Sage Journals: Discover world-class research

Abstract

The model for end-stage liver disease (MELD) and the model for end-stage liver disease excluding international normalized ratio (INR) (MELD-XI) scores, which reflect dysfunction of liver and kidneys, have been reported to be related to the prognosis of patients with right-sided “backward” failure. However, the relationship between the MELD/MELD-XI score and the in-hospital adverse events in pulmonary embolism (PE) patients was unknown. Normotensive PE patients were retrospectively enrolled at China–Japan friendship hospital from January 2017 to February 2020. The primary outcome was defined as death and clinical deterioration during hospitalization. Multivariate logistic analysis was used to explore the association between the MELD and MELD-XI scores for in-hospital adverse events. We also compared the accuracy of the MELD, MELD-XI, and the pulmonary embolism severity index (PESI) score using the time-dependent receiver operating characteristic curve and corresponding areas under the curve (AUC). A total of 222 PE patients were analyzed. Logistic regression analysis showed that the MELD score was independently associated with in-hospital adverse events (odds ratio = 1.115, 95% confidential interval = 1.022-1.217, P = .014). The MELD score has an AUC of 0.731 and was better than PESI (AUC of 0.629) in predicting in-hospital adverse events. Among PE patients with normal blood pressure on admission, the MELD score was associated with increased in-hospital adverse events.

Keywords

pulmonary embolism MELD score MELD-XI score risk stratification,in-hospital adverse events

Key Learning Points

What is Already Known?

Optimizing the early risk stratification is essential to determine which patients can be treated safely at home and which patients need surveillance and potential treatment upgrading. Right ventricle dysfunction has been shown to be an important predictor of the severity of acute pulmonary embolism (PE), and the model for end-stage liver disease (MELD)/model for end-stage liver disease excluding INR (MELD-XI) score has been proven to be associated with poor prognosis in different cohorts of right-sided “backward” failure.

What this Study Adds?

Our study suggests that the MELD/MELD-XI score can be used as a practical predictor for in-hospital adverse events in PE patients.

Introduction

Normotensive patients with acute pulmonary embolism (PE) are a highly heterogeneous population with short-term mortality of 2.9% to 7.8%^1–3; therefore, advanced risk stratification is a highly essential and challenging component of management. Patients with low risk may be candidates for early discharge and continuation of treatment at home,^4,5 while early reperfusion treatment should be considered for patients with intermediate-high risk PE.⁶ To date, several risk stratification models for mortality have been developed. Of these, the pulmonary embolism severity index (PESI) score is the most extensively validated score.⁷ The model for end-stage liver disease (MELD) score which is based on the international normalized ratio (INR), total bilirubin (TB), and creatinine levels, and the model for end-stage liver disease excluding INR (MELD-XI) are traditionally used to reflect liver and renal dysfunction. Right-sided “backward” failure may lead to renal and hepatic congestion then injury; recently, several studies have reported the prognostic relevance of the MELD/MELD-XI score in different cohorts of right-sided “backward” failure, including patients undergoing tricuspid valve surgery,⁸ constrictive pericarditis,⁹ and right ventricular failure after undergoing left-ventricular assist device (LVAD) implantation.¹⁰ The right ventricular dysfunction has been shown to be an important prognosis predictor for patients with acute PE.^11,12 The MELD score might be a useful predictor of mortality among high-risk PE patients admitted to intensive care units.¹³ Studies also suggested that the MELD-XI score is associated with the in-hospital mortality of intermediate-to-high risk acute PE.¹⁴ However, the association of the MELD and MELD-XI scores with adverse events has not been reported in normotensive patients with acute PE.

In this study, we aimed to assess the association between MELD and MELD-XI scores and adverse in-hospital outcomes in PE patients with normal blood pressure, and compared their prognostic accuracy with the PESI score.

Methods

Study Design and Participants

Normotensive PE patients admitted to China–Japan Friendship Hospital from January 2017 to February 2020 were retrospectively enrolled. The inclusion criteria were as follows: 1. age ≥18 years; 2. the diagnosis of PE was determined by a positive test using computed tomography pulmonary angiography (CTPA) or a high probability ventilation-perfusion (V/Q) scan; 3. hemodynamic stability on admission with systemic systolic blood pressure (SBP) of at least 90 mm Hg. Patients with chronic thromboembolic pulmonary hypertension, coronary artery disease, and existing severe hepatic and renal insufficiency (chronic kidney disease stage 5 and child-C stage) were excluded from this study. The study protocol was conducted in accordance with the amended Declaration of Helsinki and was approved by the local independent Ethic Committees at China–Japan Friendship Hospital.

Data Collection

We collected the clinical data of all the patients, including age, sex, clinical presentation, vital signs on admission, and the presence of comorbidities. Laboratory panel on admission was comprised of INR, creatinine, TB, troponin I (cTNI) or troponin T (cTNT), brain natriuretic peptide (BNP) or N-terminal B-type natriuretic peptide (NT-proBNP), and arterial blood gas analysis. All INR, creatinine, and TB levels were measured before initiating any anticoagulant therapy. Troponin was defined as elevated if cTNI > 0.4 ng/ml or cTNT > 0.014 ng/ml according to the biochemical tests used in our institution. NT-ProBNP > 600 pg/ml and BNP > 100 pg/ml were considered abnormal and these values were used as cut-off values in our study. The right ventricle (RV) dysfunction was assessed by transthoracic echocardiography or CTPA and defined as follows: (1) tricuspid annular plane systolic excursion (TAPSE) < 16 mm; or (2) RV/left ventricle (LV) > 1.0; or (3) sPAP (systolic pulmonary artery pressure) > 50 mm Hg.

MELD and MELD-XI Scores

The MELD and MELD-XI scores were calculated using the following formula, as previously reported¹⁵: the MELD score = 11.2 × (ln INR) + 3.78 × (ln TB [mg/dl]) + 9.57 × (ln creatinine [mg/dl]) + 6.43. The MELD-XI score = 11.76 × ln(creatinine [mg/dl]) + 5.11 × ln(TB [mg/dl]) + 9.44. Any values <1 were given the lower limit value of 1 to prevent negative logarithmic values in the formula.¹⁶ The MELD and MELD-XI scores were calculated using laboratory data on admission before initiating anticoagulant therapy.

Definition of Outcomes

The primary outcome was in-hospital adverse events, including in-hospital death and clinical deterioration. Clinical deterioration was defined as hypotension with SBP <90 mm Hg for ≥15 min or need for catecholamine administration, thrombolysis, extracorporeal membrane oxygenation, mechanical ventilation or cardiopulmonary resuscitation during hospitalization.

Statistical Analysis

Normally distributed data were expressed as mean ± standard deviation (SD), and non-distributed data are presented as medians with interquartile ranges. Categorical variables are expressed as numbers and percentages. The statistical significance of differences was analyzed using a one-way analysis of variance for parametric continuous variables and the Kruskal–Wallis rank-sum test for non-parametric continuous variables. The χ² test was used to compare differences in categorical variables. Univariate logistic analysis was performed and statistically significant variables were entered into a multivariate logistic regression model to assess the association with in-hospital outcomes. Model 1 was adjusted for age and gender. Model 2 was additionally adjusted for heart rate ≥110 beats/min, elevated troponin, elevated BNP or NT-pro BNP levels, and PaO₂/FiO₂ < 300. The performance of MELD, MELD-XI, and PESI scores for predicting in-hospital adverse events was examined using receiver operating characteristic (ROC) curve analysis.

A two-tailed P < .05 was considered statistically significant. All statistical analyses were performed using SPSS (IBM SPSS Statistics for Windows, version 225.0; IBM Corporation).

Results

Baseline Characteristics

In total, 222 patients hospitalized for acute PE were included (Figure 1). Overall, the mean age of the patients was 68 years + SD, and 44.6% were male. The distributions of MELD-XI and MELD scores are shown in Figure 2. In our study, the mean MELD score was 7.8 and 196 patients (94.2%) had MELD score <15, and 12 patients (5.8%) with MELD ≥15.

Figure 1.

Flowchart of the participants.

Figure 2.

Distribution of model for end-stage liver disease excluding international normalized ratio (MELD-XI) and model for end-stage liver disease (MELD) scores across the cohort.

Compared to the patients without in-hospital adverse events, patients with adverse events had more symptoms such as chest pain and syncope, lower diastolic blood pressure, and higher heart rate. Patients with in-hospital adverse events had higher troponin and BNP levels and lower PaO₂/FiO₂ (Table 1). Patients with in-hospital adverse events had higher PESI and MELD scores than patients without in-hospital adverse events (101 vs 82 and 9.7 vs 7.6, respectively). However, there was no significant difference among these groups in liver dysfunction, renal insufficiency, and RV dysfunction.

Table 1.

Clinical Characteristics.

Characteristics	All (n = 222)	Patients with Adverse Event (n = 35)	Patients without Adverse Event (n = 187)	P Value
Age (years)	68 ± 19	66 ± 21	69 ± 18	.467
Male sex	95 (44.6%)	14 (40.0%)	85 (45.5%)	.686
Former smoking	33 (15.5%)	4 (11.4%)	29 (15.5%)	.814
Smoking	26 (11.3%)	4 (11.4%)	22 (11.8%)	1
Dyspnea	170 (77.0%)	31 (88.6%)	139 (74.3%)	.068
Chest pain	76 (35.2%)	6 (17.1%)	70 (37.4%)	.020
Syncope	37 (16.7%)	14 (40.0%)	23 (12.3%)	<.001
Unilateral lower limb gall	32 (14.4%)	4 (11.4%)	28 (15.0%)	.584
Hemoptysis	23 (10.4%)	4 (11.4%)	19 (10.2%)	.829
Comorbidities
DVT	111 (50.9%)	16 (48.5%)	95 (51.4%)	.762
Ischemic stroke	42 (18.9%)	8 (22.9%)	34 (18.2%)	.517
Surgical history	38 (17.1%)	7 (20.0%)	31 (16.6%)	.622
Heart failure	37 (16.7%)	9 (25.7%)	28 (15.0%)	.118
Malignant	37 (16.7%)	9 (25.7%)	28 (15.0%)	.118
Chronic lung disease	30 (13.5%)	5 (14.3%)	25 (13.4%)	.884
Atrial fibrillation/atrial flutter	17 (7.7%)	5 (14.3%)	12 (6.4%)	.108
SBP (mm Hg)	129 ± 18	125 ± 20	130 ± 17	.183
DBP (mm Hg)	75 ± 13	69 ± 16	77 ± 13	.012
Heart rate (bpm)	86 ± 18	95 ± 24	85 ± 17	.022
Respiratory rate (beats/min)	20 ± 2	21 ± 2	20 ± 2	.069
Laboratory test
cTn elevated	115 (52.5%)	28 (80.0%)	87 (47.3%)	.001
BNP/nt elevated	106 (48.6%)	23 (65.7%)	83 (45.4%)	.027
PaO₂/FiO₂⁺	81 (38.0%)	23 (65.7%)	58 (32.6%)	.003
Creatinine (mg/dl)	0.89 ± 0.85	1.13 ± 1.49	0.85 ± 0.66	.279
TB (mg/dl)	0.72 ± 0.61	1.12 ± 1.16	0.65 ± 0.40	.022
INR	1.19 ± 0.41	1.43 ± 0.68	1.15 ± 0.32	.021
Imaging parameters
TAPSE (mm)	18.24 ± 5.11	19.86 ± 4.74	18.66 ± 4.59	.447
sPAP (mm Hg)	49.22 ± 24.36	46.78 ± 13.56	38.96 ± 5.37	.126
RV/LV >1.0	45 (20.5%)	7（31.8%）	38 (26.6%)	.607
RV dysfunction	126 (59.2%)	24 (68.6%)	102 (57.3%)	.440
PESI	85 ± 28	101 ± 41	82 ± 23	.009
MELD	7.8 (6.8-9.5)	9.7 (7.7-12.8)	7.6 (6.8-8.9)	.005
MELD-XI	9.4 (9.4-10.0)	9.4 (9.4-12.4)	9.4 (9.4-9.7)	.044

Abbreviations: DVT, deep venous thrombosis; SBP, systolic blood pressure; DBP, diastolic blood pressure; D-D, D-dimer; cTn, cardiac troponin; BNP, brain natriuretic peptide; TAPSE, tricuspid annular plane systolic excursion; sPAP: systolic pulmonary artery pressure; RV, right ventricle; LV, left ventricle; INR, international normalized ratio; TB, total bilirubin.

The Association Between MELD and MELD-XI and In-Hospital Adverse Events

Adverse events were recorded in 35 (15.8%) patients during hospitalization, including 7 in-hospital death (3.2%) and 28 clinical deterioration (12.6%), including SBP <90 mm Hg for ≥15 min (26 cases, 11.7%), need for catecholamine administration (21 cases, 9.5%), thrombolysis (13 cases, 5.9%), mechanical ventilation (19 cases, 8.6%), or cardiopulmonary resuscitation (7 cases, 3.2%). Univariate analysis showed that in-hospital adverse events were associated with pulse ≥110 beats/min (odds ratio [OR] = 3.536, 95% confidential interval [CI] = 1.477-8.471), positive troponin (OR = 4.460, 95% CI = 1.855-10.724), elevated BNP levels (OR = 2.309, 95% CI = 1.084-4.919), and PaO₂/FiO₂ < 300 (OR = 1.835, 95% CI = 1.441-7.077) (Table S1). Multivariate logistic regression analysis indicated that MELD was independently associated with in-hospital adverse events even after adjusting for age, gender, and these covariates (Table 2).

Table 2.

Association of MELD, MELD-XI, and PESI Scores With In-Hospital Adverse Events.

	UnadjustedOR (95% CI)	P	Model 1OR (95% CI)	P	Model 2OR (95% CI)	P
MELD	1.157 (1.058-1.266)	.001	1.157 (1.057-1.268)	.002	1.115 (1.022-1.217)	.015
MELD-XI	1.149 (1.033-1.278)	.011	1.144 (1.029-1.271)	.013	1.113 (0.993-1.248)	.065
PESI	1.030 (1.016-1.045)	.001	1.029 (1.015-1.044)	.001	1.026 (1.008-1.043)	.003

Model 1: adjusted for age and gender.

Model 2: adjusted for age, gender, heart rate ≥110 beats/min, elevated troponin, elevated BNP or NT-pro BNP levels, and PaO₂/FiO₂ < 300.

Table 3 summarizes the unadjusted and adjusted analysis of the association between MELD score and individual outcomes.

Table 3.

Relative Effect of MELD and MELD-XI Scores on Primary and Secondary Outcomes.

Outcome	MELDUnadjusted OR (95% CI)	P	Adjusted OR (95% CI)		MELD-XIUnadjusted OR (95% CI)	P	Adjusted OR (95% CI)	P
In-hospital adverse events	1.165 (1.063-1.276)	.001	1.115 (1.022-1.217)	.015	1.149 (1.033-1.278)	.011	1.113 (0.993-1.248)	.065
Death	1.039 (0.945-1.142)	.429	1.038 (0.919-1.171)	.551	1.022 (0.889-1.173)	.763	1.016 (0.842-1.226)	.869
Shock	1.113 (1.032-1.201)	.006	1.120 (1.026-1.223)	.011	1.105 (1.009-1.210)	.032	1.144 (1.107-1.287)	.026
Catecholamine administration	1.118 (1.035-1.207)	.005	1.149 (1.044-1.265)	.004	1.108 (1.011-1.215)	.028	1.163 (1.028-1.317)	.017
Thrombolysis	1.142 (1.052-1.240)	.002	1.096 (0.993-1.209)	.068	1.137 (1.033-1.253)	.009	1.063 (0.916-1.233)	.421
ECMO support	1.097 (0.991-1.215)	.074	1.175 (0.954-1.448)	.129	1.102 (0.959-1.266)	.171	1.203 (0.897-1.614)	.218
Mechanical ventilation	1.124 (1.039-1.215)	.003	1.153 (1.045-1.271)	.005	1.107 (1.009-1.214)	.032	1.145 (1.012-1.296)	.031
Cardiopulmonary resuscitation	1.108 (1.018-1.206)	.018	1.086 (0.974-1.211)	.137	1.121 (1.007-1.249)	.037	1.119 (0.966-1.297)	.135

Adjusted for age, gender, heart rate ≥110 beats/min, elevated troponin, elevated BNP or NT-pro BNP levels, and PaO₂/FiO₂ < 300.

Abbreviation: ECMO, extracorporeal membrane oxygenation.

Figure 3 depicts the effects graphically to emphasize our findings. Even after correction for relevant clinical confounders, both MELD and MELD-XI scores were associated with SBP <90 mm Hg for ≥15 min, catecholamine administration, and mechanical ventilation.

Figure 3.

Odds ratios (ORs) of model for end-stage liver disease (MELD) and model for end-stage liver disease excluding international normalized ratio (MELD-XI) scores for the primary outcome and secondary outcomes.

Comparison of the Predictive Value of MELD, MELD-XI, and PESI for In-Hospital Adverse Events

Figure 4 depicts the ROC curves of MELD score, MELD-XI score, and PESI score. The area under the curve of the MELD score for in-hospital adverse events was better 0.731 (95% CI = 0.636-0.827) than the PESI score (0.629, 95% CI = 0.514-0.744) (Table S2). However, the MELD-XI score (0.618, 95% CI = 0.505-0.730) is less effective than the PESI score in predicting adverse events during hospitalization. The cut-off points of MELD score 9.4 had a sensitivity of 60.0% and a specificity of 80.9%.

Figure 4.

Area under the receiver operating characteristic (ROC) curve of model for end-stage liver disease (MELD), model for end-stage liver disease excluding international normalized ratio (MELD-XI), and pulmonary embolism severity index (PESI) score predicting in-hospital adverse events.

Discussion

In this single center retrospective study of normotensive PE patients, we had two major findings. First, high MELD score was significantly associated with the increased risk of in-hospital adverse events in normotensive patients with acute PE. The cutoff values of the MELD for predicting in-hospital adverse events were 9.4 compared to PESI; MELD score had better predictive performance in predicting in-hospital adverse events.

Accurate risk-stratification assessments are valuable tools that guide physicians to determine appropriate therapeutic management decisions. The MELD score, which is calculated utilizing bilirubin, creatinine, and INR, reflects dysfunction of liver and kidneys. As a modified MELD score, the MELD-XI score excludes INR and thus could be used in patients on anticoagulants. They were developed to predict clinical outcomes of patients with advanced liver disease^17,18 and cardiac diseases.^9,19,20 A small study (n = 104)¹⁴ of intermediate-to-high PE patients has found MELD-XI to be a predictor of mortality and the optimal cut-off was 10.2. Furthermore, Kadir İdin et al¹³ have shown MELD is an independent predictor of 30-day mortality in high-risk patients with acute PE admitted to intensive care units. In the present study, we focus on the various in-hospital outcomes of normotensive acute PE patients, and it also may lead to the optimal cut-off of MELD-XI score ≥12.1 higher than previously reported by Orçun et al.³

While most risk scoring systems assess cardiopulmonary variables, such as PESI,⁷ sPESI,²¹ Bova,²² and FAST (H-FABP, Syncope and tachycardia) score,²³ evidence is mounting that liver^24,25 and renal dysfunction^26,27 are predictors of prognosis and adverse factors in acute PE. Moreover, the Hestia criteria, which require an assessment of decreasing of liver and kidney functions, could effectively identify acute PE patients who were at low risk of mortality for outpatient treatment or early discharge.²⁸

The pathophysiological connection between MELD, MELD-XI, and PE might be complex. In PE patients, relative hypoxia,^29,30 ischemia,³¹ and passive venous congestion²⁹ are suggested to be the primary driving renal and hepatic injury. First, acute RV dysfunction, triggered by acute PE, usually results in increased central venous pressure and could potentially lead to passive congestion in the liver and kidneys, along with functional impairment of these organs.^24,32 Second, dysfunction of the RV can alleviate the load on the LV, subsequently leading to a decrease in stroke volume, which further reduces renal blood flow and liver perfusion.³³ Third, systemic arterial hypoxemia due to acute PE results in liver and kidney dysfunction.³⁴ In addition, it is likely that MELD/MELD-XI serves as a surrogate marker of general multiorgan dysfunction and mirrors severity of illness. They have been shown to correlate with other scores of poor functional status such as Acute Physiology And Chronic Health Evaluation and to predict outcomes including mortality in the critically ill population.^35,36

The MELD/MELD-XI score is dynamic and reflective of the patient's current severity of illness. Whether active thrombolysis is required for intermediate high-risk PE is controversial, in addition to identification of intermediate high-risk PE patients, the score might have a potential role in guiding best timing for the reperfusion. Of note, preoperative improvement in MELD score has been found to improve outcomes for patients with congestive heart failure undergoing LVAD implantation.³⁷ Only a portion of the identified risk factors for adverse events of PE are modifiable, whether clinical optimization reflected by improved MELD/MELD-XI scores improves outcomes of PE patients has not been investigated. In addition, further studies are warranted to determine whether MELD score can be used as a selection tool for outpatient treatment.

Although no significant improvement was found when compared with PESI, the MELD and MELD-XI scores only consist of two or three parameters, which can be easily measured using inexpensive, routine laboratory tests, so they are simpler and practical risk assessment tools. In conclusion, our findings reinforce the concept of integrating the functional status of the liver and kidney into the risk stratification of acute PE.

Limitations

Our study has a number of limitations that need to be discussed. First, this is a retrospective single-center study, and the sample size was relatively small. Therefore, these conclusions should be verified in different regions and in different populations with larger samples. Second, we could not analyze the association between the MELD/MELD-XI score and long-term prognosis. Additionally, the MELD/MELD-XI score is dynamic and reflective of the patient's current severity of illness, whether preoperative clinical optimization reflected by improved MELD/MELD-XI scores improves outcomes after receiving anticoagulation has not been investigated. Third, INR could artificially elevated by antagonizing vitamin K-dependent pathways, so we collected the biochemical data on admission before initiating anticoagulant therapy. We also assessed the association between the MELD-XI (excluding INR) score and outcomes in order to eliminate the deviation of some patients with heart failure and atrial fibrillation using warfarin. Lastly, despite the fact that a multivariate analysis was conducted, a residual confounding from unmeasured factors may exist, especially liver and kidney biomarkers, gamma-glutamyltransferase, cystatin C, kidney injury molecule-1, and so on, which might affect the study's ultimate results.

Conclusion

Among normotensive patients with acute PE, both the MELD scores are associated with in-hospital adverse events. These results suggest that MELD/MELD-XI score can be used as a practical predictor for in-hospital adverse events in PE patients and further studies are needed to validate these findings.

Footnotes

Data Availability Statement

The data underlying this article will be shared on reasonable request to the corresponding author.

Declaration of Conflicting Interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by the Capital Health Research and Development of Special Fund (grant number 2020-2-4065).

ORCID iD

Siqi Jiao

References

Becattini

Vedovati

Pruszczyk

, et al. Oxygen saturation or respiratory rate to improve risk stratification in hemodynamically stable patients with acute pulmonary embolism. J Thromb Haemostasis. 2018;16(12):2397-2402.

Jaureguízar

Jiménez

Bikdeli

, et al. Heart rate and mortality in patients with acute symptomatic pulmonary embolism. Chest. 2022;161(2):524-534.

Zhai

Wang

Lei

, et al. Trends in risk stratification, in-hospital management and mortality of patients with acute pulmonary embolism: an analysis from the China pUlmonary thromboembolism REgistry study (CURES). Eur Respir J. 2021;58(4):2002963.

Barco

Schmidtmann

Ageno

, et al. Early discharge and home treatment of patients with low-risk pulmonary embolism with the oral factor Xa inhibitor rivaroxaban: an international multicentre single-arm clinical trial. Eur Heart J. 2020;41(4):509-518.

Barco

Mahmoudpour

Planquette

Sanchez

Konstantinides

Meyer

. Prognostic value of right ventricular dysfunction or elevated cardiac biomarkers in patients with low-risk pulmonary embolism: a systematic review and meta-analysis. Eur Heart J. 2019;40(11):902-910.

Meyer

Vicaut

Danays

, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med. 2014;370(15):1402-1411.

Aujesky

Obrosky

Stone

, et al. Derivation and validation of a prognostic model for pulmonary embolism. Am J Respir Crit Care Med. 2005;172(8):1041-1046.

Ailawadi

LaPar

Swenson

, et al. Model for end-stage liver disease predicts mortality for tricuspid valve surgery. Ann Thorac Surg. 2009;87(5):1460-1468.

Diaz Soto

Mauermann

Lahr

Schaff

Luis

Smith

. MELD and MELD XI scores as predictors of mortality after pericardiectomy for constrictive pericarditis. Mayo Clin Proc. 2021;96(3):619-635.

10.

Yost

Coyle

Bhat

Tatooles

. Model for end-stage liver disease predicts right ventricular failure in patients with left ventricular assist devices. J Artif Organs. 2016;19(1):21-28.

11.

Kucher

Rossi

De Rosa

Goldhaber

. Prognostic role of echocardiography among patients with acute pulmonary embolism and a systolic arterial pressure of 90 mm Hg or higher. Arch Intern Med. 2005;165(15):1777-1781.

12.

Becattini

Agnelli

Vedovati

, et al. Multidetector computed tomography for acute pulmonary embolism: diagnosis and risk stratification in a single test. Eur Heart J. 2011;32(13):1657-1663.

13.

İdin

Dereli

Kaya

, et al. Modified model for end-stage liver disease score predicts 30-day mortality in high-risk patients with acute pulmonary embolism admitted to intensive care units. Scand Cardiovasc J. 2021;55(4):237-244.

14.

Çiftci

Çelik

ÇO

Uzar

Küpeli

Müderrisoğlu

İH

. MELD-XI score predicts in-hospital mortality independent of simplified pulmonary embolism severity index among patients with intermediate-to-high risk acute pulmonary thromboembolism. Tuberk Toraks. 2019;67(3):169-178.

15.

Martin

Bartels

Hauss

Fangmann

. Overview of the MELD score and the UNOS adult liver allocation system. Transplant Proc. 2007;39(10):3169-3174.

16.

Kawahira

Tamaki

Yamada

, et al. Prognostic value of impaired hepato-renal function and liver fibrosis in patients admitted for acute heart failure. ESC Heart Fail. 2021;8(2):1274-1283.

17.

Kamath

Wiesner

Malinchoc

, et al. A model to predict survival in patients with end-stage liver disease. Hepatology. 2001;33(2):464-470.

18.

Salerno

Merli

Cazzaniga

, et al. MELD score is better than Child-Pugh score in predicting 3-month survival of patients undergoing transjugular intrahepatic portosystemic shunt. J Hepatol. 2002;36(4):494-500.

19.

Yang

Kato

Shulman

, et al. Liver dysfunction as a predictor of outcomes in patients with advanced heart failure requiring ventricular assist device support: use of the model of end-stage liver disease (MELD) and MELD excluding INR (MELD-XI) scoring system. J Heart Lung Transplant. 2012;31(6):601-610.

20.

Zhang

Lin

Zhang

Zhao

Chen

. MELD-XI score predict no-reflow phenomenon and short-term mortality in patient with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. BMC Cardiovasc Disord. 2022;22(1):113.

21.

Jiménez

Aujesky

Moores

, et al. Simplification of the pulmonary embolism severity index for prognostication in patients with acute symptomatic pulmonary embolism. Arch Intern Med. 2010;170(15):1383-1389.

22.

Bova

Sanchez

Prandoni

, et al. Identification of intermediate-risk patients with acute symptomatic pulmonary embolism. Eur Respir J. 2014;44(3):694-703.

23.

Lankeit

Friesen

Schäfer

Hasenfuß

Konstantinides

Dellas

. A simple score for rapid risk assessment of non-high-risk pulmonary embolism. Clin Res Cardiol. 2013;102(1):73-80.

24.

Aslan

Meral

Akgun

, et al. Liver dysfunction in patients with acute pulmonary embolism. Hepatol Res. 2007;37(3):205-213.

25.

Kırış

Yazıcı

Durmuş

, et al. The relation between international normalized ratio and mortality in acute pulmonary embolism: a retrospective study. J Clin Lab Anal. 2018;32(1):e22164.

26.

Kostrubiec

Pływaczewska

Jiménez

, et al. The prognostic value of renal function in acute pulmonary embolism—a multi-centre cohort study. Thromb Haemost. 2019;119(1):140-148.

27.

Chopard

Jimenez

Serzian

, et al. Renal dysfunction improves risk stratification and may call for a change in the management of intermediate- and high-risk acute pulmonary embolism: results from a multicenter cohort study with external validation. Crit Care. 2021;25(1):57.

28.

Roy

Penaloza

Hugli

, et al. Triaging acute pulmonary embolism for home treatment by Hestia or simplified PESI criteria: the HOME-PE randomized trial. Eur Heart J. 2021;42(33):3146-3157.

29.

Henrion

Minette

Colin

Schapira

Delannoy

Heller

. Hypoxic hepatitis caused by acute exacerbation of chronic respiratory failure: a case-controlled, hemodynamic study of 17 consecutive cases. Hepatology. 1999;29(2):427-433.

30.

Subramanian

Ramadurai

Arthur

Gopalan

. Hypoxia as an independent predictor of adverse outcomes in pulmonary embolism. Asian Cardiovasc Thorac Ann. 2018;26(1):38-43.

31.

Van den Broecke

Van Coile

Decruyenaere

, et al. Epidemiology, causes, evolution and outcome in a single-center cohort of 1116 critically ill patients with hypoxic hepatitis. Ann Intensive Care. 2018;8(1):15.

32.

Pływaczewska

Pruszczyk

Kostrubiec

. Does kidney function matter in pulmonary thromboembolism management? Cardiol J. 2022;29(5):858-865.

33.

Mauritz

Marcus

Westerhof

Postmus

Vonk-Noordegraaf

. Prolonged right ventricular post-systolic isovolumic period in pulmonary arterial hypertension is not a reflection of diastolic dysfunction. Heart. 2011;97(6):473-478.

34.

Elliott

. Pulmonary physiology during pulmonary embolism. Chest. 1992;101(4, Supplement):163S-171S.

35.

Wernly

Lichtenauer

Franz

, et al. Model for end-stage liver disease excluding INR (MELD-XI) score in critically ill patients: easily available and of prognostic relevance. PLOS ONE. 2017;12(2):e0170987.

36.

Wernly

Lichtenauer

Vellinga

, et al. Model for end-stage liver disease excluding INR (MELD-XI) score is associated with hemodynamic impairment and predicts mortality in critically ill patients. Eur J Intern Med. 2018;51:80-84.

37.

Amione-Guerra

Cruz-Solbes

Gonzalez Bonilla

, et al. Melding a high-risk patient for continuous flow left ventricular assist device into a low-risk patient. Asaio J. 2017;63(6):704-712.

The Predictive Value of the MELD Scores for In-Hospital Adverse Events in Normotensive Patients with Acute Pulmonary Embolism

Abstract

Keywords

Key Learning Points

What is Already Known?

What this Study Adds?

Introduction

Methods

Study Design and Participants

Data Collection

MELD and MELD-XI Scores

Definition of Outcomes

Statistical Analysis

Results

Baseline Characteristics

The Association Between MELD and MELD-XI and In-Hospital Adverse Events

Comparison of the Predictive Value of MELD, MELD-XI, and PESI for In-Hospital Adverse Events

Discussion

Limitations

Conclusion

Footnotes

Data Availability Statement

Declaration of Conflicting Interests

Funding

ORCID iD

References