Clinical and Experimental Evidence for a Strain-Based Classification of Left Bundle Branch Block-Induced Cardiac Remodeling.


Journal

Circulation. Cardiovascular imaging
ISSN: 1942-0080
Titre abrégé: Circ Cardiovasc Imaging
Pays: United States
ID NLM: 101479935

Informations de publication

Date de publication:
11 2022
Historique:
pubmed: 5 11 2022
medline: 19 11 2022
entrez: 4 11 2022
Statut: ppublish

Résumé

Septal strain patterns measured by echocardiography reflect the severity of left bundle branch block (LBBB)-induced left ventricular (LV) dysfunction. We investigated whether these LBBB strain stages predicted the response to cardiac resynchronization therapy in an observational study and developed a sheep model of LBBB-induced cardiomyopathy. The clinical study enrolled cardiac resynchronization therapy patients who underwent echocardiographic examination with speckle-tracking strain analysis before cardiac resynchronization therapy implant. In an experimental sheep model with pacing-induced dyssynchrony, LV remodeling and strain were assessed at baseline, at 8 and 16 weeks. Septal strain curves were classified into 5 patterns (LBBB-0 to LBBB-4). The clinical study involved 250 patients (age 65 [58; 72] years; 79% men; 89% LBBB) with a median LV ejection fraction of 25 [21; 30]%. Across the stages, cardiac resynchronization therapy resulted in a gradual volumetric response, ranging from no response in LBBB-0 patients (ΔLV end-systolic volume 0 [-12; 15]%) to super-response in LBBB-4 patients (ΔLV end-systolic volume -44 [-64; -18]%) ( The strain-based LBBB classification reflects a pathophysiological continuum of LBBB-induced remodeling over time and is associated with the extent of reverse remodeling in observational cardiac resynchronization therapy-eligible patients.

Sections du résumé

BACKGROUND
Septal strain patterns measured by echocardiography reflect the severity of left bundle branch block (LBBB)-induced left ventricular (LV) dysfunction. We investigated whether these LBBB strain stages predicted the response to cardiac resynchronization therapy in an observational study and developed a sheep model of LBBB-induced cardiomyopathy.
METHODS
The clinical study enrolled cardiac resynchronization therapy patients who underwent echocardiographic examination with speckle-tracking strain analysis before cardiac resynchronization therapy implant. In an experimental sheep model with pacing-induced dyssynchrony, LV remodeling and strain were assessed at baseline, at 8 and 16 weeks. Septal strain curves were classified into 5 patterns (LBBB-0 to LBBB-4).
RESULTS
The clinical study involved 250 patients (age 65 [58; 72] years; 79% men; 89% LBBB) with a median LV ejection fraction of 25 [21; 30]%. Across the stages, cardiac resynchronization therapy resulted in a gradual volumetric response, ranging from no response in LBBB-0 patients (ΔLV end-systolic volume 0 [-12; 15]%) to super-response in LBBB-4 patients (ΔLV end-systolic volume -44 [-64; -18]%) (
CONCLUSIONS
The strain-based LBBB classification reflects a pathophysiological continuum of LBBB-induced remodeling over time and is associated with the extent of reverse remodeling in observational cardiac resynchronization therapy-eligible patients.

Identifiants

pubmed: 36330792
doi: 10.1161/CIRCIMAGING.122.014296
doi:

Types de publication

Observational Study Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e014296

Commentaires et corrections

Type : CommentIn

Auteurs

Simon Calle (S)

Department of Cardiology, University Hospital Ghent, Belgium (S.C., M.D.B., J.D.P., F.T.).

Jürgen Duchenne (J)

Department of Cardiovascular Sciences, KU Leuven, Belgium (J.D., A.S.B., I.S., A.P., J.-U.V.).
Department of Cardiovascular Diseases, University Hospital Leuven, Belgium (J.D., A.P., J.-U.V.).

Ahmed S Beela (AS)

Department of Cardiovascular Sciences, KU Leuven, Belgium (J.D., A.S.B., I.S., A.P., J.-U.V.).
Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, the Netherlands (A.S.B.).
Department of Cardiovascular Diseases, Suez Canal University, Egypt (A.S.B.).

Ivan Stankovic (I)

Department of Cardiovascular Sciences, KU Leuven, Belgium (J.D., A.S.B., I.S., A.P., J.-U.V.).
Clinical Hospital Centre Zemun, Faculty of Medicine, University of Belgrade, Serbia (I.S.).

Alexis Puvrez (A)

Department of Cardiovascular Sciences, KU Leuven, Belgium (J.D., A.S.B., I.S., A.P., J.-U.V.).
Department of Cardiovascular Diseases, University Hospital Leuven, Belgium (J.D., A.P., J.-U.V.).

Stefan Winter (S)

Department of Cardiology, St. Vinzenz Hospital, Germany (S.W., W.F.).

Wolfgang Fehske (W)

Department of Cardiology, St. Vinzenz Hospital, Germany (S.W., W.F.).

Marit Aarones (M)

Department of Medicine, Diakonhjemmet Hospital, Norway (M.A.H.).

Marc De Buyzere (M)

Department of Cardiology, University Hospital Ghent, Belgium (S.C., M.D.B., J.D.P., F.T.).

Jan De Pooter (J)

Department of Cardiology, University Hospital Ghent, Belgium (S.C., M.D.B., J.D.P., F.T.).

Jens-Uwe Voigt (JU)

Department of Cardiovascular Sciences, KU Leuven, Belgium (J.D., A.S.B., I.S., A.P., J.-U.V.).
Department of Cardiovascular Diseases, University Hospital Leuven, Belgium (J.D., A.P., J.-U.V.).

Frank Timmermans (F)

Department of Cardiology, University Hospital Ghent, Belgium (S.C., M.D.B., J.D.P., F.T.).

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