Abstract
Introduction
The pulmonary artery pulsatility index (PAPI) is a newer hemodynamic index used for assessment of right ventricular performance. We hypothesized that PAPI predicts morbidity and mortality in acute systolic heart failure (HF).
Methods
The ESCAPE trial was utilized to identify the prognostic value of PAPI at different time points in patients hospitalized with acute systolic HF who received care assisted with central hemodynamic monitoring.
Results
Among 167 patients (age 57 years, 71% men), PAPI significantly increased from admission to optimum hemodynamic day (from 2.88 to 4.09, P < 0.001) and final day (from 3.24 to 3.91, P = 0.032), and the magnitude of increase was strongly associated with markers of decongestion. Discharge PAPI was higher among survivors compared to non-survivors (median 3.1 vs. 2.0, P = 0.0008) and among patients who did not require rehospitalization compared to re-hospitalized patients (median 3.33 vs. 2.67, P = 0.017), both at 6-months. Discharge PAPI predicted mortality with AUC of 0.631 (P = 0.0207), rehospitalization (AUC 0.598, P = 0.0303), and composite of death, rehospitalization, cardiac transplant (AUC 0.621, P = 0.0101). An optimal cutoff value of discharge PAPI ≤2 had the highest sensitivity and specificity in predicting 6-month mortality, rehospitalization and the composite endpoint. Discharge PAPI, had a higher (though non-significant) AUC in predicting death and composite endpoint compared to admission PAPI, next day PAPI and optimal day PAPI. Cox proportional hazard analysis showed that discharge PAPI remained an independent predictor of the composite endpoint (hazard ratio 0.890, 95% CI 0.819–0.967, P = 0.006) after covariate adjustment.
Conclusions
Discharge PAPI ≤2 is a marker of intermediate-term morbidity and mortality in acute systolic HF.
Keywords: Heart failure, Pulmonary artery pulsatility index, Mortality
1. Introduction
Heart failure (HF) continues to be a growing public health concern both in the United States and globally due to the increasing prevalence over the last decade. Data from the 2015 release of the National Health and Nutrition Examination Survey (NHANES) demonstrated a rise from 5.7 million cases in 2009 to 2012 to 6.5 million cases from 2011 to 2014 among Americans over the age of 20 [1]. The overall disease burden of HF is only estimated to rise, with a projected 46% increase in prevalence by year 2030 resulting in over 8 million affected [1]. HF remains the most common reason for hospital admission and accounted for over 1 million hospital discharges in 2010 [2]. Despite advances in evidenced based medical therapy, mortality in HF continues to remain significantly elevated with a 5-year survival rate of only around 50%, which is worse than many cancers [3,4]. Acute exacerbations requiring hospital admission marks a significant event in a patient's disease course and is marker of poor prognosis, as 30-day mortality following hospital admission is over 10% [5].
Current risk stratification models look primarily at measurements and data obtained noninvasively, such as common laboratory values, comorbid conditions, and echocardiographic parameters [[6], [7], [8]]. Now, however, more attention is being placed on identifying other values associated with HF mortality that more adequately represent the physiology and hemodynamic changes occurring with disease progression. One novel value, the pulmonary artery pulsatility index (PAPI) is an evolving parameter of cardiovascular hemodynamics [9]. PAPI is calculated as follows: . PAPI first emerged in 2008 in a study evaluating right ventricular (RV) systolic dysfunction following acute inferior myocardial infarction. A lower PAPI was associated with a statistically significant increased risk of RV systolic dysfunction and need for placement of a right ventricular assist device (RVAD) [10]. Since this initial study, PAPI is now being increasingly utilized in the left ventricular assist device (LVAD) population. Low PAPI values are associated with increased risk of RV failure requiring inotropic therapy and RVAD placement following LVAD placement [11,12]. Given the incorporation of surrogate markers that approximate right and left heart filling pressures, PAPI serves as a simple, invasive marker of cardiac hemodynamics.
Based on this previous literature, we hypothesize that PAPI can also be used as a prognostic marker in patients admitted with acute decompensated HF with reduced ejection fraction to identify subjects at risk of death or rehospitalization. We further hypothesize that PAPI calculated at final hemodynamic day (i.e. after optimal decongestion) is a better predictor of post-discharge outcomes in patients hospitalized with HF, compared with the same index calculated on admission. Because this time point was closest to the discharge, we use the term “discharge PAPI” and "final PAPI" interchangeably, although in fact, the measurement was done few days prior to discharge.
2. Methods
2.1. The ESCAPE trial
The Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial was conducted at 26 sites in the United States and Canada between 2000 and 2003 and randomized 433 patients with acute HF to either clinical assessment guided by pulmonary artery catheters (PAC) versus clinical assessment alone. All patients were classified to have New York Heart Association class IV symptoms and had a left ventricular ejection fraction <30%, 3 months of symptoms despite appropriate therapy, a systolic blood pressure <125 mm Hg and at least one symptom and sign of congestion. Cases with creatinine > 3.5 mg/dL, and those who required dobutamine/dopamine 3 g/kg/min or milrinone before randomization were excluded. The study showed that PAC did not significantly alter the number of days alive and out of the hospital for 6 months after randomization. Results from the ESCAPE trial have been previously published [13].
2.2. PAPI and study endpoints
We hypothesized that PAPI calculated at final hemodynamic day (i.e. after optimal decongestion) is a predictor of short and intermediate-term post-discharge outcomes in patients hospitalized with acute HF. In the ESCAPE trial, hemodynamic variables were measured via the PAC at baseline, and serially until the catheter was removed (on the next day after insertion of PAC, on the day of optimal hemodynamics, and on the last day of PAC presence). Follow-up occurred after hospital discharge at 1 week, 2 weeks, then at 1, 2, 3, and 6 months. For the purpose of the current analysis, only subjects who had central hemodynamic measurements recorded via PAC were included. The study endpoints were all-cause mortality, all-cause rehospitalization, the composite endpoint of death, cardiac rehospitalization, cardiac transplant and the composite endpoint of death, any rehospitalization and cardiac transplant, all up to 6 months following randomization.
2.3. Statistical analysis
Demographics, clinical, laboratory, echocardiographic and central hemodynamic findings, were summarized as counts and percentages for categorical variables and as medians with interquartile range (IQR) for continuous variables. Since majority of variables were not normally distributed as assessed by the Shapiro-Wilk test, the Mann Whitney U test was used to compare continuous variables. Categorical variables were compared via the Chi square test. The prognostic effect of PAPI calculated at final hemodynamic day on the study endpoints was assessed by calculating the area under the curve (AUC) of the receiver operating characteristics (ROC) curve. The optimum cutoff points were those who provide the maximum combined sensitivity and specificity. Comparison of the AUC of the admission PAPI, next day PAPI, optimum day PAPI and final PAPI was performed, using the Hanley and McNeil method as implemented in the MedCalc software. Cox proportional hazard analysis was performed to identify whether discharge PAPI independently predicted a composite of death rehospitalization and cardiac transplant. Factors included in the model included those that were significant on univariate analysis. Statistical analysis was performed using IBM SPSS 21.0 statistical software (IBM SPSS Version 21.0. Armonk, NY). All statistical significance was assessed using a 2-sided P values. A P-value < 0.05 was considered statistically significant.
3. Results
3.1. Patient characteristics
A total of 198 cases were randomized to receive PAC, among which 167 (84%) patients (age 57 years, 71% men) had recorded values for pulmonary artery systolic pressure (PASP), pulmonary artery diastolic pressure (PADP) and right atrial pressure (RAP) at multiple time points, and hence the ability to calculate their PAPI. 87.4% of these patients were classified as New York Heart Association function class IV at baseline, with median ejection fraction of 18%, median pulmonary capillary wedge pressure (PCWP) of 24 mm Hg, and median RAP of 12 mm Hg. 22.2% (37/167) died and 58.7% (98/167) were rehospitalized, at 6 month following randomization. The detailed characteristics of these 167 patients are listed in Table 1.
Table 1.
Demographics, clinical, laboratory, echocardiographic and central hemodynamic characteristics of ESCAPE trial patients with calculated PAPI on discharge.
| Demographics | |
| Age (years, median, IQR) | 57 (48, 67) |
| Male sex n (%) | 118/167 (70.7%) |
| BMI (kg/m2, median, IQR) | 27.4 (23.5, 32.6) |
| Black race n (%) | 48/167 (28.7%) |
| White race n (%) | 99/167 (59.3%) |
| Comorbidities | |
| Ischemic etiology of HF n (%) | 87/167 (47.9%) |
| CABG n (%) | 50/167 (29.9%) |
| COPD n (%) | 26/167 (15.6%) |
| IDDM n (%) | 29/167 (17.4%) |
| Atrial fibrillation n (%) | 51/167 (30.5%) |
| ICD n (%) | 47/167 (28.1%) |
| Admission physical exam | |
| Elevated JVP > 12 cm n (%) | 95/162 (58.6%) |
| S3 gallop n (%) | 107/167 (64.1%) |
| Positive HJR n (%) | 129/161 (80.1%) |
| At least 2+ edema n (%) | 66/167 (39.5%) |
| NYHA class IV n (%) | 146/167 (87.4%) |
| Admission laboratory tests | |
| Na (meq/L, median, IQR) | 137 (135, 140) |
| K (meq/L, median, IQR) | 4.2 (3.8, 4.6) |
| BUN (mg/dL, median, IQR) | 29 (20, 43) |
| Creatinine (mg/dL, median, IQR) | 1.4 (1.1, 1.8) |
| ALT (IU/L, median, IQR) | 27 (18, 39) |
| Total bilirubin (mg/dL, median, IQR) | 0.8 (0.4, 1.2) |
| Direct bilirubin (mg/dL, median, IQR) | 0.3 (0.2, 0.6) |
| BNP (pg/dL, median, IQR) | 545 (213, 1244) |
| Admission echocardiographic variables | |
| EF (%, median, IQR) | 18 (13, 26) |
| LVEDD (cm, median, IQR) | 6.5 (5.9, 7.3) |
| LVESD (cm, median, IQR) | 5.8 (5.2, 6.6) |
| IVC inspiration (cm, median, IQR) | 1.7 (1, 2.2) |
| IVC expiration (cm, median, IQR) | 2.3 (1.7, 2.6) |
| IVC collapsibility index (%, median, IQR) | 24 (15, 47) |
| Admission central hemodynamic variables | |
| PCWP (mm Hg, median, IQR) | 24 (20, 30) |
| RAP (mm Hg, median, IQR) | 12 (8, 18) |
| PASP (mm Hg, median, IQR) | 55 (45, 66) |
| PADP (mm Hg, median, IQR) | 25 (20, 34) |
| Cardiac output (L/min, median, IQR) | 3.7 (2.9, 4.6) |
| PAPI final day (median, IQR) | |
BMI: body mass index, CABG: coronary artery bypass graft, COPD: chronic obstructive pulmonary disease, IDDM: insulin dependent diabetes mellitus, ICD: implantable cardiac defibrillator, JVP: jugular venous pressure, HJR: hepatojugular reflux, BNP: B-type natriuretic peptide, EF: ejection fraction, LVEDD: left ventricular end-diastolic dimension, LVESD: left ventricular end-systolic dimension, IVC: inferior vena cava, PCWP: pulmonary capillary wedge pressure, RAP: right atrial pressure, PASP: pulmonary artery systolic pressure, PADP: pulmonary artery diastolic pressure, COP: cardiac output: PAPI: pulmonary artery pulsatility index.
3.2. Longitudinal values of PAPI throughout hospitalization
Using paired sample t-test, there was a significant increase in PAPI from admission to optimum hemodynamic day (from 2.88 to 4.09, P < 0.001), and from admission to final hemodynamic day (from 3.24 to 3.91, P = 0.032). Fig. 1 shows the longitudinal values of PAPI from admission to final hemodynamic day.
Fig. 1.
The longitudinal values of pulmonary artery pulsatility index (PAPI) from admission to discharge among patients enrolled in the ESCAPE trial. The five horizontal lines represent the 10th, 25th, 50th, 75th and 90th percentiles of PAPI from bottom to top, excluding outliers which are shown as circles, and extreme outliers shown as one asterisk. §P < 0.05 and §§P < 0.01 (both relative to admission PAPI).
3.3. Association of longitudinal increase in PAPI with markers of decongestion
To investigate whether PAPI increased longitudinally with decongestion, Spearman's correlation analysis was utilized to study association between rise in PAPI from admission to final hemodynamic day and degree of decongestion throughout hospitalization from admission to discharge. The magnitude of rise in PAPI from admission to final hemodynamic day was associated with admission to discharge change in RAP (n = 159, r = −0.752, P < 0.001), PCWP (n = 136, r = −0.357, P < 0.001), inferior vena cava (IVC) diameter during inspiration (n = 51, r = −0.348, P = 0.012), IVC diameter during expiration (n = 54, r = −0.427, P = 0.001) and weight change (n = 141, r = −0.178, P = 0.034).
3.4. Association of final PAPI on study endpoints
PAPI on final hemodynamic day was significantly higher in survivors compared with non-survivors: [median (IQR): 3.05 (2.32, 4.81) vs. 2 (1.38, 3.91), P = 0.008, in both groups, respectively], and in those who were rehospitalized compared with those not rehospitalized: [median (IQR): 3.33 (2.43, 5.67) vs. 2.67 (1.9, 4), P = 0.017, in both groups, respectively]. Also, PAPI on final day was significantly higher in subjects without the composite endpoint of death, cardiac rehospitalization, cardiac transplant (P = 0.019) and in those without the composite endpoint of death, any rehospitalization and cardiac transplant (P = 0.005), compared with those with the composite endpoints, all up to 6 months following randomization. Fig. 2 compares values of discharge PAPI among subjects with or without the study endpoints.
Fig. 2.
Box and whisker plots of the discharge pulmonary artery pulsatility index (PAPI) among ESCAPE trial patients according to death (panel a), all-cause rehospitalization (panel b), composite endpoint of death, cardiac rehospitalization, cardiac transplant (panel c) and composite endpoint of death, any rehospitalization and cardiac transplant (panel d). The five horizontal lines represent the 10th, 25th, 50th, 75th and 90th percentiles of PAPI calculated on final hemodynamic day, from bottom to top, excluding outliers which are shown as circles and extreme outliers shown as one asterisk.
ROC curves showed that discharge PAPI had an AUC of 0.631 (95% CI 0.553–0.705, P = 0.0207), and an optimum cutoff value ≤2 had a 54.1% sensitivity and 69.2% specificity for predicting death. With regards to all-cause rehospitalization, discharge PAPI had an AUC 0.598 (95% CI 0.520–0.673, P = 0.0303) and an optimum cutoff value ≤2 had a 42.9% sensitivity and 73.9% specificity for predicting rehospitalization. Discharge PAPI also had an AUC 0.593 (95% CI 0.514–0.668, P = 0.0353) and an optimum cutoff value ≤3 had a 65.9% sensitivity and 48.7% specificity for predicting composite endpoint of death, cardiac rehospitalization and cardiac transplant. Discharge PAPI had an AUC 0.621 (95% CI 0.543–0.695, P = 0.0101) and an optimum cutoff ≤2 had a 41.4% sensitivity and 76.5% specificity for predicting a composite of death, any rehospitalization and cardiac transplant (Fig. 3).
Fig. 3.
Receiver operator characteristics curves showing area under curve of discharge pulmonary artery pulsatility index (PAPI) in predicting death (panel a), rehospitalization (panel b), composite of death, cardiac rehospitalization, cardiac transplant (panel c) and composite of death, any rehospitalization and cardiac transplant (panel d).
3.5. Comparison of PAPI at different time points on outcomes
Discharge PAPI had higher (though non-significant) AUC for predicting death (AUC 0.619) compared with admission PAPI (P = 0.605), next day PAPI (P = 0.585) and optimum day PAPI (P = 0.596). Also discharge PAPI had higher (though non-significant) AUC for predicting all-cause rehospitalization (AUC 0.617) compared with admission PAPI (P = 0.523), next day PAPI (P = 0.572) and optimum day PAPI (P = 0.594) (Fig. 4).
Fig. 4.
Comparison of area under curve of admission pulmonary artery pulsatility index (PAPI), next day PAPI, optimum day PAPI and final day PAPI in predicting death and rehospitalization.
3.6. Comparison of final PAPI and final RAP and pulmonary artery pulse pressure
Since PAPI is a ratio, we attempted to compare final PAPI versus final pulmonary artery pulse pressure and final RAP in predicting death. We found that final PAPI had a superior, although non-significant AUC of 0.631 in predicting death versus pulmonary artery pulse pressure which had an AUC of 0.557. On the other hand, comparison of final PAPI and final RAP in predicting death revealed that RAP had a superior, although non-significant AUC of 0.688 versus final PAPI which had an AUC of 0.631 (Fig. 5).
Fig. 5.
Comparison of area under curve of final day PAPI and final day pulmonary artery pulse pressure (panel a) and right atrial pressure (panel b) in predicting death.
3.7. Prognostic role of PAPI on 6-month outcomes after acute heart failure
Univariate and multivariate Cox regression analysis for discharge predictors of the composite of death, rehospitalization, and cardiac transplant is presented in Table 2. On Univariate analysis, the total duration of initial hospitalization, presence of peripheral edema on discharge, discharge Na, discharge BUN, discharge creatinine, final RAP, final PCWP, final PADP, and final day PAPI were significantly associated with the composite endpoint. After adjustment for other significant risk factors including discharge BUN, discharge Na and duration of hospitalization, final day PAPI remained an independent predictor of the composite endpoint (hazard ratio 0.890, 95% CI 0.819–0.967, P = 0.006).
Table 2.
Discharge determinants of 6-month death rehospitalization or cardiac transplant among ESCAPE study patients.
| Variable | Univariable analysis |
Multivariable analysis |
||
|---|---|---|---|---|
| HR (95% CI) | P-value | HR (95% CI) | P-value | |
| Age | 1.003 (0.994–1.012) | 0.481 | ||
| Men | 0.995 (0.764–1.297) | 0.973 | ||
| Discharge weight | 0.999 (0.993–1.006) | 0.834 | ||
| White race | 1.065 (0.839–1.353) | 0.604 | ||
| Black race | 1.194 (0.925–1.542) | 0.173 | ||
| Duration of hospitalization | 1.032 (1.016–1.048) | <0.001 | 1.023 (0.990–1.056) | 0.174 |
| Discharge +ve HJR | 1.284 (0.985–1.673) | 0.064 | ||
| Discharge hepatomegally | 1.251 (0.956–1.637) | 0.103 | ||
| Discharge peripheral edema | 1.306 (1.079–1.579) | 0.006 | ||
| Discharge 6MWD | 0.999 (0.999–1.000) | 0.137 | ||
| Discharge Na | 0.965 (0.938–0.994) | 0.017 | 0.956 (0.911–1.004) | 0.072 |
| Discharge BUN | 1.017 (1.012–1.023) | <0.001 | 1.011 (1.001–1.020) | 0.030 |
| Discharge creatinine | 1.170 (1.057–1.296) | 0.003 | ||
| Discharge bilirubin | 0.962 (0.658–1.408) | 0.844 | ||
| Discharge IVC diameter (ins) | 1.081 (0.858–1.364) | 0.508 | ||
| Discharge IVC diameter (exp) | 1.061 (0.822–1.366) | 0.652 | ||
| Discharge right atrial area | 1.012 (0.992–1.033) | 0.246 | ||
| Discharge RV area (systole) | 0.999 (0.974–1.026) | 0.958 | ||
| Discharge LVEDD | 1.051 (0.901–1.227) | 0.526 | ||
| Discharge LVEF | 0.981 (0.961–1.001) | 0.064 | ||
| Final PAC SBP | 0.993 (0.983–1.003) | 1.181 | ||
| Final PAC DBP | 1.000 (0.988–1.012) | 0.974 | ||
| Final RAP | 1.064 (1.031–1.099) | <0.001 | ||
| Final PCWP | 1.039 (1.011–1.069) | 0.007 | ||
| Final PASP | 1.008 (0.993–1.022) | 0.299 | ||
| Final PADP | 1.026 (1.002–1.050) | 0.032 | ||
| Final CI | 0.866 (0.638–1.177) | 0.359 | ||
| Final COP | 0.938 (0.810–1.087) | 0.395 | ||
| Final PAPI | 0.909 (0.846–0.976) | 0.009 | 0.890 (0.819–0.967) | 0.006 |
HJR: hepatojugular reflux, 6MWD: 6-minute walk distance, IVC: inferior vena cava, RV: right ventricle, LVEDD: left ventricular end-diastolic dimension, LVEF: left ventricular ejection fraction, PAC: pulmonary artery catheter, SBP: systolic blood pressure, DBP: diastolic blood pressure, RAP: right atrial pressure, PCWP: pulmonary capillary wedge pressure, PASP: pulmonary artery systolic pressure, PADP: pulmonary artery diastolic pressure, CI: cardiac index, COP: cardiac output: PAPI: pulmonary artery pulsatility index.
bold means "significant" i.e P < 0.05.
4. Discussion
The idea of using PAPI as a prognostic marker in advanced HF is a relatively new clinical concept. Lower PAPI reflects poorer RV function. Our results demonstrate that PAPI prior to discharge measured following optimized hemodynamics is a useful predictor of morbidity and mortality among patients with advanced HF. At 6-month follow up, a lower PAPI on discharge from index hospitalization was associated with increased risk of mortality, all cause hospitalization as well as the 2 composite end points. Our findings remained unaltered after covariate adjustment. A cutoff value of discharge PAPI ≤2 was the optimal value to predict the study endpoints. We have also shown that PAPI increases longitudinally throughout hospitalization, with decongestion being a determinant of rising PAPI. Comparison of AUC suggests that the prognostic value of PAPI in acute HF is driven mainly by the component of RAP rather than pulmonary artery pulse pressure.
Our findings also demonstrate that PAPI changes significantly in the course of one hospital admission. It means that when PAPI is used for assessment of RV function, the index should be used very carefully. If the value of PAPI is calculated in a severely congested patient, elevated PADP will bring the index down. It has to be re-calculated based on the measurements obtained after the hemodynamics is optimized. This is particularly important in evaluation of candidacy for LVAD.
In the LVAD population, PAPI was found to be significantly lower and predictive of development of RV failure and need for RVAD following placement of an LVAD [11,12]. One of these studies demonstrated that 74% of patients with a PAPI of <2 prior to insertion of LVAD device required placement of a RVAD [12]. Another study evaluating use of PAPI in acute inferior wall myocardial infarctions found that absolute PAPI values were significantly lower among patients who developed severe RV dysfunction and need for a percutaneous right ventricular assist device (pRVSD) [10]. In this same study a PAPI of <0.9, was 100% sensitive and 98% specific in predicting in-hospital mortality, as well as pRSVD placement [10]. Despite the multitude of data surrounding PAPI in predicting RV failure, it has not been thoroughly evaluated in patients with advanced left ventricular HF who are not undergoing device placement.
Given the variables used in calculating PAPI (PASP, PADP, RAP), it likely serves not only as a marker for RV dysfunction, but also as a predictor of worsening LV dysfunction as well. By incorporating the pulmonary artery diastolic pressure (PADP) in the equation we are evaluating LV hemodynamics in addition to RV hemodynamics, as PADP can be used a surrogate marker for left atrial pressure which in turn reflects LV diastolic filling pressure. By using the PADP along with the RAP, we are inherently evaluating the overall cardiac function by looking at combined left ventricular and right ventricular hemodynamics on a more global perspective. This zoomed out evaluation is what drives the utility of this index in patients with decompensated systolic HF.
Kochav and colleagues studied the prognostic value of PAPI on HF mortality and rehospitalization in the same population of the ESCAPE trial [14]. Unlike us, they studied baseline PAPI, with all measurements performed in acutely decompensated patients. We found that PAPI after decongestion would be more valuable in predicting post-discharge outcomes and would be considered as patient's “ideal PAPI” to be targeted during future hospitalization. This is the same rational as with B-type natriuretic peptide (BNP), where discharge BNP is considered by many as “baseline”, and treatment should be targeted to maintain BNP level close to this value. Multiple studies showed that discharge variables area superior to admission variables in predicting acute HF outcomes, including a study by our team showing that discharge BNP is superior to admission BNP in predicting mortality after acute systolic HF [15]. In the current analysis, ROC curve comparison indeed showed that discharge PAPI had a higher (though non-significant) AUC in predicting mortality, and composite endpoint relative to PAPI measured at all other timepoints.
4.1. Study limitations
Study limitations include the retrospective nature and relatively small population of patients. Calculating PAPI requires invasive hemodynamic monitoring and therefore this index is valuable only in hospitalized advanced heart failure patients undergoing central hemodynamic monitoring. The study included patient with acute HF with EF ≤ 30% and so findings can't be generalized to all HF population.
5. Conclusion
PAPI is a novel hemodynamic index that can be utilized for risk stratification of patients with systolic heart failure. This index changes longitudinally throughout hospitalization and hence can be a surrogate marker for decongestion. Discharge PAPI ≤ 2 should be utilized to identify those at highest risk of re-hospitalization and mortality following a hospitalization for advanced heart failure where central hemodynamic monitoring is utilized.
Declaration of competing interest
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Acknowledgments
Acknowledgement
The ESCAPE trial is conducted and supported by the NHLBI in collaboration with the ESCAPE Study Investigators. This article was prepared using a limited access dataset obtained from the NHLBI and does not necessarily reflect the opinions or views of the ESCAPE trial investigators or the NHLBI. We would like to thank Amit Lale for revision of this work.
Footnotes
No financial support was used.
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