circulatory support, although every patient must be evaluated individually for their own specific management plan.

Figure 7.

Figure 7.

Patients who are at INTERMACS 1, that is, who are in life-threatening cardiogenic shock, may be rescued by a short-term device, which in the majority of cases will be VA-ECMO. In some situations, particularly in the catheterization laboratory or coronary care unit, rescue with alternate short-term devices (eg, IABP, Impella, or TandemHeart) may be attempted but inevitably converted to VA-ECMO on site or in the OR. If patients are deemed to be viable from a neurologic standpoint, they will be supported and closely monitored for possible cardiac recovery and VA-ECMO weaning. If cardiac recovery is negligible or slow, they may be converted to a CentriMag device to allow organ recovery and possible circulatory weaning. If this appears unlikely, the patient will be evaluated for a durable VAD or TAH as BTT or DT.

Patients who are at INTERMACS 2, that is, who are developing progressive organ dysfunction, are generally evaluated for a durable VAD or TAH as BTT or DT. If they deteriorate more rapidly, they may undergo interim support with a CentriMag device pending evaluation for a durable VAD or TAH as BTT or DT.

Patients who are at INTERMACS 3, that is, who are stable but dependent on inotropic support, are generally evaluated for a durable VAD or TAH as BTT or DT ab initio.

It should be noted that in some patients with a durable VAD as DT, conditions may improve to allow them to enter the BTT pathway. Conversely, in some patients with a durable VAD as BTT, conditions may deteriorate to preclude OHT and force a change to DT. In either situation, complications may occur that cause consideration of device deactivation (see below).

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Ethical and Psychosocial Issues in Durable Device Placement

Durable device placement is increasingly considered as a standard of care for older patients with intractable end-stage heart failure who are not candidates for heart transplantation. The most recent INTERMACS report on more than 15,000 patients reveals an 80% 1-year and 70% 2-year survival with durable CF-VADs.4 However, what caregivers may interpret as a therapeutic success may not necessarily translate into improved QOL for the patient, which after all is the primary goal of durable device implantation.

Ethical issues in device placement include appropriate patient evaluation and selection; fully informed consent for device initiation; and end-of-life decision making, that is, device deactivation.73

The Centers for Medicare and Medicaid Services (CMS) have clearly defined medical criteria for durable device placement, but psychosocial criteria—unlike those well established for heart transplantation—remain generic and institution dependent. Key issues of focus must include drug, alcohol, or tobacco abuse or psychiatric illness; capacity for learning and problem solving; previous compliance with medical regimens; the quality of psychosocial, family, and financial support after implantation; and the adequacy of health insurance coverage.74 These concerns particularly apply to older patients with impaired functional or cognitive reserve (frailty) that affects their ability to take care of their device.

Understanding of their full implications of device insertion among patients and families remains extremely limited. Patient acceptance may be automatic (“There was no other choice”) or reflective (“I thought about it an awful lot”) and inform their subsequent postoperative expectations, including rejection versus acceptance of device deactivation in the context of their QOL.75

Careful discharge planning is essential with regard to device and battery management, anticoagulation regimen, 24/7 emergency contacts, and the potential for complications such as device malfunction, bleeding, infection, and stroke.74 In this regard, routine palliative care consultation at the time of evaluation can be very helpful in establishing patient and family goals of care and expectations.76

Predictive outcome models tend to focus on mortality rather than (uncertain) patient QOL or its economic effect, measured by quality-adjusted life years. Patient perception of good QOL relates to successful hospital discharge, ambulation, adequate sleep, and acceptance of their artificial support; the obverse is associated with increasing anxiety and depression. In interviews, patients express VAD insertion as “a new lease on life,” while acknowledging its limitations on their lifestyle, the care burden placed on the spouse or caregiver (especially during the early postdischarge period), time spent in follow-up care, and anxiety about access to VAD-trained providers. They also emphasize the importance of developing support groups with other VAD recipients.76

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Durable Device Withdrawal

The ethics of durable device withdrawal remain controversial, even in situations where advance care planning has been well documented or discontinuation is requested by the patient.77 Current advanced directives or “living wills” do not specify “no mechanical circulatory support” as opposed to “do not resuscitate” or “do not intubate.” Relatives of incapacitated loved ones who are placed in a situation of substituted judgment may feel that they have “no choice” but to allow durable VAD placement even though the patient may previously have expressed a desire not to be on life support.78 It has been suggested that, in uncertain situations, a time-limited trial of device support could be offered, that is, reevaluated based on whether the condition of the patient improves or deteriorates—a judgment that should be made by the patient as well as the medical team.78

The fundamental question is whether device deactivation represents physician-assisted death (an act of commission) versus allowing natural death to proceed (an act of omission). In the former argument, the VAD is considered as a constitutive (integral) life-sustaining intervention; it should be discontinued only when unrelated lethal conditions such as irreversible coma, refractory shock, or multiple organ system failure coexist.79 These considerations may be modified in countries and states that permit physician-assisted death under specified circumstances. In the latter argument, withdrawal of mechanical circulatory support is considered no different than the withdrawal of other types of life support such as mechanical ventilation or renal replacement therapy. Regardless, when device deactivation is planned, a multidisciplinary team (ethics, palliative care, chaplaincy) should support the medical team, patient, and family to ensure a peaceful, dignified, and compassionate death.

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The past decade has seen an exponential increase in the application and development of durable long-term as well as nondurable short-term mechanical circulatory support for cardiogenic shock, acute heart failure, and chronic heart failure. Support has evolved from BTT to destination therapy, bridge to rescue, bridge to decision making, and “bridge to a bridge.” Noticeable trends include device miniaturization, minimally invasive and/or percutaneous insertion, and efforts to superimpose pulsatility on continuous flow. We can certainly anticipate that innovation will accelerate in the months and years to come. However, despite—or perhaps because of—the enhanced equipment now available, mechanical circulatory support is an expensive, complex, resource-intensive modality that requires considerable expertise, perhaps best confined to highly specialized centers. Anticoagulation to prevent device-induced thrombosis begets bleeding, and coagulopathy, embolic and hemorrhagic stroke, sepsis, and multisystem failure continue to be formidable risks in these very sick patients. Patient psychosocial and QOL aspects of device placement and withdrawal necessitate greater attention, and study as the primary role of mechanical circulatory support becomes increasingly established in cardiogenic shock, acute heart failure, and chronic heart failure.

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Name: Robert N. Sladen, MBChB, FCCM

Contribution: The author designed, prepared, and reviewed the manuscript.

This manuscript was handled by: W. Scott Beattie, PhD, MD, FRCPC.

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