Abstract
Background: Right ventricular (RV) dysfunction negatively affects mitral valve transcatheter edge-to-edge repair (M-TEER) outcomes in patients with ventricular secondary mitral regurgitation (vSMR). However, RV dysfunction occurs in the late phase of heart failure, when it may not respond to interventions. The pulsatile component of RV afterload, pulmonary artery (PA) compliance, is a sensitive parameter that decreases before RV dysfunction occurs. We explored the utility of PA compliance in predicting cardiac events after M-TEER.
Methods and Results: We analyzed 107 patients with vSMR who underwent M-TEER and in whom right heart catheter parameters were measured in a conscious state. Twenty-four patients had a cardiac event. There were no differences in patient characteristics or echocardiographic parameters between groups with and without cardiac events. PA compliance was significantly reduced in the event group, but other RV function parameters did not differ between the 2 groups. Receiver operating characteristic curve analysis revealed an optimal prognostic cut-off value for PA compliance of 2.7 mL/mmHg. In multivariate Cox regression, reduced PA compliance (<2.7 mL/mmHg) was strongly associated with cardiac events. Kaplan-Meier analysis revealed PA compliance had significant prognostic power for the composite outcome of cardiac events (log-rank P<0.01).
Conclusions: Reduced PA compliance (hemodynamically derived in the conscious state) was a strong prognostic indicator in patients with vSMR who underwent M-TEER.
Although mitral valve transcatheter edge-to-edge repair (M-TEER) for ventricular secondary mitral regurgitation (vSMR) was proven to reduce rehospitalization and mortality in the COAPT (Cardiovascular Outcomes Assessment of the MitraClip Percutaneous Therapy for Heart Failure Patients With Functional Mitral Regurgitation) trial, >30% of those patients who underwent M-TEER were hospitalized for heart failure within 1 year even after M-TEER treatment.1,2 Previous studies have suggested that the presence of right ventricular (RV) dysfunction detected by echocardiography, such as RV-pulmonary artery (PA) uncoupling before the procedure, negatively affects outcomes in patients undergoing M-TEER.3–6 However, echocardiographic measurement of RV function measurement is technically demanding and can be limited, especially in the case of various preload conditions and in the presence of tricuspid regurgitation (TR).7 Moreover, RV dysfunction appears in the late phase of heart failure, when patients may not respond to M-TEER. PA compliance, a pulsatile component of RV afterload, decreases early in the disease process when pulmonary vascular resistance is normal and is a sensitive parameter to detect cardiac event before RV dysfunction occurs.8
The aim of this study was to explore the utility of preprocedural invasive hemodynamic assessment in vSMR patients to predict cardiac events after M-TEER.
Methods
Study Population
This study is a retrospective analysis of data from a single center. We reviewed 182 consecutive patients with symptomatic mitral regurgitation (MR) who were admitted to the National Cerebral and Cardiovascular Center and underwent M-TEER with the MitraClipTM
system (Abbott Vascular, Santa Clara, CA, USA) between October 2015 and January 2023. All patients were symptomatic with Grade 3/4+ MR and were considered suitable for the MitraClip procedure by our heart team. Patients with cardiogenic shock who need mechanical support or who were inotrope dependent were not included in the study because M-TEER with the MitraClipTM
system in these patients is off-label use according to the Ministry of Health, Labor, and Welfare of Japan. The study flowchart is shown in Figure 1. Patients with primary MR with preserved ejection fraction ≥50%, dynamic MR with less than moderate MR at rest, residual MR Grade 3/4+ after the MitraClip procedure and/or no right heart catheterization performed in a stable condition before M-TEER were excluded from the study. We defined as primary MR as the presence of some sort of leaflet degeneration, such as mitral valve billowing or the myxomatous change, leaflet degeneration with reduced ejection fraction (left ventricular ejection fraction [LVEF] <50%), known as mixed etiology, was defined as secondary MR, as in a previous study.9
After applying the exclusion criteria, there were 107 patients with vSMR who underwent right heart catheterization in a stable state before M-TEER who were included in this study. Clinical data, including patient characteristics, laboratory data, heart failure etiology, Society of Thoracic Surgeons predicted risk of mortality (STS) score, echocardiography data, and medications, were collected on admission. All patients underwent transthoracic echocardiography before M-TEER. Baseline MR severity was assessed using quantitative assessment (regurgitant fraction and volume using the volumetric method). Tricuspid annular plane systolic excursion (TAPSE) was evaluated in an apical 4-chamber view with M-mode ultrasound to measure the displacement of the tricuspid annular plane in the longitudinal direction towards the RV apex. RV-PA coupling was assessed by dividing TAPSE by echocardiographic PA systolic pressure, obtained by estimating the peak systolic TR gradient from the peak TR velocity using the Bernoulli equation and adding the estimated right atrial pressure, as described previously.3
Hemodynamic Parameters
Right-sided heart catheterization was performed in the cardiac catheterization laboratory while patients were conscious and stable, as per our routine preprocedural evaluation, within 1 month before M-TEER. Cardiac pressure was measured for at least 3 and 5 beats at end-expiration for sinus and atrial fibrillation rhythms, respectively. Pressure measurements were confirmed by typical waveforms using a balloon-tipped Swan-Ganz catheter while patients were supine. Care was taken to avoid Valsalva maneuvers during measurements. The variables measured were the mean and V wave of pulmonary capillary wedge pressure (m/vPCWP), PA systolic pressure (PASP), mean PA pressure (mPAP), PA diastolic pressure (PADP), and mean right atrial pressure (mRAP). Cardiac output (CO) was calculated using the direct Fick method as the current gold standard, with the cardiac index (CI) calculated by dividing CO by body surface area. Oxygen uptake and ventilatory gas exchange were measured using a custom breath-by-breath system (AE-310S; Minato Medical Science). Hemodynamic formulas for assessing RV function have been proposed previously.10 Stroke volume (SV) was calculated by dividing CO by heart rate, and SV index was divided by body surface area. The hemodynamic formulas used to evaluate RV function and RV afterload indices in the present study were as follows:
PAPi = (PASP − PADP) / mRAP
where PAPi is the PA pulsatility index.
PVR = (mPAP − mPCWP) / CO
where PVR is pulmonary vascular resistance.
RVSWI = (mPAP − mRAP) × SV index × 0.0136
where RVSWI is the RV stroke work index.
PA compliance = SV / (PASP − PADP)
An interdisciplinary heart team, which included an interventional cardiologist, cardiac surgeon, echocardiologist, and cardiac anesthetist, discussed each participant’s eligibility for M-TEER. All patients underwent the MitraClip procedure as described previously.11 Patients were followed up for 1 year after the procedure, and information on cardiac events (heart failure hospitalization, cardiovascular death, or insertion of a left ventricular assist device [LVAD]) was collected.
This observational study was approved by the National Cerebral and Cardiovascular Center Institutional Review Board (R20106-2).
Statistical Analysis
Continuous data are presented as the median with interquartile range (IQR) and were compared using Mann-Whitney U test. Categorical data are presented as absolute and relative frequencies and were compared using the Chi-squared or Fisher’s exact test. Survival and event-free survival were estimated using the Kaplan-Meier method, and group differences were assessed using the log-rank test. The optimal PA compliance cut-off value for predicting survival was determined via receiver operating characteristic (ROC) curve analysis. All hemodynamic parameters were dichotomized as described in the literature.8 The independent association between PA compliance (modeled as a continuous variable or as a binary variable based on the cut-off value determined using ROC analysis) and prognosis, including cardiac events (heart failure rehospitalization, insertion of an LVAD, or all-cause mortality) during the follow-up period, was assessed using Cox proportional hazard models. Multivariate analysis was performed using models adjusted for LVEF, MR severity, mPCWP, mPAP, and cardiac index. Other Cox proportional hazard analysis was performed using models adjusted for binary variables of mPCWP, mPAP, and cardiac index based on cut-off values reported in previous studies to reduce multicollinearity among hemodynamic variables.8 Statistical significance was set at P<0.05.
All statistical analyses were performed using EZR (Saitama Medical Center, Jichi Medical University, Saitama, Japan), which is a graphical user interface for R (R Foundation for Statistical Computing, Vienna, Austria). More precisely, EZR is a modified version of R commander designed to add statistical functions frequently used in biostatistics.12
Results
In total, 107 patients with vSMR who underwent hemodynamic assessment in a conscious state before M-TEER were included in this study. During the follow-up period (mean [±SD] 318±100 days), 24 patients experienced cardiac events, including hospitalization due to heart failure, cardiovascular death, or LVAD insertion.
Patient characteristics and echocardiographic data at baseline for the groups with and without cardiac events are presented in Table 1. There were no differences in patient background, including age, sex, percentage of New York Heart Association Class III/IV, heart failure medication status, or laboratory data, between the 2 groups. In the study cohort, no patients had restrictive lung disease based on respiratory function tests. Although the STS score were slightly higher but not significant in the event group, STS scores for both groups were in the range of high risk for 30-day mortality. This may reflect differences in patient backgrounds, including LVEF. Preoperative echocardiography revealed no significant differences in left ventricular (LV) size or left atrial volume index. Although MR grades were comparable between the 2 groups, MR regurgitant fraction and regurgitant volume determined by quantitative assessment were higher in the cardiac event group. The cardiac event group had significantly lower LVEF than the non-event group (median 30% [IQR 20–50%] vs. 33% [IQR 21–50%]; P=0.03). Of the right heart function parameters assessed by echocardiography, there were no significant differences between the cardiac event and non-event groups in estimated PA pressure, TR grade, TAPSE, or RV-PA coupling. In terms of procedural characteristics, there were no differences between the 2 groups in the number of clips implanted and MV mean pressure gradient after the procedure, but the MR grade at discharge was slightly higher (but not significant) in the cardiac event group.
Table 1.
Patient Characteristics and Echocardiographic Data at Baseline With and Without Cardiac Events During 1-Year Follow-up
| |
Cardiac events
(n=24) |
No cardiac events
(n=83) |
P value |
| Clinical characteristics |
| Age (years) |
79 [44–90] |
76 [41–91] |
0.35 |
| Male sex |
14 (58.3) |
58 (69.9) |
0.33 |
| Body surface area (m2) |
1.5 [1.1–2.2] |
1.6 [0.4–2.1] |
0.32 |
| Ischemic cardiomyopathy |
20.8 (5) |
38.6 (32) |
0.15 |
| NYHA Class III/IV |
50 (12) |
35.9 (29) |
0.23 |
| SBP (mmHg) |
102 [72–123] |
101 [70–152] |
0.53 |
| DBP (mmHg) |
62 [47–79] |
59 [37–100] |
0.69 |
| Heart rate (beats/min) |
72 [50–100] |
69 [48–92] |
0.07 |
| Atrial fibrillation |
42 (10) |
43 (36) |
1.00 |
| STS score (%) |
10.6 [0.8–46.1] |
8.2 [0.6–35.3] |
0.09 |
| CRT |
25 (6) |
24.1 (20) |
1.00 |
| Medications |
| ACE-I/ARB |
13 (54.2) |
61 (73.5) |
0.08 |
| β-blocker |
22 (91.7) |
78 (94.0) |
0.65 |
| MRA |
14 (58.3) |
57 (68.7) |
0.46 |
| Anticoagulant |
13 (54.2) |
53 (63.9) |
0.48 |
| Laboratory data |
| BNP (pg/mL) |
636 [87–5,174] |
429 [15–4,753] |
0.24 |
| Creatinine (mg/dL) |
1.4 [0.7–6.2] |
1.7 [0.4–7.8] |
0.29 |
| eGFR (mL/min/1.73 m2) |
23 [11–90] |
34 [11–160] |
0.13 |
| TTE findings at baseline |
| LV end-diastolic diameter (mm) |
63 [47–91] |
62 [44–91] |
0.55 |
| LV end-systolic diameter (mm) |
56 [28–87] |
52 [27–86] |
0.22 |
| LVEF (%) |
30 [20–50] |
33 [21–50] |
0.03 |
| IVS (mm) |
8.0 [4.0–15.0] |
8.0 [3.0–14.0] |
0.87 |
| LAVI (mL/m2) |
82 [44–199] |
85 [290–232] |
0.75 |
| MR grade |
3.5 [2.5–4.0] |
3.5 [2.5–4.0] |
0.54 |
| MR Grade III |
42 (10) |
47 (39) |
0.82 |
| MR Grade IV |
58 (14) |
53 (44) |
|
| MR regurgitant fractionA (%) |
59 (12) |
54 (11) |
0.03 |
| MR regurgitant volumeA (mL) |
58 [40–82] |
51 [30–79] |
0.04 |
| TR grade |
1.5 [0.0–3.0] |
1.0 [0.0–3.0] |
0.23 |
| TR pressure gradient (mmHg) |
36.0 [22.0–65.0] |
36.0 [19.0–63.0] |
1.00 |
| TAPSE (mm) |
14.6 [8.0–22.6] |
15.8 [7.1–115.0] |
0.29 |
| RV-PA coupling (mm/mmHg) |
0.43 [0.21–0.94] |
0.43 [0.14–4.11] |
0.41 |
| Procedural characteristics |
| No. clips implanted |
1.0 [1.0–2.0] |
1.0 [1.0–3.0] |
0.35 |
| MR grade at discharge |
1.5 [0.5–2.5] |
1.5 [0.0–2.5] |
0.06 |
| MV mPG at discharge (mmHg) |
2.1 [1.3–8.8] |
2.0 [1.0–7.3] |
0.45 |
Unless indicated otherwise, data are given as the median [interquartile range] or % (n). ADetermined using the volumetric method. ACE-I, angiotensin-converting enzyme inhibitor; APS, acute procedure success; ARB, angiotensin receptor blocker; BNP, B-type natriuretic peptide; CRT, cardiac resynchronization therapy; DBP, diastolic blood pressure; eGFR, estimated glomerular filtration rate; IVS, interventricular septum thickness; LAVI, left atrial volume index; LV, left ventricle; LVEF, left ventricular ejection fraction; mPG, mean pressure gradient; MR, mitral regurgitation; MRA, mineralocorticoid receptor antagonist; MV, mitral valve; NYHA, New York Heart Association; PA, pulmonary artery; RV, right ventricular; SBP, systolic blood pressure; STS score, Society of Thoracic Surgeons predicted risk of mortality score; TAPSE, tricuspid annular plane systolic excursion; TR, tricuspid regurgitation; TTE, transthoracic echocardiography.
Hemodynamic data recorded in patients in a stable conscious state before M-TEER are presented in Table 2. mPCWP (median 21.0 [IQR 8.0–46.0] vs. 17.0 [IQR 5.0–36.0] mmHg; P=0.02) and mPAP (median 31.0 [IQR 14.0–55.0] vs. 225.0 [IQR 10.0–52.0] mmHg; P=0.06) were higher in the cardiac event than non-event group, although the difference in mPAP was not statistically significant. There were no significant differences between the 2 groups in vPCWP, mRAP, and cardiac index. With respect to right heart function and RV afterload indices from hemodynamic assessments, there were no significant differences between the 2 groups in PAPi, PVR, and the RVSWI, but PA compliance was significantly lower in the event than non-event group (median 1.6 [IQR 0.3, 3.2] vs. 2.2 [IQR 0.7, 6.4] mL/mmHg; P=0.01).
Table 2.
Hemodynamic Data in a Stable Conscious State Before M-TEER According to the Presence of Cardiac Events During the 1-Year Follow-up
Catheter measurements
before M-TEER |
Cardiac events
(n=24) |
No cardiac events
(n=83) |
P value |
| Aortic pressure mean (mmHg) |
77.5 [55.0, 113.0] |
80.0 [49.0, 130.0] |
0.97 |
| PCWP (mmHg) |
| V wave |
32.0 [10.0, 65.0] |
25.0 [6.0, 68.0] |
0.08 |
| Mean (mmHg) |
21.0 [8.0, 46.0] |
17.0 [5.0, 36.0] |
0.02 |
| mPAP (mmHg) |
31.0 [14.0, 55.0] |
25.0 [10.0, 52.0] |
0.06 |
| mRAP (mmHg) |
6.50 [1.0, 15.0] |
5.0 [1.0, 16.0] |
0.21 |
| Cardiac index (L/min/m2) |
2.15 [0.90, 3.46] |
2.13 [1.38, 3.48] |
0.50 |
| PAPi |
4.3 [2.3, 30.0] |
4.7 [1.5, 33.0] |
0.75 |
| PVR (Wood units) |
2.9 [0.9, 8.4] |
2.7 [−0.3, 8.5] |
0.48 |
| RVSWI (mL · mmHg/m2) |
14.7 [3.5, 26.8] |
13.2 [4.2, 35.1] |
0.60 |
| PA compliance (mL/mmHg) |
1.6 [0.3, 3.2] |
2.2 [0.7, 6.4] |
0.01 |
Unless indicated otherwise, data are given as the median [interquartile range]. mPAP, mean pulmonary artery pressure; mRAP, mean right atrial pressure; M-TEER, mitral valve transcatheter edge-to-edge repair; PA, pulmonary artery; PAPi, pulmonary artery pulsatility index; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; RVSWI, right ventricular stroke work index.
As indicated in Figure 2, ROC curve analysis indicated that the optimal cut-off value of PA compliance for predicting cardiac events was 2.66 mL/mmHg, which had a sensitivity of 0.91, a specificity of 0.59, and an area under the curve of 0.672 (95% confidence interval [CI] 0.562–0.782). Survival curves after M-TEER for patients with preprocedural PA compliance ≥2.7 and <2.7 mL/mmHg are shown in Figure 3. Patients with PA compliance <2.7 mL/mmHg had a significantly higher rate of cardiac events than with PA compliance ≥2.7 mL/mmHg (log-rank P=0.0065). Cox proportional hazards regression models were used to test the independent association between PA compliance and cardiac events, using PA compliance as both a continuous variable (Table 3) and a binary variable based on a cut-off value of <2.7 mL/mmHg from our study (Table 4). Using PA compliance as a continuous variable, the analysis that PA compliance was significantly associated with cardiac events after adjusting for LVEF (Model 2), MR regurgitant fraction (Model 3), and mPAP (Model 5), but not mPCWP (Model 4). However, Cox proportional hazards regression analysis of hemodynamic parameters using binary variables of mPCWP, mPAP, and cardiac index based on cut-off values reported in previous studies (Table 3) revealed that PA compliance was a stronger indicator of poor prognosis than high mPCWP (Model 7), high mPAP (Model 8), or low cardiac index (Model 9). Moreover, this trend was consistent in multivariate analyses using binary PA compliance with a cut-off value of <2.7 mL/mmHg. Models using hemodynamic parameters as continuous variables (Table 4), including mPCWP (Model 4) and mPAP (Model 5), were not significant, whereas high mPCWP (Model 7), high mPAP (Model 8), and low cardiac index (Model 9) were significant indicators of cardiac events.
Table 3.
Cox Proportional Hazard Regression Models to Test Independent Associations Between PA Compliance as a Continuous Variable and Cardiac Events
| |
PA compliance
(per 0.1-mL/mmHg increase) |
P value |
| HR |
95% CI |
| Model 1 (age, sex) |
0.52 |
0.33–0.82 |
<0.01 |
| Model 2 (age, sex, LVEF) |
0.57 |
0.35–0.92 |
0.02 |
| Model 3 (age, sex, MR regurgitant fraction) |
0.58 |
0.36–0.96 |
0.03 |
| Model 4 (age, sex, mPCWP) |
0.30 |
0.3–1.07 |
0.08 |
| Model 5 (age, sex, mPAP) |
0.47 |
0.23–0.96 |
0.04 |
| Model 6 (age, sex, cardiac index) |
0.48 |
0.28–0.83 |
0.01 |
| Model 7 (age, sex, mPCWP >15 mmHg) |
0.54 |
0.31–0.93 |
0.03 |
| Model 8 (age, sex, mPAP ≥25 mmHg) |
0.46 |
0.24–0.88 |
0.02 |
| Model 9 (age, sex, cardiac index <2.5 L/min/m2) |
0.55 |
0.34–0.89 |
0.01 |
CI, confidence interval; HR, hazard ratio. Other abbreviations as in Tables 2,3.
Table 4.
Cox Proportional Hazard Regression Models to Test the Independent Associations Between PA Compliance as a Binary Variable and Cardiac Events
| |
PA compliance <2.7 mL/mmHg |
P value |
| HR |
95% CI |
| Model 1 (age, sex) |
4.80 |
1.42–16.2 |
0.01 |
| Model 2 (age, sex, LVEF) |
3.83 |
1.09–13.5 |
0.04 |
| Model 3 (age, sex, MR regurgitant fraction) |
3.54 |
1.01–12.5 |
0.05 |
| Model 4 (age, sex, mPCWP) |
3.48 |
0.92–13.2 |
0.07 |
| Model 5 (age, sex, mPAP) |
3.92 |
0.96–16.0 |
0.06 |
| Model 6 (age, sex, cardiac index) |
4.82 |
1.33–17.4 |
0.02 |
| Model 7 (age, sex, mPCWP >15 mmHg) |
4.01 |
1.07–15.1 |
0.04 |
| Model 8 (age, sex, mPAP ≥25 mmHg) |
4.63 |
1.18–18.2 |
0.03 |
| Model 9 (age, sex, cardiac index <2.5 L/min/m2) |
4.19 |
1.22–14.5 |
0.02 |
CI, confidence interval; HR, hazard ratio. Other abbreviations as in Tables 2,3.
Discussion
In our study, we measured echocardiographic and hemodynamic RV function and afterload parameters in patients with vSMR, and examined their associations with cardiac events. The main findings of this study are that RV function derived from both echocardiography and invasive measurements was comparable between the cardiac event and non-event groups and that reduced PA compliance (a pulsatile component of RV afterload), derived from invasive hemodynamic measurements before M-TEER, was associated with 1-year cardiac events after the procedure.
Previous reports have shown that reduced RV function, as determined by tissue Doppler imaging13 and TAPSE,4,5,14 is closely related to poor prognosis after M-TEER. More recently, Stolz et al. revealed that RV-PA uncoupling is associated with the poor prognosis after M-TEER in vSMR.3 In contrast, in the present study, there were no differences in RV function parameters, determined from both echocardiographic and hemodynamic data, and the presence of cardiac events. This discrepancy may be due to differences in patient selection. In our study, only 15% of patients presented with RV failure with RV-PA coupling <0.274 mm/mmHg, compared with 29% of patients presenting with RV failure in the study of Stolz et al.3 This difference indicates that our patients were at an earlier stage of cardiac damage. Moreover, in their report at 1 year, they found no differences in prognosis among patients with earlier cardiac damage (Stage 1–3) before RV failure occurred. However, when RV failure occurred, 1-year survival decreased to 67%,3 indicating that one-third of patients die even after M-TEER. This shows the limitations of current staging using echocardiographic parameters and emphasizes the need for new parameters to predict cardiac events before RV dysfunction occurs.
RV dysfunction associated with left heart failure does not become clear until late in disease progression, indicating that waiting for RV dysfunction may be too late for intervention.3 LV failure can directly increase RV afterload through passive (pulmonary venous pressure elevation) and reactive (pulmonary vasoconstriction and remodeling) components; thus, afterload-sensitive RVs are at increased risk of RV failure, even in the absence of intrinsic damage.15 PASP and PVR, which are commonly used as measures of RV afterload, may not accurately describe afterload because the contribution of pulsatile loading has not been taken into account.16 As the antegrade blood flow flows from the RV into the lungs, it encounters retrograde flow generated from the pulmonary vasculature, which reduces antegrade flow and increases peak PASP.17 Thus, elevated LV filling pressures directly increase RV afterload, reduce PA compliance, and increase PA resistance through acute vasoconstriction and chronic vascular remodeling.16 It has also been shown that, in the early stages of the disease during therapy for pulmonary hypertension, PVR and PA compliance remain inversely related, and a decrease in PA compliance is larger and more easily observed than an increase in PVR.18 These findings suggest that PA compliance is reduced at an earlier stage than PVR is elevated or RV dysfunction occurs, and demonstrate that PA compliance is a more sensitive marker to detect cardiac event than PVR. In fact, PA compliance is a strong prognostic indicator in patients with chronic heart failure and systolic LV dysfunction, regardless of PVR.8 In 724 patients with LV dysfunction, Dupont et al. determined that PA compliance (but not PVR) was an independent predictor of all-cause mortality and cardiac transplantation.19 Pellegrini et al. showed that PA compliance was associated with survival more than any other hemodynamic variable, whether high or normal PVR,8 suggesting that PA compliance is reduced at earlier stage than PVR is elevated or RV dysfunction occurs.
Our findings agree with those of previous studies. We found that PA compliance was significantly lower in the group with cardiac events, whereas there was no difference in PVR between the 2 groups. This result remained significant even in the multivariate model. More interestingly, echocardiography-derived RV-PA uncoupling, as well as RV function based on hemodynamic parameters, did not differ between the 2 groups, suggesting that reduced PA compliance may predict cardiac events in the early phase before RV dysfunction and even before PVR reduction occur.
A recent study from Bou Chaaya et al. demonstrated that pulmonary effective arterial elastance, derived from PASP/SV as well as PA compliance, was a strong predictor of outcomes after M-TEER both in primary and secondary MR, with approximately 43% of patients having secondary MR.20 Pulmonary effective arterial elastance mimics PA compliance, and both parameters reflect pulsatile RV afterload.21 In their study, Bou Chaaya et al. found that patients with high elastance (low PA compliance) had a poor prognosis after 2 years, regardless of pulmonary hypertension.20 They also found that the prognosis was dependent on the etiology of MR. Prognosis after M-TEER was better for primary MR with low elastance than for secondary MR, but similar to secondary MR for primary MR with high elastance.20 However, Bou Chaaya et al. did not distinguish secondary MR according to pulsatile RV afterload including elastance and PA compliance. Our findings align with their results and contribute to furthering the discussion by focusing on secondary MR. In addition, our study is the first to demonstrate a relationship between PA compliance and cardiac events in vSMR patients.
M-TEER for vSMR is a safe and effective procedure. However, there may be some hesitation in using M-TEER in some patients, such as those with extreme hypotension, impaired respiratory function, or the presence of esophageal varices. Measuring hemodynamic-derived PA compliance in a conscious state may aid in the clinical decision making by the heart team in such difficult cases.
Study Limitations
This study has several limitations. First, this was a single-center retrospective study with a relatively small sample size; therefore, sampling error may occur, and selection bias cannot be ruled out. Second, reasonable time frames were arbitrarily set for clinical and echocardiographic values related to catheterization. However, we performed hemodynamic assessment within 30 days before the M-TEER procedure and the hemodynamic fluctuations were relatively small. Third, quantitative measurements of residual MR were not made in every patient. Although there was no significant difference in residual MR after M-TEER, because quantitative measurements of residual MR were not made in all patients, the possibility remains a of larger residual MR in the event group that may have affected prognosis after M-TEER. Finally, the results do not apply to patients with primary MR or atrial functional MR with normal systolic function. Future multicenter studies are warranted to support our findings.
Conclusions
PA compliance assessed with invasive catheter measurements in a conscious state before M-TEER in vSMR may play an important role in predicting post-M-TEER cardiac events.
Sources of Funding
This work was supported by JSPS KAKENHI Grant no. JP20K08440.
Disclosures
M.A. is a clinical proctor of transcatheter edge-to-edge repair for Abbott Medical and has received consultant fees and remuneration for presentations from Abbott Medical. K.Y. and C.I. are members of Circulation Journal’s Editorial Team. The other authors declare no conflicts of interest.
IRB Information
This observational study was approved by the National Cerebral and Cardiovascular Center Institutional Review Board (R20106-2).
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