Heart transplantation remains the treatment of choice for patients with end-stage heart failure, allowing high survival rates and improved quality of life.1  Worldwide, more than 6,000 heart transplantations are performed annually, with 1-yr posttransplant survival around 85% and median survival now exceeding 12 yr.2  The progressive improvement in posttransplant outcome that has been observed during these years is mostly driven by a dramatic drop in the early posttransplant mortality.2  However, the first weeks after heart transplantation remain critical, with an 8% 1-month mortality in contemporary cohorts.2  The perioperative period remains at very high risk due to the increasing proportion of candidates bridged to transplant with durable mechanical circulatory supports and an increasing number of sensitized patients.3,4  In addition, the prioritization of high-risk candidates on extracorporeal membrane oxygenation (ECMO) support and the broader eligibility for both recipient- and donor-related risk factors of primary graft dysfunction (older age, comorbidities) also contribute to increase the challenges of the perioperative period.2,5  The role of the cardiothoracic anesthesiologist–intensivist in the early management of heart transplant recipients is crucial both during surgery and in the intensive care unit (ICU).6  Guidelines focused on the perioperative management of heart transplant recipients are still lacking, and the area of knowledge required is vast. This includes the management of hemodynamic instability, transfusion and hemostatic disorders, immunosuppression, and infectious complications (prevention and treatment) in addition to acute kidney injury and renal replacement therapy. This review aims to summarize the latest knowledge in the field of perioperative management of heart transplant recipients in order to guide cardiothoracic anesthesiologist–intensivists.

Vasoplegia

Defining Vasoplegia

A refractory vasoplegic syndrome (a persistent low vascular resistance requiring intravenous vasopressors) is observed in 11 to 60% of heart transplantation patients.7,8  There is currently no standard consensus on the definition of vasoplegic syndrome after cardiac surgery or more specifically after heart transplantation, but hypotension occurring within 24 h of heart transplantation with a cardiac index greater than 2.2 l/kg/m2 and a systemic vascular resistance of less than 800 dyne.s/cm5 is generally considered characteristic of this situation.7,9  The pathophysiology of vasoplegic syndrome remains poorly understood, but it could be associated with cytokine release, adrenergic receptor desensitization, increased nitric oxide synthesis, relative deficiency of vasopressin, activation of adenosine triphosphate–sensitive potassium channels, vascular smooth muscle cell membrane hyperpolarization, dysfunction of the renin–angiotensin system, and endothelial glycocalyx alteration.10 

Risk Factors

Age, history of thyroid disease or chronic kidney disease, ventricular-assist device before transplant, duration of cardiopulmonary bypass, and intraoperative blood products are associated with this condition.8,11,12  Treatment with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers is associated with vasoplegia after cardiac surgery,13  although this is less well-documented after heart transplantation.8  Nevertheless, the presence of a vasoplegic syndrome may be associated with an unfavorable prognosis in heart transplantation patients,14  and the consequences of the vasoplegia do not appear to differ after heart transplantation and after standard cardiac surgery.15 

Management of Vasoplegia

As highlighted in the recent guidelines of the International Society for Heart and Lung Transplantation (Chicago, Illinois), the first-line choice in the treatment of vasoplegia is norepinephrine16  (see figure in Supplemental Digital Content 1, https://links.lww.com/ALN/D159). However, the management of post–heart transplantation vasoplegia is most often extrapolated from the literature related to this condition after standard cardiac surgery, due to the lack of specific data. In a recent Brazilian single-center study, Hajjar et al. randomized 330 patients with vasoplegic shock after cardiac surgery to receive vasopressin or norepinephrine.17  Mortality or severe complications occurred in 32% of patients receiving vasopressin, compared with 49% receiving norepinephrine, but the extrapolation of these findings has been questioned. Moreover, acute renal failure occurred in only 10.3% of patients receiving vasopressin, compared with 35.8% of patients receiving norepinephrine.17  In heart transplantation patients with vasoplegia syndrome, vasopressin was shown to decrease norepinephrine requirements, but the level of evidence remains low.18  Similarly, the use of methylene blue, hydroxocobalamin, or angiotensin II could be of interest in this population but, up to now, efficacy of these therapies has only been substantiated by cases reports.10,19–23 

Primary Graft Dysfunction

Defining Primary Graft Dysfunction

The International Society of Heart and Lung Transplant defined primary graft dysfunction after heart transplantation as a failure of the transplanted heart, necessitating high doses of catecholamines and/or temporary mechanical circulatory support to achieve an adequate cardiac index in the recipient, and diagnosed within 24 h of completion of surgery in the absence of a discernible alternate cause such as hyperacute rejection, pulmonary hypertension, or surgical complications.24,25  Primary graft dysfunction can be further characterized as predominantly left-sided or right-sided, as well as mild, moderate, or severe, depending on the level of cardiac dysfunction and the extent of inotrope and mechanical support required (table 1). The most recent data suggest an incidence of 10 to 36% with severe primary graft dysfunction occurring in 8 to 18% of heart transplantation patients. Primary graft dysfunction is associated with increased 30-day and 1-yr mortality.25 

Table 1.

Severity Scale for Primary Graft Dysfunction

Severity Scale for Primary Graft Dysfunction
Severity Scale for Primary Graft Dysfunction

Risk Factors

The risk factors for primary graft dysfunction include factors related to the donor, the recipient, and the surgical procedure itself (table 2). The Right atrial pressure, recipient Age, Diabetes mellitus, Inotrope dependence, donor Age, Length of ischemic time (RADIAL) score was developed from a cohort of 621 heart transplantation patients in which six risk factors were identified using multivariable analysis: (1) recipient risk factors include right atrial pressure 10 mmHg or greater, age 60 yr or greater, diabetes mellitus, and dependence toward inotropes, and (2) donor risk factors are age 30 yr or greater, and length of ischemic time 240 min or greater.26  The RADIAL score allows heart transplantation patients to be stratified into groups with an incremental incidence of primary graft dysfunction.27  In patients bridged to heart transplantation with continuous-flow left ventricular assist devices, the RADIAL score did not accurately predict severe primary graft dysfunction. In this group, the risk factors for primary graft dysfunction included mechanical support duration more than 1 yr, elevated pre–heart transplantation creatinine plasma levels, elevated central venous pressure or pulmonary capillary wedge pressure ratio, and use of amiodarone before heart transplantation.28 

Table 2.

Risk Factors for Primary Graft Dysfunction

Risk Factors for Primary Graft Dysfunction
Risk Factors for Primary Graft Dysfunction

Management of Primary Graft Dysfunction

Despite the lack of high-level evidence supporting their efficacy, inotropic drugs and vasopressors (including dobutamine, dopamine, milrinone, epinephrine, and norepinephrine) remain the first-line treatment for primary graft dysfunction. These medications may potentially be combined with vasopressin and inhaled nitric oxide8  (see figure in Supplemental Digital Content 1, https://links.lww.com/ALN/D159). The use of milrinone as a bridge to transplantation has been reported in a few cohort studies, but the data regarding the treatment of primary graft dysfunction using this medication are extremely limited.29,30  Weis et al. assessed the effect of levosimendan in 12 heart transplantation patients with primary graft dysfunction, with good results on hemodynamic parameters such as cardiac index, mean arterial pressure, or mean pulmonary artery pressure.31  In this cohort of patients with primary graft dysfunction, survival at day 30 was 93%. When cardiac output remains inadequate despite high doses of inotropes and/or vasopressors, the use of temporary mechanical circulatory support is needed to provide systemic perfusion and oxygenation, allowing the graft to recover and maintaining the other organs. For patients needing a temporary mechanical circulatory support, venoarterial ECMO seems to be associated with shorter assistance duration, lower incidence of major bleeding, lower incidence of renal failure requiring renal replacement therapy, and reduced mortality compared with patients supported with a continuous-flow external ventricular assist device.32  The ideal timing for ECMO implantation in patients with primary graft dysfunction is not known. However, as with the timing for ECMO implantation in postcardiotomy cardiogenic shock, it can be assumed that early implantation is beneficial. Thus, in a cohort of 347 patients assisted with postcardiotomy venoarterial ECMO, including 59 primary graft dysfunction patients, postoperative implantation of venoarterial ECMO was independently associated with an increased risk of Kidney Disease Improving Global Outcomes stage 3 acute kidney injury.33  In a retrospective study involving 135 primary graft dysfunction patients including 66 assisted with venoarterial ECMO, delayed initiation of venoarterial ECMO was independently associated with in-hospital mortality.34  Thus, venoarterial ECMO implantation appears to be an efficient strategy for the management of severe primary graft dysfunction, in spite of a significant impact on long-term quality of life.35  Finally, although there are data pointing to a beneficial effect of left ventricle unloading in patients assisted by venoarterial ECMO, there is little specific evidence in transplant patients.36  Indeed, in a recent study from the Extracorporeal Life Support Organization (Ann Arbor, Michigan) registry on the association between left ventricle unloading and in-hospital mortality, transplantation was an exclusion criterion.36 

Right heart failure remains a frequent and potentially severe complication after heart transplantation and contributes significantly to morbidity and mortality. When a discernible cause can be identified, right heart failure is related to a secondary graft dysfunction. Usual etiologies include hyperacute rejection (see Treatment of Cardiac Allograft Rejection section), known surgical complication, or pulmonary hypertension. As the presence of pretransplant pulmonary hypertension in heart recipients increases the risk of posttransplant right heart failure, the selection of transplant recipients and their pretransplant hemodynamic optimization is essential. A single-center retrospective study reported an incidence of 5.9% for severe right heart failure after heart transplantation, while increased pulmonary capillary wedge pressure and mean pulmonary arterial pressure were identified as risk factors.37  The International Society for Heart and Lung Transplantation suggests that a pulmonary vasodilator challenge with inhaled (nitric oxide or prostacyclins) or intravenous (nitroglycerin or nitroprusside) vasoactive agents should be administered when the systolic pulmonary artery pressure is 50 mmHg or greater and when the transpulmonary gradient is 15 mmHg or greater or the pulmonary vascular resistance is greater than 3 Wood units. Meanwhile, systolic arterial blood pressure should be maintained greater than 85 mmHg. Although the right and left filling pressures decrease within weeks after heart transplantation, an elevated mean pulmonary arterial pressure after transplantation is an independent prognostic factor for long-term mortality.38,39 

The management of right heart failure relies on the preservation of coronary perfusion through the maintenance of an adequate mean arterial pressure using norepinephrine infusion, optimization of the right ventricle preload with careful monitoring to avoid congestion, reduction of the right ventricle afterload by decreasing pulmonary vascular resistance, and limitation of pulmonary vasoconstriction through ventilator settings (avoiding hypoxia and hypercarbia)40  (see figure in Supplemental Digital Content 1, https://links.lww.com/ALN/D159). Inhaled nitric oxide is unique in that it allows selective pulmonary vasodilatation and is effective in improving stroke volume as a result of right ventricle afterload reduction.41  However, there is currently no clear evidence that this medication may improve long-term outcome in patients, and the cost/benefit ratio is questioned.42  Finally, it was recently suggested, in a retrospective cohort of cardiac surgical patients with pulmonary hypertension or right ventricular failure, that the combination of inhaled milrinone and epoprostenol was associated with beneficial effects on hemodynamics.43 

The severe forms of primary graft dysfunction are traditionally managed with venoarterial ECMO, but up to 45% of patients with primary graft dysfunction have isolated right ventricular dysfunction.27  In these patients, percutaneous right ventricular support, for example through the Protek Duo cannula (CardiacAssist Inc., USA) or with the Abiomed Impella RP device (ABIOMED, USA), could be particularly useful, allowing mechanical support of the right ventricle without the detrimental effects of venoarterial ECMO (nonphysiologic circulation with reduced pulmonary flow, risk of intravascular pulmonary thrombosis, increased left ventricular afterload).44,45 

The mechanisms for arrhythmogenesis in heart transplant patients are related to several factors including surgical technique, graft ischemia duration, autonomic denervation, immune rejection, cardiac allograft vasculopathy, and graft dysfunction. The loss of parasympathetic input from the vagus nerve results in a higher resting heart rate for transplant patients (90 to 100 beats/min) and a significantly reduced heart rate variability. Graft ischemia exceeding 240 min and the biatrial surgical technique are associated with increased rates of postoperative atrial fibrillation. Atrial fibrillation, atrial flutter, and supraventricular tachycardia are the most common posttransplant arrhythmias and are associated with decreased long-term survival.46,47  Despite their frequency, atrial arrhythmias occur in heart transplant recipients at a much lower rate (2 to 4%) than in other post–cardiac surgery patients (overall incidence of 26.7%, from 22.9% for coronary artery bypass graft to 45.2% for combined procedures).46,48  The majority of atrial fibrillation episodes occur within 2 weeks of transplantation, whereas atrial flutter most commonly presents after the first 2 weeks. Atrial fibrillation and flutter may be associated with acute rejection and/or cardiac allograft vasculopathy, particularly when arrhythmias persist beyond the postoperative period.46,47  Ventricular arrhythmias and sudden cardiac arrest represent 10% of deaths after heart transplantation, with an incidence of 1.30 per 100 person-years.49,50  Treated rejection and cardiac allograft vasculopathy were described as risk factors for sudden cardiac death in heart transplant patients.51  The management of atrial fibrillation after heart transplantation is similar to that of other cardiac surgery patients. A treatment strategy of rate versus rhythm control is determined by the presence of symptoms and the effect of atrial fibrillation on systolic function. Rate control may be achieved with β-blockers, with short half-life drugs being preferred at the onset of treatment in this setting to ensure tolerance. Rhythm control may consist in electrical or pharmacologic cardioversion.52  It should be remembered, however, that treatment of the recipient with amiodarone before heart transplantation is a well-established factor for primary graft dysfunction.45,53,54  Finally, as these patients are frequently on inotropes, it may be strategic to decrease the inotropes and to look for other pharmacologic methods for rate or rhythm control. There are no specific guidelines for anticoagulation after heart transplantation, and a decision should be made after considering the Congestive heart failure, Hypertension, Age, Diabetes mellitus, Stroke or transient ischemic attack, Vascular disease, Age, Sex (CHA2DS2-VASc) score according to current guidelines.55  Sinus node dysfunction and atrioventricular block requiring pacemaker implantation are present in 2 to 15% of heart transplant patients.56–58  In addition to the biatrial surgical technique, risk factors for early pacemaker implantation (less than 3 months) are donor age, ischemic time, cellular rejection, and amiodarone use before heart transplantation.59  Late pacemaker implantation (more than 3 months) risk factors include donor age and cardiac allograft vasculopathy.60 

Tricuspid regurgitation is the most common valvular abnormality after heart transplantation (19 to 84%), and has been associated with increased morbidity and mortality.61,62  The risk of mortality is greater in case of tricuspid regurgitation due to primary graft dysfunction or rejection.63  Therefore, if the effects of subclinical tricuspid regurgitation remain controversial, the more severe forms could be associated with chronic fluid congestion, lower extremity edema, liver congestion, and finally renal failure.64 

Although there may be other factors that could be responsible for a functional tricuspid regurgitation (allograft rejection, preoperative abnormal transpulmonary gradient, and vascular resistance), the main risk factor seems to be the biatrial surgical technique.65  Hence, Aziz et al. observed a higher incidence of tricuspid regurgitation among patients who underwent a biatrial surgical technique versus patients who underwent a bicaval approach (41% at 1 month and 52% at 24 months vs. 15% at 1 month and 30% at 24 months).66  Tricuspid regurgitation can also be the consequence of the anatomic disruption of the subvalvular apparatus. Specifically, endomyocardial biopsy, performed to detect allograft rejection, is a procedure particularly at risk of creating valvular lesions. Although the majority of patients are asymptomatic, moderate to severe tricuspid regurgitation can induce progressive right ventricle cavity enlargement, elevated right-side pressures, and eventually symptoms of right heart failure. Diuretics remain the cornerstone treatment for patients with tricuspid regurgitation. However, a surgical intervention could be indicated in refractory cases to prevent ventricular failure and the systemic consequences of severe tricuspid regurgitation.67 

Allograft rejection remains an important cause of graft dysfunction, patient mortality, and morbidity after heart transplantation.68  The immunosuppressive regimen must balance the risk between allograft rejection and the complications of overimmunosuppression, particularly infectious complications occurring early after heart transplantation.

The principle of an induction therapy is to induce a profound and rapid immunosuppression to lower the risk of rejection. Three approaches are widely used (sorted by the level of immunosuppression required): (1) no induction therapy, (2) nondepletive monoclonal induction using IL-2 receptor antagonists, and (3) polyclonal induction with antithymocyte globulins (T-cell depletion therapy). The practice is variable across centers and countries.68  No study ever proved a survival benefit of one strategy over another at the population level.69  The benefit–risk ratio of each approach should be discussed for every patient at the time of listing. Table 3 summarizes the doses, side effects, and monitoring of each drug.

Table 3.

Doses, Side Effects, and Monitoring of Immunosuppressive Drug for Heart Transplantation in the Context of the Intensive Care Unit

Doses, Side Effects, and Monitoring of Immunosuppressive Drug for Heart Transplantation in the Context of the Intensive Care Unit
Doses, Side Effects, and Monitoring of Immunosuppressive Drug for Heart Transplantation in the Context of the Intensive Care Unit

Allosensitization represents a major barrier to heart transplantation. The presence of antibodies to human leukocyte antigens is associated with increased risk of waitlist mortality. The proportion of allosensitized patients awaiting heart transplantation continues to increase, possibly due to the increasing exposition to procedures before transplant, including durable mechanical circulatory support, homografts, and blood products.4 

Virtual cross-matches at the time of organ proposal (i.e., the analysis of the immunological compatibility of the donor and the recipient: comparison of anti–human leukocyte antigens antibody developed by the recipient to the human leukocyte antigens of the donor) allow an accurate and early evaluation of the immunological risk of rejection. The exclusion of grafts from donors with human leukocyte antigens against which the recipient has developed donor-specific antibodies helps avoiding hyperacute rejection of the transplanted organ. In addition, donor-specific antibodies might induce acute and chronic injuries due to antibody-mediated rejection or cardiac allograft vasculopathy.70,71  The downside of this selection process is that the higher the number of unacceptable antigens, the narrower the donor pool.3  The definition of what is an unacceptable antigen is therefore essential but remains highly controversial (level of mean fluorescence intensity, in vitro complement fraction C1q binding, dilution).72 

Since heart transplantation is a vital therapeutic option, some centers opt to cross human leukocyte antigens barriers and manage donor specific antibodies subsequently.73  A perioperative combination of plasmapheresis and high-dose intravenous immunoglobulins can be used to reduce donor-specific antibodies plasma levels in patients at moderate immunological risk. For higher-risk patients, an intensification of the immunosuppression may be required. The early inhibition of the complement cascade is an attractive approach due its major implication in antibody-related acute allograft injury.

The early maintenance immunosuppressive therapy usually relies on a triple drug regimen: calcineurin inhibitor (tacrolimus, cyclosporine), cell-cycle inhibitor (mycophenolate mofetil, mycophenolic acid), and corticosteroids.16 Table 3 summarizes the doses, side effects, and monitoring of each drug with a particular focus on short-term management in the ICU.

The pathologic evaluation of endomyocardial biopsies remains the accepted standard to monitor, diagnose, and classify heart allograft rejection. The International Society for Heart and Lung Transplantation working formulations classify acute cellular rejection from 0R to 3R according to the importance of lymphocytes infiltrates and signs of myocyte injury (fig. 1A) and antibody-mediated rejection from 0 to 3 according to the presence of histologic (microvascular inflammation) and immunopathologic (complement C4d deposition in capillaries, presence of intravascular macrophages) signs of antibody-mediated rejection (fig. 1B).74,75 

Fig. 1.

Summary of the management of the heart transplant patient over time. CO, cardiac output; ICU, intensive care unit; IV, intravenous; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography; VTE, venous thromboembolism.

Fig. 1.

Summary of the management of the heart transplant patient over time. CO, cardiac output; ICU, intensive care unit; IV, intravenous; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography; VTE, venous thromboembolism.

Close modal

This international classification is the guide to rejection therapies. The presence of an acute allograft dysfunction is always considered as a marker of the severity of an ongoing rejection and should prompt aggressive immunosuppressive strategies. While the treatment of acute cellular rejection is well described and consensual (corticosteroids, antithymocyte globulin in the case of severe graft dysfunction),16  the treatment of antibody-mediated rejection remains controversial.76  Plasmapheresis and high doses of intravenous immunoglobulins represent the first-line therapy, but a more aggressive immunosuppressive strategy may be required, particularly in case of allograft dysfunction77,78  (table 3).

Infections are the leading cause of death within the first year after heart transplantation and justify targeted prophylaxis.79  The development of infection can be facilitated by the level of immunosuppression, drug-induced leukopenia, or immunomodulation by viral infection such as cytomegalovirus.80  A classic timeline describes three distinct periods of infection after solid organ transplantation: (1) the postoperative period within the first month is characterized by nosocomial and donor-derived infections (cytomegalovirus, Epstein–Barr virus, or Toxoplasma species); (2) the second period, up to 6 months after surgery, is characterized by opportunistic infections; and (3) after 6 months, community-acquired or rare infectious agents are expected. However, epidemiologic data are scarce, not recent (older than 10 yr), with various methodologies and from a limited number of centers, which makes generalization difficult. The two most recent cohorts, with a follow-up between 3 months and 1 yr, found a high incidence of infection (60 to 80%) after heart transplantation, with the highest rate within the first month.81,82  Among infectious agents, bacteria were the most frequently involved (greater than 50%), and viruses were also frequent (30%), whereas fungal infection accounted for only 13 to 14%. The predominant pathogens were Enterobacteriaceae and herpesviruses. Multidrug-resistant bacteria were frequent (15 to 20% of the cases). The respiratory tract and bloodstream were the most frequent bacterial infection sites, whereas viral infections were mostly mucocutaneous and respiratory. Although less represented, surgical site infections may be more prevalent (9 to 10%) after heart transplant than other cardiac surgeries.81,83  Interestingly, cannulation site infection may be a frequent complication (37%) in patients supported by ECMO after heart transplantation.84 

Preventive strategies based on pharmacologic prophylaxis according to serologic status of the donor or recipient are recommended by the International Society of Heart and Lung Transplantation guidelines for the care of heart transplant recipients,16  and are summarized in table 4. Prophylaxis against Pneumocystis jirovecii and Toxoplasma gondii is recommended during the early postoperative period, usually with trimethoprim or sulfamethoxazole, if not contraindicated. Antifungal prophylaxis to prevent mucocutaneous candidiasis or aspergillosis is not routinely recommended but may be considered in case of specific risk factors for aspergillosis. High-risk patients for cytomegalovirus infection (seronegative patients with seropositive donors) should benefit from antiviral prophylaxis (ganciclovir or valganciclovir) within 10 days after the transplantation for at least 3 months.85  Seropositive patients may benefit from antiviral prophylaxis or from a preemptive strategy according to the center preference.86  In the latter, cytomegalovirus viral load is quantified by nucleic acid amplification testing at least weekly in the whole blood, and an antiviral treatment is initiated only when a predetermined threshold is achieved. However, no specific threshold can be recommended given the interassay and patient-related factors variabilities. A preemptive strategy might prevent late cytomegalovirus infection, prevent drug toxicity, and reduce cost. Conversely, universal prophylaxis is easier to implement, prevents other herpesvirus infections, and may prevent opportunistic infections or graft rejection.85  Antimicrobial prophylaxis before the surgery with activity against skin flora, including Staphylococcus aureus, is recommended to prevent surgical site infections.16  If a chronic infection of ventricular assist device, pacemaker, or defibrillator is present, a perioperative antibiotic therapy based on known microbiologic susceptibilities should be initiated after consultation of an infectious disease specialist. Nonpharmacologic strategies range from standard precaution to protective isolation. Standard precautions are recommended for all patient care and include hand hygiene, personal protective equipment in case of possible exposure to infectious material, respiratory hygiene, adequate environment cleaning, adequate handling and disinfection of patient care equipment and instrument, and safe injection practices. Despite the lack of evidence, protective isolation seems very frequent in heart transplant centers across the world with an important variability in the measures used, with high-touch surface disinfection, private rooms, and daily linen change being the more frequent measures used.87 

Table 4.

Perioperative Antibacterial, Antiviral, Antifungal, and Antiprotozoal Prophylaxis in Heart Transplant Recipients

Perioperative Antibacterial, Antiviral, Antifungal, and Antiprotozoal Prophylaxis in Heart Transplant Recipients
Perioperative Antibacterial, Antiviral, Antifungal, and Antiprotozoal Prophylaxis in Heart Transplant Recipients

The treatment of postoperative hemorrhage and transfusion protocols after transplantation are poorly described. Furthermore, these patients are largely underrepresented and seldom studied in prospective trials investigating bleeding and transfusion in cardiac surgery.88–92  In the absence of specific data and guidelines, perioperative hemostasis and transfusion management in heart transplantation should probably follow current guidelines for cardiac surgery, including preoperative management of antithrombotic drugs, cardiopulmonary bypass optimization, algorithm-guided therapy for perioperative bleeding, and use of viscoelastic testing.93,94  A suggested perioperative bleeding management protocol is provided (see figure in Supplemental Digital Content 2, https://links.lww.com/ALN/D160).

Preoperative vitamin K antagonists should be reversed during surgery using vitamin K and international normalized ratio-guided four-factor prothrombin complex concentrates.16,95  In the situation where a direct oral anticoagulant is preferred over vitamin K antagonists, it is appropriate to choose dabigatran rather than anti-Xa direct oral anticoagulants, in combination with a protocol for reversal using idarucizumab.96  While aspirin can safely be continued, uninterrupted P2Y12 inhibitors might increase postoperative bleeding and should be avoided in patients awaiting heart transplantation.16,97  In the case of a formal indication for dual antiplatelet therapy, thienopyridines (clopidogrel, prasugrel) should be preferred due to the inefficacy of platelet transfusion in neutralizing ticagrelor when the last intake is less than 24 h before surgery.98  Antiplatelet agents’ reversal using platelet concentrates should be considered in case of severe perioperative bleeding and may be guided by platelet function testing.98 

Overall, heart transplant seems to be associated with a risk of severe perioperative bleeding and a high exposition to allogeneic transfusion, especially in the setting of redo surgery and bridge to transplantation using ECMO or ventricular assist device support.99–102  In accordance with cardiac surgery guidelines, postoperative bleeding should be managed using a tailored goal-directed hemostatic protocol, in coordination with the hemostasis specialist (see figure in Supplemental Digital Content 2, https://links.lww.com/ALN/D160). Special attention should be paid to a patient supported by ECMO or ventricular assist device, which are associated with platelet function defects and acquired von Willebrand syndrome, although little evidence is available regarding the impact of platelet transfusion or von Willebrand factor concentrate in this setting.103,104 

In the absence of specific data, a restrictive erythrocyte transfusion strategy (hemoglobin threshold between 7.5 and 8 g/dl) should probably be used for heart transplantation, potentially tailored to tissue perfusion or oxygenation values, including central venous oxygen saturation.93,105  As for patients with chronic heart failure, including those awaiting heart transplantation, postoperative anemia and iron deficiency warrant particular attention and may justify intravenous iron therapy in case of significant bleeding and/or postoperative iron deficiency.106,107 

Heart transplantation patients are at increased risk of venous thromboembolism and should receive pharmacologic prophylaxis, primarily using low molecular weight heparin.108  Antiplatelet therapy using low-dose aspirin is usually initiated early after surgery and would seem to be associated with a reduction of cardiac allograft vasculopathy.109 

In the absence of specific data in heart transplantation patients, ventilation strategies recommendations can be inferred from cardiac surgery literature. Intraoperative protective ventilation with tidal volume between 6 and 8 ml/kg of predicted body weight and positive end-expiratory pressure at 5 cm H2O may be recommended according to studies performed in noncardiac major surgery.110  However, open-lung ventilation with higher positive end- expiratory pressure and lung recruitment maneuvers or ventilation during bypass remain controversial to date.111–113  Interestingly, mechanical ventilation before heart transplantation is strongly associated with increased mortality.114  Early extubation within 6 h of ICU admission should be achieved whenever possible.115  Importantly, extubation may be also achieved safely in patients on venoarterial ECMO with clinical benefit.116 

Early postoperative acute kidney injury is frequent in the first 7 days after heart transplantation, with an incidence between 40 to 76% according to Kidney Disease: Improving Global Outcomes classification. Renal replacement therapy is required in 7 to 19% of patients.117–119  Furthermore, recent studies demonstrate a trend toward an increased incidence of all Kidney Disease: Improving Global Outcomes stages of acute kidney injury over time.117,118  The preoperative factors independently associated with early acute kidney injury include higher body mass index, diabetes, and chronic kidney disease.117,118,120,121  In addition, longer cardiopulmonary bypass time, postoperative hemodynamic instability, ECMO support, severe bleeding, and early initiation of calcineurin inhibitors are independent predictors of early acute kidney injury.117,118,120  The pathogenesis of heart transplantation–associated acute kidney injury mainly involves type 1 and type 2 cardiorenal syndrome.122  Among potential mechanisms, close attention should be paid to right heart hemodynamics, especially preoperative pulmonary hypertension, postoperative right ventricular failure, and renal congestion, which appears as a strong predictor of early acute kidney injury.119,123–125  Severe postoperative acute kidney injury is associated with a higher incidence of chronic kidney disease, rejection, and mortality at 1 yr after heart transplant.117,118,126  Although there is no single pharmacologic treatment, heart transplant patients might benefit from early prediction and recognition of postoperative acute kidney injury and multimodal bundle implementation.119,127,128  Specific actions might include postponing calcineurin inhibitors, providing both left and right ventricle support (inotropes, pulmonary vasodilators, circulatory support), and minimizing renal congestion.

Nutritional status is crucial but often underestimated in heart failure patients. Yet cachexia and sarcopenia may occur in at least 10 to 20% of ambulatory patients with systolic heart failure.129  Therefore, the Heart Failure Society of America (Rockville, Maryland) proposed in a recent consensus statement a nutritional evaluation and counseling for patients with heart failure proposed for heart transplantation.129  In the postoperative period, early enteral nutrition is recommended including also patients receiving extracorporeal membrane oxygenation.130  Oral intake should be the preferred route whenever possible. In patients with uncontrolled shock, enteral feeding must be delayed, but a low dose of enteral nutrition can be started as soon as shock is controlled. However, in the case of low cardiac output requiring inotropic support, the risk of acute mesenteric ischemia requires cautious enteral nutrition introduction, or even delayed introduction.131  In addition, heart transplantation is frequently associated with hyperglycemia in both diabetic and nondiabetic patients, requiring continuous insulin infusion in ICU to maintain glycemic control.16,132 

Conclusions

Early postoperative mortality after heart transplantation remains high despite substantial improvements during recent years. Therefore, optimal perioperative management of these patients is crucial. Unfortunately, most of the evidence supporting the current recommendations is mainly based on retrospective studies with limited sample size or is adapted from general cardiac surgery practices. Therefore, collaborative research networks at the international level should be strongly encouraged to improve the knowledge and, hopefully, the outcome of heart transplant patients.

Acknowledgments

The authors express their gratitude to Mary Regan, M.D., (Sorbonne University, Clinical Research Group in Perioperative Anesthesia and Resuscitation, Public Hospitals of Paris, Department of Anesthesiology and Critical Care, Cardiology Institute, Pitié-Salpêtrière Hospital, Paris, France) for proofreading.

Research Support

Support was provided solely from institutional and/or departmental sources.

Competing Interests

Dr. Mansour received payments made to his institution from i-SEP (Nantes, France) for consulting fees, and from French Fractionating and Biotechnologies Laboratory (Les Ulis, France), Aguettant (Lyon, France), and Pfizer (Paris, France) for lecture fees. Dr. Cholley received payments from Orion Pharma (Issy-les-Moulineaux, France), Nordic Pharma (Paris, France), Edwards Life Sciences (Guiyancourt, France), and AOP Orphan (Meudon La Foret, France) for participation in advisory boards and lectures at industry symposia. Dr. Bouglé received payments from Fresenius (Sevres, France) and French Fractionating and Biotechnologies Laboratory for lecture fees. The other authors declare no competing interests.

Supplemental Digital Content 1: Potential summarized postoperative shock assessment and management, https://links.lww.com/ALN/D159

Supplemental Digital Content 2: Potential perioperative bleeding management protocol, https://links.lww.com/ALN/D160

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Corrigendum to: 2021 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: Developed by the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure of the European Society of Cardiology (ESC) with the special contribution of the Heart Failure Association (HFA) of the ESC.
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