Right heart failure after left ventricular assist device implantation: latest insights and knowledge gaps on mechanism and prediction

Heart failure is a global health concern, with many patients being unresponsive to medical therapies. In end-stage disease, left ventricular assist devices (LVADs) offer an alternative to transplantation, yet their clinical course remains unfavorable, with up to one in four patients dying within a year. Although LVAD implantation aims to alleviate left-sided congestion and reduce right ventricular burden, a significant proportion of patients develop RHF, which is a major driver of morbidity and mortality. The underlying mechanisms leading to RHF remain a subject of debate, with no definitive conclusions reached. Due to the heterogeneity of heart failure pathophysiology, clinical data varies, and the translation of preclinical findings into effective bedside management remains challenging. These factors collectively hinder the precise characterization of RHF mechanisms, with some proposed explanations remaining speculative. Assessing the risk of RHF development based on pathophysiological insights is essential. However, predicting the progression of RHF following LVAD implantation remains difficult due to complex hemodynamic interactions and the lack of established guidelines, often leading to missed opportunities for timely right ventricular (RV) support device implantation. To reduce the incidence of RHF, this review aims to provide insights into RV failure mechanisms and propose a refined predictive approach. Although data in this field is rapidly evolving, explanations and assessment methods have not been significantly updated. This paper consolidates recent findings, presents updated perspectives, and identifies remaining gaps in knowledge.

1 Introduction

Heart failure (HF) affects more than 65 million worldwide, with many patients being unresponsive to medical therapies (1). For those with end-stage HF, mechanical circulatory support (MCS), in the form of left ventricular assist devices (LVADs), has emerged as a bridge to transplantation, to a decision, or to myocardial recovery, as well as destination therapy in patients in whom cardiac transplantation is contraindicated (2).

Despite advances in LVAD indications, the incidence of right heart failure (RHF) after LVAD implantation remains a major concern, where the dysfunctional right ventricle (RV) undermines hemodynamic stability and is a driver of morbidity and mortality (3, 4). Previous studies report that 10%–35% of patients experience RHF within one month following LVAD placement (5–8) and the in-hospital mortality rate of LVAD recipients requiring right ventricular assist device (RVAD) was up to 50%, while patients undergoing planned biventricular assist device (BiVAD) placement face a mortality rate of 30% (6).

Considering that LVADs relieve congestion in the left-side heart and, consequently, the right side, the underlying mechanism of RHF is challenging to fully elucidate. Several contributing factors have been discussed in previous reviews, including excessive LVAD suction disrupting ventricular interdependence and increased LVAD flow elevating RV preload, yet adequate evidence supporting some of these phenomena is lacking, with speculative components included. Additionally, it remains unclear which mechanisms are well supported by firm evidence and which remain hypothetical (9). Most of the current evidence relies on load-dependent functional parameters, further raising concerns about their reliability in LVAD patients, where loading conditions fluctuate dramatically (10–12).

Additionally, planned BiVAD implantation potentially improves the outcomes as mentioned previously (6), yet the definitive indication for simultaneous LV and RV support device implantation is unclear. Although numerous factors have been proposed as predictors for RHF after LVAD implantation, their reproducibility remains inconsistent.

To advance our understanding of the mechanism and possibly improve the prediction of post-LVAD RHF, this review aims to: (i) examine the recently proposed pathophysiological mechanistic evidence from the human pressure-volume (PV) loops to capture load-independent functional parameters such as RV end-systolic elastance (Ees) and end-diastolic pressure volume relation (EDPVR); (ii) evaluate existing functional assessment approaches and risk scores to predict RHF development, and consolidate the key factors; and, (iii) clarify the current knowledge gaps and future research directions. To capture the latest insights, we conducted an extensive literature search in PubMed MEDLINE, Scopus, Embase, and ClinicalTrials.gov using controlled keywords, primarily “LVAD” and “RHF.”

Figure 1 illustrates the principal concepts discussed in this review. The goal of this review is to assist clinicians in optimizing LVAD management and guiding research, ultimately to improve patient outcomes.

Figure 1

Figure 1. Graphical abstract. Illustration outlines the primary impact of an LVAD on the RV, including underlying mechanisms driving post-LVAD RHF. The table at the bottom summarizes changes in RV function and loading conditions following LVAD implantation. The column on the right identifies strong predictors for RHF including non-cardiac factors, all of which are incorporated into at least two representative risk scores and have been identified as significant predictors in large scale multivariable analyses. LVAD, left ventricular assist device; TR, tricuspid regurgitation; RV, right ventricle; RHF, right heart failure; MCS, mechanical circulatory support; RV LS, right ventricular longitudinal strain; RVSWi, right ventricular stroke work index; PAPi, pulmonary artery pulsatility index; RAP, right atrial pressure; PCWP, pulmonary capillary wedge pressure.

2 RHF definition

The Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) and the updated Mechanical Circulatory Support—Academic Research Consortium (MCS–ARC) definitions of RHF have been widely accepted (13, 14). In the most recent consensus statement from 2020, RHF is classified into three categories based on the timing of symptom onset (Table 1) (14):

1. Early acute RHF,

- requiring concomitant implantation of a temporary VAD or

- requiring RVAD with an LVAD implantation

2. Early post-implantation RHF,

- requiring a RVAD <30 days or

- failing to wean from inotropes, vasopressors or nitric oxide within 14 days, or

- death attributable to RHF <14 days from an LVAD implantation

3. Late RHF,

- requiring a RVAD more than 30 days or

- requiring hospitalization for RHF >30 days after an LVAD implantation

Table 1

Table 1. MCS-ARC definition of right heart failure.

In addition to these categories, the diagnostic criteria also include multiple clinical indicators, such as hemodynamic parameters (elevated central venous pressure, reduced cardiac index, and reduced venous oxygen saturation), right heart failure symptoms (e.g., edema, ascites), and end-organ dysfunction (e.g., kidney dysfunction, liver failure) (14). Furthermore, the statement also recommends classifying RHF incidence into three categories based on its associations: (1) patient-related (e.g., valvular heart disease, pulmonary disease, cardiorenal syndrome); (2) management-related (e.g., surgical procedures, inotrope withdrawal, volume overload); and (3) device-related (e.g., pump malfunction, outflow graft compromise). Early RHF occurs most frequently. In a recent study using the STS INTERMACS database, the prevalence of de novo RHF at one month (i.e., early RHF) was as high as 24% (8).

Although the overall prevalence of late RHF remains stable and less than early RHF at a rate of 8%–10% over their three-year surveillance, it cannot be underestimated (8). This is because late RHF is also associated with the least favorable outcome (8, 15). Takeda et al. demonstrated the prognostic significance of late RHF after continuous-flow LVAD implantation, with the survival of patients with RHF progressively worsening compared to that of patients without RHF (Figure 2) (16).

Figure 2

Figure 2. Comparison of survival rate between patients with and without right heart failure five-year kaplan-meier curve between patients with and without RHF.. RHF was defined as rehospitalization and medical treatment because of recurrent RHF or patients who required continuous inotropic support because of persistent RHF >4 weeks after implantation. The survival curve gap between the two groups widens year by year. Reproduced with permission from “Comparison of survival: non-RHF group versus RHF group. RHF, right heart failure” by Koji Takeda, Hiroo Takayama, Paolo C. Colombo, Ulrich P. Jorde, Melana Yuzefpolskaya, Shinichi Fukuhara, Donna M. Mancini and Yoshifumi Naka, licensed under CC-BY-NC-ND.

This definition is widely adopted in most studies and is therefore used in this review.

3 Mechanisms of RHF

This section outlines the impact of implantation of an LVAD on the RV and discusses the potential mechanisms driving RHF. In the later part of the section, PV loop data from clinical studies are summarized, as it accurately reflects afterload and preload on RV and provide load-independent functional parameters such as Ees and EDPVR (Figure 3). Moreover, PV loops also provide pulmonary artery (PA) effective arterial elastance (Ea) and the RV Ees/Ea ratio, commonly referred to as “RV-PA coupling,” which serve as valuable indices of RV contractility in relation to the afterload imposed by the PA (17). These approaches will contribute to a more comprehensive understanding of RHF mechanisms.

Figure 3

Figure 3. Pressure-Volume loop and right ventricular and pulmonary artery coupling. The steady-state RV PV loop (black line) illustrates the relationship between pressure and volume during a cardiac cycle. The enclosed area by the PV loop represents RV stroke work. By reducing preload (e.g., via inferior vena cava occlusion or the Valsalva maneuver), multiple PV loops can be generated, from which Ees and EDPVR can be derived. Effective pulmonary arterial elastance (Ea; blue) is a determinant of RV afterload. The RV Ees/Ea ratio describes RV-PA coupling, assessing contractility relative to load. An optimal ratio (1.5–2.0) ensures cardiac efficiency, whereas uncoupling (0.6–1.0) signifies RV decompensation (17, 20). RV, right ventricle; PV, pressure volume; Ees, end-systolic elastance; EDPVR, end-diastolic pressure volume relationship; Ea, effective arterial elastance.

A fundamental understanding of interventricular interaction is essential to grasp this section, as it plays a critical role in the pathophysiology of post-LVAD RHF. The Torrent-Guasp helical model describes the entire heart as composed of two interconnected loops of the myocardium (18, 19). One loop has muscle fibers wrapping around both ventricles in parallel with a short axis at their basement, and the other loop has fibers spiraling around the left ventricle (LV), including the interventricular septum. The RV is constructed from these two fiber systems, with the free wall formed by the first (wrapping) myocardial loop and the septal wall formed by the second (helical) structure. This structure is crucial because the “helical” or “twisting” motion of the secondary loop significantly contributes to the RV systolic function. This LV “twisting” contributes to longitudinal motion of RV, while wrapping myocardium primarily facilitates “transverse (radial)” movement of RV free wall (20, 21).

According to studies in a canine model by Hoffman and colleagues, where the RV free wall was replaced with a xenograft pericardial patch, LV motion accounted for 24%–35% of RV stroke work (SW) (22). Thus, RV function can be significantly influenced by the LV through the septal wall, which is key factor in the occurrence of RHF after LVAD implantation.

3.1 LVAD-specific effects on RV

The following mechanisms can act individually or in combination: (1) Loss of LV twist, (2) Leftward shift of the interventricular septum, (3) Changes in RV Loading Conditions Due to LVAD, (4) Worsening of functional tricuspid regurgitation (TR), (5) Aortic insufficiency (AI). Notably, these mechanisms remain incompletely characterized in the literature, as studying the mechanisms of RHF in patients is challenging presumably due to the heterogeneity of LVAD candidates' pathophysiology and the lack of accurate human data.

3.1.1 Loss of LV twist

- Decrease in RV contractility

In LVAD patients, LV twisting motion is primarily impaired due to two factors: (1) loss of constraint following pericardiotomy, and (2) constraining of the LV apex and septum.

The relationship between pericardial constraint and LV twist has been frequently discussed in the past. A preclinical study demonstrated a decline in LV twist, measured by LV speckle tracking, following pericardiotomy—due to the loss of pericardial constraint, suggesting that this constraint plays a significant role in LV twist. This study was specifically designed to investigate the role of the pericardium and further revealed that the decline in LV twist was restored after pericardial closure (23). Additionally, impaired longitudinal motion of the RV after pericardiotomy has been reported in clinical settings including mitral valve surgery, heart transplantation and coronary artery bypass graft (CABG) surgery, whereas other thoracic surgeries, such as lung transplantation, did not demonstrate a similar effect. Given that LV twist plays a significant role in the longitudinal movement of the RV, RHF after LVAD implantation may be attributable to the loss of LV twist. Long-term follow-up studies have reported that this reduction in longitudinal motion persists for more than one month even after chest closure (23–26). Clinical data linking the loss of LV twist to pericardiotomy specifically in LVAD implantation remain sparse, highlighting the need for further data accumulation to support this explanation.

Additionally, the LVAD replacement to the LV apex can also constrain the LV apex and septum, potentially impairing LV twisting movement (Figure 1). This deformation is considered to negatively affect RV outflow although clinical research on this impact remain limited (20). However, data directly supporting this mechanism also remain scarce, making this impact somewhat speculative. More detailed data on LV twist in LVAD patients are needed.

3.1.2 Leftward shift of interventricular septum

- Decrease in RV contractility - Improvement in RV diastolic compliance

In an LVAD configuration, suction within the LV displaces the interventricular septum leftward, altering its geometry, reducing septal motion, and consequently diminishing RV contractility, while simultaneously improving RV diastolic compliance (9).

A decline in RV contractility by leftward shift of the interventricular septum is the subject of debate (27), and preclinical studies support this expectation (28, 29). Since the interventricular septum plays a pivotal role in RV systolic function, as previously mentioned, excessive LVAD suction can impair septal wall motion, thereby compromising RV function. A study on PV loops and septal strain for RV contractility assessment in LVAD patients found that alterations in RV Ees during ramp test were significantly correlated with RV septal strain (r = 0.78, p = 0.02) but not with free wall strain (r = 0.45, p = 0.26), highlighting the critical role of the interventricular septum in RV contractility (30). Impaired septal movement can be compensated by the RV free wall; however, this mechanism fails in patients with a high afterload. In this context, contractile impairment significantly affects RV SV, resulting in RV-PA uncoupling (20).

In contrast to contractility, leftward septal deformation can enhance RV compliance. Left-sided suction allows the RV to expand further, even under low end-diastolic pressure, thereby increasing diastolic compliance, a mechanism that will be discussed later in the PV loop part (3–2. PV loop in patients with LVAD). This effect is beneficial to the RV, and does not directly contribute to RHF (31).

3.1.3 Changes in RV loading conditions due to LVAD

- Decrease(/Increase) in RV afterload - Decrease/Increase in RV preload

To avoid confusion, this paper defines afterload/preload as end-systolic pressure (ESP) and end-diastolic pressure (EDP), respectively as per Guyton and Hall Textbook (32). LVAD unloading generally relieves the load on the RV. However, preload can increase in specific conditions, such as RV dysfunction, TR, and LVAD-induced AI. Since claims especially regarding changes in preload after LVAD implantation vary depending on review papers (33, 34), we present actual hemodynamic data of ESP and EDP to support our discussion.

RV afterload

Since an LVAD relieves congestion on the left side of the heart and in the pulmonary circulation, RV afterload is generally expected to decrease following device placement. Below, we have listed three papers that report a reduction in RV afterload (ESP) or related components, including pulmonary capillary wedge pressure (PCWP) and mean PA pressure.

1. Data from Brener and colleagues demonstrated a slight but significant decrease in RV afterload during a temporary increase in LVAD speed (RV ESP 31.58 ± 9.75–29.58 ± 9.41 mmHg: p = 0.02) (35).

2. Regarding factors related to RV afterload, Masri and colleagues reported pulmonary artery catheter (PAC) data showing a significant reduction in PCWP (23.2 ± 7.6–14.9 ± 7.3 mmHg; p < 0.01) and mean PA pressure (from 35.9 ± 9.9 to 23.3 ± 7.7 mmHg; p < 0.01) within 72 h after LVAD implantation with a volume displacement pump (63%), axial pump (26%), and centrifugal pumps (11%) (36).

3. This trend generally continues over the long-term, as another study reported sustained decreases in PCWP (from 23 [1st and 3rd interquartile 17, 30] to 12 [7, 17] mmHg) and in effective arterial elastance (Ea; from 1.31 [0.7, 1.62] to 0.59 [0.42, 0.9] mmHg/ml) over six months after implantation of axial pumps (28%) and centrifugal pumps (72%) (37).

However, specifically in cases of AI, afterload may increase. Hemodynamic data comparing pressure parameters showed that patients who developed AI had higher mean PA pressure and PCWP compared to those without AI (38, 39).

RV preload

Preload, or RV end-diastolic pressure (EDP), decreases or remains stable immediately after LVAD implantation because of LVAD suction.

Below, we have listed three papers that report a reduction or stabilization in RV preload.

1. PV loop data from Brener and colleagues also demonstrated a slight decrease in preload (RV EDP 7.95 ± 3.55–7.42 ± 3.29 mmHg: p = 0.04).

2. Right atrial pressure (RAP) also generally decreases or stabilizes in the short term (RAP: 11.8 ± 6.5–10.1 ± 5.4 mmHg) after LVAD implantation with volume displacement pump, axial pump, and centrifugal pumps (36)

3. This trend generally continues over the long-term (RAP: 11 [1st and 3rd interquartile 5, 16], 10 [5, 15] mmHg) after implantation of axial pump and centrifugal pump (37).

Changes aforementioned are slight and biologically insignificant, suggesting that RV preload remains unchanged after LVAD implantation. However, in the presence of RV dysfunction, functional TR, or AI, preload may increase (40). The impact of AI and TR on the RV is discussed later in sections “3-1-4. Worsening of Functional Tricuspid Regurgitation” and “3-1-5. Aortic Insufficiency”.

Notably, there is an explanation suggesting that RV preload increases due to LVAD flow (34), probably based on data showing an increase in RV EDV (41). However, the studies examining changes in RV EDP, RAP, or CVP, not EDV, immediately after LVAD implantation or during ramp test, generally demonstrate either a decrease or stability in these values (35, 42, 43). An increase in RV EDV may result from improved RV compliance due to LVAD-induced suction; therefore, careful interpretation of these parameters is necessary to accurately assess true RV preload following LVAD implantation.

However, excessive LVAD speed remains a potential concern in LVAD management, because excessive LVAD speed may significantly impair RV contractility by disrupting LV twist and septal motion. In this dysfunctional RV, increased preload may be required to maintain stroke volume and circulatory equilibrium (41).

3.1.4 Worsening of functional tricuspid regurgitation

- Increase in preload

Leftward shift of the septal wall can enlarge the tricuspid annulus, potentially inducing functional TR (44, 45). However, the real-world data has shown that over 50% of moderate-severe TR improves following LVAD implantation, attributed to the reduction in afterload (46–48). A particular proportion of patients (30%) still have persistent TR, and 6%–20% develops significant TR following surgery (46–48), both of which are associated with RHF development (44). Nakanishi and colleagues identified preprocedural tricuspid valve annular diameter as a predictor of persistent or worsening TR (49) and atrial fibrillation (AF) has also been reported as a potential predictor (48, 50). However, a large registry study from INTERMACS did not demonstrate a prognostic benefit of tricuspid valve procedures at the time of LVAD implantation, suggesting that the extent to which TR contributes to the development of right heart failure (RHF) remains unclear. Rather, TR may be a consequence of right heart enlargement secondary to RHF (51).

3.1.5 Aortic insufficiency

- Increase in preload and afterload

AI increases preload on the LV and, ultimately RV (52). Indeed, AI has been linked to worsening mitral regurgitation following LVAD implantation, further supporting significant volume overload on the LV and subsequent negative effects on RV (53). Given its gradual progression, AI may contribute to late RHF.

Aortic insufficiency (AI) can develop over time due to LVAD outflow into the aorta. According to the STS INTERMACS registry, 15% of patients developed AI ≥moderate at 2 years after LVAD implantation, which was associated with poor outcomes (53). Importantly, this percentage gradually rose after LVAD implantation, having reached 37.6% within three years (54, 55).

At the time of LVAD implantation, it is reasonable to consider concomitant procedures on the aortic valve for more than mild AI and the outflow graft anastomosis should be oriented downstream to prevent the development of or progression of AI. However, outcome data on these interventions remain conflicting, and the effectiveness has not been clearly demonstrated (56). Following implantation, optimizing LVAD flow is also required to avoid excessive output to the aorta (54).

3.2 PV loop in patients with LVAD

This section summarizes data on the RV PV loop during a ramp test in patients with an LVAD, to capture true or intrinsic change of RV function due to LVAD suctioning.

Brener et al. published data in HeartMate3 recipients (n = 19) recruited from two sites (35). Based on the statistical analysis of ramp tests including all patients, they concluded the impact of an LVAD on the RV is as follows:

1. No significant decline in RV contractility

2. Improvement in RV diastolic compliance

3. Reduction in RV afterload

Notably, contractility did not significantly change, which contradicts the commonly held view that RV contractility declines due to loss of LV twist and impaired septum motion. In their study population, as pump speed was increased from 5,000 to 5,800 rpm, the RV PV loop expanded rightward and shifted downward, indicating an increase in SV and SW in response to higher pump speed. This change is attributed to “an improvement in diastolic compliance (EDPVR), also referred to as adaptive diastolic compliance in response to LVAD suctioning,” as well as “a reduction in afterload” (Figure 4A). From this perspective, therefore, the RV may accommodate the increased flow generated by the LVAD through enhanced diastolic function. In contrast, part of RVs in their study show inability to improve EDPVR, referred to inadaptive diastolic compliance, and only afterload is decreased in response to increased LVAD flow (Figure 4B), where PV loop shifts only downwards without rightward shift. These RVs failing to increase RV diastolic compliance, may be unable to generate a comparable SV, which may result in compromised hemodynamics and RHF.

Figure 4

Figure 4. Transformation in right ventricular pressure-volume loop during ramp test. Depicted is the schematic illustration of RV PV loop transformation based on the current study (35). With the increase in LVAD pump speed, the EDPVR curve leans downwards, and the inclination of Ea line gets smaller (rightward/downward shift in RV PV loop), meaning that diastolic compliance improves, and afterload decreases (A) However, they identified certain recipients whose EDPVR does not improve and only RV afterload decreases (only downward shift) in response to pump speed, susceptive of inadaptive diastolic compliance, which may compromise hemodynamics and causes RHF (B) RV, right ventricle; PV, pressure-volume; Ea, effective arterial elastance; Ees, end-systolic elastance; EDPVR, end-diastolic pressure-volume relationship; SW, stroke work; SV, stroke volume; LVAD, left ventricular assist device; RVSWi, right ventricular stroke work index; RHF, right heart failure.

Although the authors (35) concluded that contractility did not change, this interpretation should be treated with caution given the study limitation: (1) all patients were stable outpatients in a late postoperative phase, with a median of 144.5 days (interquartile range: 53.5–357 days) after LVAD implantation; (2) the small sample size (n = 19) limits the generalizability of the findings: and (3) only temporary changes were considered in this study, leaving uncertainty regarding the chronic impact of LVAD support. Further research with a larger, more heterogeneous cohort and longitudinal assessments is needed to draw more definitive conclusions about systolic function.

Besides, Scheel et al. also reported the measurement of RV Ees using conductance catheters in HeartMate 3 (Abbott, Chicago, IL) and HeartWare (Medtronic, Minneapolis, MN) recipients (n = 13) (30). During their ramp test (low, intermediate, and high speeds, increased by 100–200 rpm), RV Ees declined in specific cases. These findings differ from those reported by Brener et al., suggesting a heterogeneous impact on a case-by-case basis and underscoring that the negative effect of LVAD pump suction on RV contractility still cannot be overlooked.

Of note, all cases studied in the above reports were stable outpatients from 1 to 12 months after LVAD implantation, and thus their RVs may have been stable and managed well. Based on these results and previous data, we summarized the impact of LVAD on RV in the table on Figure 1.

3.3 RHF mechanism and knowledge gaps

Based on the latest evidence, we propose the following LVAD-specific mechanisms of RHF:

1. Inadequate Adaptation of Diastolic Function to Increased Flow: While diastolic compliance generally improves to accommodate the increased flow and generate more SV comparable to LVAD-generated SV, some RVs with unchanged diastolic compliance fail to provide the necessary SV, possibly leading to RHF (Figure 4B).

2. Reduced Contractility: RV contractility declines due to the loss of LV twist and reduced mobility of the septal wall caused by LVAD suction. Compromised contractility leads to RV-PA uncoupling and RHF, particularly in patients with high afterload, where the RV free wall fails to compensate for impaired septal movement.

3. Elevation of Preload: Dysfunctional RV and other factors (e.g., functional TR and AI) can increase preload chronically and result in RHF.

This represents the simplest scenario; however, other factors—such as the progression of underlying RV or pulmonary vessel diseases and de novo AF—can further compromise RV function and hemodynamic conditions. HF is invariably heterogenous.

The knowledge gap identified from the literature search is the scarcity of firm clinical evidence on proposed mechanisms, particularly on LV twist, and load-independent functional assessments using PV loop derived parameters such as Ees, EDPVR and Ees/Ea in real-world LVAD recipients. These limitations restrict the understanding of RHF within the expected range. Further data from human studies, including heterogenous patients are required to achieve a more definitive understanding.

4 Functional parameters and predictive value

Functional assessment of RV is essential to predict the likelihood of RHF following LVAD implantation (6). Severely depressed RV function prior to LVAD placement is one of the most significant predictors [odds ratio [OR] 1.60; 95% confidence interval [CI] 1.17–2.20; p = 0.004] in the multivariable analysis of STS–INTERMACS database (5–8). However, accurately assessing RV function remains a long-standing challenge. In end-stage HF, loading conditions fluctuate dramatically, undermining the reliability of functional parameters. To enhance the prediction of post-LVAD RHF, this section summarizes the relevant functional parameters, highlighting their utility and identifying the existing knowledge gaps.

The latest consensus statement recommends evaluating tricuspid annular plane systolic excursion (TAPSE), systolic tissue Doppler velocity of the tricuspid annulus (RV S'), right ventricular fractional area change (RV FAC), and right ventricular longitudinal strain (RV LS) prior to LVAD implantation (57). Echocardiography is the initial imaging modality of choice accessible for severely ill patients, with CT and MRI considered if echocardiographic findings remain inconclusive. Beyond these imaging modalities, right heart catheterization (RHC) parameters provide incremental value for assessing RV function in a load-independent manner, such as RVSWi, and pulmonary artery pulsatility index (PAPi) (58, 59). Although RAP/PCWP does not typically reflect RV function, it is included in this section as it is also derived from a RHC. This section highlights the predictive value (Tables 2–6), and limitations of these indices.

Table 2

Table 2. Performance of systolic function parameters.

Table 3

Table 3. Performance of diastolic function parameters.

Table 4

Table 4. Performance of RVSWi.

Table 5

Table 5. Performance of PAPi.

Table 6

Table 6. Performance of RAP (CVP)/PCWP.

4.1 Systolic function

TAPSE, RV S', RV FAC, and RV LS are the most commonly used parameters for measuring RV systolic function. A meta-analysis demonstrated that TAPSE, RV FAC, and RV global longitudinal strain (GLS) reliably distinguish between patients who do and do not develop RHF (60). Among these parameters, RV free-wall longitudinal strain (FWLS) is specifically recommended for evaluating subclinical RV dysfunction in LVAD candidates (57). Indeed, RV LS generally demonstrates superior performance in predicting RHF and adverse events, in comparison to TAPSE, RV FAC (Table 2).

Limitations: However, it is important to note that these parameters represent geographic or volumetric changes in the RV, rather than “contractility” or “Ees” derived from the PV loop, strictly speaking (61). Consequently, they have load-dependency, which is a critical limitation in capturing intrinsic RV function data in severe heart failure, where afterload and preload can dramatically fluctuate (10–12). Although Ees derived from the PV loop is considered the gold standard for assessing contractility independently of loading conditions, its routine use in daily clinical practice is limited by the invasiveness, analytical complexity, and high cost (62).

Additionally, all these assess only regional function, and TAPSE and RV S' have angle dependency, thus requiring clinicians to be cautious when interpreting actual values (61). Given the complex structure of the RV, three-dimensional ejection fraction would be ideal to capture more global motion (63), yet this approach is technically challenging to accurately visualize and is not widely available in real-world clinical settings, as indicated in current guidelines (64).

Moreover, the median values of TAPSE (1.03–1.61 cm), RV FAC (18.7%–40.4%), and RV GLS (6.7%–12.6%) in patients who developed RHF vary widely across studies (60), suggesting their unreliability as definitive predictors of RHF. Therefore, careful consideration of simultaneous loading conditions, or other load-dependent indices is highly recommended.

4.2 Diastolic function

Given the discussion in the previous section of pathophysiology, the adaptability of diastolic function can be a key contributor to post-LVAD RHF development, yet the data remains particularly scarce (65). In echocardiography or MRI, trans-tricuspid E/A ratio, deceleration time of peak E velocity, E/e', RV diastolic strain rate (DSR), or right atrial (RA) strain are used to assess RV diastolic function (66). E/e' is associated with RV filling pressure, and E/e' > 10 may be helpful in predicting post-LVAD RHF. However, the supporting evidence is limited to univariable analysis, and further investigation is warranted (67). In addition, impaired peak RA strain, which also reflects RV filling pressure or RA reservoir function, was reported as another independent predictor of subsequent RVAD implantation (68). Their analysis demonstrated excellent predictive values of diastolic functional parameters including peak RA strain and late diastolic strain rate, outperforming RV LS.

Furthermore, catheter-derived RA waveforms show better predictive values for RHF. A deeper Y descent compared to X descent, indicative of impaired RV diastolic compliance, demonstrated a high OR of 10.5 (95% CI 1.75–63.5), surpassing other catheter-derived parameters such as central venous pressure (CVP)/PCWP, PAPi, and RVSWi (69).

Limitations: As a significant knowledge gap, evidence pertaining to diastolic function remains extremely limited, and even studies investigating systolic function often do not compare their findings to diastolic function parameters (Table 3). However, the data on diastolic function parameters identified thus far have demonstrated excellent utility in predicting post-LVAD RHF or mortality, comparable or even superior to RV LS, and further studies are strongly warranted.

4.3 RV-PA coupling

RV Ees/Ea, or RV-PA coupling, serves as a mediator of RV contractility while accounting for PA elastance or afterload, and is primarily measured using a conductance catheter and PV loop. Scheel and colleagues demonstrated that a lower RV Ees/Ea (below 0.35) was associated with more frequent heart failure symptoms compared to a RV Ees/Ea ≥0.35 (71% vs. 17%, p = 0.048), suggesting that this parameter effectively captures an uncoupled, abnormal RV state by incorporating loading conditions (30, 42). However, as previously mentioned, data obtained using conductance catheters and PV loops remains limited.

Recently, the ratio of echocardiographic systolic parameters, such as TAPSE, RV S', RV LS, and approximated pulmonary artery systolic pressure (PASP), have been employed as a surrogate of RV Ees/Ea (61). This echocardiographic surrogate has been adopted across various patient populations (70), yet the utility in LVAD population is unclear, with studies indicating that this parameter lacks predictive value for RHF development (71–73).

Limitations: A few limitations should be considered: (1) PASP estimation is challenging in cases of severe or greater TR due to the widened regurgitant orifice, which hinders the accurate capture of the pressure gradient; (2) TAPSE, RV S', and RV LS do not fully capture global RV systolic function, as they provide only regional assessments, which is problematic in an enlarged, dysfunctional RV; (3) in end-stage RV dysfunction, PASP may not increase as expected due to the RV's inability to generate sufficient flow and pressure, being critical to use PASP as a surrogate of Ea (66, 70). Although RV-PA coupling is reliable indices, adoption of echocardiography estimate in LVAD is not clearly explored.

4.4 RVSWi

The right ventricular stroke work index (RVSWi) reflects the RV external workload, representing the area enclosed by the PV loop. It is obtained from PV loops using a conductance catheter or estimated using RHC-derived parameters based on the following formula:

$$\begin{gathered} \mathrm{RVSWI}=(\mathrm{mean}\mathrm{PA}\mathrm{pressure} \\ \mathrm{ndashCVP})\times \mathrm{SVindex}(\times 0.0136) \end{gathered}$$

RVSWi is considered a load-independent parameter and is particularly useful in evaluating complex pathophysiology, where loading conditions are highly variable (74). In general, RVSWi decreases in dysfunctional RV because low Ees and impaired EDPVR are unable to generate sufficient external workload (74). Specifically, RVSWi <250, 300, or 400 mmHg L/m² are used for cut-off points for predicting post-LVAD RHF (75–77).

The recent meta-analysis demonstrated the highest standard mean difference of RVSWI (0.58) among various RV hemodynamic and functional parameters such as TAPSE, RV FAC, and RV LS, although PAPi and RAP/PCWP were not included in this analysis (7).

Limitations: RVWSi is frequently used in LVAD populations (Table 4), yet most RVSWi measurements used in clinical, or research settings are derived from RHC-derived parameters. These estimations do not necessarily capture true workload as measured from PV loops and are susceptible to errors in hemodynamic measurements (77). Moreover, there are also some studies that have shown limited predictive capacity of RVSWi in multivariable analyses (78). The specific situation or population where its performance becomes unreliable is still unclear, it should be noted that functional assessment should be multifaceted.

4.5 PAPi

The pulmonary artery pulsatility index (PAPi) is a measure initially developed for use in MI and MCS conditions and it has demonstrated a good predictive value for RHF development or mortality after LVAD implantation either (79). PAPi is calculated using the following formula:

$\mathrm{PAPi}=(\mathrm{systolic}\text{-}\mathrm{diastolic}\mathrm{PA}\mathrm{pressure})/\mathrm{RA}\mathrm{pressure},$

where PA pulse pressure provides an estimate of RV pulsatile load and contractile strength, and RA pressure acts as a mediator of preload (80). Lower PAPi indicates impaired RV function. A systematic review incorporating 32 studies found that patients who developed RHF had a significantly lower preoperative PAPi than those who did not (2.17 vs. 2.87; p < 0.001) (79) (Table 5).

In analysis on PAPi, the utility of simulation test has been proposed in addition to the resting value. Cacioli and colleagues reported PAPi measured after administering sodium nitroprusside (NTP) had the potential to predict RHF development. By administrating the vasodilator and reducing pulmonary vascular resistance, post-NTP PAPi was considered capable of assessing (1) reversibility of pulmonary hypertension and (2) the reserve in RV function. Indeed, the post-NTP PAPi improved predictive value, and when combined with RV FAC and systolic PA pressure, the area under the curve (AUC) increased up to 0.95 in their study (81). Hsi and colleagues also reported the efficacy of PAPi measured in a micro-axial flow pump (mAFP) test to predict RHF before LVAD implantation (82). These dynamic changes in parameters during simulation testing may help capture the intrinsic adaptability of the RV and improve the prediction of RHF (83). Although this was also suggested in the study by Brener and colleagues where they proposed RVSWi (35), available data remains limited.

Limitations: A concern regarding PAPi is that pulmonary circulation factors—including resistance and compliance—can significantly affect its value. Not only RV dysfunction but also pulmonary embolism and PA diseases can diminish PAPi value since pulse pressure declines in these conditions (84).

Another concern is the variable cutoff value reported in literature. From 0.88 to 3.3 have been reported as an effective cutoffs, and median values also vary across studies (85). Even small changes in RA pressure can significantly affect PAPi, precise measurement of catheter parameters is essential.

4.6 RAP (CVP)/PCWP

RAP (or CVP)/PCWP includes the LV component when evaluating the RV preload, thereby reflecting right-sided preload relative to the left side and implying RV's adaptability towards certain volume condition, not representing RV function (86). With respect to prediction, RAP/PCWP ratio shows excellent predictive values (87, 88). A higher RAP/PCWP ratio indicates excessively accumulated preload in the RV, suggesting inadequate adaptation of RV to certain volume conditions or afterloads. In general, 0.55–0.6 are considered as cutoff values (58) (Table 6).

Regarding this parameter, data are available not only for its resting value at a single time point but also from a simulation test of LVAD suctioning. In terms of this parameter, there is a data of utility by simulation test of LVAD, not only rest value at one point. Hsi and colleagues reported the efficacy of a simulation test with mAFP in assessing the RAP/PCWP ratio either (82). In their study, the ratio decreased significantly after mAFP insertion in patients who did not develop RHF, compared to those who did (non-RHF group: 0.61 → 0.38; RHF group: 0.46 → 0.40) (82). Simulation test performed before implantation may further improve the predictive value of this parameter as PAPi. RAP/PCWP is simple to obtain and has a high predictive reliability; therefore, its assessment is reasonable and recommended.

Limitations: As a limitation, this ratio can be low when PCWP is particularly high. Amsallem and colleagues reported that 43% of patients with a low RAP/PAWP ratio (≤0.54) and high RAP (≥15 mmHg) developed RHF after LVAD implantation, suggesting that the absolute value of RAP itself should also be considered (89).

5 Risk sores and significant items for prediction

Various scoring models, many of which do not focus solely on RV factors, have been developed to predict the incidence of post-LVAD RHF. Although incorporating the non-RV-centered factors helps further identify high-risk patients for developing RHF prior to LVAD implantation, comprehensive validation of these models and comparisons of their performance remains limited.

This section outlines several risk scores validated externally (Table 7). Components of these scores can be classified as follows: (1) baseline characteristics/presentation; (2) treatment-related factors (e.g., vasopressors, inotropes, MCS); (3) right heart conditions (hemodynamics, and RV function); (4) laboratory data. Most scores define RHF as the need for MCS or RVAD, iNO ≥48h, or inotropes ≥14 days, same as MCS-ARC early RHF definition (14).

Table 7

Table 7. Summary of existing risk scores.

As summarized in Table 7, the discrimination performances of most scores are generally “fair” or “moderate,” with C-index or AUC values less than 0.7, and comparable results observed in external validations. Scores relatively recently developed, including STOP-RVF Score, EUROMACS Score, and CRITT, are derived from cohort all with continuous flow pump, whereas that for other scores included pulsatile flow pump. Kalogeropoulos and colleagues compared six existing risk scores in their cohort who were all recipients of continuous flow LVAD, with the Michigan Right Ventricular Failure Risk Score (RVFRS) achieving the highest C-index of 0.62 (Figure 5). They attribute the limited performance to: (1) Variability in RHF definitions, (2) The inclusion of non-RV markers as surrogates for RV dysfunction, and (3) Differences in the cohorts used for model derivation, as older scoring systems included fewer patients receiving destination therapy and continuous-flow pumps (90).

Figure 5

Figure 5. Comparison of discrimination of risk scores. Kalogeropoulos et al. compared existing risk scores in 116 patients with continuous-flow LVAD, either the HeartMate II (Thoratec, Inc.) or the HeartWare HVAD (Heart-Ware, Inc.), in single center. Although the Michigan score showed the highest value, the C-indexes of all scores remained around 0.6. Reproduced with permission from “Comparative Receiver Operating Characteristic Curve Plots with Right Ventricular Failure Prediction as the Outcome of Interest for the Scores Evaluated” by Andreas P. Kalogeropoulos, Anita Kelkar, Jeremy F. Weinberger, Alanna A. Morris, Vasiliki V. Georgiopoulou, David W. Markham, Javed Butler, J. David Vega and Andrew L. Smith, licensed under CC-BY-NC-ND.

The most recent risk prediction model, called “STOP-RVF score”, derived using a machine learning approach, has demonstrated superior performance, achieving a C-statistic of 0.75 even in external validation, outperforming other scores such as the Kormos et al. score [C statistic, 0.5 (75)] and score from the University of Utah [C statistic, 0.627 (91)] (87).

Noticeably, four items—(1) liver/renal dysfunction, (2) MCS/catecholamine dependency (or INTERMACS profile 1/2) before implantation, (3) pre-existing severe RV dysfunction, and (4) high RAP/PCWP—are included in at least two scoring models and thus, should be incorporated certainly when evaluating the RHF risk (Figure 1). Meta-analysis or large-scale registry studies (n > 1,000) conducting multivariable analysis for the incidence of post-LVAD RHF, also demonstrated the statistical significance of the aforementioned four factors (7, 8, 92, 93).

Unfortunately, “severe RV dysfunction” is not clearly defined in most studies including risk score deviation paper (76, 88, 94), yet, given their superior predictive capacities discussed in previous section, RV LS, RVSWi, and PAPi should be evaluated. Considering preimplantation RV LS ≥16% (77), RVSWi <250–300 mmHg L/m² (75–77), or PAPi <2.0–3.0 (95) as a critical factor strongly indicative of RV dysfunction, patients with additional risk factors—such as liver/renal dysfunction, MCS/catecholamine dependency, or high RAP/PCWP (0.5–0.6)—should be strongly considered for RVAD implantation.

6 Conclusion

This review consolidates the latest insights into the pathophysiology of and predictive models for RHF following LVAD implementation.

As highlighted in Figure 1, both the loss of LV twist and LVAD suction on the septal wall are LVAD-specific factors that negatively impact RV contractility. Although LVAD suction improves diastolic compliance, insufficient adaptation to increased flow may contribute to RHF. Furthermore, functional TR and AI can additionally promote congestion.

To predict this unfavorable outcome, guidelines and expert consensus recommend several RV functional parameters from imaging modalities or RHC. Among these, RV LS, RVSWi, and PAPi, exhibit strong predictive value in large-scale studies. Since none of these parameters alone provide definitively high predictive accuracy, and each reflects different aspects of RV function, considering multiple parameters in combination may enhance the prediction of RHF.

Although several risk scores have been developed for prediction, most have demonstrated only “fair” performance in discriminating RHF during external validation. Across these score models, four specific factors recur and have demonstrated consistent performance in meta-analysis either, thereby we propose multiparametric approach for RHF prediction, specifically focusing on four factors—(1) liver/renal dysfunction, (2) MCS/catecholamine dependency (or INTERMACS profile 1/2), (3) pre-existing severe RV dysfunction (impairment in RV LS, RVSWi, and PAPi), and (4) high RAP/PCWP (Figure 1).

We identified the following knowledge gaps and future directions:

1. Incomplete Clinical Evidence on RV Pathophysiology in LVAD Candidates

The proposed pathophysiological mechanisms are largely derived from preclinical studies or estimations based on imaging modalities or RHC, where contractility and diastolic compliance cannot be accurately assessed. More robust evidence on proposed mechanisms, particularly the loss of LV twist, along with comprehensive, larger-scale evaluations of the RV PV loop in human patients, is needed.

2. Evaluation of Diastolic Compliance

Although diastolic compliance may significantly influence how the RV adapts to the increased flow from an LVAD, standard assessment methods via imaging modality or RHC for diastolic function remain limited. Further research is required to collect data on current diastolic function metrics and develop reliable parameters.

3. Simulation and Intraoperative Testing

Simulation studies that replicate LVAD hemodynamics, as well as short-term intraoperative tests just before LVAD implantation, could enhance predictive accuracy by providing more precise assessments of RV functional reserve. However, comprehensive and refined data are still needed.

Addressing these gaps is crucial for improving LVAD management and enhancing quality of life for patients reliant on LVAD support.

Author contributions

HN: Conceptualization, Investigation, Visualization, Writing – original draft, Writing – review & editing. LL: Conceptualization, Data curation, Methodology, Writing – original draft, Writing – review & editing. NO: Supervision, Writing – review & editing. JS: Supervision, Writing – review & editing. DM: Supervision, Visualization, Writing – original draft, Writing – review & editing. JPF: Conceptualization, Methodology, Resources, Supervision, Writing – original draft, Writing – review & editing. JFF: Supervision, Writing – original draft, Writing – review & editing.

Funding

The author(s) declare that financial support was received for the research and/or publication of this article. HN is supported by The Prince Chales Hospital Foundation through his PhD scholarship (2024-01).

Acknowledgments

Figure 1 was created by illustrator Nick Valmas. We thank him for his cooperation.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Generative AI statement

The author(s) declare that no Generative AI was used in the creation of this manuscript.

Publisher's note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

References

1. Lippi G, Sanchis-Gomar F. Global epidemiology and future trends of heart failure. AME Med J. (2020) 5:15. doi: 10.21037/amj.2020.03.03

Crossref Full Text | Google Scholar

2. Members ATF, McMurray JJ, Adamopoulos S, Anker SD, Auricchio A, Böhm M, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: the task force for the diagnosis and treatment of acute and chronic heart failure 2012 of the European Society of Cardiology. Developed in collaboration with the heart failure association (HFA) of the ESC. Eur Heart J. (2012) 33(14):1787–847. doi: 10.1093/eurheartj/ehs104

PubMed Abstract | Crossref Full Text | Google Scholar

3. de By TM, Mohacsi P, Gummert J, Bushnaq H, Krabatsch T, Gustafsson F, et al. The European registry for patients with mechanical circulatory support (EUROMACS): first annual report. Eur J Cardiothorac Surg. (2015) 47(5):770–7. doi: 10.1093/ejcts/ezv096

PubMed Abstract | Crossref Full Text | Google Scholar

4. Lam KM-T, Ennis S, O'Driscoll G, Solis JM, MacGillivray T, Picard MH. Observations from non-invasive measures of right heart hemodynamics in left ventricular assist device patients. J Am Soc Echocardiogr. (2009) 22(9):1055–62. doi: 10.1016/j.echo.2009.06.006

PubMed Abstract | Crossref Full Text | Google Scholar

5. Baumwol J, Macdonald PS, Keogh AM, Kotlyar E, Spratt P, Jansz P, et al. Right heart failure and “failure to thrive” after left ventricular assist device: clinical predictors and outcomes. J Heart Lung Transplant. (2011) 30(8):888–95. doi: 10.1016/j.healun.2011.03.006

PubMed Abstract | Crossref Full Text | Google Scholar

6. Takeda K, Naka Y, Yang JA, Uriel N, Colombo PC, Jorde UP, et al. Outcome of unplanned right ventricular assist device support for severe right heart failure after implantable left ventricular assist device insertion. J Heart Lung Transplant. (2014) 33(2):141–8. doi: 10.1016/j.healun.2013.06.025

PubMed Abstract | Crossref Full Text | Google Scholar

7. Bellavia D, Iacovoni A, Scardulla C, Moja L, Pilato M, Kushwaha SS, et al. Prediction of right ventricular failure after ventricular assist device implant: systematic review and meta-analysis of observational studies. Eur J Heart Fail. (2017) 19(7):926–46. doi: 10.1002/ejhf.733

PubMed Abstract | Crossref Full Text | Google Scholar

8. Kapelios CJ, Lund LH, Wever-Pinzon O, Selzman CH, Myers SL, Cantor RS, et al. Right heart failure following left ventricular device implantation: natural history, risk factors, and outcomes: an analysis of the STS INTERMACS database. Circ Heart Fail. (2022) 15(6):e008706. doi: 10.1161/CIRCHEARTFAILURE.121.008706

PubMed Abstract | Crossref Full Text | Google Scholar

9. Moon MR, Bolger AF, DeAnda A, Komeda M, Daughters GT, Nikolic SD, et al. Septal function during left ventricular unloading. Circulation. (1997) 95(5):1320–7. doi: 10.1161/01.CIR.95.5.1320

PubMed Abstract | Crossref Full Text | Google Scholar

10. Ho SY, Nihoyannopoulos P. Anatomy, echocardiography, and normal right ventricular dimensions. Heart. (2006) 92 Suppl 1(Suppl 1):i2–13. doi: 10.1136/hrt.2005.077875

PubMed Abstract | Crossref Full Text | Google Scholar

11. Schlangen J, Petko C, Hansen JH, Michel M, Hart C, Uebing A, et al. Two-Dimensional global longitudinal strain rate is a preload independent Index of systemic right ventricular contractility in hypoplastic left heart syndrome patients after fontan operation. Circ Cardiovasc Imaging. (2014) 7(6):880–6. doi: 10.1161/CIRCIMAGING.114.002110

PubMed Abstract | Crossref Full Text | Google Scholar

12. Yuchi Y, Suzuki R, Kanno H, Saito T, Teshima T, Matsumoto H, et al. Influence of heart rate on right ventricular function assessed by right heart catheterization and echocardiography in healthy anesthetized dogs. BMC Vet Res. (2022) 18(1):166. doi: 10.1186/s12917-022-03271-y

PubMed Abstract | Crossref Full Text | Google Scholar

13. STS-INTERMACS. Appendix A—adverse event definitions.: UAB School of Medicine).

Google Scholar

14. Kormos RL, Antonides CF, Goldstein DJ, Cowger JA, Starling RC, Kirklin JK, et al. Updated definitions of adverse events for trials and registries of mechanical circulatory support: a consensus statement of the mechanical circulatory support academic research consortium. J Heart Lung Transplant. (2020) 39(8):735–50. doi: 10.1016/j.healun.2020.03.010

PubMed Abstract | Crossref Full Text | Google Scholar

15. Rame JE, Pagani FD, Kiernan MS, Oliveira GH, Birati EY, Atluri P, et al. Evolution of late right heart failure with left ventricular assist devices and association with outcomes. J Am Coll Cardiol. (2021) 78(23):2294–308. doi: 10.1016/j.jacc.2021.09.1362

PubMed Abstract | Crossref Full Text | Google Scholar

16. Takeda K, Takayama H, Colombo PC, Jorde UP, Yuzefpolskaya M, Fukuhara S, et al. Late right heart failure during support with continuous-flow left ventricular assist devices adversely affects post-transplant outcome. J Heart Lung Transplant. (2015) 34(5):667–74. doi: 10.1016/j.healun.2014.10.005

PubMed Abstract | Crossref Full Text | Google Scholar

17. Brener MI, Masoumi A, Ng VG, Tello K, Bastos MB, Cornwell WK, et al. Invasive right ventricular pressure-volume analysis: basic principles, clinical applications, and practical recommendations. Circ Heart Fail. (2022) 15(1):e009101. doi: 10.1161/CIRCHEARTFAILURE.121.009101

PubMed Abstract | Crossref Full Text | Google Scholar

18. Torrent-Guasp FF, Whimster WF, Redmann K. A silicone rubber mould of the heart. Technol Health Care. (1997) 5(1-2):13–20. doi: 10.3233/THC-1997-51-202

PubMed Abstract | Crossref Full Text | Google Scholar

19. Buckberg GD, RESTORE Group. The ventricular septum: the lion of right ventricular function, and its impact on right ventricular restoration. Eur J Cardiothorac Surg. (2006) 29(Supplement_1):S272–S8. doi: 10.1016/j.ejcts.2006.02.011

PubMed Abstract | Crossref Full Text | Google Scholar

20. Houston BA, Shah KB, Mehra MR, Tedford RJ. A new “twist” on right heart failure with left ventricular assist systems. J Heart Lung Transplant. (2017) 36(7):701–7. doi: 10.1016/j.healun.2017.03.014

PubMed Abstract | Crossref Full Text | Google Scholar

21. Surkova E, Kovács A, Tokodi M, Lakatos BK, Merkely B, Muraru D, et al. Contraction patterns of the right ventricle associated with different degrees of left ventricular systolic dysfunction. Circ Cardiovasc Imaging. (2021) 14(10):e012774. doi: 10.1161/CIRCIMAGING.121.012774

PubMed Abstract | Crossref Full Text | Google Scholar

22. Hoffman D, Sisto D, Frater RW, Nikolic SD. Left-to-right ventricular interaction with a noncontracting right ventricle. J Thorac Cardiovasc Surg. (1994) 107(6):1496–502. doi: 10.1016/S0022-5223(12)70150-2

PubMed Abstract | Crossref Full Text | Google Scholar

23. Chang SA, Kim HK, Kim YJ, Cho GY, Oh S, Sohn DW. Role of pericardium in the maintenance of left ventricular twist. Heart. (2010) 96(10):785–90. doi: 10.1136/hrt.2009.182345

PubMed Abstract | Crossref Full Text | Google Scholar

24. Wranne B, Pinto FJ, Hammarström E, St Goar FG, Puryear J, Popp RL. Abnormal right heart filling after cardiac surgery: time course and mechanisms. Br Heart J. (1991) 66(6):435–42. doi: 10.1136/hrt.66.6.435

PubMed Abstract | Crossref Full Text | Google Scholar

25. Raina A, Vaidya A, Gertz ZM, Susan C, Forfia PR. Marked changes in right ventricular contractile pattern after cardiothoracic surgery: implications for post-surgical assessment of right ventricular function. J Heart Lung Transplant. (2013) 32(8):777–83. doi: 10.1016/j.healun.2013.05.004

PubMed Abstract | Crossref Full Text | Google Scholar

26. Unsworth B, Casula RP, Kyriacou AA, Yadav H, Chukwuemeka A, Cherian A, et al. The right ventricular annular velocity reduction caused by coronary artery bypass graft surgery occurs at the moment of pericardial incision. Am Heart J. (2010) 159(2):314–22. doi: 10.1016/j.ahj.2009.11.013

PubMed Abstract | Crossref Full Text | Google Scholar

27. Damiano RJ Jr, La Follette P Jr, Cox JL, Lowe JE, Santamore WP. Significant left ventricular contribution to right ventricular systolic function. Am J Physiol. (1991) 261(5 Pt 2):H1514–24. doi: 10.1152/ajpheart.1991.261.5.H1514

PubMed Abstract | Crossref Full Text | Google Scholar

28. Park CH, Nishimura K, Kitano M, Matsuda K, Okamoto Y, Ban T. Analysis of right ventricular function during bypass of the left side of the heart by afterload alterations in both normal and failing hearts. J Thorac Cardiovasc Surg. (1996) 111(5):1092–102. doi: 10.1016/S0022-5223(96)70386-0

PubMed Abstract | Crossref Full Text | Google Scholar

29. Apitz C, Honjo O, Humpl T, Li J, Assad RS, Cho MY, et al. Biventricular structural and functional responses to aortic constriction in a rabbit model of chronic right ventricular pressure overload. J Thorac Cardiovasc Surg. (2012) 144(6):1494–501. doi: 10.1016/j.jtcvs.2012.06.027

PubMed Abstract | Crossref Full Text | Google Scholar

30. Scheel PJ, III C, Salazar IM, Friedman S, Haber L, Mukherjee M, et al. Occult right ventricular dysfunction and right ventricular-vascular uncoupling in left ventricular assist device recipients. J Heart Lung Transplant. (2024) 43(4):594–603. doi: 10.1016/j.healun.2023.11.015

PubMed Abstract | Crossref Full Text | Google Scholar

31. Sack KL, Dabiri Y, Franz T, Solomon SD, Burkhoff D, Guccione JM. Investigating the role of interventricular interdependence in development of right heart dysfunction during LVAD support: a patient-specific methods-based approach. Front Physiol. (2018):9:520. doi: 10.3389/fphys.2018.00520

PubMed Abstract | Crossref Full Text | Google Scholar

32. Khonsary SA. Guyton and Hall: textbook of medical physiology. Surg Neurol Int. (2017) 8:275. doi: 10.4103/sni.sni_327_17 eCollection 2017.

Crossref Full Text | Google Scholar

33. Ali HR, Kiernan MS, Choudhary G, Levine DJ, Sodha NR, Ehsan A, et al. Right ventricular failure post-implantation of left ventricular assist device: prevalence, pathophysiology, and predictors. Asaio J. (2020) 66(6):610–9. doi: 10.1097/MAT.0000000000001088

PubMed Abstract | Crossref Full Text | Google Scholar

34. Bravo CA, Navarro AG, Dhaliwal KK, Khorsandi M, Keenan JE, Mudigonda P, et al. Right heart failure after left ventricular assist device: from mechanisms to treatments. Front Cardiovasc Med. (2022) 9:1023549. doi: 10.3389/fcvm.2022.1023549

PubMed Abstract | Crossref Full Text | Google Scholar

35. Brener MI, Kanwar MK, Lander MM, Hamid NB, Raina A, Sethi SS, et al. Impact of interventricular interaction on ventricular function: insights from right ventricular pressure-volume analysis. JACC Heart Fail. (2024) 12(7):1179–92. doi: 10.1016/j.jchf.2023.12.001

PubMed Abstract | Crossref Full Text | Google Scholar

36. Masri SC, Tedford RJ, Colvin MM, Leary PJ, Cogswell R. Pulmonary arterial compliance improves rapidly after left ventricular assist device implantation. Asaio J. (2017) 63(2):139–43. doi: 10.1097/MAT.0000000000000467

PubMed Abstract | Crossref Full Text | Google Scholar

37. Houston BA, Kalathiya RJ, Hsu S, Loungani R, Davis ME, Coffin ST, et al. Right ventricular afterload sensitivity dramatically increases after left ventricular assist device implantation: a multi-center hemodynamic analysis. J Heart Lung Transplant. (2016) 35(7):868–76. doi: 10.1016/j.healun.2016.01.1225

PubMed Abstract | Crossref Full Text | Google Scholar

38. Sayer G, Sarswat N, Kim GH, Adatya S, Medvedofsky D, Rodgers D, et al. The hemodynamic effects of aortic insufficiency in patients supported with continuous-flow left ventricular assist devices. J Card Fail. (2017) 23(7):545–51. doi: 10.1016/j.cardfail.2017.04.012

PubMed Abstract | Crossref Full Text | Google Scholar

39. Rubinstein GAL, Moeller CM, Lotan DOR, Slomovich S, Fernandez-Valledor A, Ranard LS, et al. The hemodynamic effects of aortic regurgitation in patients supported by a HeartMate 3 left ventricular assist device. J Card Fail. (2024) 30(1):95–9. doi: 10.1016/j.cardfail.2023.08.010

PubMed Abstract | Crossref Full Text | Google Scholar

40. Haddad F, Hunt SA, Rosenthal DN, Murphy DJ. Right ventricular function in cardiovascular disease, part I. Circulation. (2008) 117(11):1436–48. doi: 10.1161/CIRCULATIONAHA.107.653576

PubMed Abstract | Crossref Full Text | Google Scholar

41. Moon MR, Castro LJ, DeAnda A, Tomizawa Y, Daughters GT, Ingels NB, et al. Right ventricular dynamics during left ventricular assistance in closed-chest dogs. Ann Thorac Surg. (1993) 56(1):54–67. doi: 10.1016/0003-4975(93)90402-4

PubMed Abstract | Crossref Full Text | Google Scholar

42. McCarthy PM, Savage RM, Fraser CD, Vargo R, James KB, Goormastic M, et al. Hemodynamic and physiologic changes during support with an implantable left ventricular assist device. J Thorac Cardiovasc Surg. (1995) 109(3):409–17. discussion 17-8. doi: 10.1016/S0022-5223(95)70271-7

PubMed Abstract | Crossref Full Text | Google Scholar

43. Uriel N, Sayer G, Addetia K, Fedson S, Kim GH, Rodgers D, et al. Hemodynamic ramp tests in patients with left ventricular assist devices. JACC Heart Fail. (2016) 4(3):208–17. doi: 10.1016/j.jchf.2015.10.001

PubMed Abstract | Crossref Full Text | Google Scholar

44. Mitra A, Siddique A. Tricuspid regurgitation in the setting of LVAD support. Front Cardiovasc Med. (2023) 10:1090150. doi: 10.3389/fcvm.2023.1090150

PubMed Abstract | Crossref Full Text | Google Scholar

45. Piacentino V III, Williams ML, Depp T, Garcia-Huerta K, Blue L, Lodge AJ, et al. Impact of tricuspid valve regurgitation in patients treated with implantable left ventricular assist devices. Ann Thorac Surg. (2011) 91(5):1342–7. doi: 10.1016/j.athoracsur.2011.01.053

PubMed Abstract | Crossref Full Text | Google Scholar

46. Veen KM, Mokhles MM, Soliman O, de By T, Mohacsi P, Schoenrath F, et al. Clinical impact and ‘natural’ course of uncorrected tricuspid regurgitation after implantation of a left ventricular assist device: an analysis of the European registry for patients with mechanical circulatory support (EUROMACS). Eur J Cardiothorac Surg. (2021) 59(1):207–16. doi: 10.1093/ejcts/ezaa294

PubMed Abstract | Crossref Full Text | Google Scholar

47. Mulzer J, Mueller M, Knierim J, Lanmueller P, Potapov E. Myocardial function recovery interventional assessment and surgical pump removal. Ann Cardiothorac Surg. (2021) 10(3):402–4. doi: 10.21037/acs-2020-cfmcs-12

PubMed Abstract | Crossref Full Text | Google Scholar

48. Itzhaki Ben Zadok O, Ben-Avraham B, Barac YD, Hammer Y, Rubachevski V, Shaul A, et al. Natural history and prognosis of patients with unrepaired tricuspid regurgitation undergoing implantation of left ventricular assist device. Asaio J. (2022) 68(4):508–15. doi: 10.1097/MAT.0000000000001521

PubMed Abstract | Crossref Full Text | Google Scholar

49. Nakanishi K, Homma S, Han J, Takayama H, Colombo PC, Yuzefpolskaya M, et al. Prevalence, predictors, and prognostic value of residual tricuspid regurgitation in patients with left ventricular assist device. J Am Heart Assoc. (2018) 7(13):e008813. doi: 10.1161/JAHA.118.008813

PubMed Abstract | Crossref Full Text | Google Scholar

50. Anwer LA, Tchantchaleishvili V, Poddi S, Daly RC, Joyce LD, Kushwaha SS, et al. Atrial fibrillation should guide prophylactic tricuspid procedures during left ventricular assist device implantation. ASAIO Journal. (2018) 64(5):586–93. doi: 10.1097/MAT.0000000000000698

PubMed Abstract | Crossref Full Text | Google Scholar

51. Mullan C, Caraballo C, Ravindra NG, Miller PE, Mori M, McCullough M, et al. Clinical impact of concomitant tricuspid valve procedures during left ventricular assist device implantation. J Heart Lung Transplant. (2020) 39(9):926–33. doi: 10.1016/j.healun.2020.05.007

PubMed Abstract | Crossref Full Text | Google Scholar

52. Boulet J, Nayak A, Mehra MR. Hemodynamic aberrancies in left ventricular assist device-associated heart failure syndromes. J Card Fail. (2022) 28(12):1738–40. doi: 10.1016/j.cardfail.2022.09.007

PubMed Abstract | Crossref Full Text | Google Scholar

53. Truby LK, Garan AR, Givens RC, Wayda B, Takeda K, Yuzefpolskaya M, et al. Aortic insufficiency during contemporary left ventricular assist device support: analysis of the INTERMACS registry. JACC Heart Failure. (2018) 6(11):951–60. doi: 10.1016/j.jchf.2018.07.012

PubMed Abstract | Crossref Full Text | Google Scholar

54. Jorde UP, Uriel N, Nahumi N, Bejar D, Gonzalez-Costello J, Thomas SS, et al. Prevalence, significance, and management of aortic insufficiency in continuous flow left ventricular assist device recipients. Circ Heart Fail. (2014) 7(2):310–9. doi: 10.1161/CIRCHEARTFAILURE.113.000878

PubMed Abstract | Crossref Full Text | Google Scholar

55. Cowger J, Pagani FD, Haft JW, Romano MA, Aaronson KD, Kolias TJ. The development of aortic insufficiency in left ventricular assist device-supported patients. Circ Heart Fail. (2010) 3(6):668–74. doi: 10.1161/CIRCHEARTFAILURE.109.917765

PubMed Abstract | Crossref Full Text | Google Scholar

56. Acharya D, Kazui T, Al Rameni D, Acharya T, Betterton E, Juneman E, et al. Aortic valve disorders and left ventricular assist devices. Front Cardiovasc Med. (2023) 10:1098348. doi: 10.3389/fcvm.2023.1098348

PubMed Abstract | Crossref Full Text | Google Scholar

57. Cameli M, Aboumarie HS, Pastore MC, Caliskan K, Cikes M, Garbi M, et al. Multimodality imaging for the evaluation and management of patients with long-term (durable) left ventricular assist devices: a clinical consensus statement of the European association of cardiovascular imaging of the European Society of Cardiology. Eur Heart J Cardiovasc Imaging. (2024) 25(10):e217–e40. doi: 10.1093/ehjci/jeae165

PubMed Abstract | Crossref Full Text | Google Scholar

58. Adamopoulos S, Bonios M, Ben Gal T, Gustafsson F, Abdelhamid M, Adamo M, et al. Right heart failure with left ventricular assist devices: preoperative, perioperative and postoperative management strategies. A clinical consensus statement of the heart failure association (HFA) of the ESC. Eur J Heart Fail. (2024) 26(11):2304–22. doi: 10.1002/ejhf.3323

PubMed Abstract | Crossref Full Text | Google Scholar

59. Saeed D, Feldman D, Banayosy AE, Birks E, Blume E, Cowger J, et al. The 2023 international society for heart and lung transplantation guidelines for mechanical circulatory support: a 10- year update. J Heart Lung Transplant. (2023) 42(7):e1–e222. doi: 10.1016/j.healun.2022.12.004

PubMed Abstract | Crossref Full Text | Google Scholar

60. Chriqui L-E, Monney P, Kirsch M, Tozzi P. Prediction of right ventricular failure after left ventricular assist device implantation in patients with heart failure: a meta-analysis comparing echocardiographic parameters. Interact Cardiovasc Thorac Surg. (2021) 33(5):784–92. doi: 10.1093/icvts/ivab177

PubMed Abstract | Crossref Full Text | Google Scholar

61. Nonaka H, Rätsep I, Obonyo NG, Suen JY, Fraser JF, Chan J. Current trends and latest developments in echocardiographic assessment of right ventricular function: load dependency perspective. Front Cardiovasc Med. (2024) 11:1365798. doi: 10.3389/fcvm.2024.1365798

PubMed Abstract | Crossref Full Text | Google Scholar

62. Hsu S. Coupling right ventricular-pulmonary arterial research to the pulmonary hypertension patient bedside. Circ Heart Fail. (2019) 12(1):e005715.30616361

PubMed Abstract | Google Scholar

63. Tanaka T, Sugiura A, Kavsur R, Öztürk C, Vogelhuber J, Wilde N, et al. Right ventricular ejection fraction assessed by computed tomography in patients undergoing transcatheter tricuspid valve repair. Eur Heart J Cardiovasc Imaging. (2023) 24(11):1501–8. doi: 10.1093/ehjci/jead102

PubMed Abstract | Crossref Full Text | Google Scholar

64. Stainback RF, Estep JD, Agler DA, Birks EJ, Bremer M, Hung J, et al. Echocardiography in the management of patients with left ventricular assist devices: recommendations from the American society of echocardiography. J Am Soc Echocardiogr. (2015) 28(8):853–909. doi: 10.1016/j.echo.2015.05.008

PubMed Abstract | Crossref Full Text | Google Scholar

65. Rodenas-Alesina E, Brahmbhatt DH, Rao V, Salvatori M, Billia F. Prediction, prevention, and management of right ventricular failure after left ventricular assist device implantation: a comprehensive review. Front Cardiovasc Med. (2022) 9:1040251. doi: 10.3389/fcvm.2022.1040251

PubMed Abstract | Crossref Full Text | Google Scholar

66. Rudski LG, Lai WW, Afilalo J, Hua L, Handschumacher MD, Chandrasekaran K, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American society of echocardiography endorsed by the European association of echocardiography, a registered branch of the European Society of Cardiology, and the Canadian society of echocardiography. J Am Soc Echocardiogr. (2010) 23(7):685–713. quiz 86-8. doi: 10.1016/j.echo.2010.05.010

PubMed Abstract | Crossref Full Text | Google Scholar

67. Kato TS, Jiang J, Schulze PC, Jorde U, Uriel N, Kitada S, et al. Serial echocardiography using tissue Doppler and speckle tracking imaging to monitor right ventricular failure before and after left ventricular assist device surgery. JACC Heart Failure. (2013) 1(3):216–22. doi: 10.1016/j.jchf.2013.02.005

PubMed Abstract | Crossref Full Text | Google Scholar

68. Charisopoulou D, Banner NR, Demetrescu C, Simon AR, Rahman Haley S. Right atrial and ventricular echocardiographic strain analysis predicts requirement for right ventricular support after left ventricular assist device implantation. Eur Heart J Cardiovasc Imaging. (2019) 20(2):199–208. doi: 10.1093/ehjci/jey065

PubMed Abstract | Crossref Full Text | Google Scholar

69. Samura T, Yoshioka D, Asanoi H, Toda K, Miyagawa S, Yoshikawa Y, et al. Right atrial pressure waveform predicts right ventricular failure after left ventricular assist device implantation. Ann Thorac Surg. (2019) 108(5):1361–8. doi: 10.1016/j.athoracsur.2019.04.050

PubMed Abstract | Crossref Full Text | Google Scholar

70. Li Q, Zhang M. Echocardiography assessment of right ventricular-pulmonary artery coupling: validation of surrogates and clinical utilities. Int J Cardiol. (2024) 394:131358. doi: 10.1016/j.ijcard.2023.131358

PubMed Abstract | Crossref Full Text | Google Scholar

71. Amsallem M, Aymami M, Hiesinger W, Zeigler S, Moneghetti K, Marques M, et al. Right ventricular load adaptability metrics in patients undergoing left ventricular assist device implantation. J Thorac Cardiovasc Surg. (2019) 157(3):1023–33.e4. doi: 10.1016/j.jtcvs.2018.08.095

PubMed Abstract | Crossref Full Text | Google Scholar

72. Shah H, Maharaj V, Kenny B, Kalra R, Rafei AE, Duval S, et al. Non-Invasive TAPSE/PASP ratio is not predictive of early right ventricular failure post LVAD implantation. J Heart Lung Transplant. (2020) 39(4):S427–S8. doi: 10.1016/j.healun.2020.01.218

Crossref Full Text | Google Scholar

73. Beneyto M, Martins R, Galand V, Kindo M, Schneider C, Sebestyen A, et al. Right ventriculoarterial coupling surrogates and long-term survival in LVAD recipients: results of the ASSIST-ICD multicentric registry. J Card Fail (2025) 31(2):388–96. doi: 10.1016/j.cardfail.2024.05.007

PubMed Abstract | Crossref Full Text | Google Scholar

74. Sanz J, Sánchez-Quintana D, Bossone E, Bogaard HJ, Naeije R. Anatomy, function, and dysfunction of the right ventricle: JACC State-of-the-Art Review. J Am Coll Cardiol. (2019) 73(12):1463–82. doi: 10.1016/j.jacc.2018.12.076

PubMed Abstract | Crossref Full Text | Google Scholar

75. Kormos RL, Teuteberg JJ, Pagani FD, Russell SD, John R, Miller LW, et al. Right ventricular failure in patients with the HeartMate II continuous-flow left ventricular assist device: incidence, risk factors, and effect on outcomes. J Thorac Cardiovasc Surg. (2010) 139(5):1316–24. doi: 10.1016/j.jtcvs.2009.11.020

PubMed Abstract | Crossref Full Text | Google Scholar

76. Fitzpatrick JR III, Frederick JR, Hsu VM, Kozin ED, O'Hara ML, Howell E, et al. Risk score derived from Pre-operative data analysis predicts the need for biventricular mechanical circulatory support. J Heart Lung Transplant. (2008) 27(12):1286–92. doi: 10.1016/j.healun.2008.09.006

PubMed Abstract | Crossref Full Text | Google Scholar

77. Gumus F, Durdu MS, Cakici M, Kurklu TST, Inan MB, Dincer I, et al. Right ventricular free wall longitudinal strain and stroke work index for predicting right heart failure after left ventricular assist device therapy. Interact Cardiovasc Thorac Surg. (2018) 28(5):674–82. doi: 10.1093/icvts/ivy328

PubMed Abstract | Crossref Full Text | Google Scholar

78. Frankfurter C, Molinero M, Vishram-Nielsen JKK, Foroutan F, Mak S, Rao V, et al. Predicting the risk of right ventricular failure in patients undergoing left ventricular assist device implantation. Circ Heart Fail. (2020) 13(10):e006994. doi: 10.1161/CIRCHEARTFAILURE.120.006994

PubMed Abstract | Crossref Full Text | Google Scholar

79. Essandoh M, Kumar N, Hussain N, Dalia AA, Wang D, Al-Qudsi O, et al. Pulmonary artery pulsatility index as a predictor of right ventricular failure in left ventricular assist device recipients: a systematic review. J Heart Lung Transplant. (2022) 41(8):1114–23. doi: 10.1016/j.healun.2022.04.007

PubMed Abstract | Crossref Full Text | Google Scholar

80. Kapur NK, Esposito ML, Bader Y, Morine KJ, Kiernan MS, Pham DT, et al. Mechanical circulatory support devices for acute right ventricular failure. Circulation. (2017) 136(3):314–26. doi: 10.1161/CIRCULATIONAHA.116.025290

PubMed Abstract | Crossref Full Text | Google Scholar

81. Cacioli G, Polizzi V, Ciabatti M, Cristiano E, Pergolini A, Distefano G, et al. Prediction of right ventricular failure after left ventricular assist device implantation: role of vasodilator challenge. Eur Heart J Acute Cardiovasc Care. (2022) 11(8):629–39. doi: 10.1093/ehjacc/zuac085

PubMed Abstract | Crossref Full Text | Google Scholar

82. Hsi B, Joseph D, Trachtenberg B, Bhimaraj A, Suarez EE, Xu J, et al. Degree of change in right ventricular adaptation measures during axillary impella support informs risk stratification for early, severe right heart failure following durable LVAD implantation. J Heart Lung Transplant. (2022) 41(3):279–82. doi: 10.1016/j.healun.2021.11.007

PubMed Abstract | Crossref Full Text | Google Scholar

83. Tadokoro N, Koyamoto T, Tonai K, Yoshida Y, Hirahsima K, Kainuma S, et al. The outcomes of a standardized protocol for extracorporeal mechanical circulatory support selection-left ventricular challenge protocol. J Artif Organs. (2024) 27(4):358–67. doi: 10.1007/s10047-023-01427-7

PubMed Abstract | Crossref Full Text | Google Scholar

84. Iannaccone M, Gamardella M, Fumarola F, Mangione R, Botti G, Russo F, et al. Pulmonary artery pulsatility index evaluation in intermediate-to-high and high-risk pulmonary embolism patients underwent transcatheter intervention. Eur Heart J. (2024) 45(Supplement_1). doi: 10.1093/eurheartj/ehae666.2324

Crossref Full Text | Google Scholar

85. Yim IHW, Khan-Kheil AM, Drury NE, Lim HS. A systematic review and physiology of pulmonary artery pulsatility index in left ventricular assist device therapy. Interdisciplin Cardiovasc Thorac Surg. (2023) 36(5):ivad068. doi: 10.1093/icvts/ivad068

Crossref Full Text | Google Scholar

86. Rajagopalan N, Borlaug Barry A, Bailey Alison L, Eckman Peter M, Guglin M, Hall S, et al. Practical guidance for hemodynamic assessment by right heart catheterization in management of heart failure. JACC Heart Fail. (2024) 12(7):1141–56. doi: 10.1016/j.jchf.2024.03.020

PubMed Abstract | Crossref Full Text | Google Scholar

87. Taleb I, Kyriakopoulos CP, Fong R, Ijaz N, Demertzis Z, Sideris K, et al. Machine learning multicenter risk model to predict right ventricular failure after mechanical circulatory support: the STOP-RVF score. JAMA Cardiol. (2024) 9(3):272–82. doi: 10.1001/jamacardio.2023.5372

PubMed Abstract | Crossref Full Text | Google Scholar

88. Soliman OI, Akin S, Muslem R, Boersma E, Manintveld OC, Krabatsch T, et al. Derivation and validation of a novel right-sided heart failure model after implantation of continuous flow left ventricular assist devices: the EUROMACS (European registry for patients with mechanical circulatory support) right-sided heart failure risk score. Circulation. (2018) 137(9):891–906. doi: 10.1161/CIRCULATIONAHA.117.030543

PubMed Abstract | Crossref Full Text | Google Scholar

89. Amsallem M, Aymami M, Hiesinger W, Zeigler S, Moneghetti K, Marques M, et al. Right ventricular load adaptability metrics in patients undergoing left ventricular assist device implantation. J Thorac Cardiovasc Surg. (2019) 157(3):1023–33.e4. doi: 10.1016/j.jtcvs.2018.08.095

PubMed Abstract | Crossref Full Text | Google Scholar

90. Kalogeropoulos AP, Kelkar A, Weinberger JF, Morris AA, Georgiopoulou VV, Markham DW, et al. Validation of clinical scores for right ventricular failure prediction after implantation of continuous-flow left ventricular assist devices. J Heart Lung Transplant. (2015) 34(12):1595–603. doi: 10.1016/j.healun.2015.05.005

PubMed Abstract | Crossref Full Text | Google Scholar

91. Drakos SG, Janicki L, Horne BD, Kfoury AG, Reid BB, Clayson S, et al. Risk factors predictive of right ventricular failure after left ventricular assist device implantation. Am J Cardiol. (2010) 105(7):1030–5. doi: 10.1016/j.amjcard.2009.11.026

PubMed Abstract | Crossref Full Text | Google Scholar

92. Bahl A, Qureshi B, Zhang K, Bravo C, Mahr C, Li S. Explainable machine learning analysis of right heart failure after left ventricular assist device implantation. ASAIO J. (2023) 69(5):417–23.36730914

PubMed Abstract | Google Scholar

93. Mehra MR, Nayak A, Morris AA, Lanfear DE, Nemeh H, Desai S, et al. Prediction of survival after implantation of a fully magnetically levitated left ventricular assist device. JACC Heart Fail. (2022) 10(12):948–59. doi: 10.1016/j.jchf.2022.08.002

PubMed Abstract | Crossref Full Text | Google Scholar

94. Atluri P, Goldstone AB, Fairman AS, MacArthur JW, Shudo Y, Cohen JE, et al. Predicting right ventricular failure in the modern, continuous flow left ventricular assist device era. Ann Thorac Surg. (2013) 96(3):857–64. doi: 10.1016/j.athoracsur.2013.03.099

PubMed Abstract | Crossref Full Text | Google Scholar

95. Akamkam A, Galand V, Jungling M, Delmas C, Dambrin C, Pernot M, et al. Association between pulmonary artery pulsatility and mortality after implantation of left ventricular assist device. ESC Heart Fail. (2024) 11(4):2100–12. doi: 10.1002/ehf2.14716

PubMed Abstract | Crossref Full Text | Google Scholar

96. Raymer DS, Moreno JD, Sintek MA, Nassif ME, Sparrow CT, Adamo L, et al. The combination of tricuspid annular plane systolic excursion and HeartMate risk score predicts right ventricular failure after left ventricular assist device implantation. Asaio J. (2019) 65(3):247–51. doi: 10.1097/MAT.0000000000000808

PubMed Abstract | Crossref Full Text | Google Scholar

97. Patil NP, Mohite PN, Sabashnikov A, Dhar D, Weymann A, Zeriouh M, et al. Preoperative predictors and outcomes of right ventricular assist device implantation after continuous-flow left ventricular assist device implantation. J Thorac Cardiovasc Surg. (2015) 150(6):1651–8. doi: 10.1016/j.jtcvs.2015.07.090

PubMed Abstract | Crossref Full Text | Google Scholar

98. Dandel M, Potapov E, Krabatsch T, Stepanenko A, Löw A, Vierecke J, et al. Load dependency of right ventricular performance is a Major factor to be considered in decision making before ventricular assist device implantation. Circulation. (2013) 128(11_suppl_1):S14–23. doi: 10.1161/CIRCULATIONAHA.112.000335

PubMed Abstract | Crossref Full Text | Google Scholar

99. Morita Y, Lencho T, Gunasekaran S, Modak R. Modified tricuspid annular plane systolic excursion using transesophageal echocardiography and its utility to predict postoperative course in heart transplantation and left ventricular assist device implantation. J Cardiothorac Vasc Anesth. (2018) 32(3):1316–24. doi: 10.1053/j.jvca.2017.11.024

PubMed Abstract | Crossref Full Text | Google Scholar

100. Raina A, Seetha Rammohan HR, Gertz ZM, Rame JE, Woo YJ, Kirkpatrick JN. Postoperative right ventricular failure after left ventricular assist device placement is predicted by preoperative echocardiographic structural, hemodynamic, and functional parameters. J Card Fail. (2013) 19(1):16–24. doi: 10.1016/j.cardfail.2012.11.001

PubMed Abstract | Crossref Full Text | Google Scholar

101. Liang LW, Jamil A, Mazurek JA, Urgo KA, Wald J, Birati EY, et al. Right ventricular global longitudinal strain as a predictor of acute and early right heart failure post left ventricular assist device implantation. ASAIO J. (2022) 68(3). doi: 10.1097/MAT.0000000000001467

PubMed Abstract | Crossref Full Text | Google Scholar

102. Dufendach KA, Zhu T, Diaz Castrillon C, Hong Y, Countouris ME, Hickey G, et al. Pre-implant right ventricular free wall strain predicts post-LVAD right heart failure. J Card Surg. (2021) 36(6):1996–2003. doi: 10.1111/jocs.15479

PubMed Abstract | Crossref Full Text | Google Scholar

103. Magunia H, Dietrich C, Langer HF, Schibilsky D, Schlensak C, Rosenberger P, et al. 3D Echocardiography derived right ventricular function is associated with right ventricular failure and mid-term survival after left ventricular assist device implantation. Int J Cardiol. (2018) 272:348–55. doi: 10.1016/j.ijcard.2018.06.026

PubMed Abstract | Crossref Full Text | Google Scholar

104. Cameli M, Lisi M, Righini FM, Focardi M, Lunghetti S, Bernazzali S, et al. Speckle tracking echocardiography as a new technique to evaluate right ventricular function in patients with left ventricular assist device therapy. J Heart Lung Transplant. (2013) 32(4):424–30. doi: 10.1016/j.healun.2012.12.010

PubMed Abstract | Crossref Full Text | Google Scholar

105. Grant ADM, Smedira NG, Starling RC, Marwick TH. Independent and incremental role of quantitative right ventricular evaluation for the prediction of right ventricular failure after left ventricular assist device implantation. J Am Coll Cardiol. (2012) 60(6):521–8. doi: 10.1016/j.jacc.2012.02.073

PubMed Abstract | Crossref Full Text | Google Scholar

106. Scheel PJ III, Cubero Salazar IM, Friedman S, Haber L, Mukherjee M, Kauffman M, et al. Occult right ventricular dysfunction and right ventricular-vascular uncoupling in left ventricular assist device recipients. J Heart Lung Transplant. (2024) 43(4):594–603. doi: 10.1016/j.healun.2023.11.015

PubMed Abstract | Crossref Full Text | Google Scholar

107. Ruiz-Cano MJ, Morshuis M, Koster A, Lauenroth V, Prashovikj E, Gummert J, et al. Risk factors of early right ventricular failure in patients undergoing LVAD implantation with intermediate intermacs profile for advanced heart failure. J Card Surg. (2020) 35(8):1832–9. doi: 10.1111/jocs.14696

PubMed Abstract | Crossref Full Text | Google Scholar

108. Akin S, Soliman O, de By T, Muslem R, Tijssen JGP, Schoenrath F, et al. Causes and predictors of early mortality in patients treated with left ventricular assist device implantation in the European registry of mechanical circulatory support (EUROMACS). Intensive Care Med. (2020) 46(7):1349–60. doi: 10.1007/s00134-020-05939-1

PubMed Abstract | Crossref Full Text | Google Scholar

109. Rivas-Lasarte M, Kumar S, Derbala MH, Ferrall J, Cefalu M, Rashid SMI, et al. Prediction of right heart failure after left ventricular assist implantation: external validation of the EUROMACS right-sided heart failure risk score. Eur Heart J Acute Cardiovasc Care. (2021) 10(7):723–32. doi: 10.1093/ehjacc/zuab029

PubMed Abstract | Crossref Full Text | Google Scholar

110. Kumar S, Rivas-Lasarte M, Rashid S, Scatola A, Rochlani Y, Murthy S, et al. External validation and comparison of the EUROMACS and right ventricular failure risk score for right ventricular failure prediction after left ventricular assist device. J Heart Lung Transplant. (2020) 39(4):S38. doi: 10.1016/j.healun.2020.01.1196

Crossref Full Text | Google Scholar

111. Shah H, Murray T, Schultz J, John R, Martin CM, Thenappan T, et al. External assessment of the EUROMACS right-sided heart failure risk score. Sci Rep. (2021) 11(1):16064. doi: 10.1038/s41598-021-94792-3

PubMed Abstract | Crossref Full Text | Google Scholar

112. Matthews JC, Koelling TM, Pagani FD, Aaronson KD. The right ventricular failure risk score: a pre-operative tool for assessing the risk of right ventricular failure in left ventricular assist device candidates. J Am Coll Cardiol. (2008) 51(22):2163–72. doi: 10.1016/j.jacc.2008.03.009

PubMed Abstract | Crossref Full Text | Google Scholar