Historical note
The first left ventricular assist device (LVAD) was implanted in 1963 by Dr. DeBakey in a patient with postcardiotomy shock. As the incidence of heart failure rose to epidemic proportions, the LVAD emerged as a new solution to this devastating disease, and superiority over medical treatment was demonstrated in the Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure (REMATCH) trial. The first-generation devices were pulsatile, in an attempt to replicate native cardiac physiology. When compared to medical management alone, therapy with these devices showed improved survival. However, their large size limited patient selection to mainly male patients, required large pneumatic drivers, and demonstrated limited durability.
Thus, second- and third-generation devices were developed using continuous-flow pumps. These devices were smaller, allowing implantation in a broader population including women and children. The improved technology allowed for lengthened battery life, longer support times, and overall better quality of life for patients with advanced heart failure. Continuous-flow devices have continued to dominate the market since their introduction and are implanted in over 90% of patients with advanced heart failure.
Principles of device selection
Chronic support of the left ventricle (LV) requires long-term reliability and durability, portability, and adequate cardiac flow for active patients. Three devices currently on the market are widely used: the HeartMate II (HMII) LVAS (Abbott, Lake Bluff, IL, USA), the Heartware HVAD (Medtronic, Minneapolis, MN, USA), and the newly approved HeartMate 3 (HM3) LVAS (Abbott, Lake Bluff, IL, USA). All three pumps have inflow cannulas that are placed in the LV apex. The inflow cannula is connected to a pump body, which then is attached to an outflow cannula and graft that is subsequently sewn onto the ascending aorta. An electrical driveline from the pump exits the patient via a subcutaneous tunnel in the upper abdomen.
These pumps differ in several significant ways. The HMII, a second-generation device, uses an axial flow pump and, in general, requires a preperitoneal pocket for placement. Both the HVAD and HM3, third-generation devices, utilize centrifugal flow in a smaller configuration allowing for intrapericardial implantation. While the survival outcomes are similar for the HMII and HVAD, complication rates differ. The HVAD has a higher stroke rate, while the HMII has a higher rate of driveline infection and hemolysis/thrombosis, all with significant clinical impact (see also Chapter 13 ). The smaller size of the HVAD is more conducive to a minimally invasive approach via thoracotomy, either at the initial operation or if a redo operation is required. Additionally, biventricular configuration of the HVAD has been reported, which is not feasible with the HMII. Early results with the HM3 are promising, as this device appears to have a lower rate of hemolysis/thrombosis. However, survival and disabling stroke rates are similar when compared to the HMII. Ultimately, it appears that device selection must be individualized for each patient, underscoring the importance of patient selection.
Preoperative assessment and preparation
Indication for LVAD placement varies by individual patient and continues to evolve. Historically, LVAD implantation has been indicated for patients with New York Heart Association Class IV heart failure refractory to medical treatment and may include those patients with intractable arrhythmias and/or angina, end-organ dysfunction attributed to heart failure, or postcardiotomy shock. Patients are classified by therapy goals into bridge to transplantation, destination, bridge to recovery, and bridge to decision therapy.
The Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) scoring system is useful to identify appropriate patients and timing of LVAD support. Optimal patient selection is crucial for the success of chronic LVAD implantation and is achieved through an array of diagnostic studies.
Assessment is divided into cardiac and noncardiac considerations. Cardiac considerations include right ventricular (RV) function, valvular function and structure, intracardiac shunting, apical thrombus, and arrhythmias. Transesophageal echocardiography (TEE) is an essential part of the preoperative evaluation. Irreversible, advanced right heart failure is a contraindication to the placement of an isolated LVAD, and these patients may be considered for biventricular ventricular assist devices (VADs), total artificial heart placement, or heart transplantation. Noncardiac considerations include end-organ function (particularly pulmonary, renal, and hepatic), nutrition, body habitus, and social and psychiatric issues. End-organ function must be optimized through the use of inotropes and potentially intra-aortic balloon pump and/or extracorporeal membrane oxygenation if shock is present.
Implant operation
Hemodynamic monitoring is performed using a pulmonary artery catheter, arterial line, and TEE. After induction and skin preparation, a midline sternotomy incision is performed. A preperitoneal pocket is made using sharp and blunt dissection in the case of HMII implantation. As VAD placements are frequently repeat sternotomies, accurate dissection of the LV from surrounding scar tissue is required. Following this dissection, the patient is systemically heparinized.
Aortic cannulation should be placed as high as possible, close to the arch. Single two-stage venous cannulation will suffice in the majority of cases. If more dissection of the LV is required, it is performed during cardiopulmonary bypass (CPB) with the heart beating but decompressed. The driveline is tunneled percutaneously under the rectus muscle to exit usually over the left upper quadrant of the abdomen and can be done prior to heparinization.
The heart is elevated, bringing the LV to the midline of the wound. Pledgeted braided polyester sutures are placed from the myocardium through the sewing ring around a chosen spot for the inflow cannula ( Fig. 11.1 ), which must point toward the mitral valve and parallel to the septum ( Fig. 11.2 ). The sutures are then placed through the sewing ring, which is then seated and tied down. In the case of HMII implantation, coring can be performed prior to placement of the sewing ring.
The patient is placed in the Trendelenburg position in preparation for coring. Strong suction is maintained on an aortic needle vent to capture any air that may be ejected from the ventricle. The heart is emptied and a cruciate incision is made at the apex. The coring tool is used to perform the left ventriculotomy ( Fig. 11.3 ), removing a core of LV muscle. The ventricle is inspected for crossing fibers, thrombus, or obstructing muscle, which, if identified, is removed or resected. Once clear, the heart is deaired, and the inflow cannula of the pump is inserted ( Fig. 11.4 ). Continuous surveillance for air in the ascending aorta is maintained by the echocardiographer or anesthesiologist during this portion of the operation. The pump is secured after proper orientation is confirmed, and the heart is then placed back in normal anatomic position in the chest.
Further deairing is then performed through the outflow graft. The bend relief and outflow graft can be placed inside a 20-mm woven Dacron graft for further protection during subsequent explant for transplantation. The graft is then measured, clamped, and cut. A partial occluding clamp is placed on the greater curvature of the ascending aorta. After aortotomy, the outflow graft is anastomosed to the ascending aorta with continuous polypropylene suture ( Fig. 11.5 ).
Normal ventilation is resumed, and inhaled nitric oxide or prostaglandin and inotropes are initiated. The driveline is passed off the field and connected to the system controller. Following rewarming to normothermia, thorough deairing of the heart and pump is again performed, and CPB is weaned while increasing the LVAD pump speed to achieve adequate flow.
After weaning from CPB, the right heart should be assessed before reversing heparin. Pulmonary hypertension by itself is not an indication for RV support unless accompanied by RV failure. Destabilizing bleeding, with ongoing transfusion requirement, will often lead to RV failure and should be corrected before weaning from bypass. Protamine infusion is administered, and the patient is decannulated. Left pleural, mediastinal, and right pleural drains are inserted. Once adequate hemostasis is achieved, the chest is closed.
Intraoperative considerations
Valvular Incompetence and Repair
The intraoperative management of native valvular incompetence during LVAD insertion remains an area of controversy. The expected duration of LVAD support and patient characteristics both influence the decision to repair insufficient native valves. However, since the duration of support can never be certain, it seems advisable to correct severe forms of aortic, mitral, and tricuspid insufficiency at the time of implantation, especially if the physiologic response to LV support appears unlikely to improve the insufficiency, and if it can be accomplished without additional mortality and morbidity. During and after LVAD implantation, both the right and the left native valves are subjected to new demands that can influence their performance acutely and chronically. In general, a greater likelihood of recovery should prompt serious consideration for repair of severely insufficient atrioventricular or aortic valves. However, consensus has not been reached on the specific indications for repair.
Tricuspid Regurgitation
Correction of tricuspid regurgitation (TR) reinforces the integrity of the RV pumping complex, which comprises the RV and the pulmonary vascular resistance (PVR). Tricuspid insufficiency in LVAD recipients is multifactorial; advancing age, chronic atrial fibrillation, and pulmonary hypertension with chronic right heart pressure and volume overload can all dilate the tricuspid annulus. In patients with a compliant interventricular septum, increased venous return to the right heart following LVAD insertion can be accompanied by a septal shift to the left. The increased RV volume can exacerbate existing TR. The TR in LVAD recipients is also often worsened by the adverse effects of the transvalvular lead components of automatic internal cardioverter defibrillators and pacemakers ( Fig. 11.6 ). Both the incidence and the degree of TR increase with the number and size of the transvalvular leads. These leads can develop clots within days, inflammation within weeks, and sclerosis within a year. Usually, the posterior leaflet is affected. Perforation can occur, as can entanglement of the subvalvular apparatus. Secondary TR may abate over time if the LV–LVAD complex is functioning properly and is accompanied by important reduction in pulmonary hypertension and pulmonary insufficiency.
An INTERMACS analysis reported a 40% incidence of moderate to severe TR at the time of implantation. The impact of surgical treatment of TR on survival and functional outcome has not been established. The controversy is confounded by the finding that moderate–severe TR is a marker for less good survival post implantation, but in two multi-institutional studies, tricuspid valve repair did not improve short or longer term survival, suggesting that moderate to severe TR is a marker for greater derangement of RV function. Furthermore, moderate to severe TR usually improves with LVAD implant alone, since reactive pulmonary hypertension and RV afterload are reduced. Some data suggest that leaving severe TR is associated with worsening RV function and progressive TR over time.
In practice, the actual threshold for repairing the tricuspid valve varies among surgeons; approximately one-third of patients with severe TR at implantation undergo TV repair. The threshold is lower for patients who are not expected to recover RV and/or tricuspid valve function. There does appear to be growing consensus that if preimplant TR is severe and tricuspid valve annulus is > 40 mm, TV repair is advisable.
Tricuspid annuloplasty can be effective in decreasing TR resulting from annular dilatation. However, if leaflet tethering is severe, annuloplasty is not usually successful. In instances where annuloplasty is not possible, tricuspid valve replacement, using a bioprosthesis inserted over existing pacemaker leads without excision of the tricuspid apparatus, has produced good long-term results. The disadvantage of having a bioprosthesis in the right heart is the increased possibility of incurring a prosthetic infection and potential heterograft degeneration. Because the post-LVAD RV afterload is usually reduced, transvalvar flow patterns and reduced pressures are likely to favor longer durability of bioprostheses in the tricuspid position.
Mitral Regurgitation
With continuous-flow pumps, the mitral valve may remain open throughout the entire natural cardiac cycle. This is especially noticeable in the early postoperative period when native LV function is most compromised. As the LV recovers, attenuated pulsatile flow becomes the norm. The reduced pressure reduces the work demands on the mitral valve.
The impact of severe mitral regurgitation (MR) on long-term outcome remains controversial. It is also unknown if these abnormal pressure and flow patterns affect the native mitral valve function and whether this impacts long-term prognosis. However, there are increasing data that repair of severe MR may improve overall survival.
MR caused by chordal tethering is diminished during LVAD support because LV volumes are reduced and the interpapillary muscle distance is lessened by the functioning LVAD. Annular dilation and contraction may recover as LV function recovers. However, if MR is > 2 +, an annuloplasty ring can be placed and provides a secure remedy at a low risk. In rare cases where structural valve leaflet abnormalities exist, repair is advised using standardized techniques, including chordal replacement, edge-to-edge repair, and annuloplasty. The edge-to-edge repair, although not a perfect solution, can be performed effectively through the LV apex at the time of apical cannula insertion. In some patients, mitral valve replacement may be necessary, in which case a bioprosthetic valve should be used.
Management of mechanical mitral valve prostheses with LVAD implantation is controversial. Minimizing the potential for thrombus on the prosthesis depends on intermittent pulsatile flows to wash areas of stasis. In recipients of long-term LVAD support, the chronic bleeding consequences imposed by LVADs may necessitate temporary cessation of anticoagulation, with a potentially adverse effect on implanted mechanical valves. However, successful LVAD support in patients with mechanical mitral prosthetic valves has been reported for up to 689 days.
Aortic Valve
The new functional demands on the native aortic valve during LVAD support are not physiologic. Aortic root flow conditions favoring stasis have been observed with continuous-flow VADs and are more severe as the distance from the aortic entry of the outflow graft to the aortic valve is increased. Thrombus has been observed on the noncoronary cusp and in the left coronary sinus in patients with previous coronary bypass grafting and in patients with aortic root closure, presumably due to the static flow conditions. This thrombotic liability can result in systemic or coronary artery embolization.
Aortic insufficiency (AI) can lead to failure of the LV to reduce in size and progressive congestive heart failure with chronically elevated left atrial pressure in VAD patients. In vitro studies have shown an increase in leaflet stress during LVAD support. Radial stress was greater than circumferential stress in a model using a continuous-flow pump in an LVAD support configuration. The clinical importance of AI during LVAD support depends on its severity and the underlying native LV function (see also Chapter 13 on Adverse Events During VAD Support). As AI progresses, more blood recirculates centrally through the LV–LVAD complex and causes systemic hypoperfusion and progressive LV volume loading. Patients with progressive or significant AI may have signs of low systemic flow and high LVAD flows with increased pulmonary capillary wedge pressure (PCWP) and pulmonary congestion. The severity of this malady can be confirmed by measuring right heart output and finding that it is less than the flows calculated from the LVAD performance interpretation displayed on the VAD console.
No absolute rules currently exist to guide treatment of AI seen in the operating room. However, aortic valve repair or closure should be considered when more than moderate (and perhaps moderate) AI is noted on the pre-CPB TEE. If the heart is maintained in a beating state during implantation, important AI will also be apparent when viewed through the apical cannulation site.
An effective technique for aortic valve closure is that described by Adamson et al. ( Fig. 11.7 ). In patients with sclerotic valves where progression is unlikely, central suture closure of insufficient leaflets may suffice, but central coaptation sutures in otherwise normal valves do not prevent progression of AI and its sequelae.
