IMR Press / RCM / Volume 22 / Issue 1 / DOI: 10.31083/j.rcm.2021.01.214
Open Access Review
Transcatheter mitral valve repair with MitraClip in patients with pulmonary hypertension: hemodynamic and prognostic perspectives
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1 Division of Cardiology, Fondazione IRCCS Policlinico San Matteo and University of Pavia, 27100 Pavia, Italy
2 Cardiocentro Ticino Institute, Ente Ospedaliero Cantonale, 6900 Lugano, Switzerland
3 Division of Cardiology and Cardiac Intensive Care Unit, San Paolo Hospital, 17100 Savona, Italy
4 Cardiocentro Ticino, 6900 Lugano, Switzerland
5 Interventional Cardiology Unit, Cardio-Thoraco Vascular Department (DICATOV), IRCCS Ospedale Policlinico San Martino, Genova, Italy; IRCCS Italian Cardiovascular Network & Department of Internal Medicine, University of Genova, 16122 Genova, Italy
6 National Kapodistrian University of Athens, Medical School, 106 71 Athens, Greece
7 University of Iowa, Section of Advanced Heart Failure and Transplantation, Iowa City, IA 52242, USA

These authors contributed equally.

Rev. Cardiovasc. Med. 2021 , 22(1), 33–38; https://doi.org/10.31083/j.rcm.2021.01.214
Submitted: 18 January 2021 | Revised: 11 March 2021 | Accepted: 12 March 2021 | Published: 30 March 2021
Copyright: © 2021 The Authors. Published by IMR Press.
This is an open access article under the CC BY 4.0 license (https://creativecommons.org/licenses/by/4.0/).
Abstract

Transcatheter mitral valve repair with MitraClip has emerged as a possible therapeutic option for patients with severe mitral regurgitation (MR) with high risk for surgical valve repair. MitraClip intervention has demonstrated to improve haemodynamics and clinical outcomes in selected patients in observational and randomized studies. Preoperative pulmonary hypertension (PH) is known to affect prognosis in patients undergoing surgical mitral valve intervention. The aim of the present review is to discuss the available literature focused on the haemodynamic and clinical effects of MitraClip in patients with severe MR and PH.

Keywords
MitraClip
Pulmonary hypertension
Mitral valve reurgitation
1. Introduction

Mitral regurgitation (MR) is the second most frequent indication for valve surgery in Europe [1] with an estimated prevalence of 5% among the adult population [2,3]. The most widely used classification distinguishes between primary and secondary (or functional) MR: the former is caused by a damage to the mitral valve leaflets or chordae tendinae, whereas the latter presents a normal valve apparatus and is the consequence of annular enlargement/dysfunction and leaflet tethering caused in the majority of cases by left ventricular dysfunction [4].

Long-term increase in left-sided filling pressures due to MR can lead to pulmonary hypertension (PH). The prevalence of PH in patients with severe primary MR is 23%, while the prevalence among patients with secondary MR is unknown. PH due to any left heart disease (LHD) is the most common form of PH [5], representing the second group of the WHO classification and being characterized by a mean pulmonary arterial pressure (mPAP) 20 mmHg and a pulmonary arterial wedge pressure (PAWP) > 15 mmHg (i.e. post-capillary PH) [6]. Indeed, severe MR induces an increase in left ventricular filling pressures and a reduction in left atrial compliance, causing an increase in left atrial pressure and causes pulmonary vascular congestion. Long-standing elevations in pulmonary pressures can cause an initial reactive vasoconstriction, which can eventually lead to irreversible remodelling of both pulmonary arterioles and veins [7], thus causing the evolution from an isolated post-capillary PH to a combined pre- and post-capillary PH, representing an advanced stage of the disease.

No pharmacological strategy showed to reduce mortality in patients with corrected MR and PH [8,9] and the cornerstone in the management of these patients is represented by treating the valvular defect [10].

Preoperative PH is known to affect prognosis in patients undergoing surgical mitral valve intervention [11]. Most of the studies on the effect of PH on outcomes after mitral valve surgery are retrospective and used different definitions of PH. However, regardless of the invasive or non-invasive measurement or the defined thresholds [12], PH has been associated with significant reduction in post-operative left ventricular ejection fraction in patients with primary MR [13] and with increased mortality in both primary and secondary MR [11,14].

Transcatheter mitral valve repair (TMVR) with MitraClip (Abbott Vascular, Inc.) has emerged as a possible therapeutic option for patients at high risk for surgical mitral valve repair. In primary MR, MitraClip is reserved for patients with symptoms who present contraindications to surgery [15]. In the setting of secondary MR, MitraClip has demonstrated to be effective in reducing symptoms and improving clinical outcomes in selected patients in observational and randomized studies [16,17].

Since PH represents an important risk factor for right ventricular (RV) failure and peri-operative mortality in patients undergoing mitral valve surgery [18], great interest has been raised for TMVR in these high-risk patients.

The aim of the present review is to expose the available literature focused on MitraClip in patients with severe MR and PH, specifically evaluating the haemodynamic and clinical effects of MitraClip in this setting.

2. Haemodynamic effects of MitraClip

MitraClip intervention has been associated with favourable acute hemodynamic changes in patients with severe MR [19-21] (Fig. 1).

Fig. 1.

Haemodynamic effects of MitraClip. The green column shows the favourable haemodynamic effects after MitraClip; the yellow one the effects whose hemodynamic significance is still controversial; the red one the negative effects. Legend. CI, cardiac index; CO, cardiac output; iASD, iatrogenic atrial septal defect; mPAP, mean pulmonary artery pressure; MVPG, mitral valve pressure gradient; PAWP, pulmonary artery wedge pressure; PVR, pulmonary vascular resistance; RVSWI, right ventricular stroke work index.

A successful reduction of MR causes a decrease of the regurgitant volume, which yields unloading of left atrium. An initial concern of TMVR was the possible increase in left ventricular (LV) afterload following elimination of the low resistance regurgitant flow into the left atrium, possibly resulting in a post-procedural low cardiac output (CO) [22,23]. However, the first studies focused on the hemodynamic effects of MitraClip, performed by repeating right heart catheterization before and after the procedure, reported an acute increase in CO and cardiac index (CI) [21,24,25] (Table 1).

Table 1. Main studies investigating the haemodynamic effects of MitraClip on pulmonary circulation and RV
Study (year) (reference) Patients (n) MR aetiology Time of assessment Hemodynamic effects
Siegel et al. (2011) [21] 107 Degenerative 79% Intraprocedural, CO
Functional 21% Under general anaesthesia CI
LVEDP
Gaemperli et al. (2012) [24] 50 Degenerative 30% Intraprocedural, CI
Functional 56% Under general anesthesia mPAP
Mixed 14% PAWP
Kottenberg et al. (2014) [20] 81 Degenerative 55% Intraprocedural,
Functional 42% Under general anesthesia - Overall:
Mixed 3% CI
mPAP
PVR
RVSWi
- Subgroup analysis in patients with PH:
mPAP
PVR
RVSWi
PAWP
Crimi et al. (2018) [26] 3 Functional 100% Before and 6 months after MitraClip, CI
(case series of patients with end-stage CHF not eligible for HTx) Conscious patients mPAP
PAWP
PVR
CHF, cardiac heart failure; CI, cardiac index; CO, cardiac output; LVEDP, left ventricular end-diastolic pressure; mPAP, mean pulmonary artery pressure; PAWP, pulmonary artery wedge pressure; PH, pulmonary hypertension; PVR, pulmonary vascular resistances; RVSWi, right ventricular stroke work index.

Data on the hemodynamic effects of MitraClip in patients with severe MR and PH are limited. In a cohort of patients with baseline low CI and elevated mean pulmonary artery pressure (mPAP), Kottenberg et al. showed that MitraClip resulted in CI, mPAP and right ventricular stroke work index (RVSWI) improvement at the end of the procedure [20]. These results allowed to assume that eliminating the regurgitant flow into the left atrium and pulmonary veins can improve cardiac forward output and reduce pulmonary pressures. Interestingly, the decrease in PAP values were reported in the first 90 days after MitraClip in patients with FMR and PH receiving hemodynamic telemonitoring with an implanted PAP sensor [27] RVSWI is a surrogate parameter for RV function, representing the pressure-volume work of the right ventricle [28]. In this study RVSWi increase was mainly driven by decreased pulmonary vascular resistance (PVR) [20]. Indeed, in patients with PH, in whom the right ventricle chronically works against high pulmonary artery pressures, a reduction in PVR may be linked with an improvement in RV function by reducing RV afterload. This finding is particularly relevant in patients with chronic heart failure (HF), where the negative impact of PH on prognosis is mainly driven by the eventual worsening of RV function [29].

The reduction of PVR may be of particular relevance for patients with advanced HF who are not eligible for heart transplantation (HTx) due to elevated PVR. HTx represents the treatment of choice for end-stage HF [30], but patients with PH and elevated PVR are not suitable for HTx because of the risk of post-operative RV failure and poor outcome [26]. In this setting, a persistent reduction of PVR may lead to eligibility for HTx. Thus, since MitraClip has been associated with a sustained reduction of PVR, it has been proposed as a “bridge to candidacy” strategy [31-33]. The selected use of MitraClip as a bridge strategy to HTx has been recently investigated by a multicenter registry, which reported that 15% of patients underwent elective HTx, 15.5% became suitable for HTx and 23.5% was removed from HTx list because of clinical improvement [34].

By approximating the two mitral valve leaflets, MitraClip can increase mitral valve pressure gradient (MVPG) thus counterbalancing the benefit of unloading the left atrium by MR reduction [35,36]. Indeed, the residual MVPG after MitraClip implantation can influence long-term outcome proportionally to the degree of the MVPG. Neuss et al. found that MVPG > 5 mmHg after MitraClip implantation was associated with poor long-term outcomes [37]. Interestingly, also a reduction in mitral valve area (MVA) after MitraClip can influence patients’ hemodynamics and outcome. In particular, Utsunomiya et al. showed that a post-procedural MVA 1.94 cm2 was independently associated with a blunted post-procedural decrease in systolic PAP (sPAP), as well as with increased all-cause mortality and hospitalization for HF [36]. For these reasons, it is crucial to carefully assess MVPG during the intervention by echocardiography, thus guiding the operators for MitraClip repositioning and implantation.

MitraClip procedure requires inter-atrial trans-septal access of the left atrium with a steerable 24F sheath, sometimes leading to the development of a post-procedural iatrogenic atrial septal defect (iASD). The persistence of iASD has been described in up to 50% patients after interventional mitral valve repair [37]; however, the clinical and hemodynamic relevance of this iASD remains debated [38,39]. Theoretically, a left-to-right shunting may increase RV preload and, in the presence of PH, this could further worsen RV loading and function. However, Eden et al. recently found that MitraClip did not induce a relevant inter-atrial left-to-right shunt through the iASD in a cohort of patients including both degenerative and functional MR [39]. However, data on the hemodynamic effects of iASD are non-conclusive and the eventual indication for post-procedural iASD closure still remains unsettled.

Data on hemodynamic effects of MitraClip are limited. Indeed, most hemodynamic studies included both patients with degenerative and functional MR, in which the pathophysiologic and hemodynamic contribution of MR and, consequently, the hemodynamic effects of mitral valve intervention may be different. Furthermore, the hemodynamic effects of MitraClip have been collected acutely at the end of the procedure, during general anaesthesia and with different dosages of inotropes and vasopressors, which could influence measurements. Importantly, previous studies did not consider PH sub-types (isolated post-capillary and combined pre- and post-capillary PH), which have significant pathophysiologic differences and may have different hemodynamic responses to MitraClip. Beyond all these considerations, the promising results from the early studies focused on the hemodynamic modifications after MitraClip should prompt future research in collecting invasive data, in order to characterize preoperative PH and to identify specific hemodynamic effects for specific subsets of patients.

3. Prognostic impact of PH in patients treated with MitraClip

Data regarding the prognostic impact of pre-operative PH in MitraClip patients are limited. Randomized clinical trials focused on MitraClip intervention did not systematically investigate the prognostic impact of pre-operative PH [16,17,40]. The EVEREST II trial did not report outcomes based on pre-operative PH [16], while sPAP > 70 mmHg represented an exclusion criterion in the COAPT trial [17]. Literature on PH in MitraClip patients is mostly based on retrospective studies which evaluated the prognostic differences between patients with and without PH, using different cut-offs for PH definition, including both degenerative and functional MR, and reporting controversial results [41-44].

Matsumoto et al. [41] stratified 91 patients undergoing MitraClip into two groups based on pre-operative sPAP estimated with echocardiography: 50 mmHg was used as a cut-off to define patients with PH. The two groups showed similar reduction in sPAP, as well as similar safety and short-term mortality. However, all-cause mortality was higher in the PH-group at long-term follow-up (84.7% vs 63.0% at 2 years, 84.7% vs 45.4% at 3 years, log-rank P-value = 0.005). In the German Transcatheter Mitral valve Interventions (TRAMI) registry, including 643 patients, Tigges et al. [42] divided the study population into three groups based on sPAP (group 1 36 mmHg, group 2 from 37-50 mmHg, group 3 > 50 mmHg). They found no significant difference among the groups in 30-day mortality or 30-day major adverse cardiac events (MACCEs) defined as the composite of death, myocardial infarction and stroke. However, the study showed a significant difference in MACCEs among groups after 1 year (34.7% in group 3 vs 33.1% in group 2 vs 20.3% in group 1, P < 0.01). An analysis of the Society of Thoracic Surgery/American College of Cardiology Transcatheter Therapy (STS/ACC TVT) registry stratified 4071 patients treated with MitraClip into four groups based on pre-operative mPAP assessed invasively (group 1 < 25 mmHg, group 2 25-34 mmHg, group 3 35-44 mmHg, group 4 > 45 mmHg). In-hospital, 30-day and 1-year mortality all significantly and progressively worsen across the groups, with an hazard ratio of 1,05 every 5 mmHg increase in mPAP (95% CI: 1.01-1.09, P = 0,017) [43]. However, a retrospective analysis from the National Inpatient Sample (NIS), which studied 1037 patients undergoing MitraClip, found that in-hospital mortality and all the secondary outcomes (vascular complications, bleeding requiring transfusion, ischemic stroke, acute kidney injury requiring dialysis, deep venous thrombosis and infectious complications) where comparable between patients with and without pre-operative PH [44].

Recently, a post-hoc analysis of the COAPT trial reported the prognostic implication of echocardiographic evidence of elevated sPAP [45]. The Authors investigated the relationship between sPAP and prognosis by evaluating sPAP as a both continuous and dichotomized variable (50 mmHg was used as cut-off). Patients treated with MitraClip and optimal medical therapy showed a lower incidence of the combined endpoint (death and HF-related hospitalization) at 2 years follow-up across sPAP values (when considered as continuous variable) and in both groups (group with sPAP < 50 mmHg: adjusted hazard ratio 0.59; 95% confidence interval: 0.42-0.82; group with sPAP > 50 mmHg: adjusted hazard ratio 0.49; 95% confidence interval: 0.32-0.72. P for interaction = 0.45) compared with patients treated only with medical therapy. Of note, a higher sPAP was associated with higher incidence of the composite endpoint at 2-years follow-up regardless of the intervention arm of the study, confirming that patients with PH are at higher risk of mortality and hospitalization for HF. This study is of great importance since, for the first time, it shows that MitraClip could improve prognosis in patients with functional MR and PH. Nevertheless, it is important to underline that the study defined PH based on sPAP evaluated by echocardiography, which represents an incomplete evaluation as it does not provide a complete characterization of the patients’ hemodynamics and pathophysiology. Indeed, PH is not a single disease and it would be of utmost importance to understand whether clinical benefit after MitraClip is present in both patients with isolated post-capillary PH and with combined pre- and post-capillary PH, or it is limited to patients without elevated PVR. However, this study importantly expands the knowledge on the usefulness of MitraClip in patients with PH and should encourage research in this area.

4. Conclusions

MitraClip represents a promising therapeutic option for selected patients with MR at high surgical risk. For patients with pre-operative PH, there is no conclusive evidence in literature on the clinical and hemodynamic effects and the appropriateness of MitraClip. Despite the promising results shown by recent analyses focusing on hemodynamic and clinical outcomes, the available studies are methodologically heterogeneous and, specifically, they do not consider the different pathophysiological entities which are collected under the name of PH. Invasive hemodynamic data could provide a comprehensive hemodynamic evaluation and PH characterization in patients with MR, thus helping in identifying hemodynamic features showing probable benefit from MitraClip and supporting clinical evaluations for patient selection.

Author contributions

EA, AB, SC conceived and designed the content; AMM, LT, LA, AD, AS, GT, GC, wrote the manuscript; EA, AB, SC supervised and prepared the final version for submission.

Ethics approval and consent to participate

Not applicable.

Acknowledgment

We thank the two anonymous reviewers for excellent criticism of the article.

Funding

This research received no external funding.

Conflict of interest

The authors have no relationship with industry to disclose.

References
[1]
Iung B, Baron G, Butchart EG, Delahaye F, Gohlke-Bärwolf C, Levang OW, et al. A prospective survey of patients with valvular heart disease in Europe: the Euro Heart Survey on Valvular Heart Disease. European Heart Journal. 2003; 24: 1231-1243.
[2]
Nkomo VT, Gardin JM, Skelton TN, Gottdiener JS, Scott CG, Enriquez-Sarano M. Burden of valvular heart diseases: a population-based study. Lancet. 2006; 368: 1005-1011.
[3]
Monteagudo Ruiz JM, Galderisi M, Buonauro A, Badano L, Aruta P, Swaans MJ, et al. Overview of mitral regurgitation in Europe: results from the European Registry of mitral regurgitation (EuMiClip). European Heart Journal - Cardiovascular Imaging. 2018; 19: 503-507.
[4]
Levine RA, Schwammenthal E. Ischemic mitral regurgitation on the threshold of a solution: from paradoxes to unifying concepts. Circulation. 2005; 112: 745-758.
[5]
Hoeper MM, Humbert M, Souza R, Idrees M, Kawut SM, Sliwa-Hahnle K, et al. A global view of pulmonary hypertension. The Lancet Respiratory Medicine. 2016; 4: 306-322.
[6]
Simonneau G, Montani D, Celermajer DS, Denton CP, Gatzoulis MA, Krowka M, et al. Haemodynamic definitions and updated clinical classification of pulmonary hypertension. European Respiratory Journal. 2019; 53: 1801913.
[7]
Naeije R, Gerges M, Vachiery JL, Caravita S, Gerges C, Lang IM. Hemodynamic phenotyping of pulmonary hypertension in left heart failure. Circulation: Heart Failure. 2017; 10: e004082.
[8]
Bonderman D, Ghio S, Felix SB, Ghofrani HA, Michelakis E, Mitrovic V, et al. Riociguat for patients with pulmonary hypertension caused by systolic left ventricular dysfunction: a phase IIb double-blind, randomized, placebo-controlled, dose-ranging hemodynamic study. Circulation. 2013; 128: 502-511.
[9]
Bermejo J, Yotti R, García-Orta R, Sánchez-Fernández PL, Castaño M, Segovia-Cubero J, et al. Sildenafil for improving outcomes in patients with corrected valvular heart disease and persistent pulmonary hypertension: a multicenter, double-blind, randomized clinical trial. European Heart Journal. 2018; 39: 1255-1264.
[10]
Galiè N, Humbert M, Vachiery JL, Gibbs S, Lang I, Torbicki A, et al. 2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: the Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS): endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT). European Heart Journal. 2016; 37: 67-119.
[11]
Kainuma S, Taniguchi K, Toda K, Funatsu T, Kondoh H, Nishino M, et al. Pulmonary hypertension predicts adverse cardiac events after restrictive mitral annuloplasty for severe functional mitral regurgitation. The Journal of Thoracic and Cardiovascular Surgery. 2011; 142: 783-792.
[12]
Le Tourneau T, Richardson M, Juthier F, Modine T, Fayad G, Polge A, et al. Echocardiography predictors and prognostic value of pulmonary artery systolic pressure in chronic organic mitral regurgitation. Heart. 2010; 96: 1311-1317.
[13]
Yang H, Davidson WR Jr, Chambers CE, Pae WE, Sun B, Campbell DB, et al. Preoperative pulmonary hypertension is associated with postoperative left ventricular dysfunction in chronic organic mitral regurgitation: an echocardiographic and hemodynamic study. Journal of the American Society of Echocardiography. 2006; 19: 1051-1055.
[14]
Ghoreishi M, Evans CF, DeFilippi CR, Hobbs G, Young CA, Griffith BP, et al. Pulmonary hypertension adversely affects short- and long-term survival after mitral valve operation for mitral regurgitation: implications for timing of surgery. Journal of Thoracic and Cardiovascular Surgery. 2011; 142: 1439-1452.
[15]
Baumgartner H, Falk V, Bax JJ, De Bonis M, Hamm C, Holm PJ, et al. 2017 ESC/EACTS Guidelines for the management of valvular heart disease. European Heart Journal. 2017; 38: 2739-2791.
[16]
Feldman T, Kar S, Elmariah S, Smart SC, Trento A, Siegel RJ, et al. Randomized comparison of percutaneous repair and surgery for mitral regurgitation: 5-year results of EVEREST II. Journal of the American College of Cardiology. 2015; 66: 2844-2854.
[17]
Stone GW, Lindenfeld J, Abraham WT, Kar S, Lim DS, Mishell JM, et al. Transcatheter mitral-valve repair in patients with heart failure. The New England Journal of Medicine. 2018; 379: 2307-2318.
[18]
Cevese PG, Gallucci V, Valfrè C, Giacomin A, Mazzucco A, Casarotto D. Pulmonary hypertension in mitral valve surgery. The Journal of Cardiovascular Surgery. 1980; 21: 7-10.
[19]
Tempe DK, Hasija S, Datt V, Tomar AS, Virmani S, Banerjee A, et al. Evaluation and comparison of early hemodynamic changes after elective mitral valve replacement in patients with severe and mild pulmonary arterial hypertension. Journal of Cardiothoracic and Vascular Anesthesia. 2009; 23: 298-305.
[20]
Kottenberg E, Dumont M, Frey UH, Heine T, Plicht B, Kahlert P, et al. The minimally invasive MitraClipTM procedure for mitral regurgitation under general anaesthesia: immediate effects on the pulmonary circulation and right ventricular function. Anaesthesia. 2014; 69: 860-867.
[21]
Siegel RJ, Biner S, Rafique AM, Rinaldi M, Lim S, Fail P, et al. The acute hemodynamic effects of MitraClip therapy. Journal of the American College of Cardiology. 2011; 57: 1658-1665.
[22]
Rankin JS, Nicholas LM, Kouchoukos NT. Experimental mitral regurgitation: effects on left ventricular function before and after elimination of chronic regurgitation in the dog. The Journal of Thoracic and Cardiovascular Surgery. 1975; 70: 478-488.
[23]
Detaint D, Sundt TM, Nkomo VT, Scott CG, Tajik AJ, Schaff HV, et al. Surgical correction of mitral regurgitation in the elderly: outcomes and recent improvements. Circulation. 2006; 114: 265-272.
[24]
Gaemperli O, Moccetti M, Surder D, Biaggi P, Hurlimann D, Kretschmar O, et al. Acute haemodynamic changes after percutaneous mitral valve repair: relation to mid-term outcomes. Heart. 2012; 98: 126-132.
[25]
Gaemperli O, Biaggi P, Gugelmann R, Osranek M, Schreuder JJ, Bühler I, et al. Real-time left ventricular pressure-volume loops during percutaneous mitral valve repair with the MitraClip system. Circulation. 2013; 127: 1018-1027.
[26]
Mehra MR, Canter CE, Hannan MM, Semigran MJ, Uber PA, Baran DA, et al. The 2016 International Society for Heart Lung Transplantation listing criteria for heart transplantation: a 10-year update. The Journal of Heart and Lung Transplantation. 2016; 35: 1-23.
[27]
Herrmann E, Ecke A, Herrmann E, Eissing N, Fichtlscherer S, Zeiher AM, et al. Daily non-invasive haemodynamic telemonitoring for efficacy evaluation of MitraClip® implantation in patients with advanced systolic heart failure. ESC Heart Failure. 2018; 5: 780-787.
[28]
Slaughter MS, Pagani FD, Rogers JG, Miller LW, Sun B, Russell SD, et al. Clinical management of continuous-flow left ventricular assist devices in advanced heart failure. The Journal of Heart and Lung Transplantation. 2010; 29: S1-S39.
[29]
Ghio S, Temporelli PL, Klersy C, Simioniuc A, Girardi B, Scelsi L, et al. Prognostic relevance of a non-invasive evaluation of right ventricular function and pulmonary artery pressure in patients with chronic heart failure. European Journal of Heart Failure. 2013; 15: 408-414.
[30]
Ammirati E, Oliva F, Cannata A, Contri R, Colombo T, Martinelli L, et al. Current indications for heart transplantation and left ventricular assist device: a practical point of view. European Journal of Internal Medicine. 2014; 25: 422-429.
[31]
Crimi G, Gritti V, Ghio S, Crescio V, Magrini G, Scelsi L, et al. MitraClip procedure as ‘bridge to list’, the ultimate therapeutic option for end-stage heart failure patients not eligible for heart transplantation due to severe pulmonary hypertension. Pulmonary Circulation. 2018; 8: 2045894018791871.
[32]
Berardini A, Biagini E, Saia F, Stolfo D, Previtali M, Grigioni F, et al. Percutaneous mitral valve repair: the last chance for symptoms improvement in advanced refractory chronic heart failure? International Journal of Cardiology. 2017; 228: 191-197.
[33]
Garatti A, Castelvecchio S, Bandera F, Medda M, Menicanti L. MitraClip procedure as a bridge therapy in a patient with heart failure listed for heart transplantation. The Annals of Thoracic Surgery. 2015; 99: 1796-1799.
[34]
Godino C, Munafò A, Scotti A, Estévez-Loureiro R, Portolés Hernández A, Arzamendi D, et al. MitraClip in secondary mitral regurgitation as a bridge to heart transplantation: 1-year outcomes from the International MitraBridge Registry. The Journal of Heart and Lung Transplantation. 2020; 39: 1353-1362.
[35]
Patzelt J, Zhang W, Sauter R, Mezger M, Nording H, Ulrich M, et al. Elevated mitral valve pressure gradient is predictive of long-term outcome after percutaneous edge-to-edge mitral valve repair in patients with degenerative mitral regurgitation (MR), but not in functional MR. Journal of the American Heart Association. 2019; 8: e011366.
[36]
Utsunomiya H, Itabashi Y, Kobayashi S, Rader F, Hussaini A, Makar M, et al. Effect of percutaneous edge-to-edge repair on mitral valve area and its association with pulmonary hypertension and outcomes. The American Journal of Cardiology. 2017; 120: 662-669.
[37]
Neuss M, Schau T, Isotani A, Pilz M, Schöpp M, Butter C. Elevated mitral valve pressure gradient after MitraClip implantation deteriorates long-term outcome in patients with severe mitral regurgitation and severe heart failure. JACC: Cardiovascular Interventions. 2017; 10: 931-939.
[38]
Schueler R, Öztürk C, Wedekind JA, Werner N, Stöckigt F, Mellert F, et al. Persistence of iatrogenic atrial septal defect after interventional mitral valve repair with the MitraClip system. JACC: Cardiovascular Interventions. 2015; 8: 450-459.
[39]
Eden M, Leeb L, Frey N, Rosenberg M. Haemodynamics of an iatrogenic atrial septal defect after MitraClip implantation. European Journal of Clinical Investigation. 2020; 50: e13295.
[40]
Obadia JF, Messika-Zeitoun D, Leurent G, Iung B, Bonnet G, Piriou N, et al. Percutaneous repair or medical treatment for secondary mitral regurgitation. New England Journal of Medicine. 2018; 379: 2297-2306.
[41]
Matsumoto T, Nakamura M, Yeow WL, Hussaini A, Ram V, Makar M, et al. Impact of pulmonary hypertension on outcomes in patients with functional mitral regurgitation undergoing percutaneous edge-to-edge repair. The American Journal of Cardiology. 2014; 114: 1735-1739.
[42]
Tigges E, Blankenberg S, von Bardeleben RS, Zürn C, Bekeredjian R, Ouarrak T, et al. Implication of pulmonary hypertension in patients undergoing MitraClip therapy: results from the German transcatheter mitral valve interventions (TRAMI) registry. European Journal of Heart Failure. 2018; 20: 585-594.
[43]
Al-Bawardy R, Vemulapalli S, Thourani VH, Mack M, Dai D, Stebbins A, et al. Association of pulmonary hypertension with clinical outcomes of transcatheter mitral valve repair. JAMA Cardiology. 2020; 5: 47-56.
[44]
Ahmed A, Akintoye E, Adegbala O, Yassin A, Subahi A, Bangura L, et al. In-hospital outcomes of transcatheter mitral valve repair with MitraClip in patients with pulmonary hypertension: insights from the National Inpatient Sample. Catheterization and Cardiovascular Interventions. 2019; 94: E30-E36.
[45]
Ben-Yehuda O, Shahim B, Chen S, Liu M, Redfors B, Hahn RT, et al. Pulmonary hypertension in transcatheter mitral valve repair for secondary mitral regurgitation: the COAPT trial. Journal of the American College of Cardiology. 2020; 76: 2595-2606.
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