Careful clinical assessment for objective signs of advanced RHF is the first and simplest step in pre-LVAD implantation. Long-standing distended jugular veins and peripheral oedema are indicators of RHF that require special attention and possible optimisation before proceeding with the procedure. Potapov et al. [11] reported that visible ascites and discolouration of the skin of the legs due to haemosiderosis already progressing above the knees are supportive of long-standing RHF with poor chances of reversibility. These clinical findings make the option of biventricular mechanical support inevitable.

Furthermore, the background of HF seems to play a significant role in the incidence of RV dysfunction after LVAD implantation. Patients with non-ischemic HF have been shown to have an increased risk (absolute value of 5.1%) of early RHF compared to patients with ischemic HF, although the long-term impact of these diseases on late RV function is still unclear [12].

Other markers of pre-implantation patient severity are associated with a higher risk of RHF, including preoperative ventilator support, multiple inotropes, extracorporeal membrane oxygenator (ECMO) support and non-elective intra-aortic balloon pump (IABP) [13].

Abnormal biochemical values including serum creatinine $>$1.9–2.0 mg/dL, blood urea nitrogen $>$44.5 mg/dL and total bilirubin $>$2.0 mg/dL [14, 15, 16] are predictors of RV impairment after left ventricular support. In addition, a meta-analysis [17] found that patients on continuous renal replacement therapy or on mechanical ventilation at the time of LVAD placement were more likely to have persistent RHF. Similarly, a pro-inflammatory milieu (with a PCT cut-off of 0.09 ng/mL) and significantly low haemoglobin levels [18] have been shown to be detrimental, although they require further validation, since they have been tested on a limited sample size of thirteen patients who developed RHF after LVAD placement.

Such findings are likely to reflect the presence of RHF-related end-organ dysfunction, anaemia or subclinical infection, or simply an inflammatory status (which is very common in patients receiving temporary support with Impella (Abiomed, Inc., Danvers, MA, USA) devices or ECMO), which may or may not be fully reversible after LVAD implantation, thereby complicating postoperative management.

Echocardiography is the easiest diagnostic modality to perform and repeat. It can provide insight into RV morphology, function and associated structural or functional abnormalities and their dynamic changes that may lead to the development of RHF.

Several echocardiographic parameters have been tested in clinical trials for their prognostic power for early RV dysfunction in the context of LVAD implantation.

Starting with standard two-dimensional transthoracic echocardiography (2D-TTE), the simple presence of a dilated tricuspid annulus has recently been recognised as an independent predictor of late RV dysfunction after LVAD placement [19], while the impact of the RV/LV ratio is far from unanimous [20, 21]: despite using the same measurement technique, Kukucka found a positive correlation between the ratio and RHF development. However, as only 13% of patients in their cohort suffered from serious post-LVAD RHF, their conclusion is less reliable.

A recent meta-analysis by Chriqui et al. [22] in a total of 1561 patients showed that RV fractional area change (FAC) and RV global longitudinal strain (RVGLS) are likely to be strong predictors of RHF after LVAD implantation; moreover, in contrast to previous single studies including a limited number of patients in different haemodynamic conditions [21, 23], tricuspid annular plane systolic excursion (TAPSE) emerged as a reliable factor in predicting RHF. The already existing uncertainty about the real role of TAPSE is that it describes apex-to-base shortening and thus reflects only one plane of RV contraction; moreover, it is strongly influenced by changes in volume and preload and increases in response to dobutamine infusion [24]; perhaps its combination with other values represents a suggestive way to strengthen its significance, as suggested by Benedetto et al. [24], whose systematic review describes a trend of statistical correlation between TAPSE, FAC and RVGLS with RHF event after LVAD placement. Peak systolic velocity of the tricuspid annulus by pulsed-wave tissue Doppler imaging has been observed to provide prognostic information for RHF after LVAD implantation, with cut-off values ranging from 8.0 to 8.8 cm/s, although data are conflicting [25]. An alternative to overcome the limitations of TAPSE and FAC is the use of 2DTTE with electronic plane rotation, which allows multi-plane quantification of the RV wall for TAPSE and tricuspid annular peak systolic velocity (RV-S’) measurements, which may reveal differences in regional RV wall function [26].

Speckle-tracking echocardiography has been used in LVAD recipients to assess its ability to predict early postoperative RHF: more specifically, lower values of RVGLS [27] and RV free wall strain (with a cut-off value $\le$–15.5%, [15]) are associated with an increased risk of developing RV failure; interestingly, only TTE-derived strain parameters, but not those derived from transesophageal echocardiography (TOE), were found to be significant [28]. Similar conclusions were drawn in the cohort of Aymami [29], who found that the quantitative evaluation of both RV size and function with the association of RV end-diastolic area index and free-wall longitudinal strain was a prognostic marker for RHF after LVAD implantation. Following the conclusions of two other retrospective studies [18, 30], RV free wall strain rather than global longitudinal strain appears to play a more important role in influencing post-LVAD RHF.

Based on the same optic of combining both morphological and functional aspects of the RV to strengthen the predictive power of TTE in the selection of adequate candidates for LVAD, a kind of hybrid echocardiographic index represented by the pressure-dimension one (calculated by dividing the systolic pulmonary artery pressure by the square of the RV minor diameter) has been identified as a possible new marker of an overburdened RV more prone to experience early failure after left assistance [31].

Another interesting measure is represented by the interventricular-septal output (ISO), calculated as (systolic interventricular septum – diastolic interventricular septum) $\times$ heart rate, whose decrease by 25% or more from pre-implant to hospital discharge seems to be associated with RHF [32]. Such a conclusion confirms the strong influence of mechanical ventricular interdependence on RV function and highlights the paramount role of the septal wall.

Concerning TOE, the application of three-dimensional technology seems promising, as 3D-RV ejection fraction and free wall strain have shown a high discriminatory ability (0.876 and 0.914, respectively) in the detection of RHF after LVAD, although tested in a small cohort of patients [33]. 3D measurement of RV end-diastolic volume index (both on TTE and TOE) and end-systolic volume on TTE (with a cut-off of $>$47 mm/m² identified by Kiernan) are associated with the postoperative development of RHF [34, 35]. However, 3D RV ejection fraction showed no predictive value in Kiernan’s cohort.

Silverton et al. [36] and Alfirevic et al. [19] have analysed the impact of several intraoperative TOE-derived parameters on the subsequent occurrence of RHF: interestingly, and in contrast to the same indices calculated at TTE, TAPSE, RV-S’, tricuspid annular displacement and RV strain failed to predict RV impairment, whereas reduced post-bypass FAC was significantly associated with RVF but with poor discrimination. A possible explanation for such conflicting results may be that RV function is highly dependent on haemodynamic conditions and filling; thus, as the patient is under general anaesthesia during intraoperative TOE examination, the performance of RV indices may be confounding.

To overcome the problem of RV load dependence, two TTE-derived dynamic measures, represented by the RV load adaptation index (LAI_RV) and the RV load-corrected peak global systolic longitudinal strain rate (PSSrL $\times$ $\mathrm{\Delta }$P_RV-RA), appear very promising, showing very high predictive values ($\ge$87%) for both RHF and freedom from RHF after LVAD placement for their composite use [37].

In conclusion, the echocardiographic assessment of a patient candidate for LVAD support is far from simple and often requires the association of standard 2D basal values integrated with 3D reconstructions, TOE incidences and speckle-tracking technology.

Although TAPSE, FAC and RV free wall strain appear to correlate well with post-implantation RHF development, the dynamic variables represented by LAI and PSSrL provide greater reliability by incorporating the patient’s overall loading status, which has an important impact on RV characteristics and performance (Table 1).

Currently, CT is not widely used in the preoperative evaluation of the RV in patients scheduled for LVAD implantation, mainly due to the potential nephrotoxicity of the contrast and the need for a stable cardiac rhythm with a low heart rate for image acquisition [4].

Nevertheless, contrast-enhanced electrocardiogram-gated CT angiography (cine-CT)—in which multiple CT images are acquired over the entire cardiac cycle—can be used to perform RV volumetric assessment, and values have been validated against CMR. Scott et al. [38] decided to apply this diagnostic tool in a small cohort of patients on the LVAD waiting list, and showed that CT-derived RV end-systolic and end-diastolic volume indices were the strongest predictors of RHF compared with demographic, echocardiographic and right heart catheterisation (RHC) data, with areas under the receiver operating curve of 0.79 and 0.76, respectively. Although these results are encouraging, the very limited number (7) of patients experiencing RHF and the difficulty of performing cardiac CT in unstable or assisted patients make it difficult to apply this method on a large scale.

CMR is the current gold standard for assessing RV volumes and function. However, CMR remains a relatively expensive diagnostic tool that is not readily available for bedside use. It is also contraindicated in patients with metallic implants (most patients with end-stage HF have a defibrillator or multi-chamber pacemaker) and is limited to haemodynamically stable conditions. For this reason, 3D echocardiography is becoming widely used in clinical practice due to its low cost and availability, although its validation against CMR in quantifying RV volumes and function is still limited, with poor data on inter-observer variability; this issue warrants further investigation [39].

To our knowledge, only one study [40] in the available literature has attempted to compare the accuracy of RV ejection fraction assessment prior to assist device placement using first pass radionuclide angiography: the results were unsatisfactory, with a moderate correlation between angiographic values and reference standard parameters calculated by CMR and echocardiography.

RHC before LVAD implantation is a standard diagnostic procedure to assess RV function, and several invasive haemodynamic variables have been identified as possible markers of early postoperative RHF development. These include an elevated right atrial pressure (RAP, $>$15 mmHg), reflecting increased RV preload [18], a low mean pulmonary artery pressure with impaired RV systolic function, an RAP/PCWP ratio $>$0.63, as well as increased pulmonary vascular resistance (PVR) and an elevated ($>$0.55) cardiac filling pressure ratio (mean right atrial to mean pulmonary capillary wedge pressure ratio) which showed an acceptable area under the curve value of 68% [16, 37, 41, 42]. The isolated finding of reduced pulmonary capillary wedge pressure (PCWP) also appears to be a significant predictor of postoperative RHF within one year [27], probably related to the predominance of precapillary pulmonary hypertension leading to a permanent increase in pulmonary resistance. Interestingly, both higher pulmonary arterial pressure and pulmonary arterial pulse pressure seem to protect against RV failure [13], probably because they act as a training condition for the RV, which is forced to muscularise and push against an important obstacle.

Recently, clinicians’ attention has focused on the potential role of the pulmonary artery pulsatility index (PAPi), a simple haemodynamic calculation [(systolic PA-dyastolic PA)/mean right atrial pressure] initially studied to predict RV dysfunction in adults after acute inferior myocardial infarction [43]. In the context of paediatric LVAD placement, the need for inotropes/pulmonary vasodilators in the postoperative period can be predicted by pre-implantation RV intrinsic contractile reserve as assessed by PAPi rather than by markers of RV afterload [44]. In the adult population, the association between PAPi and post-assistance RHF seems to exist, although not unanimously: on the one hand, Kiernan et al. [45] suggested that patients with a PAPi less than 1.85 have an increased risk of RHF after LVAD; similarly, another study has demonstrated an association of low preoperative PAPi (2.84) with a higher risk of early mortality after the left device placement without affecting 2-year outcomes in survivors [46], as well as a more robust predictive power for RHF when postoperative PAPi (with a cut-off value 1.56) is included in the Michigan score [47]. On the contrary, Alfirevic et al. [19] did not find any reliability of intraoperative PAPi. Again, it can be argued that the measurement of haemodynamic variables concerning the RV under general anaesthesia cannot be compared to a preoperative RHC under “physiological” conditions. It is impossible to detect the reason why different studies identified such a large discrepancy in the discriminating threshold of PAPi, even though the value of 1.85 seems to be the most reliable, as it emerges from a large cohort of around 10,000 LVAD patients [45].

Other parameters derived from RHC, such as RV stroke work index (RVSWi) of $>$300 mmHg $\times$ mL/m² preoperatively, minimise the risk of perioperative RV assist, thus confirming it as a reliable predictor of RHF after LVAD with an area under the curve of 63% [48]. The important role of RVSWi is confirmed by Gumus et al. [15], although they identified a different cut-off value (400 mmHg $\times$ mL/m²) to anticipate an adverse RV outcome.

Table 2 summarises the different RHC variables and their predictive power.

Given the complexity of global RV assessment, risk scoring studies have emerged since the 2000s to better predict RV behaviour after implantation. By incorporating clinical, laboratory and haemodynamic factors, they attempt to take into account the full complexity of end-stage HF patients, focusing on the degree of RV involvement in the process.

The Michigan right ventricular failure risk score developed by the authors is the first model for preoperative risk stratification of RV failure in LVAD candidates [14]. The score is composed of four variables: preoperative vasopressor use (add 4 points), creatinine $>$2.3 mg/dL (add 3 points), bilirubin $>$2 mg/dL (add 2.5 points) and aspartate aminotransferase $>$80 UI/dL (add 2 points); scores above 5.5 are associated with a higher risk of RV failure after LVAD implantation. In the original validation study, this model showed very effective discriminatory power (area under the curve - AUC of 0.73), but a more recent cohort analysis [19] was less satisfactory, similar to PAPi and other echocardiographic variables.

In the same year, the Penn RVAD risk score was developed by Fitzpatrick et al. [49]. This study established a risk model by showing that a low preoperative cardiac index and RVSWi, severe pre-LVAD RV dysfunction, high creatinine level, previous cardiac surgery and hypotension increased the risk of RHF after LVAD implantation. Analysis of this risk score showed that patients with a low score were predicted to have successful LVAD support, whereas patients with a high score were likely to have biventricular assist device (BiVAD) placement.

The UTAH score, elaborated with multivariate regression analysis, identified the need for preimplantation intra-aortic balloon counterpulsation, increased PVR and destination therapy as significant predictors of RHF [50]. With a remarkable AUC of 0.743, the UTAH score is among the more powerful risk models for both RHF and reduced survival at days 30, 180 and 365 after LVAD implantation.

In 2010, Kormos et al. [48] evaluated the incidence, risk factors, and impact on outcomes of RHF in patients implanted with a HeartMate II (Abbott, Plymouth, MN, USA), the so-called Kormos score. Multivariate analysis showed that a RAP/PCWP greater than 0.63, preoperative ventilatory support and a blood urea nitrogen level greater than 39 mg/dL were independent predictors of RHF, although the rates of need for temporary RV assist devices were low compared with previous results with pulsatile LVADs, supporting the use of new-generation continuous-flow devices.

An alternative high performance risk model (AUC 0.74) is the CRITT one [51], which includes RAP $>$15 mmHg, severe RV dysfunction, preoperative intubation, severe tricuspid regurgitation (TR) and tachycardia. By assigning a score of 1 to each variable, Atluri et al. [51] showed that 80% of patients with a score of 4 or higher required BiVAD. A particularly appreciated feature of the CRITT model is that it can be easily calculated at the bedside.

More recently, Raina et al. [23] and Aissaoui et al. [52] proposed two risk models (the TTE and ARVADE scores, respectively) based mainly on echocardiographic parameters, concluding that the combination of different echocardiographic variables could reflect global left ventricular systolic and diastolic dysfunction and RV congestion, thus estimating suitability for LVAD implantation with good reliability.

In 2018, a simple and easy-to-remember risk stratification tool (the ALMA score) [53] was introduced to determine whether an isolated continuous-flow LVAD could be tolerated. A five-point risk score was developed based on clinical variables identified by multivariate logistic regression analysis as follows: the destination therapy intention, PAPi 2, RVSWi 300 mL/m², RV/left ventricle ratio $>$0.75, and model for end-stage liver disease excluding international normalized ratio (MELD-XI) score $>$17. BiVAD was recommended for patients with a score of 4 or 5.

Finally, the EUROMACS-RHF score was tested in a large population from the EUROMACS database [54]. It is composed of severe RV dysfunction, RAP/PCWP ratio $\ge$0.54, advanced INTERMACS classes 1–3, need for $\ge$3 intravenous inotropes and haemoglobin 10 g/dL. A 5-point composite score predicted early RHF after LVAD implantation, and the risk of both RHF and mortality increased as the score increased. Although the authors claimed that the EUROMACS-RHF risk model outperformed previously published scores, its AUC was good (0.75) when applied to the cohort implanted with the HeartMate II, but dropped to an unsatisfactory 0.66 for the latest-generation HeartMate III. Its limited discriminatory power was later confirmed in two external cohorts [13, 55], with AUCs of 0.64 and 0.58 respectively, casting doubt on its true clinical utility. The reasons for such different performances in different populations and devices are difficult to identify. Some hypotheses may include the tendency to better prepare patients for implantation more recently, for example by ensuring they have a higher haemoglobin concentration before surgery, the absence of preoperative RAP/PCWP measurement in patients under ECMO support, and their percentage in the whole population. Another possibility is the need for a learning curve in the management of the “new” HeartMate III, which may have impacted the occurrence of postoperative RHF.

An attempt to compare the predictive performance of each model was made by Peters et al. [56] who retrospectively applied different scores, decision trees and echocardiographic metrics to their cohort of 93 LVAD patients. Interestingly, the older and more established Michigan score, which emphasises preoperative haemodynamic instability and target end-organ dysfunction, remained a superior predictor of postoperative RHF as well as of short- and long-term mortality when compared to the Utah and EUROMACS models. The Michigan RHF score was also the best predictor of in-hospital mortality and long-term survival.

However, these conclusions failed to be confirmed in a more recent retrospective single-centre analysis [57], which found that the EUROMACS-RHF risk score was superior to the Michigan and CRITT models in predicting RHF. The authors took the opportunity to develop a new model based on four variables selected for the best reduced logistic model: INTERMACS level, number of inotropes used, RAP/PCWP ratio and echocardiographic RV/left ventricle diameter ratio. This model showed significant discrimination of RHF with an AUC of 0.9, probably due to the addition of a more objective parameter of RV function assessment, but further testing in different populations is needed.

The currently available risk scores and their receiver operating curves are summarised in Table 3 (Ref. [13, 29, 53, 55]).

To our knowledge, only one study has focused on the intraoperative evaluation of some haemodynamic and echocardiographic measures that could predict the development of severe RHF after LVAD implantation. Gudejko et al. [58], in their cohort of 110 LVAD patients, identified RAP and PAPi after chest closure as reliable factors associated with RHF, whereas quantitative echocardiographic metrics of right heart geometry and function acquired after cardiopulmonary bypass were weakly correlated. Although such considerations are quite appealing, caution must be exercised in drawing simple conclusions, since the early post-implantation period is a very unstable time, experiencing rapid and unexpected changes related to bleeding, adjustment of pump speed, degree of filling, importance of inotropic support, which can alter haemodynamic parameters independently of real RV function.

Assessment of RV contractile reserve by pharmacological stress or exercise testing appears to be key in the evaluation of impaired resting RV function. For example, Guazzi et al. [59] measured TAPSE at rest and at peak exercise: patients with impaired RV function at rest but preserved contractile reserve had better RV-pulmonary coupling, ventilatory efficiency and functional capacity. Even in the context of screening for future LVAD support (which can be thought of as a stress test, since it restores normal left cardiac output and forces the RV to adapt to the new situation), and if the patient’s general condition allows for stress testing, the presence of improved RV contractility during exercise may predict a good RV response to LVAD support.

Remaining in the field of pre-implant pharmacological testing, the cohort of Read et al. [60] underwent vasodilator testing with nitroprusside during their pre-LVAD RHC. Multivariable analysis revealed that peak stroke volume index (SVI) was significantly associated with early RHF, with a 16% increased risk of early RHF per 1 mL/m² decrease in SVI. In addition, follow-up of 10 consecutive patients showed that all patients were appropriately classified as having early RHF or no RHF according to this index. Moreover, resting haemodynamics demonstrated no discriminatory power.

DLCO reduction is a common finding in HF and is associated with a worse prognosis. Its correlations with pulmonary hypertension, and in particular with higher PVR and diastolic pulmonary gradient, have been described prior to LVAD implantation, suggesting that it may be an expression of persistent lung damage in combined post- and capillary pulmonary hypertension; however, DLCO impairment failed to predict early development of RHF or significant morbidity after left support placement [61].

To corroborate their findings and compare different tools for predicting the early occurrence of RHF after LVAD support, many authors have attempted to evaluate the performance of different pre-implant features in the same cohort of patients.

Liang et al. [27] found that echocardiographic RV strain (AUC 0.86) outperformed more invasive conventional haemodynamic measures (including PAPi and RVSWi), as well as the Michigan RV and CRITT scores, both of which were highly specific for RHF at higher values, but were not sensitive.

These conclusions are in complete contrast to those of Peters et al. [56] who found that the Michigan score was superior to PAPi, preoperative RV dysfunction, RAP and PVR in predicting RHF after LVAD. In another group of LVAD patients, preoperative transpulmonary gradient, cardiac index and postoperative PAPi were the only haemodynamic variables associated with the development of RHF. However, the best predictive power was obtained when the Michigan score was combined with post-implant PAPi, with an area under the receiver operating characteristic curve of 0.73 [47].

Sert et al. [62] described the performance of different risk scores and their combinations (Michigan, Pennsylvania, CRITT, ALMA and EUROMACS) in a retrospective study of 71 patients who underwent continuous-flow LVAD placement between 2013 and 2016. Each model alone showed poor discrimination (AUC below 0.7), with slightly better performance for the CRITT and EUROMACS scores. The addition of the Michigan and Pennsylvania models did not improve their predictive power, while the association of TAPSE + Pennsylvania was found to have the highest sensitivity (85%), while TAPSE + Michigan + RAP/PCWP appeared to be the most specific combination.

Once again, it is clear that unanimity is far from being achieved. This may be due to the retrospective nature of the cited validation studies and their application to small populations (100 included patients).

Several parameters have been identified as strong predictors of the development of RHF after LVAD:

(1) Patients with a small left ventricle (with a cut-off left ventricular end-diastolic diameter of 59 mm) have an increased risk of requiring temporary RV mechanical support, as well as a higher incidence of late RHF, poorer short- and medium-term survival, and more frequent readmissions due to gastrointestinal bleeding and low flow alarms [63].

(2) Pre-operative atrial fibrillation appears to show a trend (although not statistically significant) towards an association with a higher rate of early RHF after implantation [64].

(3) The role of residual mitral regurgitation after LVAD support may be important: in their cohort of 155 consecutive patients, Sharma et al. [65] describe an expected improvement in the severity of both tricuspid and mitral insufficiency as a result of effective left ventricular unloading in the majority, although about 15% of device recipients had persistent significant residual mitral regurgitation, which is associated with RV dysfunction and higher long-term mortality. This may be predicted by preoperative greater left ventricular end-systolic diameter, right ventricular end-diastolic diameter, left atrial volume index and ischaemic aetiology. A recent meta-analysis [66] confirmed the effect of LVAD in improving left ventricular haemodynamics and promoting resolution of mitral regurgitation. Furthermore, the authors showed that the presence of pre-deployment moderate to severe mitral insufficiency (grade II–III) did not affect mortality or morbidity, but increased the risk of developing RHF.

(4) Tricuspid regurgitation (TR) is common in patients with end-stage HF and is part of an interplay with other risk factors (e.g., RV dysfunction, pulmonary hypertension, and renal or hepatic impairment). Many questions remain unanswered, including the impact of tricuspid insufficiency after device implantation on long-term mortality and the impact of concomitant surgical correction on postoperative outcome and in particular on the development of RHF [67]; current guidelines recommend consideration of tricuspid valve surgery in the presence of moderate to severe regurgitation at baseline. However, the key seems to be appropriate patient selection, taking into account the aetiology of TR, the severity of RV dysfunction (it is important to remember that closing a retrograde exit door in an impaired RV can be detrimental) and the underlying myocardial disease. Primary TR (e.g., caused by a defibrillator or pacemaker lead) may not decrease spontaneously after LVAD placement, whereas functional TR is likely to do so. However, functional TR can be caused not only by annular dilatation but also by valve tethering, which will not be completely reduced by annuloplasty. Overall, TR decreases after device implantation regardless of pre-LVAD pulmonary hypertension or RV function. Therefore, additional tricuspid surgery may be redundant in most patients, even considering that it has been associated with an increased risk of RV dysfunction at 3-month follow-up, possibly indicating a subtle, unrecognised RV impairment in these patients [68].

(5) Concerning molecular mechanisms potentially involved, preliminary data suggest a role for SPARC-related modular calcium-binding 2 protein (SMOC2) and TRAPP6AC in favouring RHF after LVAD, although further confirmation in larger populations is needed [69].

(6) A mini-invasive approach through a limited thoracotomy appears to significantly protect against the occurrence of RHF after LVAD placement, thereby reducing the incidence of all-cause mortality, acute renal failure and stroke [70].

(7) The development and application of artificial intelligence and machine learning is a promising area, although its performance is currently far from ideal [71].

IABP remains a simple and widely used mechanical assistance that can help to stabilise decompensated patients with advanced HF. Some evidence in the medical literature [72, 73] described that IABP, placed through the femoral or subclavian approach, improved some parameters reflecting RV function, allowing a lower rate of RHF development in case of LVAD support. These data were confirmed by a report from the INTERMACS registry [74] showing that patients with IABP prior to LVAD, despite having a more advanced HF stage including worse RV function, had the same outcomes compared to the less severe patients who did not require pre-LVAD IABP, suggesting a protective role of the balloon against RHF development. The physiological mechanisms underlying such a phenomenon may include an increase in oxygen delivery to the right myocardium, improvement in right coronary perfusion and, more generally, a reduction in diastolic pulmonary artery pressure and PCWP; logically, these benefits become less likely the more fibrotic the RV free wall is [75].