Systematic Reviews Open Access
Copyright ©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 21, 2025; 31(27): 107740
Published online Jul 21, 2025. doi: 10.3748/wjg.v31.i27.107740
Cardiovascular risk assessment and predictors of cardiac decompensation after transjugular intrahepatic portosystemic shunt in patients with cirrhosis
Davide R Tomassoni, Department of General Medicine, Eastern Health, Melbourne 3128, Victoria, Australia
Tamar Schildkraut, Rohit Sawhney, Department of Gastroenterology, Eastern Health, Melbourne 3128, Victoria, Australia
Vivekananda Ramachandran, Department of Radiology, Eastern Health, Melbourne 3128, Victoria, Australia
Jennifer C Cooke, Department of Cardiology, Eastern Health, Melbourne 3128, Victoria, Australia
Jennifer C Cooke, Rohit Sawhney, Eastern Health Clinical School, Monash University, Melbourne 3128, Victoria, Australia
ORCID number: Rohit Sawhney (0000-0002-8131-2182).
Author contributions: Tomassoni DR was the predominant writer, performed literature search, extraction, evaluation and synthesis; Schildkraut T was secondary author, co-evaluator for literature reviewed, edited the article, provided assistance with producing figures; Ramachandran V provided radiological expertise, assistant editor; Cooke JC provided cardiology expertise, assistance with formulation of figure 4, assistant editor; Sawhney R provided research oversight, key gastroenterology consultation and major structuring of review as well as editing.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
PRISMA 2009 Checklist statement: The authors have read the PRISMA 2009 Checklist, and the manuscript was prepared and revised according to the PRISMA 2009 Checklist.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Rohit Sawhney, Associate Professor, Department of Gastroenterology, Eastern Health, 3 West, Building B, Box Hill Hospital, 8 Arnold Street, Box Hill, Melbourne 3128, Victoria, Australia. rohit.sawhney@easternhealth.org.au
Received: March 30, 2025
Revised: May 16, 2025
Accepted: July 1, 2025
Published online: July 21, 2025
Processing time: 115 Days and 10 Hours

Abstract
BACKGROUND

Portal hypertension (PH) is a major complication of chronic liver disease and a leading cause of mortality and morbidity in patients with cirrhosis. Transjugular intrahepatic portosystemic shunt (TIPS) is an established treatment for PH-related complications, including refractory ascites, variceal bleeding, hepatic hydrothorax and Budd-Chiari syndrome. However, post-TIPS cardiac decompensation has been reported in up to 25% of patients, often due to haemodynamic shifts revealing occult cardiac dysfunction. Current approaches to pre-procedural cardiac assessment and risk stratification remain inconsistent. This systematic review examines current recommendations and emerging strategies for cardiovascular evaluation in patients with cirrhosis prior to a TIPS.

AIM

To identify the key predictive factors for cardiac decompensation following a TIPS in patients with cirrhosis.

METHODS

A systematic review of available literature, using PubMed (including MEDLINE), Embase and Cochrane databases. Results were searched comprehensively, without exclusion criteria, from inception to May 2025. Given the predominance of retrospective cohort studies, risk of bias assessment was primarily performed using the ROBINS-E tool.

RESULTS

Thirteen studies were included (n = 1674 patients), with a pulled mean decompensation rate of 8.8%. Due to the variability in TIPS timing, study quality and heterogeneity, a meta-analysis was not feasible, therefore results were synthesised narratively. Multiple diastolic dysfunction parameters independently and integrated through the American Society of Echocardiography guidelines demonstrated predictive value. Newly validated risk score, heart failure with preserved ejection fraction, and biomarkers such as N-terminal pro-B-type natriuretic peptide ≥ 125 pg/mL consistently highlight cardiac dysfunction amongst the literature. Our review also explored left-atrial strain imaging as well as recent advances in cardiac magnetic resonance imaging and potential genetic contributors.

CONCLUSION

Multiple predictors of cardiac decompensation following TIPS exist, however studies are of limited quality. Implementing reliable markers may enable early risk stratification, candidate selection and guide pre-procedural optimisation.

Key Words: Portal hypertension; Transjugular intrahepatic portosystemic shunt; Pre-emptive transjugular intrahepatic portosystemic shunt; Diastolic dysfunction; N-terminal pro-B-type natriuretic peptide; Echocardiography; Left atrial strain; Multidisciplinary team; Risk stratification; Heart failure

Core Tip: Diastolic dysfunction, particularly when defined using American Society of Echocardiography criteria, consistently correlates with post-transjugular intrahepatic portosystemic shunt (TIPS) heart failure. N-terminal pro-B-type natriuretic peptide ≥ 125 pg/mL, clinical history and examination, 12-lead electrocardiography, transthoracic echocardiography can improve pre-TIPS risk stratification, optimise patient selection, and enable early cardiac optimisation. Employing additional tools, such as the heart failure with preserved ejection fraction score and left-atrial strain imaging may further characterise cardiac dysfunction however, requires further validation. Future research should clarify the role of cardiac magnetic resonance imaging and precision medicine in this cohort.



INTRODUCTION

Portal hypertension (PH) is a common complication of advanced chronic liver disease, defined as an elevation of portal-to-systemic pressure gradient, and is a major contributor to morbidity and mortality in patients with cirrhosis[1,2]. It leads to life-threatening complications such as variceal bleeding, refractory ascites, hepatic hydrothorax, hepatorenal syndrome and veno-occlusive disease. Transjugular intrahepatic portosystemic shunt (TIPS) placement is an established procedure that effectively decompresses the portal venous system in patients with PH refractory to medical therapy. Indications for TIPS include acute and recurrent variceal bleeding, refractory ascites, hepatic hydrothorax and Budd-Chiari syndrome; with emerging data for hepatorenal syndrome, hepatopulmonary syndrome and prevention of further decompensation[3-6]. More recently, the early or pre-emptive use of TIPS (typically performed within 24-72 hours of admission) has demonstrated improved survival and reduced rebleeding rates in high-risk patients with acute variceal haemorrhage[7,8]. Despite the benefits of TIPS, up to 25% of patients experience cardiac decompensation or new heart failure (HF) post-procedure[9-12]. However, there is a lack of consensus regarding pre-procedural cardiac assessment to guide patient selection. This systematic review explores current recommendations and emerging strategies to improve cardiovascular risk stratification in patients with cirrhosis undergoing a TIPS procedure.

Concern over cardiac complications

The placement of a TIPS in cirrhotic patients raises concerns over cardiac complications owing to TIPS-induced haemodynamic changes. The TIPS procedure functions by directly connecting the high-pressure splanchnic venous system to the systemic venous return through an interventional radiology-guided insertion of a polytetrafluoroethylene coated shunt[13]. The increased volume in systemic venous return can, however, result in increased preload and systemic volume overload[14]. The accompanying demand for increased cardiac output may unmask or induce worsening cardiac dysfunction. This is especially concerning in patients with cirrhotic cardiomyopathy who demonstrate a blunted cardiac response to stimuli and electrophysiologic changes[9,15,16]. Cardiac complications include pulmonary oedema, cardiac failure, arrhythmias and worsening pulmonary hypertension. A significant proportion, 10%-25% of patients suffer cardiac failure due to cardiac decompensation 3-12 months after undergoing TIPS[9-12]. Given the drastic cardiovascular alterations witnessed following a TIPS procedures, it is unsurprising that severe congestive HF, severe untreated valvular heart disease and moderate-severe pulmonary hypertension are absolute contraindications to TIPS placement in established guidelines[17].

Haemodynamic changes seen post-TIPS

A TIPS lowers the portal venous pressure by providing a novel channel to bypass problematic sinusoidal resistance of the cirrhotic liver. Decompressing the portal venous system alleviates the underlying pathophysiological driver of complications such as gastro-oesophageal varices, ascites and hepatic hydrothorax. Additional haemodynamic effects are evident by a TIPS induced multifactorial vasodilation. This effect is partially attributable to portal-systemic shunting of vasodilatory substances from the portal circulation, normalising effective systemic blood volume, thereby decreasing stimulation of renin-angiotensin-aldosterone axis and finally increased nitric oxide production secondary to increased cardiac output[18].

Cardiac complications of TIPS-a lesson in physiology

Significant cardiovascular adaptation is encountered in advanced cirrhosis and PH which is augmented post-TIPS: An induced hyperdynamic circulatory state characterised by increased cardiac output, elevated heart rate, reduced systemic vascular resistance and low arterial blood pressure (Figure 1). This state is a product of splanchnic vasodilation, mediated by elevated levels of endogenous vasodilators as well as endocannabinoids and the development of autonomic neuropathy[19,20]. The resultant reduction in effective blood volume activates neurohumoral vasocontractile systems including the sympathetic and renin-angiotensin-aldosterone system leading to sodium and water retention. This serves to increase plasma volume and cardiac output. During TIPS, diversion of blood flow directly from splanchnic circulation into systemic circulation can cause dramatic augmentation of preload 50%-100% increase in right atrial pressure, pulmonary artery pressure, left ventricular diastolic volumes, intensification of hyperdynamic circulation and increased portosystemic shunting[7,9,21]. This effect results in a persistent increase in cardiac output in cirrhotic hearts which may result in prolonged strain and/or impaired cardiac contractility, whilst also increasing right heart pressure rise secondary to volume load[18,22]. This volume challenge can exaggerate the pre-existing hyperdynamic state and potentially worsen occult pulmonary hypertension or reveal subclinical cardiomyopathy under the guise of “cirrhotic cardiomyopathy” evidenced by reduced pre-load reserve and blunted response to stress[23-26].

Figure 1
Figure 1 Hyperdynamic alterations in advanced chronic liver disease and post-transjugular intrahepatic portosystemic shunt[30]. Depicted: Hyperdynamic changes seen in advancing chronic liver disease (grey arrows), with transjugular intrahepatic portosystemic shunt changes (green) demonstrating haemodynamic changes with resultant effects. TIPS: Transjugular intrahepatic portosystemic shunt; RA: Right atrium; LV: Left ventricle; CO: Cardiac output.

Diastolic dysfunction is an important entity in cardiology and may precipitate congestive cardiac failure symptoms in the setting of normal left ventricular systolic function[6,27]. Indeed, in the absence of intrinsic cardiac disease or dilated alcoholic cardiomyopathy, cardiac function in cirrhotic patients may appear normal, evidenced by normal conventional left ventricular ejection fraction (EF). However, the prevalence of diastolic dysfunction averages about 50% in this population[28]. Increased left ventricular diastolic pressure in cirrhotic patients is postulated to mainly result from a decreased cardiac wall compliance, a feature which concomitantly deteriorates the chronic liver disease course and prognosis whilst simultaneously worsening diastolic dysfunction with progressive liver disease[28,29]. It is unsurprising that diastolic dysfunction is a predictor of poorer survival in these patients, and should hence be identified[11,26,28].

Current recommendations and challenges for cardiac assessment

Most international guidelines recommend clinically significant congestive cardiac failure, severe untreated valvular disease and moderate-severe pulmonary hypertension despite medical therapies [mean pulmonary artery pressure > 45 mmHg on right heart catheterisation (RHC)] as absolute contraindications to a TIPS procedure[4,6,30-33].

While a TIPS is clearly contraindicated in severe cardiovascular and cardiopulmonary disease, recommendations for mild to moderate disease are less well defined. New-onset cardiac dysfunction is a recognised entity in the absence of known cardiac disease irrespective of cirrhosis aetiology but this remains difficult to predict, as the occult cardiac dysfunction becomes apparent only under physiological, pharmacologic or pathological stress[31]. Thorough cardiac evaluation during TIPS work-up is paramount to identify the outlying patients who do not have severe cardiac disease yet remain at-risk of HF or arrhythmias given pre-existing cardiac dysfunction.

Currently, there is a lack of consensus amongst international guidelines with significant variability regarding recommendations for cardiovascular workup[7,34]. The current European and American Association for the Study of Liver Diseases (EASL) advises an echocardiogram be performed in all TIPS candidates[7,17,33]. British guidelines suggest clinical evaluation, a 12-lead electrocardiography (ECG) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) as screening tools for all patients undergoing elective TIPS with further assessment, such as echocardiography, recommended if any abnormalities are identified[13].Other groups recommend pre-TIPS echocardiography in all patients with the addition of a RHC to confirm and/or define pulmonary hypertension in selected patients[31]. In addition, earlier European guidelines recommended dynamic stress testing by inducing a hyperdynamic circulatory state, systolic dysfunction and failure to increment would be unmasked[6]. This was omitted in newer recommendations, likely due to updated cirrhotic cardiomyopathy criteria in 2020 surpassing this limited finding[35]. Conversely, the Cardiovascular and Interventional Radiological Society of Europe Standards of Practice recommends ECG, echocardiography and NT-proBNP levels[32]. The Toulouse algorithm developed from a prospective study of patients with cirrhosis treated with TIPS suggests combining pre-TIPS natriuretic peptides and echocardiographic parameters of diastolic dysfunction to improve patient selection regarding the risk of post-TIPS cardiac decompensation but requires further validation[9].

Therefore, universal recommendations for cardiovascular workup pre-TIPS, which may serve to optimise risk stratification and aid in patient selection, are lacking and further studies are required for clarification. Herein, we will review the literature for both established and novel cardiac screening modalities for patients undergoing TIPS and propose a potential algorithm to aid this assessment.

MATERIAL AND METHODS

This study was developed according to the preferred reporting items for systematic reviews and meta-analyses statement 2020 the 27-item updated guideline for reporting systematic reviews[36]. All available full-text articles, translated or published in English which reported on patients with cirrhosis, undergoing the TIPS procedure and experiencing HF were included in this systematic review. No published research was omitted on the basis of study design, year of publication, number of patients, disease aetiology/type, length of follow-up or other characteristics. The systematic review protocol was not published or registered a priori. Ethics committee approval was not required, as the study involved only secondary analysis of previously published data.

Search strategy and selection criteria

Databases were most recently searched on May 13, 2025, and included PubMed (including MEDLINE), Embase and the Cochrane library. Searches spanned from inception to May 2025, using search terms “cirrhosis” combined with “transjugular intrahepatic portosystemic shunt” and “heart failure”. Abstracts and conference proceedings were included in the search results. No filters or limits were used, however search results yielded only articles published in English. Editorials and review articles were screened to identify further eligible studies not captured in the database searches. All data sought, pertained to outcomes involving HF following a TIPS procedure in patients with cirrhosis particularly research investigating predictive markers. No additional filters or variables were used which may have diminished search results. There was no contact with included study authors during the synthesis of this review.

Data extraction

Records were imported into a bibliographic management system with duplicate entries removed manually. Potential patient population overlap was assessed for in the studies, however was not identified. The first author (Tomassoni DR) independently screened titles and abstracts to determine eligibility. All studies deemed eligible at this stage had their full texts retrieved for further review. The first author independently extracted data on the patient group (P), intervention (I), comparator (C), outcome (O) and study design (S). Additional variables included study setting and region, sample size, follow-up. Data was extracted manually and solely from the published manuscript, without correspondence with study investigators. To enable consistent extraction of data, some outcome measure reporting using different units or scales were converted to common metrics where possible. Where possible, outcome definitions were harmonized to facilitate comparison across studies.

Methodological quality

The ROBIN-E risk of bias tool was utilised independently and manually by authors (Tomassoni DR and Schildkraut T) to evaluate the methodological quality of the non-randomised cohort studies reviewed. That was, after applying the framework for extending ROBINS-E to address appropriateness of the study review question[37]. There were no significant discrepancies requiring further input by a third assessor. This tool serves to appraise each study (study-level) in seven domains for potential bias, namely: Confounding, measurement of the exposure, selection of participants, post-exposure intervention, missing data, measurement of the outcome, selection of the reported result. Evaluation thereafter results in judgement of low bias (i.e. little or no concern about bias), some concern (some concerns, unclear if important risks of bias), high (important problems giving rise to high risk of bias) and very high bias (the study is very problematic in this domain).

Given the lack of validated quality assessment tools for observational studies, further assessment was performed with the National Heart, Lung, and Blood Institute (NHLBI) study quality assessment tool: Quality assessment tool for before-after (pre-post) studies with no control group was also applied[1]. Supplementary Table 1, demonstrates this tool, which is recommended for use in non-randomised, uncontrolled studies which utilise an early measure (i.e. prior to TIPS) as well as a later measure (post-TIPS)[38]. It utilises 12 criteria to illustrate study quality in domains involving: Study objective, transparency of eligibility criteria, representativeness of participants, proportion of recruitment of eligible participants, sample size, clarity in delivering consistent intervention, prespecified reliable outcome measures, blinding of assessors, follow-up, statistical analysis, features of interrupted time-series and extrapolation of individual level data or only group level. Upon review, these questions were answered with a “yes”, “no” or “other” (i.e. cannot determine, not applicable, not reported). A final, “good”, “fair” or “poor” was awarded to the study overall “quality”.

Summary measures and synthesis of results

The principal summary measures sought were risk ratios for dichotomous outcomes, and mean differences for continuous variables. Where these measures were not explicitly reported, alternative statistics such as hazard ratios (HR) or odds ratios (OR) were extracted with consideration for conversion if feasible. There were significant clinical and methodological heterogeneity, including variations in study design, outcome definitions and statistical reporting, therefore formal meta-analysis was not undertaken. Consequently, no pooled estimates or measures of statistical consistency were calculated. Rather, results were synthesized narratively with studies grouped thematically by outcome domain and stratified where relevant by intervention type, population characteristics or study features. Key findings were summarised in structured tables to facilitate comparison and identify trends across the literature included.

RESULTS
Study selection

The search of the three Databases: PubMed (including MEDLINE), Embase and Cochrane library returned a total of 309 results. Duplicates were eliminated, reducing the search results to 240 records. By screening the title and abstract for relevance to the current research question, 199 records were excluded, leaving 42 studies. Of these, 13 met the inclusion criteria, of which three were prospective studies and the remaining ten were retrospective cohort or case-control studies. One study was bicentric, the remaining studies were monocentric. Please review Figure 2, for schematic representation of study selection process.

Figure 2
Figure 2  Screening process: From identification to inclusion.
Study characteristics

The included studies were published between 2015 and 2025, cohorts ranged between 15 and 360 patients, totalling 1674 patients undergoing a TIPS procedure as summarized in Table 1. Laurenzano et al[39], was the only multi-centre study, based in the United States, representing the largest cohort a respectable 360 participants and also had the equal longest follow up. The 24-month follow up was tied only with Alla et al[40]. Alla et al[40], Billey et al[9], and Vanderschueren et al[41] all had moderate participants cohorts (180, 100 and 106 participants respectively), with very similar investigative aims: Predictive factors of cardiac decompensation following a TIPS; and utilised diastolic dysfunction parameters found also in the algorithm from American Society of Echocardiography (ASE)[42]. They differed however in design, Vanderschueren et al[41] and Alla et al[40] both produced a retrospective cohort study, the latter only available as a conference abstract at the time of writing. The study by Billey et al[9] however ran prospectively and involved risk stratification of patients utilising a novel Toulouse algorithm.

Table 1 Studies on predictors of cardiac decompensation in patients with cirrhosis post-transjugular intrahepatic portosystemic shunt study design data.
Ref.
Year
Type
Design
Setting
Population
Sample (n)
Predictors
Outcomes
Follow up (months)
Ali et al[10]2022JRetrospective cohortSingle centre (United States)Patients with cirrhosis for TIPS107TTE: RA size, LV dimensions, PASPSignificant HF, mortality3
Alla et al[40]2021CARetrospective cohortSingle centre (India)Patients with cirrhosis for TIPS164TTE: RAP, EF, E/e’; HVPG; NT-proBNP; MELD; CTPSignificant HF, mortality24
Billey et al[9]2019JProspective cohortSingle centre (France)Patients with cirrhosis for TIPS100TTE: E/A > 1.5, E/e’ > 10, LAVI > 34 mL/m2, AS; BNP > 40 pg/mL; NT-proBNP > 125 pg/mL; QTc > 440 millisecondsSignificant HF12
Filì et al[43]2015JProspective physiologicalSingle centre (Italy)Patients with cirrhosis for TIPS15TTE: LV dimensions, IVS, LVEF, LAD, E/A, DT, PASP; RHC: PASP, mPAP, pADP, PCWP, TPG, CO, PVS, SVR; NT-proBNP; QTc > 440 millisecondsHaemodynamic changes, significant HF1
Laurenzano et al[39]2024JRetrospective cohortDual centre (United States)Patients with cirrhosis for TIPS360TTE: LAVI, E/e’, TR max, septal e, lateral e, LVEF; Intraprocedural RA pressureSignificant HF, hospitalisation, mortality24
Luo et al[44]2024CARetrospective cohortSingle centre (China)Patients with cirrhosis for TIPS140TTE: LVEF, E/A, LAVI, Septal e’, lateral e’, E/e’, pro-BNPSignificant HF, mortality6
Modha et al[45]2018JRetrospective case-controlSingle centre (United States)Patients with cirrhosis for TIPS481Age; RA pressure, portal vein pressureSignificant HF, mortality1
Nguyen et al[47]2022CARetrospective cohortSingle centre (United States)Patients with cirrhosis for TIPS249MELD-Na; PMHx: IHD, CVA/TIA, HFpEFSignificant HF6
Schneider et al[11]2023JRetrospective cohortSingle centre (Germany)Patients with cirrhosis for TIPS234DD (ASE/EACVI), pathological E/A, HanDeCT algorithmSignificant HF12
Vanderschueren et al[41]2024JRetrospective cohortSingle centre (Belgium)Patients with cirrhosis for TIPS106TTE: LAVI; Age; Albumin; NT-proBNP; Toulouse algorithmSignificant HF, mortality12
Venner et al[46]2025JRetrospective cohortSingle centre (Netherlands)Patients with cirrhosis for TIPS52H2FPEF score, LA strain, HDF, QTc, E/e’ ratio, RWTSignificant HF6
Debernardi Venon et al[49]2021JRetrospective cohortSingle centre (Italy)Patients with cirrhosis for TIPS63LV diastolic dimensions, EACI/ASE DD: LA diameter, LVEF, TAPSE, E/A ratio, e’, mPAP, CVP, NT-proBNP, PRALV DD incidence, TIPS response, mortality12
Wade et al[48]2021CARetrospective cohortSingle centre (United States)Patients with cirrhosis for TIPS36MELD-Na, bilirubin, INR, TTE parameters (atrial dimensions and pressures)Significant HF12

A monocentric retrospective study by Ali et al[10], reviewed 107 patients between 2003 and 2018, also seeking predictors of HF after TIPS, however had a relatively short follow up period (90 days) and stringent HF diagnosis criteria. Despite this, they had comparable rates (10%) of HF (endpoint). Of the two remaining prospective studies, Filì et al[43] published a prospective physiological study investigating 15 patients receiving TIPS (30-days follow-up), while Luo et al[44] produced a prospective 140 participant cohort study with 6-months follow-up. Of note, neither demonstrated any HF following TIPS procedure (nor due to volume expansion by experimental means). These studies however didn’t clearly describe their method for diagnosing HF following the TIPS. In addition, these studies are unique due to the predominance of viral causes of cirrhosis.

Modha et al[45], also experienced diminutive HF endpoints (0.9% of participants) in their retrospective case-control study and also had the equal shortest follow up (tied with Filì et al[43]) at 30 days. Of the 882 patients who had received TIPS and were eligible, 8 experienced cardiac decompensation which were compared with 40 randomly selected patients. Notably, Modha et al[45] recorded 52 deaths within 7 days of TIPS which were omitted from results, as none appeared attributable to cardiac causes during investigator review. This study was limited by small sample groups, incomplete peri-procedural investigation data and lack of randomization information. Research by Venner et al[46], which employed less stringent HF diagnostic criteria and had the most prominent proportion of participants (44%) experiencing HF post-TIPS. This was also a small retrospective cohort study, of only 52 participants (follow-up 6-months), and HF diagnosis consisted of clinical or imaging or biochemical evidence of cardiac congestion. Additionally, this study explores unique and novel imaging parameters including relative wall thickness of left ventricular and diastolic haemodynamic work to predict cardiac decompensation.

Schneider et al[11] published a sizeable retrospective cohort study (234 participants) with a unique comparison of recent diagnostic algorithms such as haemodynamic decompensation following TIPS cardiac tolerance algorithm (HanDeCT), Toulouse, ASE as well applying the cirrhotic cardiomyopathy consortium (CCC) criteria with 12-months follow-up. Nguyen et al[47], reports on a retrospective cohort study with a reasonable cohort size (249 participants) and intermediate follow-up period (6-months). Of interest, this conference abstract does not expand on how their HF diagnosis is confirmed, nor elucidate the pre-TIPS investigations. Instead, it appears, predictors involving model for end-stage liver disease (MELD) score [MELD incorporating serum sodium (MELD-Na)] score and traditional cardiovascular risk factors are investigated. The study by Wade et al[48], is a small (36 participant) monocentric retrospective cohort study with one-year follow up, submitted as a conference abstract, however lacks data which may limit utility including demographics, cardiac history and TIPS indication. Finally, the study by Debernardi Venon et al[49], described the clinical impact of left ventricular diastolic dysfunction in 63 cirrhotic candidates awaiting TIPS with 12-months follow up. While this study does not explicitly include HF endpoints, subgroup analysis reports HF mortalities. This is one of four studies which exclude or limit emergent TIPS[9,10,43,49] and as such, may limit generalisability. Furthermore, the outcomes were not clearly outlined by Debernardi Venon et al[49], with HF only described in two expired patients described as part of mortality outcomes.

Risk of bias and study quality

The risk of bias tool is presented in Figure 3. Five studies were rated as “high’ risk of bias: Luo et al[44], Modha et al[45], Nguyen et al[47], Wade et al[48], and Debernardi Venon et al[49]. The remaining eight rated as moderate risk of bias, with predominant ratings of “some concerns” across several domains. None of the studies were considered to be of “low” risk of bias, however Ali et al[10], Billey et al[9], Laurenzano et al[39], and Schneider et al[11] had the most favourable profiles without high-risk domains identified. Most common sources of bias were in domains regarding confounding (D1) and missing data (D5). These findings were parallelled by the NHLBI tool presented in Supplementary Table 1. This tool rated 8 of 13 studies as “poor” quality, primarily due to methodological shortcomings such as lack of control for confounding, unclear outcome assessment and incomplete or unreported follow-up data. Appraisal found that most criteria was fulfilled by Ali et al[10], Billey et al[9], Laurenzano et al[39], and Schneider et al[11], Vanderschueren et al[41] demonstrating fewer methodological limitations which would otherwise limit the validity of the study rated as “fair” quality. None met criteria for high methodological quality. Collectively, these findings underscore the caution needed when interpreting these results given the potential for systematic error and variability in study rigour.

Figure 3
Figure 3  ROBINS-E, risk of bias tool on selected cohort studies[110].
Demographics, intervention and outcomes

Median ages within the studies ranged from 42 to 69 years, and cohorts were predominantly male, between 52%-80% as shown in Table 2. Cirrhosis aetiology varied significantly between studies: Alcohol-related cirrhosis predominated, followed by viral aetiology. Across the studies, TIPS was primarily performed in patients with Child-Pugh class B cirrhosis. MELD scores available from the studies range predominantly between 11-16, also reflecting moderate baseline liver dysfunction. Indication for TIPS, was largely impacted by some studies excluding a proportion of pre-emptive or emergent TIPS[9,10,44], or selecting only patients with refractory ascites[43,49]. Following refractory ascites, variceal bleed was the next commonest indication. Other indications for TIPS were pre-operative and hepatic hydrothorax.

Table 2 Studies on predictors of cardiac decompensation in patients with cirrhosis post-transjugular intrahepatic portosystemic shunt demographic data.
Ref.
Age (median)
Sex (men %)
Creatinine (μmol/L)
1° cirrhosis aetiology
Child-Pugh A/B/C
MELD (MELD-Na)
TIPS indication
HF%
Cardiac disease
Ali et al[10]586697.3 (35.4-238.7)Alcohol (39%)A: 11%, B: 62%, C: 27%15 (7-30)Ref.A. (50%), V.B. (42%)1017%
Alla et al[40]4379.6 vs 159Alcohol7 ± 1.2116 ± 5.322.266%
Billey et al[9]697989 ± 53Alcohol (74%)A: 25%, B: 66%, C: 9%11.5 ± 4Ref.A. (58%), pre-op (23%), V.B. (19%)2028% include AS: 10%
Filì et al[43]548079.6 vs 97.3Viral (73.3% +)A: 0%, B: 46%, C: 53.3%14.3 ± 4Ref.A. (100%)0Excluded
Laurenzano et al[39]5860Alcohol (31%)13.1 (9.7-16.7)Ref.A. (39%), V.B. (33%), H.H. (12%)8.8Excluded
Luo et al[44]Viral (56.4%)V.B. (80.7%)0Excluded
Modha et al[45]5852115 ± 94MAFL (35.4%)A: 20.8%, B: 66.7%, C: 12.5%12.0 ± 4.7Ref.A. (47.9%), V.B. (31.3%)0.925.90%
Nguyen et al[47]21 vs 1711.7
Schneider et al[11]5959100 (57.8-135.3)Alcohol (58.1%)A: 9.4%, B: 81.2%, C: 9.4%12 (10-15)Ref.A. (82.9%), V.B. (20.5%)1839.7% include AS: 8.2%
Vanderschueren et al[41]6369.893.73 (64.6-115)Alcohol (72.6%)8 (7.0-9.2)12.3 (10.2-16.5)Ref.A. (58.5%), V.B. (41.5%)11.3Yes, unclear
Venner et al[46]64 vs 57Ref.A. (50%), V.B. (40%), H.H. (6%)44
Debernardi Venon et al[49]5979113.2 ± 5.3Alcohol (49%)A: 0, B: 84%, C: 16%13.7 ± 0.55Ref.A. (100%)3Excluded
Wade et al[48]13.5 vs 17.114

There is significant heterogeneity among studies when assessing for cardiac disease preceding TIPS. Several studies opted to exclude patients with known cardiac disease and dysfunction[39,43,44,49], whilst cardiac dysfunction ranges between 17%-66%, with inclusion of structural heart disease in three studies, including aortic stenosis (AS)[9,11,41]. Pre-procedural cardiac function is undisclosed in the remaining studies[46-48]. Further, renal function, measured by creatinine ranged from mean value of 79 mmol/L to 115 mmol/L in available cohorts.

Notably, as seen in Table 3, additional risk associated with advancing age was demonstrated by three authors [HR = 1.05, (1.01-1.09), P = 0.013; OR = 1.02 (1.01-1.03), P = 0.006][41,45,46]. In addition, ischaemic heart disease and cerebrovascular accident/transient ischaemic attack history resulted in correlations with decompensation [HR = 3.48 (1.53-7.88), P = 0.002; HR = 4.45 (1.52-12.98), P = 0.006, respectively][47].

Table 3 Summary of traditional risk factors, by study.
Ref.
Advancing age (years)
MELD-Na
Portal vein pressure (mmHg)
QTc (millisecond)
IHD (previous history)
CVA/TIA (previous history)
Modha et al[45]63.6 vs 57.1 (P = 0.041)1> 25, P = 0.018
Nguyen et al[47]21 vs 17, P = 0.037; [HR = 1.08 (1.02-1.14), P = 0.014]HR = 3.48 (1.53-7.88), P = 0.002HR = 4.45 (1.52-12.98), P = 0.006
Vanderschueren et al[41]61.5 vs 67 [HR = 1.05 (1.01-1.09), P = 0.013]
Venner et al[46]64.3 vs 57.4 [OR = 1.02 (1.01-1.03), P = 0.006]453 vs 431 [OR = 1.03 (1.00-1.01), P = 0.01]
Wade et al[48]13.5 vs 17.1 (P = 0.007)

Multiple studies consistently highlighted elevated markers of left or right ventricular dysfunction as primary indicators demonstrated in Tables 4 and 5. This is evidenced by elevated early (E) to late (A) ventricular filling velocities (E/A) ratio correlating strongly in studies by Billey et al[9] [OR = 6.2 (1.7-21.4), P < 0.001] and Ali et al[10] [OR = 4.2 (1.39-12.31), P = 0.005]. Similarly, left atrial (LA) pressures demonstrated significant involvement with elevated early mitral inflow velocity (E) to early diastolic mitral annular velocity (e’), (E/e’) ratio associated with cardiac decompensation by Ali et al[10] [OR = 5.6 (1.3-23.4), P = 0.003], Billey et al[9] [OR = 6.7 (1.8-24.5), P < 0.001] and Schneider et al[11] [OR = 1.06 (1.00-1.11), P = 0.004].

Table 4 Summary of significant transthoracic echocardiography findings, by study.
Ref.
E/A ratio
E/e’ ratio
RA size (cm)
RA pressure (mmHg)
LAVI (mL/m²)
Smaller LA volume (mL)
Ali et al[10]5.5 ± 4.9 [OR: 3.26 (1.22-10.16), P = 0.03]
Alla et al[40]1.8 ± 0.9 [OR = 4.2 (3.9-12.3), P = 0.005]13 ± 5 [OR = 5.6 (3.0-23.4), P = 0.003]8 ± 3, OR = 5.7 (3.4-14.5), P-absent
Billey et al[9]> 1.5 [OR = 6.2 (1.7-21.4), P < 0.001]> 10 (OR = 6.7 (1.8-24.5), P < 0.001)> 34 mL/m2 [OR = (1.2-13.6), P = 0.031]
Modha et al[45]10.5 vs 6.6, P = 0.039
Schneider et al[11]< 0.8/> 2, HR = 2.21 (1.17-4.16), P = 0.015
Venner et al[46]11.4 vs 9.5 [OR = 1.06 (1.00-1.11), P = 0.04]
Wade et al[48]46.5 vs 67.8 (P = 0.020)
Table 5 Summary of significant transthoracic echocardiography findings, by study (continued).
Ref.
LVESD (cm)
LVEDD (cm)
LVOT VTI (cm)
TAPSE (mm)
PASP (mmHg)
RWT
Ali et al[10]3.2 vs 2.8 [OR = 5.43 (1.44-24.50), P = 0.02]5.2 vs 4.6 [OR = 4.12 (1.51-13.47), P = 0.001]≥ 31 (OR = 1.27 (1.51-13.47) P = 0.001)
Alla et al[40]30 ± 6 [OR = 3.4 (4.0-32.4) P < 0.001]30 ± 6 [OR = 3.4 (4.4-1.9), P = 0.01]
Venner et al[46]0.39 vs 0.34 [OR = 1.03 (1.02-1.30), P = 0.012]

Surrogate markers for right heart dysfunction and preload intolerance were significant in several trials Ali et al[10] [OR = 3.26 (1.22-10.16), P = 0.03], and Alla et al[40] [OR = 3.4 (1.4-32.4), P < 0.001] for increased right atrial size and pressure. Although Alla et al[40] report elevated tricuspid annular plane systolic excursion demonstrative for right ventricle dysfunction, it must be noted that the interquartile range data is incomplete [OR = 3.4 (4.4-1.9), P = 0.01]. Moreover, pulmonary artery hypertension as seen with increased pulmonary artery systolic pressure (PASP) also was predictive of post TIPS HF, Ali et al[10] [OR = 1.27 (1.15-13.47), P = 0.001]. Increased relative wall thickness was suggestive of concentric left ventricular remodelling demonstrated to have some predictive capacity by Venner et al[46] [OR = 1.03 (1.02-1.30), P = 0.012].

Biochemically, NT-proBNP elevation consistently predicted cardiac complications namely, Ali et al[10] [OR = 4.2 (2.3-9.50), P < 0.001]; Billey et al[9] median 610 vs 206 pg/mL, P = 0.005 and Vanderschueren et al[41] HR = 1.04 (1.00-1.07), demonstrated in Table 6. This effect was reflected with BNP in the Billey et al’s study[9] median 368 vs 86 pg/mL, P < 0.001. Further, perturbations in coagulation were demonstrated with elevated partial thromboplastin time (PTT) and reduced international normalised ratio (INR) by Modha et al[45] (PTT 15.0 vs 13.2 seconds, P = 0.029) and Wade et al[48] (INR 1.18 vs 1.40, P = 0.007) respectively. Modha et al[45] additionally observed elevated serum albumin levels in HF patients (5.2 vs 2.9, P = 0.028), a finding supported by multivariate regression in the Vanderschueren et al[41] study [HR = 1.10 (1.03-1.18), P = 0.009].

Table 6 Summary of significant serum markers, by study.
Ref.
NT-proBNP (pg/mL)
BNP (pg/mL)
Elevated albumin (mg/dL)
Elevated PTT (seconds)
Reduced INR
Reduced bilirubin (g/dL)
Alla et al[40]720 [OR = 4.2 (2.3-9.5), P < 0.001]1
Billey et al[9]> 125 (610 vs 206, P = 0.005)BNP > 40 (368 vs 86, P = 0.001)
Modha et al[45]5.2 vs 2.9, P = 0.02815.0 vs 13.2, P = 0.029
Vanderschueren et al[41]540 vs 150, HR = 1.04 (1.00-1.07)2HR = 1.10 (1.03-1.18), P = 0.009
Wade et al[48]1.18 vs 1.40 (P = 0.007)1.02 vs 2.05 (P = 0.022)

Regarding the risk stratification algorithms consolidated in Table 7 within this review, Schneider et al[11] identified predictive value using the ASE and European Association of Cardiovascular Imaging (EACVI) definition for diastolic dysfunction [HR = 2.22 (1.11-4.46), P = 0.025]. The HanDeCT [HR = 2.93 (1.47-5.87), P = 0.002] algorithm also demonstrated utility. The Toulouse algorithm failed to reach statistical significance for Schneider et al[11] [HR = 2.05 (0.89-4.70), P = 0.09], however was found effective at identifying high risk patients in the refractory ascites population in Vanderschueren et al’s study (P = 0.003)[41]. MELD-Na proved useful in two studies-with HR = 1.08 (1.02-1.14), P = 0.014[47,48]. The CCC criteria did not achieve significance in the single trial observing this [HR = 1.75 (0.76-4.02), P = 0.19][11].

Table 7 Summary of risk stratification tools, by study.
Ref.
DD (ASE/EACVI)
DD CCC
Risk tools
Toulouse algorithm
Schneider et al[11]HR = 2.22 (1.1-4.46), P = 0.025HR = 1.75, (0.76-4.02), P = 0.19HR = 2.93 (1.47-5.84), P = 0.0021HR = 2.05, (0.89-4.70), P = 0.09
Vanderschueren et al[41]High risk: 78%; All: P = 0.047; Ref.A. P = 0.003
Venner et al[46]OR = 1.14 (1.05-1.23), P > 0.012

An additional finding with predictive potential, reported by Modha et al[45], is a portal vein pressure > 25 mmHg, which was significantly associated with decompensated patients (P = 0.018). The porto-systemic pressure gradient was found to be elevated in the Vanderschueren et al’s study however when multivariable analyses were performed, was not found to be significant[41].

Follow-up times varied greatly between studies. The weighted mean follow-up time was approximately 13.2 months, within a range of 30 days to 24 months. Primary outcome for this review: Cardiac decompensation or HF developing after TIPS procedure ranged between 0% to 44%, with a weighted mean of 8.8%. Notwithstanding, this calculation was performed utilising incomplete data from the Debernardi Venon et al[49] study, whereby 3% (2/63 patients) incidence of HF was extrapolated from their mortality outcome within 12 months: Likely underestimating the true incidence, in the absence of complete (including HF) outcome data.

DISCUSSION

The results of this systematic review demonstrate the broad potential of multi-system predictors of cardiac decompensation ranging from demographics, serum biomarkers, echocardiographic parameters and clinical risk scores. Acknowledging these findings in the broader context of the literature may best serve to illustrate the utility of these findings and inform strategies to optimise pre-TIPS cardiac assessment and outcomes, as well as explore novel concepts for further study including uncovering contributory factors to cardiac decompensation in post-TIPS patients.

Favoured screening modalities

Transthoracic echocardiogram: Clinically significant HF often precludes patients from undergoing TIPS placement[17,39,45,50]. Stress echocardiography is a useful tool for assessing left ventricular function, especially in patients with occult diastolic dysfunction, and may serve to assess for a blunted sympathetic response on previous cirrhotic cardiomyopathy diagnosis criteria. However, EF assessment in stress echocardiography results may be unreliable in this population owing to frequent use of beta-blocker for treatment of PH and variceal prophylaxis[35].

Diastolic dysfunction indices E/A ratio: E/A ratio is demonstrated on two-dimensional echocardiography derived from the ratio of measured velocities of early maximal ventricular filling and late diastolic/atrial velocity assessing the atrial contribution to ventricular filling. An E/A < 1 represents a larger contribution of ventricular filling by the atrial “kick” during diastole, indicative of diastolic dysfunction in its earliest stages[51].

Diastolic function is commonly impaired in patients with advanced cirrhosis with marked reduction in E/A ratio described in comparison to controls, which partially improved with paracentesis, however remained abnormal[52,53]. Studies evaluating E/A ratio as an indicator of diastolic dysfunction have demonstrated significantly increased mortality risk following TIPS insertion in cirrhotic patients with an E/A ratio < 1[29,54]. These studies however, are older and additionally limited by their small, single-centred design.

Interestingly, a raised E/A ratio > 1.5 is also strongly predictive of cardiac decompensation likely given pseudo-normalisation develops (E/A 0.8-1.5, grade 2 dysfunction) followed by restricted filling (E/A > 2, grade 3) with advancing diastolic dysfunction[55]. Recent studies support abnormal E/A ratio, either < 0.8 or > 2, as being a significant risk factor for cardiac decompensation after TIPS[9,11] within the limitations of retrospective cohort studies[11]. Including both early and late E/A ratio values for diagnosis of diastolic dysfunction can identify early as well as late stages of restrictive ventricle filling thereby increasing its sensitivity[11]. It must be noted that the E/A ratio is dynamic, and can vary with changes in heart rate, cardiac filling and age[49], unlike the newer E/e’ ratio in the updated criteria[42].

Recommendations from the ASE/EACVI detailed a decision algorithm for left ventricular diastolic function assessment in patients with normal left ventricle EF utilising additional echocardiographic parameters: E/e’ ratio, early diastolic mitral annular (e’) velocity, peak tricuspid regurgitation (TR) velocity and LA volume index (LAVI)[42]. Based on these parameters, patients can be classified into normal diastolic function (< 50% positive criteria), indeterminate function (50% positive) or diastolic dysfunction (> 50% positive). The algorithm stratifies patients by assessing for elevated LA pressures (E/e’ > 14), reduced septal (e’ < 7 cm/second) or lateral (e’ < 10 cm/second) tissue Doppler velocities, increased tricuspid regurgitant velocity (> 2.8 m/second) and increased LA volume (LAVI > 34 mL/m2), albeit based on a non-cirrhotic or perioperative population[42]. These recommendations for diagnosis of cardiac diastolic dysfunction were simplified and adopted by the CCC in 2020[35]. Utilising the E/A ratio in addition to septal e’ velocity, E/e’, TR velocity and LA volume. The modified ASE criteria was proposed to stratify end-stage liver disease patients into normal, grade 1-3 or indeterminate diastolic function these however require further studies to validate use in TIPS populations. Notwithstanding, in a population with cirrhosis awaiting TIPS, an E/e’ ratio > 10 significantly increased the risk of cardiac decompensation[9]. Findings in pre-TIPS patients support ASE/EACVI recommendations for diagnosing diastolic dysfunction using LAVI > 34 mL/m2, however, an altered threshold for E/e’ ratio (> 14 vs > 10) has also been proposed[9,56].

Additional markers of systolic dysfunction, included in the latest iteration of CCC criteria is global longitudinal strain (GLS), which can unmask subclinical systolic dysfunction[35]. This is a sensitive echocardiographic measure derived from speckle-tracking imaging. In brief, it quantifies left ventricular deformation specifically percentage of shortening in longitudinal axis during systole, which typically compromises prior to radial axis function or EF decline. Normally the value is -16% to -24%, with more negative (i.e. -24%) indicating better function, -16% to -18% borderline function in adults, and less negative (i.e. -15%) denotes impaired systolic function[57]. Notably, values vary with sex and age[35], and GLS is not routinely measured by all clinical echocardiography laboratories; however, its measurement should be requested in patients with suspected dysfunction[58].

The 2020 CCC criteria included GLS < 18% (note change to absolute value for ease of interpretation) which is a sensitive marker of systolic dysfunction[59]. Currently, a single-centred, retrospective trial was unable prove significant mortality prediction when utilising GLS in cirrhotic patients following a TIPS procedure[56]. Further multi-centred prospective studies would be useful to establish the utility of GLS use in this population, given its widespread prognostic value in detecting early cardiac dysfunction general cardiac and cardio-oncology groups.

The presence of AS demonstrated on transthoracic echocardiography (TTE) has also been recognised as a major contributor to post-TIPS decompensation, reflecting a heightened risk due to latent cardiac dysfunction, and prompting enhanced evaluation or even preclusion from TIPS depending on severity[9]. Evidence pertaining to aortic valve replacement or valvuloplasty prior to a TIPS procedure is lacking, acknowledging a significant mortality risk associated with cardiac surgery (50%-100%) in advanced cirrhosis[60]. One study described a small subgroup of 10 patients with underlying asymptomatic AS prior to TIPS with 80% experiencing cardiac decompensation following TIPS insertion; half of these subsequently underwent a successful transcutaneous aortic valve replacement[9]. Further studies elucidating cardiac decompensation risk associated with AS and valvulopathies in cirrhosis patients following TIPS are lacking.

Additional echocardiographic variables associated with cardiac failure following TIPS in a small single-centre trial included right atrial size, left ventricular-end systolic and end diastolic dimensions, and estimated peak PASP[10].

Serum biomarkers: Cardiac

Brain BNP and NT-proBNP: BNP is one of the important prognostic markers in HF and following myocardial infarction, released by the left ventricle in response to increased wall stress, with plasma levels serving as a marker of left ventricular strain and elevated filling pressures. Studies suggest elevated concentration of BNP are indicative of cardiac diastolic dysfunction and severity of disease[61-63]. However, natriuretic peptide levels can be raised in instances of symptomatic and asymptomatic left ventricular dysfunction[64,65]. Notably, natriuretic peptides may be unreliable in pre-ascitic cirrhosis where normal hormone levels were detected in patients with demonstrated cardiac function abnormalities[62]. Prospective liver transplant patients, similar to TIPS candidates, in whom PH is often prevalent, a robust correlation with diastolic dysfunction has been reported[63,66].

Patients with advanced cirrhosis with ascites may exhibit elevated levels of natriuretic peptides, likely reflecting increased cardiac release[62,67]. This was correlated with prolonged QTc and TTE finding of interventricular septal thickness, increased LA volumes, lower EF and abnormal left ventricular diastolic compliance[61,68]. Whilst BNP levels > 100 pg/L have demonstrated significant correlation with TTE features of diastolic dysfunction in patients with cirrhosis, NT-proBNP is a stronger prognostic marker in HF independent to echocardiographic parameters[69,70]. It is regarded as a superior biomarker for detecting cardiac dysfunction when compared to BNP, owing to greater stability and reduced susceptibilities to rapid fluctuation. Normal values of BNP and NT-proBNP are < 35 pg/mL and < 125 pg/mL, respectively, in patients younger than 75-years, and NT-proBNP < 450 pg/mL in patients over 75-years[71,72]. Natriuretic biomarkers are independent of hyperdynamic circulation or impaired hepatic degradation however may be influenced by age and renal function[61,70]. Notably, cirrhotic patients display significantly higher plasma natriuretic peptide levels than controls, which increases further with liver disease severity, higher MELD scores and complications from PH[69,70,73]. Given the raised mean natriuretic peptide levels in cirrhosis, screening for cardiac dysfunction with conventional cut-offs of < 35 pg/mL BNP and < 125 pg/mL NT-proBNP may result in over-investigation within this population. Natriuretic peptide parameters indicating cardiac dysfunction are not standardised in cirrhosis, however EASL thresholds of BNP < 40 pg/mL and NT-proBNP < 125 pg/mL represent thresholds for patients without risk of cardiac decompensation[33]. This was also echoed by the Toulouse group who utilised conventional cut-offs and found that normal levels (< 40 pg/mL BNP and < 125 pg/mL NT-proBNP) can accurately identify patients at low risk with none of the patients below these thresholds experiencing cardiac decompensation[9]. This is further supported by a recent study[44], in which 140 patients with cirrhosis undergoing a TIPS had a mean proBNP of 110 np/L, and none developed cardiac failure following the procedure. Further, a 2024 retrospective study revealed a significant association between NT-proBNP and cardiac decompensation following TIPS placement[74]. Finally, a 2018 small prospective study with decompensated cirrhosis identified higher NT-proBNP concentrations in patients with hyperdynamic circulation with a cut-off level of 170.0 pg/mL most predictive and a tendency toward further elevations seen with concurrent diastolic dysfunction[75].

Uncertainty regarding cardiopulmonary risk could prompt further cardiac evaluation if natriuretic peptides are raised in the absence of known cardiac disease or medications including diuretics. Importantly, normal or low BNP or NT-proBNP levels have an excellent negative predictive value[9,62,71].

Troponin: Troponin is a regulatory protein integral for muscle contraction, with cardiac-specific isoforms (troponin I, troponin T) serving as highly sensitive biomarkers of myocardial injury. Elevated levels indicate myocardial cell damage and are commonly utilised in diagnosing acute coronary syndromes, although troponin levels may also be elevated in non-ischaemic conditions such as HF and sepsis.

One small, prospective study of patients with predominantly alcohol-related cirrhosis treated with TIPS, demonstrated elevated pre- and post-TIPS cardiac markers including troponin-T which were associated with increased one-year mortality risk and were a stronger predictor than Child-Pugh score[76].

Studies investigating the role of troponin-I have not demonstrated a clear correlation with severity of liver disease, severity of PH or other haemodynamic factors. A mildly elevated troponin I concentration was correlated with subclinical myocardial damage to the left ventricle in patients with cirrhosis attributed to alcohol use[77]. This finding was confounded by a reduced left ventricular mass thereby postulating alcohol related cardiac myocyte damage[77].

Other cardiac biomarkers: Cardiac and proinflammatory biomarkers, such as atrial natriuretic peptide, C-terminal portion of provasopressin peptide (copeptin), and soluble urokinase-type plasminogen activator receptor, have been associated with disease severity, PH, and prognosis in cirrhosis[78,79]. While these markers have been well-documented for detection of cardiovascular disease in the broader context of cirrhotic cardiomyopathy and systemic inflammation, their specific predictive role in post-TIPS cardiac decompensation remains unexplored[78,80]. Given the haemodynamic shifts following TIPS placement, further investigation is warranted to determine whether these biomarkers could aid in risk stratification and early detection of cardiac complications in this unique patient population.

Serum biomarkers: Vasoactive compounds

While several vasodilatory markers have been studied in cirrhosis, their specific roles as predictors for cardiac decompensation post-TIPS remain under investigation.

Nitric oxide, a potent vasodilator, is elevated in cirrhosis and contributes to systemic vasodilation and circulatory dysfunction, though its specific role in post-TIPS cardiac decompensation remains under-investigated[81]. Carbon monoxide, another endothelium-derived vasodilator, has been implicated in vascular dysregulation in cirrhosis, yet its predictive utility for post-TIPS HF also remains unclear[81,82]. Endocannabinoids, which modulate vascular tone, are elevated in cirrhotic patients and contribute to the hyperdynamic syndrome, potentially exacerbating post-TIPS haemodynamic instability[83]. Endothelin-3, a vasoconstrictor with compensatory effects, is dysregulated in cirrhosis, yet data on its association with cardiac outcomes post-TIPS are limited[84,85]. Prostacyclin, known for its vasodilatory and antithrombotic properties, is increased in PH, however, its role in predicting post-TIPS cardiovascular dysfunction remains undefined[84]. Adrenomedullin, a peptide involved in vascular homeostasis, is significantly elevated in cirrhosis and correlates with disease severity[79]. While it has been proposed as a biomarker for haemodynamic changes, its specific predictive role in post-TIPS HF has not been studied[79].

ECG

The ECG QT interval reflects ventricular systole duration, with prolongation (> 440 millisecond in males, > 460 millisecond in females) largely due to delayed repolarization. Aetiologies are varied, including several pathological congenital and acquired conditions[86]. Cardiomyopathies represent the most common acquired aetiologies of prolonged QT, and non-cardiac causes include subarachnoid haemorrhage as well as metabolic and drug related causes. Prolonged QT increases the risk of severe ventricular arrhythmias and sudden death in both congenital and acquired spheres[87].

Within cirrhotic populations, QT prolongation is seen in almost half of end-stage liver disease patients, increasing according to severity of liver disease as determined by the Child-Pugh score[61,88,89]. Post-TIPS, a small European study has demonstrated an amplification of this effect observing 29 patients, with a sustained prolongation of QT-interval beyond 1-3 months[90]. This occurs independent of deterioration in liver function or alteration in haemoglobin or serum electrolyte concentration[90]. Conversely, liver transplantation has been associated with improvement in QT interval prolongation, indicating that the pathogenic factors may be in part corrected by liver replacement[91]. Given that this effect is not universal but rather occurs in half of patients with prolonged QT following transplant, it appears other factors may be implicated. While QT prolongation in non-cirrhotic individuals is a well-established risk factor for ventricular arrhythmias, including torsades de pointes, its clinical significance in patients with cirrhosis remains incompletely understood[92]. Of interest, there appears to be a positive correlation between circulating BNP levels in cirrhotic patients and prolongation of QT interval, however not significant for QTc (QT interval corrected for heart rate)[61]. Electrocardiographic investigations revealing a prolonged QT-interval may provide further evidence of cardiac dysfunction[9], which is more prominent in severe liver disease, prompting further investigations. Following a TIPS procedure, there may be worsening of QT prolongation, and this appears associated with cardiac decompensation[9].

Emerging diagnostic modalities

The inability of the left ventricle and LA to accommodate increased preload post-TIPS is a key contributor to post-TIPS cardiac dysfunction. However, current pre-TIPS cardiac assessments primarily rely on resting echocardiographic parameters, which may fail to detect subclinical diastolic dysfunction and impaired atrial compliance.

Diastolic stress testing, which evaluates left ventricular filling pressures and compliance during exercise or pharmacologic stress, has been proposed as a tool to unmask latent diastolic dysfunction that may otherwise go undetected at rest[42]. Although extensively studied in HF with preserved EF (HFpEF), there is a lack of evidence regarding its role in cirrhotic patients undergoing TIPS and may be limited by beta-blocker medication regularly encountered in this population.

Emerging evidence suggests that LA dysfunction is an early marker of haemodynamic intolerance post-TIPS. LA reservoir strain (≤ 35%), assessed using 2D speckle-tracking echocardiography (2D-strain), has been identified as an independent predictor of mortality in cirrhotic patients undergoing TIPS[56]. LA stiffness, a novel metric reflecting atrial compliance and ventricular-atrial coupling abnormalities provides incremental prognostic value beyond the MELD score and left ventricular diastolic dysfunction grading[56]. Elevated LA stiffness correlates with increased left ventricular filling pressures, reduced cardiac reserve, and worse post-TIPS outcomes, yet its prognostic value in identifying high-risk TIPS candidates remains unexplored[56]. Additional novel imaging techniques include haemodynamic forces can detect subtle cardiac dysfunction by utilising pressure gradients and tissue deformation. A single, small, retrospective study has not found association with hemodiafiltration or 2D-strain in predicting HF following TIPS[46]. Notwithstanding, integrating speckle-tracking LA strain with Doppler-derived LA pressure estimations, may help identify latent cardiac dysfunction and improve risk stratification. While elevated LA stiffness is theoretically linked to post-TIPS haemodynamic intolerance, its role as a predictive marker remains unproven. Further studies are needed to determine whether these echocardiographic measures can reliably guide patient selection and reduce the risk of post-TIPS cardiac decompensation.

Cardiac magnetic resonance imaging: Cardiac magnetic resonance imaging (CMRI) is firmly established in clinical practice for assessment of cardiac morphology and volumes with marked accuracy and confirmed high reproducibility[93,94]. Multiparametric CMRI is emerging as a key non-invasive diagnostic modality for detection of inflammation, fibrosis and systolic dysfunction in the setting of occult cardiac disease[95]. CMRI offers several advantages over TTE in selected patients. Namely, enabling use of myocardial tag markers as well as the ability to image the whole chest with visualisation of entire heart with excellent temporal and spatial resolution, unencumbered by interference and limitations of echo window[96]. Studies highlight a significant correlation of high burden of cardiac disease in patients with liver cirrhosis detected with CMRI including myocardial inflammation, fibrosis and systolic dysfunction, even in the absence of cardiac symptoms[95]. Further, higher mean values of myocardial T1 relaxation times, extracellular volume and appearance of late gadolinium contrast enhancement (LGE) lesions corresponded with severity of liver disease (by Child-Pugh score and MELD score)[95]. Briefly, myocardial T1 relaxation times and increased extracellular volume represent diffuse myocardial fibrosis[97], which is closely related to diastolic dysfunction and non-ischaemic cardiomyopathy[28]. CMRI also assesses for longitudinal strain which suggests systolic dysfunction[95]. Notably in a prospective 2020 study of 42 patients, liver stiffness assessed by magnetic resonance elastography (cutoff > 9.2 kPa) was correlated with myocardial T1 relaxation times, and was an independent predictor for LGE lesion prevalence (OR = 1.6) absent in all controls[95].

MRI could serve along with non-invasive imaging biomarkers to identify patients at higher risk of cardiac decompensation[28,95]. This supports integrating cardiac MRI and liver stiffness into pre-TIPS risk stratification protocols particularly in advanced chronic liver disease. Studies demonstrate good correlation between CMRI and TTE in determining left ventricular diastolic function within general population[98,99]. In cirrhotic cardiomyopathy, CMRI may be more sensitive than conventional methods such as dobutamine stress echocardiography at detecting myocardial dysfunction[35]. As such, should acquisition of CMRI be unattainable, an accurate evaluation of diastolic function by echocardiography with 2D imaging plus, spectral, colour and tissue doppler imaging should be performed[28]. Ultimately, further controlled studies in larger, multicentre trials including correlation with clinical endpoints will need to be performed to validate for outcomes following TIPS procedure.

Risk scores

MELD: MELD score remains a very strong predictor of 90-day mortality after TIPS creation[100] therefore useful in assessing liver function as well as post-TIPS survival, however recent systematic review and meta-analysis are limited by lack of cardiovascular sub-group analysis[101]. No MELD cut-offs in isolation are recommended to assess TIPS candidacy in current guidelines. Rather, MELD score should be integrated into relative risk assessment specific to patient including co-morbidities, context and indication for a TIPS as well as consideration of alternate treatment options (including liver transplant)[33].

Toulouse algorithm: The Toulouse algorithm was developed in 2019, designed to categorise patients into three groups according to risk of cardiac decompensation[9]. It utilises natriuretic peptide assessment, followed by a simple or complete TTE, subject to the initial result. Unsurprisingly, a negative screen with BNP or NT-proBNP enlists the patient for a simple TTE, which if normal, risk stratifies into the “zero risk” group. Other patients are stratified using a complete TTE, into high or low risk of cardiac decompensation. Further studies aimed at validating this algorithm had mixed results: One study did not correlate appropriately with decompensated patients[11], while another demonstrated efficacy only with elective TIPS for refractory ascites[41]. Further validation is required.

HF with preserved EF score: The HF with preserved EF score (H2FPEF) score is a point-based validated tool, which serves to estimate the likelihood of HFpEF by using a composite, clinical and echocardiographic-based variables. Created in 2018, it consists of body mass index > 30 kg/m2 (yields 2 points), use of ≥ 2 antihypertensive medications, presence of atrial fibrillation (AF) (persistent AF yields 3 points), PASP > 35 mmHg, age > 60 years, elevated cardiac filling pressure (E/e’ > 9)[102]. It is highly predictive for subclinical diastolic dysfunction, stratifying risk as low (< 25%), intermediate (50%) or high (approximately 90%) for HF with preserved EF. Applicability into patients with cirrhosis has commenced, with non-alcoholic steatohepatitis cirrhosis patients demonstrating elevated scores, attributable to post-liver transplant HF[103]. This is corroborated by a recent study demonstrating significant predictive ability of H2FPEF for post-TIPS HF [OR = 1.14 (1.05-1.23), P > 0.01][46].

HanDeCT algorithm: The HanDeCT is a novel decision framework proposed for evaluation of cardiac function in context of TIPS-related (pre)load shifts. It integrates the ASE framework for diastolic dysfunction with a pathological E/A ratio. In the study, HanDeCT algorithm was able to detect patients at high risk of cardiac decompensation [HR = 2.53 (1.23-5.18), P = 0.011][11]. Although promising, this tool requires further validation ideally in prospective, large-cohort, multicentred trials.

Genetic factors

Genetic polymorphisms may contribute to cardiac decompensation in cirrhotic patients both directly, and indirectly. A 2022 study provides evidence of a common variant in the ARG1 (Arginase 1) gene contributing to increased susceptibility to the risk and features of cirrhotic cardiomyopathy in the Han Chinese population. More specifically, two of the twelve single-nucleotide polymorphisms were associated with the risk of cirrhotic cardiomyopathy in both dominant and additive inheritance models[104].

Other potential culprit disease genes such as TTN (Titin) variants may be implicated in the development or severity of dilated cardiomyopathy in response to cardiotoxins including alcohol as a first and second hit, respectively[105].

Broader literature suggest GSTT1 and GSTM1 (Glutathione S-Transferase) gene polymorphisms may be associated with increased risk of left ventricular diastolic dysfunction due to oxidative stress particularly in b-thalassemia major patients[106]. Further studies assessing GSTP1 gene polymorphism found no significant correlation with HF however[107]. Further research in this area may be pertinent given increased oxidative stress levels seen in patients with liver cirrhosis[108].

These findings highlight the potential of incorporating genetic screening into the assessment of patients with cirrhosis who may be at increased risk of cardiac decompensation. Such an approach aligns with principles of precision medicine, allowing individualised monitoring and management strategies, however further studies are required in this patient population.

Proposed pre-TIPS workup

Figure 4 illustrates a proposed pathway aligning with the 2025 EASL guidelines recommendations providing a graphical representation of the recommended cardiovascular workup.

Figure 4
Figure 4 Proposed algorithm for cardiovascular workup prior to transjugular intrahepatic portosystemic shunt procedure. TIPS: Transjugular intrahepatic portosystemic shunt; Cardiac history: History of peripheral oedema, congestive cardiac failure, pulmonary hypertension, valvular disease; ECG: Electrocardiogram; NT-proBNP: N-terminal pro-B-type natriuretic peptide; TTE: Transthoracic echocardiography; LV: Left ventricular; 2D-strain: Two-dimensional speckle-tracing echocardiography assessing for left atrial strain; RHC: Right heart catheterisation; MDT: Multi-disciplinary team gastroenterology, anaesthesiology, interventional radiology, cardiology inputs.

This approach begins with a comprehensive history and examination, with particular emphasis on cardiac history. Particularly, close monitoring for signs or history of cardiac failure left, right, biventricular, arrhythmia and ischaemia. This additionally provides an opportunity for optimising cardiovascular risk factors.

Following this stage, an ECG, NT-proBNP and TTE are to be performed. If a normal NT-proBNP (< 125 pg/mL) is returned, ECG unrevealing for significant ischaemia, arrhythmia or QT prolongation (female QTc ≤ 460 millisecond, male ≤ 440 millisecond), and TTE unremarkable with respect to normal systolic (≥ 50% LVEF), diastolic function, valvular structure and function, estimated right atrial pressure, and right ventricular systolic pressure, then this enables the patient to proceed with TIPS placement from cardiac perspective.

Investigating for diastolic dysfunction if abnormalities arise in preceding history, assessments or examination should be performed in line with the ASE 2016 criteria[42] or the similar iteration from the CCC[35]. This diagnostic algorithm monitors for diastolic dysfunction by utilising routine TTE parameters if LVEF is normal. Included parameters are septal e’ < 7 cm/second, lateral e’ < 10 cm/second, average E/e’ > 14, LA volume index > 34 mL/m², and peak TR velocity > 2.8 m/second. More than half of these parameters returning a positive result, is diagnostic for diastolic dysfunction. Less than half, clears diastolic function as normal. Half (50%) positive findings is an indeterminate result, which will likely require further testing for characterisation including, but not limited to speckle tracking imaging investigating for GLS, 2D-strain, RHC or CMRI.

Invariably, severe systolic dysfunction, moderate-severe pulmonary hypertension despite treatment (must be diagnosed with RHC), or untreated severe valvular disease are important to diagnose as these could preclude patients from receiving TIPS as per 2025 EASL guidelines[33].

Abnormalities with ECG, TTE or invasive/specialty imaging will likely benefit from multidisciplinary discussion including a cardiologist referral.

Risk scores such as the H2FPEF, may be a useful point-based validated tool, which has exhibited an impressive predictive ability in previous studies. This can be used as an adjunct, to raise suspicion of cardiac dysfunction, but does not replace the investigative process.

Alternate pathways, such as the Toulouse algorithm, which serve to stratify patients based on negative natriuretic peptides combined with simple TTE or provide a complete TTE may provide a rapid and resource friendly assessment. However, at this time, this review suggests that further validation should be performed before it can be recommended.

Ultimately, given the complexity of cardiac assessments, and uncertainty shrouding results and risk within this population, the proposed algorithm recommends multidisciplinary team (MDT) input including cardiology consult for any abnormal findings within investigations encountered to guide safe, appropriate management. Referral for an MDT to interpret cardiac findings, irrespective of the risk score applied, to appropriately assess cardiac risk, particularly when TIPS may prove life-saving or transformative, is in alignment with current guideline recommendations[17,33].

MDT input

Traditionally, MDT meeting groups include hepatogastroenterologists, interventional radiologists and occasionally anaesthetists. Whilst this serves to evaluate if contraindications are present on routine assessments, this risks an inadequate cardiovascular evaluation, beyond assessment of valvular function and left ventricular EF. Additional specialty consultation, such as by a cardiologist, is recommended in current guidelines on a case-by-case basis[17,33], especially in cases with indeterminate or uncertain cardiac parameters, could be useful for cardiovascular risk stratification or optimisation.

Presently, there is no published data demonstrating MDT input including cardiology specialty improves outcomes within TIPS patients, an area which should be further explored. This review supports the utility of MDT discussions for wholistic outcome prediction following TIPS, given the high prevalence of adverse cardiac outcomes. It must also be acknowledged that end-stage liver disease patients have significant coronary risk factors burden, occult coronary artery narrowing and features of diastolic compliance[109]. As such, MDT including a dedicated cardiology referral if cardiac screening in asymptomatic patients reveals left ventricular dysfunction should be recommended in TIPS patients, echoing recommendations for liver transplant candidates[110].

Application in clinical care

Post-TIPS cardiovascular decompensation remains a significant issue, particularly in patients with underlying cardiac dysfunction. Despite the well-recognised haemodynamic alterations following TIPS placement, there is no universally accepted consensus for pre-TIPS cardiovascular evaluation, nor risk stratification algorithms. Therefore, patients at risk of cardiac decompensation post-TIPS, may currently go undetected pre-procedurally, resulting in adverse outcomes.

Diastolic dysfunction is a critical contributor to post-TIPS cardiovascular failure and remains under-recognised. Given the higher prevalence of diastolic dysfunction in cirrhosis, a structured approach to evaluating LA strain and diastolic dysfunction is recommended. Perhaps the most widely accessible and informative investigation remains the TTE for indicators of systolic and diastolic dysfunction, with several markers demonstrating possible predictive value for post-TIPS cardiac failure in small studies[10,42,56]. In areas with scarce resources, where TTE may not be accessible, elevated NT-proBNP and prolonged QT interval could be used to prompt further assessment as seen in British guidelines and the Toulouse algorithm[9,13], however this is contrary to current European practice guidelines[33]. Emerging echocardiographic techniques including 2D-strain as well as CMRI have shown promise, however their role in routine clinical practice remains unvalidated but evolving. Ultimately, a multimodal approach integrating multiple investigative modalities may be required for optimal pre-procedural cardiovascular assessment.

Limitations

This review has several limitations. At a study level, most included studies were small retrospective cohort designs, inherently prone to selection bias, confounding and reliance on the accuracy of medical records. Many studies did not adjust for key prognostic factors, and risk of bias was frequently moderate to high. At the outcome level, there was variability in how outcomes such as cardiac decompensation were defined and reported. At a review level, we acknowledge limitations due to clinical and methodological heterogeneity and incomplete statistical reporting across studies, which precluded meta-analyses which may limit the strength and generalisability of this study’s conclusions.

Future directions

Further research is warranted to refine pre-TIPS cardiovascular risk stratification, including validating predictive cardiac markers in cirrhotic populations and developing standardised screening algorithms. Prospective studies evaluating the utility of diastolic stress testing, LA strain analysis, novel biomarkers and identification of genetic polymorphisms, useful in predicting post-TIPS decompensation are needed. Additionally, the impact of cardiology involvement in MDT discussions for indeterminate cases regarding patient selection and outcomes should be explored. Establishing consensus guidelines for pre-TIPS cardiovascular work-up could mitigate procedural risks, enhance patient safety and improve outcomes in this high-risk population.

CONCLUSION

Careful TIPS candidate selection necessitates balance between the benefits of portal decompression and the risks posed by potential cardiovascular deterioration. Despite several conflicting international recommendations for pre-TIPS work-up, the current EASL recommendations for TIPS cardiac workup: ECG, natriuretic peptides and TTE provide a safe scaffold to evaluate the cardiac function. Given the critical role of diastolic dysfunction in post-TIPS decompensation, the ASE and CCC criteria for diagnosis is recommended. Advanced cardiac imaging modalities such as 2D-strain, GLS, CMRI, biomarker analysis and genetic markers may aid in risk stratification, however more research is required in validating these further in this population. The inclusion of cardiologists in MDT discussions may enhance cardiovascular evaluation for indeterminate or complex cases, aligning TIPS work-up more closely with liver transplant protocols. Addressing these gaps through multi-centred prospective studies and guideline development will be crucial in optimising patient outcomes following TIPS procedures.

Footnotes

Provenance and peer review: Invited article; Externally peer reviewed.

Peer-review model: Single blind

Specialty type: Gastroenterology and hepatology

Country of origin: Australia

Peer-review report’s classification

Scientific Quality: Grade A, Grade B

Novelty: Grade A, Grade B

Creativity or Innovation: Grade A, Grade B

Scientific Significance: Grade A, Grade A

P-Reviewer: Li N; Zhao SR S-Editor: Fan M L-Editor: A P-Editor: Zhang L

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