Frontiers in valvular heart disease: outcomes of novel percutaneous procedures

For the podcast associated with this article, please visit https://academic.oup.com/eurheartj/pages/Podcasts. Percutaneous interventions have grown impressively from coronary angioplasty to coronary stenting, occlusion of patent foramen ovales (PFOs),1,2 atrial septal defects (ASDs),3,4 and ductus Botalli, to transarterial valve implantation5 and MitraClip®.6 Outcomes of transcatheter aortic valve implantation (TAVI) have improved and complications decreased with experience and new devices.7,8 Due to surgical bioprosthetic valve degeneration, aortic valve-in-valve (ViV) implantation is a new procedure that is increasingly performed. The long-term outcome of this procedure was previously unknown, but such data are now provided in the Fast Track ‘Long-term outcomes after transcatheter aortic valve implantation in failed bioprosthetic valves’ by Danny Dvir and colleagues from the University of Washington in Redmond, USA.9 Of 1006 aortic ViV procedures in patients with a median STS-PROM score, 7.3% were performed either with Medtronic self-expandable valves (i.e. CoreValve/Evolut, Medtronic Inc.) or with Edwards balloon-expandable valves (i.e. SAPIEN/SAPIEN XT/SAPIEN 3, Edwards Lifesciences). Survival at 8 years was 33.2% in patients with failed bioprostheses with an internal diameter ≤20 mm compared with 40.5% in those with bioprostheses of >20 mm (Figure 1). Aside from that, independent correlates for mortality included age and non-transfemoral access. There were 40 reinterventions after ViV with the following predictors: pre-existing severe prosthesis–patient mismatch; device malposition; Edwards balloon-expandable valves; and age. Thus, the size of the original failed valve may influence long-term mortality, and the type of the transcatheter valve may influence the need for reintervention after aortic ViV. These clinically important findings are put into context in an Editorial by Helmut Baumgartner from the University Hosptial Muenster in Germany.10 Kaplan–Meier model of survival after aortic valve-in-valve. (A) All patients included in the analysis. (B) Patients with small bioprostheses (i.e. true internal diameter ≤20 mm) had worse survival at 8 years. Note that bioprosthetic valves without a known standard for internal diameter size, such as homografts, were not included (from Bleiziffer S, Simonato M, Webb JG, Rodés-Cabau J, Pibarot P, Kornowski R, Kornowski S, Erlebach M, Duncan A, Seiffert M, Unbehaun A, Frerker C, Conzelmann L, Wijeysundera H, Kim W-K, Montorfano M, Latib A, Tchetche D, Allali A, Abdel-Wahab M, Orvin K, Stortecky S, Nissen H, Holzamer A, Urena M, Testa L, Agrifoglio M, Whisenant B, Sathananthan J, Napodano M, Landi A, Fiorina C, Zittermann A, Veulemans V, Sinning J-M, Saia F, Brecker S, Presbitero P, De Backer O, Søndergaard L, Bruschi G, Franco LN, Petronio AS, Barbanti M, Cerillo A, Spargias K, Schofer J, Cohen M, Muñoz-Garcia A, Finkelstein A, Adam M, Serra V, Teles RC, Champagnac D, Iadanza A, Chodor P, Eggebrecht H, Welsh R, Caixeta A, Salizzoni S, Dager A, Auffret V, Cheema A, Ubben T, Ancona M, Rudolph T, Gummert J, Tseng E, Noble S, Bunc M, Roberts D, Kass M, Gupta A, Leon LB, Dvir D. Long-term outcomes after transcatheter aortic valve implantation in failed bioprosthetic valves. See pages 2731–2742). Kaplan–Meier model of survival after aortic valve-in-valve. (A) All patients included in the analysis. (B) Patients with small bioprostheses (i.e. true internal diameter ≤20 mm) had worse survival at 8 years. Note that bioprosthetic valves without a known standard for internal diameter size, such as homografts, were not included (from Bleiziffer S, Simonato M, Webb JG, Rodés-Cabau J, Pibarot P, Kornowski R, Kornowski S, Erlebach M, Duncan A, Seiffert M, Unbehaun A, Frerker C, Conzelmann L, Wijeysundera H, Kim W-K, Montorfano M, Latib A, Tchetche D, Allali A, Abdel-Wahab M, Orvin K, Stortecky S, Nissen H, Holzamer A, Urena M, Testa L, Agrifoglio M, Whisenant B, Sathananthan J, Napodano M, Landi A, Fiorina C, Zittermann A, Veulemans V, Sinning J-M, Saia F, Brecker S, Presbitero P, De Backer O, Søndergaard L, Bruschi G, Franco LN, Petronio AS, Barbanti M, Cerillo A, Spargias K, Schofer J, Cohen M, Muñoz-Garcia A, Finkelstein A, Adam M, Serra V, Teles RC, Champagnac D, Iadanza A, Chodor P, Eggebrecht H, Welsh R, Caixeta A, Salizzoni S, Dager A, Auffret V, Cheema A, Ubben T, Ancona M, Rudolph T, Gummert J, Tseng E, Noble S, Bunc M, Roberts D, Kass M, Gupta A, Leon LB, Dvir D. Long-term outcomes after transcatheter aortic valve implantation in failed bioprosthetic valves. See pages 2731–2742). This topic is further investigated in another important manuscript entitled ‘Comparison of in-hospital outcomes and readmissions for valve-in-valve transcatheter aortic valve replacement vs. reoperative surgical aortic valve replacement: a contemporary assessment of real-world outcomes’ authored by Sameer Hirji and colleagues from the Brigham and Women’s Hospital in Boston, Massachusetts, USA. They performed a head-to-head comparison of contemporary 30-day outcomes and readmissions of 3443 ViV-TAVI and 372 matched high-risk reoperative surgical aortic valve replacements.11 Unadjusted, ViV-TAVR patients had a lower 30-day mortality of 2.7% vs. 5.0%, lower 30-day morbidity of 66.4% vs. 79%, and lower rates of major bleeding of 35.8% vs. 50%. On multivariable analysis, surgery was a risk factor for both 30-day mortality and 30-day morbidity (Figure 2). After matching, ViV-TAVR was associated with lower odds of 30-day mortality of 0.41, of 30-day morbidity of 0.53, and of major bleeding of 0.66. ViV-TAVR was also associated with 2-day shorter length of hospital stay and higher odds of routine home discharges compared with redo surgery. Thus, ViV-TAVR appears to confer an advantage over redo surgery in terms of mortality, morbidity, and bleeding. These impressive novel findings are further discussed in an insightful Editorial by Bernard Iung from the Bichat Hospital in Paris, France.12 Forest plot demonstrating the independent predictors of 30-day morbidity following re-surgical aortic valve replacement and valve-in-valve transcatheter aortic valve replacement (from Hirji SA, Percy ED, Zogg CK, Malarczyk A, Harloff MT, Yazdchi F, Kaneko T. Comparison of in-hospital outcomes and readmissions for valve-in-valve transcatheter aortic valve replacement vs. reoperative surgical aortic valve replacement: a contemporary assessment of real-world outcomes. See pages 2747–2755). Forest plot demonstrating the independent predictors of 30-day morbidity following re-surgical aortic valve replacement and valve-in-valve transcatheter aortic valve replacement (from Hirji SA, Percy ED, Zogg CK, Malarczyk A, Harloff MT, Yazdchi F, Kaneko T. Comparison of in-hospital outcomes and readmissions for valve-in-valve transcatheter aortic valve replacement vs. reoperative surgical aortic valve replacement: a contemporary assessment of real-world outcomes. See pages 2747–2755). Cardiac amyloidosis has taken centre stage as a cause of heart failure with preserved ejection fraction, thanks to the introduction of a clinically relevant staging system,13 effective drugs,14 and promising novel monoclonal15 and genetic compounds.16 There are different echocardiographic phenotypes17 and it may indeed co-exist in elderly patients with aortic stenosis.18 In those referred for TAVI, this may be particularly important, as reported in the article ‘Prevalence and outcome of dual aortic stenosis and cardiac amyloid pathology in patients referred for transcatheter aortic valve implantation’19 by Paul Scully and colleagues from the Barts Heart Centre and the Institute of Cardiovascular Sciences in London, UK. The authors characterized 200 patients with a mean age of 85 years and this dual pathology. Amyloid was found in 13% of patients with aortic stenosis and led to a reduced quality of life. In these patients, left ventricular wall thickness was greater, ECG voltages lower, and voltage/mass ratio lower, while high-sensitivity troponin T (hsTnT) and N-terminal probrain natriuretic peptide (NT-proBNP) were higher. Gender, comorbidities, 6-min walk distance, aortic stenosis severity, prevalence of disproportionate hypertrophy, and post-TAVI complication rates were the same. At 19 months of follow-up, there was no mortality difference. TAVI equally improved outcome in the overall population and in those with amyloid aortic stenosis. Thus, amyloidosis is common and differs from lone aortic stenosis. The clinical impact of these findings are put into context in an Editorial by Sharmila Dorbala and colleagues from Harvard Medical School in Boston, Massachusetts, USA.20 The clinical impact of new-onset persistent left bundle branch block (LBBB) and permanent pacemaker implantation21 in TAVI recipients remains controversial.22 In a meta-analysis entitled ‘Clinical impact of conduction disturbances in transcatheter aortic valve replacement recipients: a systematic review and meta-analysis’, Josep Rodés-Cabau and colleagues from the Quebec Heart & Lung Institute at Laval University in Québec, Canada evaluated the impact of (i) periprocedural LBBB and permanent pacemaker implantation post-TAVI on 1-year all-cause death, cardiac death, and heart failure hospitalization; and (ii) the impact of new-onset LBBB on the need for permanent pacemaker implantation at 1-year follow-up.23 The authors included 7792 patients and 42 927 patients for the evaluation of the impact of new-onset LBBB and permanent pacemaker implantation after TAVI, respectively. At 1-year follow-up, new-onset LBBB was associated with an increased risk of all-cause death with a risk ratio of 1.32, cardiac death with one of 1.46, heart failure hospitalization with one of 1.35, and permanent pacemaker implantation with one of 1.89. Periprocedural permanent pacemaker implantation was associated with a higher risk of all-cause death with a risk ratio of 1.17 and heart failure hospitalization with a risk ratio of 1.18, but not cardiac death. The clinical implications of these novel findings are further discussed in an Editorial by Vincent Auffret and colleagues from the Hopital Pontchaillou in Rennes, France.24 Patients with tricuspid regurgitation and pulmonary hypertension are often excluded from surgery,25 although they have a poor survival.26 Transcatheter tricuspid valve repair using the MitraClip® technique is a novel treatment option for such patients, as outlined by Philipp Lurz and colleagues from the University of Leipzig–Heart Center in Germany in their article ‘Clinical characteristics, diagnosis, and risk stratification of pulmonary hypertension in severe tricuspid regurgitation and implications for transcatheter tricuspid valve repair’.27 A total of 243 patients underwent transcatheter tricuspid valve repair. In 121, pulmonary hypertension had an invasively determined systolic pulmonary artery pressure ≥50 mmHg. Patients with pulmonary systolic pressure ≥50 mmHg were at higher pre-operative risk, had more severe symptoms, higher NT-pro-BNP levels, more impaired right ventricular function, and afterload-corrected RV function. Transcatheter tricuspid valve repair success was similar in those with pulmonary systolic pressure ≥50 mmHg or <50 mmHg. The echocardiographic diagnostic accuracy to detect pulmonary hypertension was only 55%. During follow-up, 35% of patients reached the endpoint of death, heart failure hospitalization, and reintervention. A discordant diagnosis of invasively or echocardiographically determined pulmonary hypertension carried the highest risk for the combined clinical endpoint, while concordant patients had a similar survival-free time from the combined endpoint. Thus, discordant echocardiographic and invasive findings of pulmonary pressures in severe tricuspid regurgitation predict outcomes after transcatheter tricuspid valve repair, provocative results that are further discussed in an Editorial by Rebecca Hahn from Columbia University in New York, USA.28 Mitral regurgitation and tricuspid regurgitation secondary to heart failure remain challenging in almost every aspect. This is comprehensively reviewed in the article ‘Secondary valve regurgitation in patients with heart failure with preserved ejection fraction, heart failure with mid-range ejection fraction, and heart failure with reduced ejection fraction’ by Georg Goliasch and colleagues from the Medical University of Vienna in Austria.29 The recent heart failure categorization, i.e. heart failure with reduced, mid-range, and preserved ejection fraction, has left secondary valve regurgitation as a determining factor undefined. This review discusses the current understanding, epidemiological considerations, impact, public health burden, mechanisms, and treatment options of secondary valve regurgitation in heart failure. Furthermore, it identifies important gaps in knowledge and future directions for research, and provides potential solutions for diagnosis and treatment. The issue is also complemented by various Discussion Forum contributions. In a piece entitled ‘Transcatheter tricuspid valve repair in patients with pulmonary hypertension’, Michele D’Alto from the Monaldi Hospital in Naples, Italy comments on the contribution ‘Clinical characteristics, diagnosis, and risk stratification of pulmonary hypertension in severe tricuspid regurgitation and implications for transcatheter tricuspid valve repair’ by Lurz et al. that is published in this issue. 27,30 Lurz et al. respond in a separate comment.31 In a contribution entitled ‘Aortic stenosis and amyloid heart disease: “the 2A dangerous liaisons”’, Dania Mohty and colleagues from the King Faisal Specialist Hospital and Research Center in Riyadh, Saudi Arabia comments on the recent contribution also contained in this issue entitled ‘Prevalence and outcome of dual aortic stenosis and cardiac amyloid pathology in patients referred for transcatheter aortic valve implantation’ by Scully et al. 19,32 The editors hope that readers of this issue of the European Heart Journal will find it of interest. With thanks to Amelia Meier-Batschelet for help with compilation of this article.