Abstract
Background
The pulmonary artery pulsatility index (PAPi) is a hemodynamic index that reflects right ventricular function. However, the association between PAPi and prognosis in patients with severe aortic stenosis who underwent transcatheter aortic valve replacement (TAVR) remains unclear.
Objectives
This study aimed to determine how periprocedural changes in the PAPi are associated with patients’ prognosis after TAVR.
Methods
Of the 405 consecutive patients who underwent TAVR for severe aortic stenosis at Hiroshima University Hospital, those with available periprocedural right heart catheter data were included in this study. Patients were divided into 2 groups with a cutoff PAPi value of 3.11 post-TAVR determined by the receiver-operating characteristic curve for the primary endpoint. The primary endpoint was the composite of all-cause mortality and hospitalization caused by heart failure. The secondary endpoint was all-cause mortality. Additionally, factors in the nonimproved PAPi group were investigated.
Results
This study enrolled 238 patients. The median follow-up was 405.5 days (Q1-Q3: 353-861 days). A lower PAPi was associated with an increased risk of the primary endpoint (23.3% vs 9.9%; log-rank P < 0.001). After multivariate Cox proportional hazard analysis, post-TAVR PAPi >3.11 was still predictive factor for the primary endpoint (HR: 3.04; 95% CI: 1.30-7.13; P = 0.011). Furthermore, the secondary endpoint was significantly increased in lower PAPi group (log-rank P = 0.010). A nonimproved PAPi predictor was pre-TAVR aortic valve mean pressure gradient in multivariate analysis (OR: 1.02; 95% CI: 1.01-1.04; P = 0.003).
Conclusions
The post-TAVR PAPi was associated with all-cause mortality and heart failure hospitalization.
Key Words: aortic stenosis, hemodynamic, right heart catheterization, right ventricular dysfunction, transcatheter aortic valve replacement
Central Illustration
Transcatheter aortic valve replacement (TAVR) is a treatment option for patients with aortic stenosis (AS) who are not amenable to aortic valve replacement surgery with a high surgical risk. In recent years, TAVR has been expanded to include patients with less than intermediate surgical risk.1,2 With the increase in TAVR for patients with low and intermediate risks,3 medium- to long-term prognoses after TAVR are increasingly being considered. Thus, classifying the risk of post-TAVR cardiac events is important.
In patients with severe AS, chronic left ventricular pressure overload may induce left atrial dilation, high pulmonary artery pressure, and ultimately right ventricular (RV) dysfunction.4 RV dysfunction is a risk factor for post-TAVR all-cause mortality or cardiovascular death.5,6 In addition, persistent post-TAVR RV dysfunction is associated with all-cause mortality and hospitalization for heart failure.7,8
The pulmonary artery pulsatility index (PAPi) is used to evaluate RV function and is easily calculated from right heart catheterization (RHC) parameters such as pulmonary artery pulse pressure and right atrial pressure (RAP). Lower PAPi is a predictor of severe RV infarction after acute myocardial infarction9 and is one of the risk factors for RV failure with left ventricular assist device implantation.10
However, the relationship between PAPi and prognosis in patients who underwent TAVR is not clearly known. Therefore, this study investigated the relationship between preoperative and postoperative PAPi and prognosis in patients who underwent TAVR.
Methods
Patient population and study design
This retrospective, observational single-center, study enrolled patients who underwent TAVR for severe AS between October 2015 and December 2022 at Hiroshima University Hospital. Severe AS was diagnosed according to the guidelines.11 Severe AS was defined as aortic valve area <1.0 cm2 (or aortic valve area <0.6 cm2/m2 indexed by the body surface area), peak aortic transit velocity at rest >4.0 m/m2, or mean pressure gradient >40 mm Hg.
The following cases were excluded from this study: 1) 3 patients who underwent other cardiac surgery (2 with coronary artery bypass graft and 1 with mitral valve plasty) simultaneously with TAVR; 2) 7 emergency cases; 3) 6 patients who underwent mitral valve transcatheter edge-to-edge repair after TAVR; 4) 1 patient who underwent percutaneous transvenous mitral commissurotomy; and 5) 150 patients without pre- or post-TAVR RHC data (Figure 1). Demographic, laboratory, and pre- and post-TAVR transthoracic echocardiographic data were collected as baseline characteristics.
Figure 1.
Patient Selection Flowchart
Patients were divided into 2 groups by post–transcatheter aortic valve replacement (TAVR) pulmonary artery pulsatility index.
This study was approved by the Ethics Committee of Hiroshima University Hospital. Written informed consent from the participants was not required because of the retrospective observational design and the use of data collected previously as part of routine clinical care.
PAPi cutoff and patient grouping
The cutoff PAPi value was determined by the receiver-operating characteristic (ROC) curve. ROC analysis predicting the composite endpoint showed that the area under curves for pre-TAVR PAPi of 0.54 and post-TAVR PAPi of 0.65. The ROC analysis of post-TAVR PAPi determined 3.11 (sensitivity 0.62, specificity 0.67) as the best cutoff PAPi. Using this cutoff value, patients were divided into 2 groups: 86 were included in the lower PAPi group and 152 in the higher PAPi group (Figure 1). With power of 80% and alpha error level of 0.05, 57 or more patients was required in the lower PAPi group and 64 or more patients was required in higher PAPi group.12 As a substudy analysis, patients were divided into 4 groups: those with pre- and post-TAVR PAPi >3.11 (group 1: unchanged higher PAPi, n = 75), those with pre-TAVR PAPi <3.11 but with post-TAVR PAPi >3.11 (group 2: increased to higher PAPi, n = 77), those with pre-TAVR PAPi >3.11 but with post-TAVR PAPi <3.11 post-TAVR (group 3: decreased to lower PAPi, n = 30), and those with both pre- and post-TAVR PAPi <3.11 (group 4: unchanged lower PAPi, n = 56) (Figure 1). Additionally, patients were divided into 2 groups: those whose post-TAVR PAPi improved and those whose post-TAVR PAPi did not improve or remained unchanged, and the factors contributing to nonimproved PAPi were investigated.
TAVR procedure
Treatment options for severe AS, including TAVR indications, were determined at a conference of our heart team consisting of cardiologists, cardiovascular surgeons, and anesthesiologists. Our heart team determined the type and size of the prosthetic valves and the access site for the TAVR. Patients received either balloon-expandable valve Sapien XT/Sapien 3 (Edwards Lifesciences) or self-expandable valve Evolut R/Evolut PRO+ (Medtronic). All patients underwent TAVR under general anesthesia. Pre- and post-TAVR peak and mean aortic valve pressure gradients were measured invasively.
RHC data collection
Invasive hemodynamic assessments by RHC were performed pre- and post-TAVR. Pre-TAVR RHC was performed at a median of 38 days (Q1-Q3: 17-67.5 days). All post-TAVR RHCs were routinely performed on the first postprocedural day using a catheter inserted during TAVR procedures. Usually, an 8-F Swan-Ganz catheter (Edwards Lifesciences) was used. RAP, systolic pulmonary artery pressure (PAP), diastolic PAP, and cardiac output were measured. Cardiac output was calculated by the Fick method. PAPi was calculated as follows: PAPi = (systolic PAP [mm Hg]−diastolic PAP [mm Hg])/RAP (mm Hg).13
Study endpoint
The primary endpoint was a composite of all-cause mortality and rehospitalization for worsening heart failure. The secondary endpoint was an all-cause mortality. Patients visited our hospital 6 and 12 months after TAVR and every 12 months thereafter. Death and rehospitalization data for heart failure were collected.
Statistical analysis
Continuous variables are presented as mean ± SD or median (Q1-Q3). Categorical variables are presented as numbers (percentages). Comparisons between 2 groups of continuous variables were performed using the Wilcoxon rank-sum test and that of 3 or more groups using the Kruskal-Wallis test. Categorical variables were compared using the chi-square or Fisher exact test. The ROC curve was applied to evaluate the usefulness of the PAPi in predicting the primary endpoint, and the cutoff value was determined. Using this cutoff value, the patients were divided into 2 groups. The Kaplan-Meier analysis was performed to evaluate the association between the PAPi and the primary and secondary endpoint. The log-rank test was used for between-group comparisons. Univariate and multivariate Cox proportional hazard models were used to analyze the primary endpoint. The proportional hazards assumption was verified by the log-log survival curve for the primary endpoint. In addition to the PAPi, transfemoral approach and covariates that have been reported to be associated with post-TAVR prognosis were included in the multivariate analysis.14, 15, 16, 17, 18 In addition, we performed multivariate analysis using covariates that reached P value <0.05 in univariate analysis.
A paired-sample Student's t-test was used to compare pre- and post-TAVR PAPi. To examine the association between pre- and post-TAVR PAPi changes and the primary endpoint, patients were classified according to PAPi changes into 4 groups: unchanged higher PAPi (group 1), increased to higher PAPi (group 2), decreased to lower PAPi (group 3), and unchanged lower PAPi (group 4). The 4 groups were evaluated through Kaplan-Meier analysis and compared using a log-rank test. In addition, to examine the factors that change pre- and post-TAVR PAPi, patients were divided into 2 groups: one with improved post-TAVR PAPi and the other with no improvement or change. Univariate and multivariate logistic regression analyses were performed to examine predictors of post-TAVR nonimproved or no changed PAPi. Analysis was adjusted using covariates previously reported to be associated with post-TAVR RV dysfunction.7,8 All statistical analyses were performed with JMP 17 (SAS Institute Inc), and a 2-sided P value <0.05 was considered significant.
Results
Baseline characteristics
From October 2015 to December 2022, 405 patients underwent TAVR for severe AS at Hiroshima University Hospital. After exclusion, a total of 238 patients were enrolled in this study. Baseline characteristics and pre-TAVR data are shown in Table 1. The median follow-up period was 406 days (Q1-Q3: 353-861 days).
Table 1.
Baseline Characteristics
| All (N = 238) | Post-PAPi >3.11 (n = 152) | Post-PAPi <3.11 (n = 86) | P Value | |
|---|---|---|---|---|
| Age, y | 84.0 ± 5.16 | 84.4 ± 4.88 | 83.3 ± 5.57 | 0.190 |
| Male | 69 (29.0) | 47 (30.9) | 22 (25.9) | 0.458 |
| Body mass index, kg/m2 | 22.7 ± 3.69 | 22.4 ± 3.41 | 23.3 ± 0.44 | 0.057 |
| NYHA functional class ≥III | 101 (42.4) | 69 (45.4) | 32 (37.2) | 0.275 |
| Clinical frailty scale score ≥4 | 172 (75.1) | 112 (74.7) | 60 (76.0) | 0.873 |
| STS score, % | 6.3 (4.3-8.1) | 6.2 (4.3-7.9) | 6.7 (4.3-8.4) | 0.476 |
| Hypertension | 210 (88.2) | 136 (89.5) | 74 (86.1) | 0.530 |
| Dyslipidemia | 142 (59.7) | 93 (61.2) | 49 (57.0) | 0.583 |
| Diabetes mellitus | 66 (27.7) | 43 (28.3) | 23 (26.7) | 0.881 |
| Chronic kidney disease | 164 (68.9) | 109 (71.7) | 55 (64.0) | 0.244 |
| Atrial fibrillation | 50 (21.0) | 28 (18.4) | 22 (25.6) | 0.246 |
| Coronary artery disease | 65 (27.3) | 42 (27.6) | 23 (26.7) | 1.000 |
| Previous percutaneous coronary intervention | 28 (11.8) | 18 (11.8) | 10 (11.6) | 1.000 |
| Previous coronary artery bypass grafting | 8 (3.36) | 6 (3.95) | 2 (2.33) | 0.714 |
| Previous pacemaker implantation | 12 (5.04) | 7 (4.61) | 5 (5.81) | 0.761 |
| History of stroke | 41 (17.2) | 27 (17.8) | 14 (16.3) | 0.859 |
| Previous cardiac surgery | 10 (4.20) | 6 (3.95) | 4 (4.65) | 0.751 |
| Echocardiography | ||||
| Left ventricular ejection fraction, % | 61.9 ± 8.91 | 61.2 ± 9.10 | 63.1 ± 8.49 | 0.133 |
| AV peak velocity, m/s | 4.64 ± 0.73 | 4.68 ± 0.691 | 4.57 ± 0.804 | 0.318 |
| AV peak pressure gradient, mm Hg | 88.4 ± 28.1 | 89.7 ± 26.8 | 86.1 ± 30.3 | 0.324 |
| AV mean pressure gradient. Mm Hg | 51.5 ± 18.3 | 52.1 ± 17.8 | 50.3 ± 19.3 | 0.431 |
| AV area, cm2 | 0.67 ± 0.20 | 0.66 ± 0.20 | 0.68 ± 0.19 | 0.318 |
| AV area index, cm2/m2 | 0.46 ± 0.14 | 0.46 ± 0.14 | 0.46 ± 0.13 | 0.474 |
| Aortic regurgitation moderate or greater | 11 (4.6) | 7 (4.6) | 4 (4.7) | 1.000 |
| Mitral regurgitation moderate or greater | 20 (8.4) | 11 (7.2) | 9 (10.4) | 0.467 |
| Tricuspid regurgitation moderate or greater | 69 (29) | 42 (27.8) | 27 (31.8) | 0.553 |
| Laboratory data | ||||
| Hemoglobin, g/dL | 12.0 ±1.65 | 12.2 ± 1.50 | 11.8 ± 1.86 | 0.050 |
| CRP, mg/dL | 0.27 ± 0.61 | 0.23 ± 0.052 | 0.33 ± 0.068 | 0.001 |
| Creatinine, mg/dL | 0.94 ± 0.34 | 0.95 ± 0.34 | 0.91 ± 0.35 | 0.300 |
| eGFR, mL/min/1.73 m2 | 52.9 ± 16.6 | 52.0 ± 16.1 | 54.4 ± 17.4 | 0.285 |
| NT-proBNP, pg/mL | 1219 (412-2462) | 1218 (481-2464) | 1221 (285-2385) | 0.587 |
| Hemodynamic data | ||||
| AV peak pressure gradient, mm Hg | 68.4 ± 32.3 | 68.8 ± 30.3 | 67.6 ± 36.0 | 0.543 |
| AV mean pressure gradient, mm Hg | 58.5 ± 22.4 | 59.0 ± 21.3 | 57.6 ± 24.6 | 0.403 |
| Heart rate, beats/min | 69.6 ± 11.5 | 68.6 ± 10.1 | 71.3 ± 13.6 | 0.267 |
| Cardiac index, L/min/m2 | 2.34 ± 9.13 | 2.30 ± 0.62 | 2.40 ± 0.67 | 0.190 |
| Systolic pulmonary artery pressure, mm Hg | 29.7 ± 9.13 | 30.2 ± 9.62 | 28.7 ± 8.15 | 0.309 |
| Diastolic pulmonary artery pressure, mm Hg | 13.3 ± 5.44 | 13.2 ± 5.38 | 13.4 ± 5.57 | 0.703 |
| Mean pulmonary artery pressure, mm Hg | 19.9 ± 6.86 | 20.1 ± 6.98 | 19.6 ± 0.72 | 0.760 |
| Right atrial pressure, mm Hg | 6.12 ± 3.28 | 5.87 ± 3.01 | 6.57 ± 3.69 | 0.216 |
| PAPi | 3.91 ± 3.71 | 4.07 ± 3.81 | 3.63 ± 3.54 | 0.018 |
Values are mean ± SD, n (%), or median (Q1-Q3).
AV = aortic valve; NT-proBNP = N-terminal pro–B-type natriuretic peptide; PAPi = pulmonary artery pulsatility index; STS = Society of Thoracic Surgeons.
Prognosis prediction ability of PAPi
The patients were divided into 2 groups: the lower PAPi group (post-TAVR PAPi <3.11, n = 86) and the higher PAPi group (post-TAVR PAPi >3.11, n = 152). The baseline characteristics of the 2 groups are shown in Table 1, and procedural and postprocedural data are shown in Table 2. No differences in age, medical history, laboratory data, echocardiographic data, or type and size of the prosthetic valve were found between the 2 groups. The pre-TAVR PAPi was lower in the lower PAPi group (3.63 ± 3.54 vs 4.07 ± 3.81; P = 0.018), although no differences in other pre-TAVR RHC data were found. The composite endpoint of all-cause mortality and heart failure hospitalization was recorded in 35 (14.7%) patients. In the lower PAPi group, the primary endpoint occurred in 23.3% of the 86 patients, all-cause mortality in 11 of 86 (12.8%), and heart failure hospitalization in 12 of 86 (13.4%). In the higher PAPi group, the primary endpoint occurred in 9.9% of the 152 patients, all-cause mortality in 8 of 152 (5.3%), and heart failure hospitalization in 10 of 152 (6.6%). In the Kaplan-Meier analysis, lower post-TAVR PAPi was associated with an increased incidence of the primary endpoint (log-rank; P < 0.001) (Figure 2). Furthermore, the secondary endpoint of all-cause mortality was significantly increased in lower PAPi group (log-rank; P = 0.010) (Figure 3).
Table 2.
Procedural and Postprocedural Data
| All (N = 238) | Post-PAPi >3.11 (n = 152) | Post-PAPi <3.11 (n = 86) | P Value | |
|---|---|---|---|---|
| Procedural variables | ||||
| Approach | ||||
| Transfemoral | 217 (91.2) | 144 (94.7) | 73 (84.9) | 0.002 |
| Transapex | 15 (6.3) | 5 (3.3) | 10 (11.6) | — |
| Trans-subclavian | 1 (0.4) | 1 (0.7) | 0 (0) | — |
| Direct aorta | 5 (2.1) | 2 (1.3) | 3 (3.5) | — |
| Valve type | ||||
| Sapien | 189 (79.4) | 121 (79.6) | 68 (79.1) | 1.000 |
| Evolut | 49 (20.6) | 31 (20.4) | 18 (20.9) | 1.000 |
| Valve diameter, mm | 23 (23-26) | 23 (23-26) | 23 (23-26) | 0.805 |
| Echocardiography | ||||
| Left ventricular ejection fraction, % | 62.4 ± 7.90 | 62.0 ± 8.01 | 63.3 ± 7.67 | 0.116 |
| AV peak velocity, mm Hg | 2.51 ± 0.50 | 2.49 ± 0.48 | 2.56 ± 0.54 | 0.280 |
| AV peak pressure gradient, mm Hg | 26.5 ± 10.7 | 25.7 ± 0.88 | 27.9 ± 11.7 | 0.180 |
| AV mean pressure gradient, mm Hg | 14.1 ± 5.85 | 13.9 ± 5.64 | 14.5 ± 6.22 | 0.526 |
| AV area, cm2 | 1.36 ± 0.36 | 1.34 ± 1.34 | 1.38 ± 0.04 | 0.616 |
| AV area index, cm2/m2 | 0.94 ± 0.25 | 0.93 ± 0.23 | 0.94 ± 0.29 | 0.926 |
| Aortic regurgitation moderate or greater | 7 (3.0) | 6 (4.1) | 1 (1.2) | 0.427 |
| Mitral regurgitation moderate or greater | 16 (7.0) | 10 (6.8) | 6 (7.2) | 1.000 |
| Tricuspid regurgitation moderate or greater | 7 (3.0) | 5 (3.4) | 2 (2.5) | 1.000 |
| Hemodynamic data | ||||
| AV peak pressure gradient, mm Hg | 6.36 ± 7.91 | 5.44 ± 6.66 | 8.19 ± 9.72 | 0.078 |
| AV mean pressure gradient, mm Hg | 12.2 ± 6.87 | 11.8 ± 6.82 | 12.8 ± 6.98 | 0.301 |
| Heart rate, beats/min | 67.3 ± 9.55 | 69.2 ± 9.32 | 69.5 ± 9.99 | 0.883 |
| Cardiac index, L/min/m2 | 2.84 ± 0.96 | 2.90 ± 1.05 | 2.72 ± 0.76 | 0.513 |
| Systolic pulmonary artery pressure, mm Hg | 26.5 ± 7.24 | 26.0 ± 7.17 | 27.4 ± 7.31 | 0.110 |
| Diastolic pulmonary artery pressure, mm Hg | 10.8 ± 4.24 | 9.51 ± 3.83 | 13.1 ± 3.98 | <0.001 |
| Mean pulmonary artery pressure, mm Hg | 16.2 ± 4.99 | 15.2 ± 4.75 | 18.0 ± 4.90 | <0.001 |
| Right atrium pressure, mm Hg | 4.39 ± 2.87 | 2.93 ± 1.70 | 6.98 ± 2.69 | <0.001 |
| PAPi | 5.43 ± 4.56 | 7.30 ± 4.81 | 2.20 ± 0.61 | <0.001 |
| Postprocedural complication | ||||
| Major bleeding | 5 (2.1) | 1 (0.7) | 4 (4.7) | 0.059 |
| Pacemaker implantation in hospital | 11 (4.6) | 5 (4.6) | 6 (7.0) | 0.211 |
| Acute kidney injury | 6 (2.5) | 2 (1.3) | 4 (4.7) | 0.193 |
| Stroke in hospital | 3 (1.3) | 1 (0.7) | 2 (2.3) | 0.297 |
| Prosthesis-patient mismatch (iEOA <0.85) | 89 (42.4) | 55 (40.2) | 34 (46.6) | 0.383 |
| Conversion to cardiac surgery | 1 (0.4) | 0 (0) | 1 (1.2) | 0.360 |
Values are mean ± SD, n (%), or median (Q1-Q3). Acute kidney injury was defined as creatinine level >0.3 mg/dL within 48 h after the procedure.
iEOA = indexed effective orifice; other abbreviations as in Table 1.
Figure 2.
Primary Outcome According to the Level of Post–Transcatheter Aortic Valve Replacement PAPi
Kaplan-Meier analysis of all-cause mortality and heart failure hospitalization with lower and higher post–transcatheter aortic valve replacement pulmonary artery pulsatility index (PAPi). Patients with PAPi <3.11 (lower PAPi) experienced more events than patients with PAPi >3.11 (higher PAPi).
Figure 3.
Secondary Outcome According to the Level of Post–Transcatheter Aortic Valve Replacement PAPi
Kaplan-Meier analysis of all-cause mortality with lower and higher post–transcatheter aortic valve replacement pulmonary artery pulsatility index (PAPi). All-cause mortality was significantly increased in lower PAPi group.
Cox proportional hazard analyses were performed to predict the primary endpoint (Table 3). In the univariate Cox proportional hazards analysis, atrial fibrillation (HR: 2.50; 95% CI: 1.24-5.06; P = 0.011), chronic kidney disease (HR: 2.96; 95% CI: 1.15-7.64; P = 0.025), pre-TAVR tricuspid regurgitation (TR) moderate or greater (HR: 2.08; 95% CI: 1.07-9.06; P = 0.030), new pacemaker implantation (HR: 2.64; 95% CI: 1.01-6.87; P = 0.005), acute kidney injury (HR: 14.8; 95% CI: 5.00-43.9; P < 0.001), and post-TAVR PAPi <3.11 (HR: 3.36; 95% CI: 1.66-6.81; P < 0.001) were associated with increased primary endpoint. Multivariate Cox proportional hazard analysis was performed with transfemoral approach, atrial fibrillation, post-TAVR aortic regurgitation moderate or greater, new pacemaker implantation, acute kidney injury, prosthesis–patient mismatch (ie, indexed effective orifice area <0.85 cm2/m2), and post-TAVR PAPi <3.11 as covariates that affected the post-TAVR prognosis.14, 15, 16, 17, 18 In the multivariate analysis, post-TAVR PAPi <3.11 was a predictive factor for the primary endpoint (HR: 3.04; 95% CI: 1.30-7.13; P = 0.011). Furthermore, in the multivariate analysis using covariates that were significant in the univariate analysis, post-TAVR PAPi <3.11 was still significantly predictive of the primary endpoint (HR: 2.80; 95% CI: 1.33-5.88; P = 0.007) (Supplemental Table 1).
Table 3.
Univariate and Multivariate Cox Regression Analyses of the Primary Endpoint
| Univariate |
Multivariate |
|||||
|---|---|---|---|---|---|---|
| HR | 95% CI | P Value | HR | 95% CI | P Value | |
| Post-TAVR PAPi <3.11 | 3.36 | 1.66-6.81 | <0.001 | 3.04 | 1.30-7.13 | 0.011 |
| Pre-TAVR PAPi <3.11 | 0.67 | 0.33-1.34 | 0.253 | |||
| Age | 0.96 | 0.33-1.34 | 0.195 | |||
| Atrial fibrillation | 2.50 | 1.24-5.06 | 0.011 | 3.45 | 1.52-7.82 | 0.003 |
| Chronic kidney disease | 2.96 | 1.15-7.64 | 0.025 | |||
| Transfemoral approach | 0.69 | 0.27-1.80 | 0.452 | 0.83 | 0.25-2.70 | 0.757 |
| Pre-TAVR AR moderate or greater | 2.99 | 0.90-9.90 | 0.074 | |||
| Pre-TAVR MR moderate or greater | 1.59 | 0.56-4.52 | 0.387 | |||
| Pre-TAVR TR moderate or greater | 2.08 | 1.07-9.06 | 0.032 | |||
| Pre-TAVR AV peak pressure gradient | 0.99 | 0.97-1.00 | 0.030 | |||
| Pre-TAVR AV mean pressure gradient | 0.98 | 1.00-1.02 | 0.080 | |||
| Post-TAVR AR moderate or greater | 1.23 | 0.30-5.46 | 0.736 | 2.19 | 0.48-10.1 | 0.313 |
| Post-TAVR MR moderate or greater | 3.12 | 1.08-9.06 | 0.036 | |||
| Post-TAVR TR moderate or greater | 2.63 | 0.62-11.14 | 0.188 | |||
| Post-TAVR AV peak pressure gradient | 1.01 | 0.97-1.05 | 0.432 | |||
| Post-TAVR AV mean pressure gradient | 0.99 | 0.94-1.03 | 0.542 | |||
| Pacemaker implantation in hospital | 2.64 | 1.01-6.87 | 0.005 | 5.32 | 1.63-17.4 | 0.006 |
| Acute kidney injury | 14.80 | 5.00-43.9 | <0.001 | 12.2 | 2.45-60.8 | 0.002 |
| Prosthesis-patient mismatch (iEOA <0.85) | 1.92 | 0.91-4.05 | 0.085 | 1.99 | 0.91-4.36 | 0.084 |
Factors associated with nonimproved or unchanged pre- and post-TAVR PAPi
Comparing pre- and post-TAVR PAPi, the PAPi increased after TAVR (from 3.92 to 5.43; P < 0.001). To investigate whether pre- and post-TAVR PAPi changes could predict the endpoints, patients were divided into 4 groups based on perioperative PAPi changes (Supplemental Table 2). Compared with group 4, group 2 was associated with a reduction in the occurrence of the primary endpoint (group 2 vs group 4; HR: 3.76; 95% CI: 1.44-9.83; log-rank; P = 0.004) (Supplemental Figure 1). There were no statistically significant differences between group 1 patients and group 3 patients. (group 1 vs group 3; HR: 0.34; 95% CI: 0.11-1.08; log-rank P = 0.056).
The 160 patients had improved PAPi post-TAVR, whereas 78 patients did not. To investigate the factors that nonimproved or no changed pre- and post-TAVR PAPi, patients were divided into 2 groups: those whose post-TAVR PAPi improve and those whose did not improve or did not change (Table 4). Univariate and multivariate logistic regression analyses were performed to evaluate factors predicting nonimproved PAPi (Table 5). In the univariate analysis, the predictors of nonimproved PAPi were pre-TAVR aortic valve pressure gradient (OR: 1.01; 95% CI: 1.01-1.02; P = 0.003), pre-TAVR aortic valve mean pressure gradient (OR: 1.02; 95% CI: 1.01-1.03; P = 0.007), pre-TAVR mitral regurgitation (MR) moderate or greater (OR: 2.76; 95% CI: 1.09-6.96; P = 0.032), and post-TAVR pulmonary hypertension (OR: 2.08; 95% CI: 1.13-3.84; P = 0.019). Multivariate analysis was performed with variables identified in univariate analysis, atrial fibrillation, post-TAVR MR moderate or greater, post-TAVR TR moderate or greater, and chronic kidney disease.7,8 In the multivariate analysis, pre-TAVR aortic valve mean pressure gradient was a predictor of nonimproved PAPi (OR: 1.02; 95% CI: 1.01-1.04; P = 0.003).
Table 4.
Baseline Characteristics of Post-TAVR PAPi Improved and Nonimproved Groups
| Improved PAPi (n = 160) | No Improvement/No Change PAPi (n = 78) | P Value | |
|---|---|---|---|
| Age, y | 84.0 ± 5.10 | 84.2 ± 5.32 | 0.834 |
| Male | 50 (31.4) | 19 (24.36) | 0.291 |
| Body mass index, kg/m2 | 23.0 ± 3.59 | 22.2 ± 3.85 | 0.124 |
| NYHA functional class ≥III | 66 (41.3) | 35 (44.9) | 0.675 |
| Clinical frailty scale score ≥4 | 116 (74.8) | 56 (75.7) | 1.000 |
| STS score, % | 6.28 ± 2.88 | 6.47 ± 3.46 | 0.891 |
| Hypertension | 142 (88.8) | 68 (87.2) | 0.831 |
| Dyslipidemia | 99 (61.9) | 43 (55.1) | 0.328 |
| Diabetes mellitus | 54 (33.8) | 12 (15.4) | 0.003 |
| Chronic kidney disease | 114 (71.3) | 50 (64.1) | 0.297 |
| Atrial fibrillation | 35 (21.9) | 15 (19.2) | 0.736 |
| Coronary artery disease | 47 (29.4) | 18 (23.1) | 0.354 |
| Previous percutaneous coronary intervention | 21 (13.1) | 7 (9.0) | 0.399 |
| Previous coronary artery bypass grafting | 7 (4.4) | 1 (1.3) | 0.200 |
| Peripheral artery disease | 19 (11.9) | 6 (7.7) | 0.375 |
| Previous pacemaker implantation | 9 (5.6) | 3 (3.9) | 0.756 |
| History of stroke | 26 (16.3) | 15 (19.2) | 0.586 |
| Previous cardiac surgery | 8 (5.0) | 2 (2.6) | 0.505 |
| Echocardiography | |||
| Left ventricular ejection fraction, % | 61.7 ± 0.71 | 62.2 ± 1.01 | 0.804 |
| AV peak velocity, m/s | 4.61 ± 0.70 | 4.73 ± 0.81 | 0.221 |
| AV peak pressure gradient, mm Hg | 86.8 ± 26.6 | 91.7 ± 30.9 | 0.248 |
| AV mean pressure gradient, mm Hg | 50.2 ± 17.5 | 54.0 ± 19.8 | 0.134 |
| Aortic valve area, cm2 | 0.68 ± 0.20 | 0.64 ± 0.20 | 0.210 |
| Aortic valve area index, cm2/m2 | 0.46 ± 0.14 | 0.45 ± 0.15 | 0.407 |
| Aortic regurgitation moderate or greater | 8 (5.0) | 3 (3.9) | 1.000 |
| Mitral regurgitation moderate or greater | 9 (5.6) | 11 (14.1) | 0.044 |
| Tricuspid regurgitation moderate or greater | 42 (26.2) | 27 (35.1) | 0.174 |
| Laboratory data | |||
| Hemoglobin, g/dL | 12.2 ± 1.61 | 11.7 ± 1.70 | 0.203 |
| CRP, mg/dL | 0.25 ± 0.62 | 0.31 ± 0.61 | 0.489 |
| Creatinine, mg/dL | 0.95 ± 0.34 | 0.92 ± 0.35 | 0.282 |
| eGFR, mL/min/1.73 m2 | 52.6 ± 17.1 | 53.4 ± 15.6 | 0.517 |
| NT-proBNP, pg/mL | 996 (389-2,409) | 1,554 (547-2,724) | 0.139 |
| Hemodynamic data | |||
| AV peak pressure gradient, mm Hg | 63.9 ± 29.7 | 78.2 (35.6) | 0.003 |
| AV mean pressure gradient, mm Hg | 55.7 ± 20.7 | 64.7 ± 24.8 | 0.010 |
| Systolic arterial pressure, mm Hg | 134.8 ± 24.3 | 130.0 ± 24.7 | 0.093 |
| Diastolic arterial pressure, mm Hg | 63.2 ± 12.5 | 67.4 ± 14.0 | 0.048 |
| Mean arterial pressure, mm Hg | 87.1 ± 13.9 | 88.4 ± 15.6 | 0.722 |
| Heart rate, beats/min | 69.8 ± 11.2 | 69.0 ± 12.2 | 0.546 |
| Cardiac index, L/min/m2 | 2.33 ± 0.64 | 2.35 ± 0.64 | 0.789 |
| Systolic pulmonary artery pressure, mm Hg | 30.2 ± 9.56 | 28.6 ± 8.13 | 0.309 |
| Diastolic pulmonary artery pressure, mm Hg | 14.2 ± 5.38 | 11.4 ± 5.09 | <0.001 |
| Mean pulmonary artery pressure, mm Hg | 20.7 ± 6.94 | 18.2 ± 6.41 | 0.006 |
| Right atrium pressure, mm Hg | 7.09 ± 3.28 | 4.14 ± 2.25 | <0.001 |
| PAPi | 2.83 ± 1.86 | 6.13 ± 5.29 | <0.001 |
Values are mean ± SD, n (%), or median (Q1-Q3).
Abbreviations as in Table 1.
Table 5.
Univariate and Multivariate Logistic Regression Analyses of Nonimproved PAPi
| Univariate |
Multivariate |
|||||
|---|---|---|---|---|---|---|
| OR | 95% CI | P Value | OR | 95% CI | P Value | |
| Age | 1.009 | 0.057-1.623 | 0.754 | |||
| Atrial fibrillation | 0.850 | 0.432-1.672 | 0.639 | 0.402 | 0.159-1.024 | 0.053 |
| Chronic obstructive pulmonary disease | 0.928 | 0.311-2.769 | 0.893 | |||
| Chronic kidney disease | 0.720 | 0.405-1.281 | 0.264 | 0.691 | 0.361-1.322 | 0.265 |
| Coronary artery disease | 0.721 | 0.385-1.350 | 0.307 | |||
| Pre-TAVR AR moderate or greater | 0.760 | 0.196-2.948 | 0.692 | |||
| Pre-TAVR MR moderate or greater | 2.755 | 1.090-6.959 | 0.032 | 2.925 | 0.703-12.167 | 0.140 |
| Pre-TAVR TR moderate or greater | 0.828 | 0.157-4.370 | 0.824 | |||
| Pre-TAVR AV peak pressure gradient | 1.014 | 1.005-1.023 | 0.003 | |||
| Pre-TAVR AV mean pressure gradient | 1.018 | 1.005-1.031 | 0.007 | 1.022 | 1.008-1.036 | 0.003 |
| Post-TAVR AR moderate or greater | 0.990 | |||||
| Post-TAVR MR moderate or greater | 2.194 | 0.790-6.095 | 0.132 | 0.668 | 0.134-3.34 | 0.624 |
| Post-TAVR TR moderate or greater | 0.828 | 0.157-4.370 | 0.824 | 1.668 | 0.224-12.408 | 0.618 |
| Post-TAVR AV peak pressure gradient, mm Hg | 0.999 | 0.963-1.036 | 1.001 | |||
| Post-TAVR AV mean pressure gradient, mm Hg | 1.023 | 0.982-1.067 | 0.977 | |||
| Pacemaker implantation in hospital | 0.442 | 0.093-2.094 | 0.303 | |||
| Acute kidney injury | 2.093 | 0.412-10.618 | 0.373 | |||
| Prosthesis-patient mismatch (iEOA <0.85) | 1.003 | 0.556-1.808 | 0.993 | |||
| Pre-TAVR pulmonary hypertension | 0.696 | 0.402-1.203 | 0.194 | |||
| Post-TAVR pulmonary hypertension | 2.081 | 1.128-3.839 | 0.019 | 1.840 | 0.828-4.087 | 0.134 |
Discussion
This study investigated whether pre- and post-TAVR PAPi predicts all-cause mortality and heart failure hospitalization. This study mainly revealed the following:
-
1.
A lower PAPi defined as post-TAVR PAPi <3.11 was associated with a higher incidence of all-cause mortality and heart failure hospitalization (Central Illustration). After multivariate analysis, a lower PAPi was still predictive of the primary endpoint.
-
2.
The pre- and post-TAVR PAPi change was associated with all-cause mortality and heart failure hospitalization. The rate of event was higher in the group with pre-TAVR PAPi <3.11 but whose PAPi did not improve post-TAVR than in the group with improved post-TAVR PAPi.
-
3.
In the univariate analysis, pre-TAVR MR moderate or greater, pre-TAVR aortic valve mean pressure gradient and post-TAVR pulmonary hypertension were predictors of nonimproved PAPi. In the multivariate analysis, pre-TAVR aortic valve mean pressure gradient was a predictor of nonimproved PAPi. To the best of our knowledge, no studies have followed changes pre- and post-TAVR and evaluated the association between RV function using PAPi and prognosis.
Central Illustration.
Prognostic Value of Post–Transcatheter Aortic Valve Replacement Pulmonary Artery Pulsatility Index
A lower pulmonary artery pulsatility index (PAPi) was associated with an increased risk of the primary endpoints, including all-cause mortality and hospitalization caused by heart failure and secondary endpoint of all-cause mortality. TAVR = transcatheter aortic valve replacement.
RV function as a prognosis predictor in patients with AS after TAVR
After they underwent TAVR, certain patients have symptoms that do not improve or have post-TAVR cardiac events.19,20 The number of patients undergoing TAVR is expected to increase3; thus, classifying the risk of post-TAVR cardiac events is important. Genereux et al12 reported a staging classification of cardiac damage assessed by echocardiography in patients with AS. Cardiac damage is classified as no cardiac damage (stage 0), left ventricular damage (stage 1), left atrial or mitral damage (stage 2), pulmonary vasculature or tricuspid valve damage (stage 3), or RV damage (stage 4). They reported that at 1-year post-TAVR or surgical aortic valve replacement, the rates of all-cause death and cardiac death significantly increased with each stage of worsening cardiac damage.12 Furthermore, Vollema et al4 reported that in patients treated with surgical or TAVR, stage 4 damage was significantly associated with both postoperative all-cause mortality and the combined outcome of all-cause mortality, stroke, and cardiac-related hospitalization. However, Koifman et al21 reported that preoperative RV dysfunction, defined by decreased tricuspid annular plane systolic excursion or change in RV fractional area, in patients with severe AS was not correlated with 1-year post-TAVR prognosis. In contrast, Galli et al22 reported that RV dysfunction, defined by decreased tricuspid annular plane systolic excursion, complicated by pre-TAVR left ventricular dysfunction was a predictor of post-TAVR mortality. Conflicting results have been reported on the association between RV dysfunction assessed by echocardiography and prognosis. The inconsistent results may be caused by the lack of the gold standard modality for accurate assessment of RV dysfunction. RV function is often assessed by echocardiography; however, accurate delineation of the right ventricle is difficult because of the complex anatomy of the RV.23 In this study, we focused on PAPi, an index that can be easily calculated from the results of RHC.
Association between PAPi and heart disease prognosis
PAPi is the ratio of the pulmonary artery pulse pressure divided by RAP and is often used in clinical practice to assess RV function in patients with cardiogenic shock.24 The physiological basis for PAPi as an index of RV function is that pulmonary artery pulse pressure is an indirect indicator of RV systolic function, and high RAP is a sign of RV failure.13 In patients with a more homogeneous pulmonary arterial and left heart status, the ratio of stroke volume to RAP becomes the dominant determinant of PAPi.13 Therefore, PAPi is a proxy for the Frank–Starling relationship in the RV.13 There are several reports of an association between PAPi and the prognosis of patients with heart disease. Korabathina et al9 reported that PAPi of ≤0.9 predicts in-hospital death or the necessity of a percutaneous RV support device in patients with acute myocardial infarction caused by proximal right coronary artery occlusion with RV infarction. Essandoh et al10 reported a systematic review of 32 studies that examined the association between PAPi and RV failure in patients who underwent left ventricular assist device implantation. They reported that patients who experienced RV failure had significantly lower preoperative PAPi than those who did not, with a mean preoperative PAPi of 2.17 in those with RV failure and 2.87 in those without RV failure. Kochav et al25 reported on the prognostic value of PAPi in patients with advanced acute heart failure using the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness trial cohort. They reported that PAPi <3.65 was a predictor of mortality and readmission rates for 6 months.
All these studies have reported the prognostic utility of PAPi; however, the reported cutoff PAPi values were different. This may be because PAPi is composed of multiple factors. Pulmonary artery pulse pressure, a component of PAPi, is determined by pulmonary artery compliance and stroke volume, and pulmonary artery compliance is influenced by pulmonary artery wedge pressure.26 PAPi is determined by RAP, pulmonary artery wedge pressure, pulmonary artery compliance, and stroke volume. Given its multiple components, establishing a universal cutoff value is difficult. The cutoff PAPi value should be considered for each patient population.
For patient populations with severe AS, the association between pre-TAVR PAPi and prognosis has been reported. According to Oshima et al,27 patients with pre-TAVR PAPi <2.1 had a higher rate of heart failure hospitalization 2 years postoperatively. Huang et al28 reported that a pre-TAVR PAPi <1.8 in emergency TAVR is a predictor of increased in-hospital mortality. Previous studies have examined the association between pre-TAVR PAPi and prognosis but have not analyzed changes in post-TAVR PAPi. In this study, the ROC analysis of post-TAVR PAPi revealed 3.11 as the best PAPi cutoff. The PAPi value in this study was higher than those in previous reports. In this study, a lower PAPi after TAVR was associated with worse clinical outcomes.
RV function assessed by echocardiography is altered after TAVR, and changes in RV function are useful in predicting post-TAVR prognosis. Asami et al7 reported that 57.4% of patients with RV dysfunction at baseline recovered it after TAVR. Poch et al8 reported that 46% of patients with RV dysfunction at baseline had improved post-TAVR RV function, and the group with improved RV function had a better prognosis than the group without. All these studies have used echocardiography to assess RV function and reported that improved RV function post-TAVR was associated with a favorable prognosis. In this study, among the groups with pre-TAVR PAPi <3.11, no improvement in post-TAVR RV function assessed by PAPi was associated with poor prognosis, similar to previous studies assessed by echocardiographic.
In addition, pre-TAVR aortic valve pressure gradient, pre-TAVR MR moderate or greater, and post-TAVR pulmonary hypertension were predictors of nonimproved PAPi in univariate analysis. Miyamoto et al29 reported that post-TAVR residual pulmonary hypertension was a prognosis predictor of clinical outcome. They also reported that atrial fibrillation and pre-TAVR TR moderate or greater were predictors of residual pulmonary hypertension, and patients with residual pulmonary hypertension were at a more advanced stage of cardiac damage at the time of TAVR. This report indicates that improving RV function in patients with advanced cardiac damage is more challenging than those without advanced cardiac damage. In this study, after multivariate analysis, pre-TAVR aortic valve mean pressure gradient was found to be a predictor of nonimproved PAPi. A greater pressure gradient represents AS severity, which may contribute to the progression of cardiac damage, and pre-TAVR cardiac damage may contribute to lower post-TAVR PAPi. In addition, the presence of prosthesis–patient mismatch is a predictor of new-onset pulmonary hypertension after TAVR.29 Sinning et al30 reported that patients diagnosed with new-onset severe pulmonary hypertension after TAVR had moderate to severe paravalvular leak.30 Although no significant differences in prosthesis–patient mismatch and post-TAVR AR, including paravalvular leak, were observed between groups according to PAPi changes, prosthesis–patient mismatch and paravalvular leak may cause pulmonary hypertension, which may subsequently cause RV dysfunction or non-improvement.
In this study, post-TAVR PAPi <3.11 was associated with an increased risk of all-cause mortality and heart failure hospitalization, and the group with an increased post-TAVR PAPi had a lower incidence of all-cause mortality and heart failure hospitalization than the group with post-TAVR PAPi that remained low. These findings suggest that improvement of RV function after TAVR may lead to a better prognosis. The PAPi used in the present study can be calculated with a simple formula; thus, it was a useful parameter for predicting post-TAVR prognosis. Given that post-TAVR PAPi was identified as a prognostic predictor, more studies are needed to investigate the causes of lower post-TAVR PAPi for patient risk classification.
Study limitations
First, this study was a single-center, retrospective, observational study of Japanese patients. Second, only patients who underwent pre- and post-TAVR RHC were included. Because the decision to perform RHC pre-TAVR was at the discretion of each attending physician and several RHC data post-TAVR could not be measured caused by accidental removal, delirium, or catheter malfunction, RHC data pre- or post-TAVR in 150 patients were not available. Therefore, selection bias could not be excluded. Third, this study excluded patients who underwent planned mitral valve transcatheter edge-to-edge repair after TAVR. Therefore, it was difficult to examine the effect of MR on PAPi. Fourth, there is no universal reference value for PAPi, and the reference value may vary depending on the disease group and endpoint. Therefore, even among patients undergoing TAVR, the best cutoff for PAPi may vary depending on the proportion of patients with a history of myocardial infarction or other cardiac diseases. Fifth, the sample size was relatively small, especially in the subgroup analysis, because this study was a retrospective study. Therefore, the performance of the ROC analysis to determine the best cutoff value of PAPi was low. If a larger sample size were obtained, the performance of the ROC analysis would improve; however, the best cutoff value of PAPi may change. Sixth, data on changes in medications after discharge were not available. Therefore, we could not rule out a prognostic effect of changes in basic heart failure medications such as beta-blockers and angiotensin-converting enzyme inhibitors. However, at least the discharge prescription medications did not differ between all groups. Finally, tricuspid annular plane systolic excursion and RV fractional area change, measures of RV function assessed by echocardiography, were not evaluated, and the prognostic value of PAPi compared with echocardiography could not be determined.
Conclusions
Decreased post-TAVR RV function as indicated by PAPi <3.11 was associated with an increased risk of all-cause mortality and heart failure hospitalization. The PAPi may be useful for risk stratification of patients with AS after TAVR.
Funding Support and Author Disclosures
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Acknowledgments
The authors did not use an artificial intelligence program.
Footnotes
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the Author Center.
Appendix
For supplemental tables and a figure, please see the online version of this paper.
Appendix
References
- 1.Mack M.J., Leon M.B., Thourani V.H., et al. Transcatheter aortic-valve replacement with a balloon-expandable valve in low-risk patients. N Engl J Med. 2019;380:1695–1705. doi: 10.1056/NEJMoa1814052. [DOI] [PubMed] [Google Scholar]
- 2.Popma J.J., Deeb G.M., Yakubov S.J., et al. Transcatheter aortic-valve replacement with a self-expanding valve in low-risk patients. N Engl J Med. 2019;380:1706–1715. doi: 10.1056/NEJMoa1816885. [DOI] [PubMed] [Google Scholar]
- 3.Yoshimura N., Sato Y., Takeuchi H., et al. Committee for Scientific Affairs, The Japanese Association for Thoracic Surgery. Thoracic and cardiovascular surgeries in Japan during 2021: annual report by the Japanese Association for Thoracic Surgery. Gen Thorac Cardiovasc Surg. 2024;72:254–291. doi: 10.1007/s11748-023-01997-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Vollema E.M., Amanullah M.R., Ng ACT, et al. Staging cardiac damage in patients with symptomatic aortic valve stenosis. J Am Coll Cardiol. 2019;74:538–549. doi: 10.1016/j.jacc.2019.05.048. [DOI] [PubMed] [Google Scholar]
- 5.Ren B., Spitzer E., Geleijnse M.L., et al. Right ventricular systolic function in patients undergoing transcatheter aortic valve implantation: a systematic review and meta-analysis. Int J Cardiol. 2018;257:40–45. doi: 10.1016/j.ijcard.2018.01.117. [DOI] [PubMed] [Google Scholar]
- 6.de Jongh M.C., Tsuruta H., Hayashida K., et al. Right ventricular dysfunction in patients with concomitant tricuspid regurgitation undergoing transcatheter aortic valve implantation. Circ J. 2024;88:451–459. doi: 10.1253/circj.CJ-22-0262. [DOI] [PubMed] [Google Scholar]
- 7.Asami M., Stortecky S., Praz F., et al. Prognostic value of right ventricular dysfunction on clinical outcomes after transcatheter aortic valve replacement. JACC Cardiovasc Imaging. 2019;12:577–587. doi: 10.1016/j.jcmg.2017.12.015. [DOI] [PubMed] [Google Scholar]
- 8.Poch F., Thalmann R., Olbrich I., et al. Changes of right ventricular function after transcatheter aortic valve replacement and association with outcomes. J Card Fail. 2021;27:1337–1344. doi: 10.1016/j.cardfail.2021.03.007. [DOI] [PubMed] [Google Scholar]
- 9.Korabathina R., Heffernan K.S., Paruchuri V., et al. The pulmonary artery pulsatility index identifies severe right ventricular dysfunction in acute inferior myocardial infarction. Catheter Cardiovasc Interv. 2012;80:593–600. doi: 10.1002/ccd.23309. [DOI] [PubMed] [Google Scholar]
- 10.Essandoh M., Kumar N., Hussain N., et al. Pulmonary artery pulsatility index as a predictor of right ventricular failure in left ventricular assist device recipients: a systematic review. J Heart Lung Transplant. 2022;41:1114–1123. doi: 10.1016/j.healun.2022.04.007. [DOI] [PubMed] [Google Scholar]
- 11.Otto C.M., Nishimura R.A., Bonow R.O., et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association joint committee on clinical practice guidelines. J Am Coll Cardiol. 2021;77(4):e25–e197. doi: 10.1016/j.jacc.2020.11.018. [DOI] [PubMed] [Google Scholar]
- 12.Genereux P., Pibarot P., Redfors B., et al. Staging classification of aortic stenosis based on the extent of cardiac damage. Eur Heart J. 2017;38:3351–3358. doi: 10.1093/eurheartj/ehx381. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Lim H.S., Gustafsson F. Pulmonary artery pulsatility index: physiological basis and clinical application. Eur J Heart Fail. 2020;22:32–38. doi: 10.1002/ejhf.1679. [DOI] [PubMed] [Google Scholar]
- 14.Sannino A., Gargiulo G., Schiattarella G.G., et al. A meta-analysis of the impact of pre-existing and new-onset atrial fibrillation on clinical outcomes in patients undergoing transcatheter aortic valve implantation. EuroIntervention. 2016;12:e1047–e1056. doi: 10.4244/EIJY15M11_12. [DOI] [PubMed] [Google Scholar]
- 15.Avvedimento M., Tang G.H.L. Transcatheter aortic valve replacement (TAVR): recent updates. Prog Cardiovasc Dis. 2021;69:73–83. doi: 10.1016/j.pcad.2021.11.003. [DOI] [PubMed] [Google Scholar]
- 16.Moriyama N., Laakso T., Raivio P., et al. Acute kidney injury following aortic valve replacement in patients without chronic kidney disease. Can J Cardiol. 2021;37:37–46. doi: 10.1016/j.cjca.2020.03.015. [DOI] [PubMed] [Google Scholar]
- 17.Compagnone M., Marchetti G., Taglieri N., et al. Long-term outcome of prosthesis-patient mismatch after transcatheter aortic valve replacement. Int J Cardiol. 2020;318:27–31. doi: 10.1016/j.ijcard.2020.06.033. [DOI] [PubMed] [Google Scholar]
- 18.Sá M.P., Jacquemyn X., Sun T., et al. Late outcomes of permanent pacemaker implantation after TAVR: meta-analysis of reconstructed time-to-event data. J Soc Cardiovasc Angiogr Interv. 2022;1 doi: 10.1016/j.jscai.2022.100434. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19.Kapadia S.R., Leon M.B., Makkar R.R., et al. 5-year outcomes of transcatheter aortic valve replacement compared with standard treatment for patients with inoperable aortic stenosis (PARTNER 1): a randomised controlled trial. Lancet. 2015;385:2485–2491. doi: 10.1016/S0140-6736(15)60290-2. [DOI] [PubMed] [Google Scholar]
- 20.Reynolds M.R., Magnuson E.A., Wang K., et al. Health-related quality of life after transcatheter or surgical aortic valve replacement in high-risk patients with severe aortic stenosis: results from the PARTNER (placement of AoRTic TraNscathetER valve) trial (Cohort A) J Am Coll Cardiol. 2012;60:548–558. doi: 10.1016/j.jacc.2012.03.075. [DOI] [PubMed] [Google Scholar]
- 21.Koifman E., Didier R., Patel N., et al. Impact of right ventricular function on outcome of severe aortic stenosis patients undergoing transcatheter aortic valve replacement. Am Heart J. 2017;184:141–147. doi: 10.1016/j.ahj.2016.09.018. [DOI] [PubMed] [Google Scholar]
- 22.Galli E., Guirette Y., Feneon D., et al. Prevalence and prognostic value of right ventricular dysfunction in severe aortic stenosis. Eur Heart J Cardiovasc Imaging. 2015;16:531–538. doi: 10.1093/ehjci/jeu290. [DOI] [PubMed] [Google Scholar]
- 23.Zaidi A., Knight D.S., Augustine D.X., et al. Echocardiographic assessment of the right heart in adults: a practical guideline from the British Society of Echocardiography. Echo Res Pract. 2020;7:G19–G41. doi: 10.1530/ERP-19-0051. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 24.Tehrani B.N., Truesdell A.G., Sherwood M.W., et al. Standardized team-based care for cardiogenic shock. J Am Coll Cardiol. 2019;73:1659–1669. doi: 10.1016/j.jacc.2018.12.084. [DOI] [PubMed] [Google Scholar]
- 25.Kochav S.M., Flores R.J., Truby L.K., Topkara V.K. Prognostic impact of pulmonary artery pulsatility index (PAPi) in patients with advanced heart failure: insights from the ESCAPE trial. J Card Fail. 2018;24:453–459. doi: 10.1016/j.cardfail.2018.03.008. [DOI] [PubMed] [Google Scholar]
- 26.Tedford R.J., Hassoun P.M., Mathai S.C., et al. Pulmonary capillary wedge pressure augments right ventricular pulsatile loading. Circulation. 2012;125:289–297. doi: 10.1161/CIRCULATIONAHA.111.051540. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 27.Oshima A., Imamura T., Tanaka S., et al. Prognostic implication of pulmonary artery pulsatility index before transcatheter aortic valve replacement. Cardiovasc Diagn Ther. 2022;12:188–195. doi: 10.21037/cdt-21-682. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 28.Huang H., Kovach C.P., Bell S., et al. Outcomes of emergency transcatheter aortic valve replacement. J Interv Cardiol. 2019;2019 doi: 10.1155/2019/7598581. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 29.Miyamoto J., Ohno Y., Kamioka N., et al. Impact of periprocedural pulmonary hypertension on outcomes after transcatheter aortic valve replacement. J Am Coll Cardiol. 2022;80:1601–1613. doi: 10.1016/j.jacc.2022.08.757. [DOI] [PubMed] [Google Scholar]
- 30.Sinning J.M., Hammerstingl C., Chin D., et al. Decrease of pulmonary hypertension impacts on prognosis after transcatheter aortic valve replacement. EuroIntervention. 2014;9:1042–1049. doi: 10.4244/EIJV9I9A177. [DOI] [PubMed] [Google Scholar]
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