Case report: takotsubo cardiomyopathy after transcatheter aortic valve-in-valve replacement.
Case report
Myocardial infarction
Stress cardiomyopathy
TAVR
Takotsubo
Journal
European heart journal. Case reports
ISSN: 2514-2119
Titre abrégé: Eur Heart J Case Rep
Pays: England
ID NLM: 101730741
Informations de publication
Date de publication:
Jan 2021
Jan 2021
Historique:
received:
11
06
2020
revised:
17
07
2020
accepted:
05
11
2020
entrez:
1
3
2021
pubmed:
2
3
2021
medline:
2
3
2021
Statut:
epublish
Résumé
Transcatheter aortic valve implantation (TAVI) has become a first-line therapeutic option in patients with severe, symptomatic aortic stenosis at increased surgical risk. Despite its success, the TAVI procedure has been associated with acute life-threatening complications as myocardial infarction secondary to periprocedural coronary occlusion, annular rupture, or vascular injury. A 79-year-old woman with a dysfunctional bioprosthetic valve following previous surgical valve replacement was hospitalized in our institution to perform a Valve-in-Valve Transcatheter Aortic Valve Replacement (ViV TAVR). Shortly after the implantation of an Evolut R valve (without complication), left ventricle dysfunction with apical akinesia and basal hyperkinesia was identified during bedside transthoracic echocardiography, in spite of a good prosthesis implantation and function. A concomitant Troponin elevation was noted, and the day-after resting electrocardiogram showed a lateral T-wave inversion. Coronary computed tomography angiography showed no coronary stenosis or occlusion, cardiac magnetic resonance imaging showed no necrosis or fibrosis, and no argument for myocarditis. The patient remained asymptomatic during her hospital stay, and the aforementioned anomalies spontaneously regressed after an in-hospital 2-week surveillance. In the presence of these transient anomalies and after ruling out myocardial infarction and myocarditis, post-procedural stress cardiomyopathy (takotsubo) was diagnosed. Post-TAVR stress-related cardiomyopathy seems to be an extremely rare entity. To our knowledge, this is the first case of a takotsubo cardiomyopathy after ViV TAVR. Though the association between the two seems likely to be causal, no clear physiopathological explanation can be formulated.
Sections du résumé
BACKGROUND
BACKGROUND
Transcatheter aortic valve implantation (TAVI) has become a first-line therapeutic option in patients with severe, symptomatic aortic stenosis at increased surgical risk. Despite its success, the TAVI procedure has been associated with acute life-threatening complications as myocardial infarction secondary to periprocedural coronary occlusion, annular rupture, or vascular injury.
CASE SUMMARY
METHODS
A 79-year-old woman with a dysfunctional bioprosthetic valve following previous surgical valve replacement was hospitalized in our institution to perform a Valve-in-Valve Transcatheter Aortic Valve Replacement (ViV TAVR). Shortly after the implantation of an Evolut R valve (without complication), left ventricle dysfunction with apical akinesia and basal hyperkinesia was identified during bedside transthoracic echocardiography, in spite of a good prosthesis implantation and function. A concomitant Troponin elevation was noted, and the day-after resting electrocardiogram showed a lateral T-wave inversion. Coronary computed tomography angiography showed no coronary stenosis or occlusion, cardiac magnetic resonance imaging showed no necrosis or fibrosis, and no argument for myocarditis. The patient remained asymptomatic during her hospital stay, and the aforementioned anomalies spontaneously regressed after an in-hospital 2-week surveillance. In the presence of these transient anomalies and after ruling out myocardial infarction and myocarditis, post-procedural stress cardiomyopathy (takotsubo) was diagnosed.
DISCUSSION
CONCLUSIONS
Post-TAVR stress-related cardiomyopathy seems to be an extremely rare entity. To our knowledge, this is the first case of a takotsubo cardiomyopathy after ViV TAVR. Though the association between the two seems likely to be causal, no clear physiopathological explanation can be formulated.
Identifiants
pubmed: 33644645
doi: 10.1093/ehjcr/ytaa457
pii: ytaa457
pmc: PMC7898568
doi:
Types de publication
Journal Article
Langues
eng
Pagination
ytaa457Informations de copyright
© The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology.
Références
Eur Heart J. 2018 Jun 7;39(22):2032-2046
pubmed: 29850871
JACC Cardiovasc Interv. 2013 May;6(5):452-61
pubmed: 23602458
JACC Cardiovasc Interv. 2009 Sep;2(9):811-20
pubmed: 19778768
N Engl J Med. 2015 Sep 3;373(10):929-38
pubmed: 26332547
JACC Cardiovasc Interv. 2016 Jun 27;9(12):1302-1304
pubmed: 27262865