Hemodynamic Assessment in Takotsubo Syndrome.


Journal

Journal of the American College of Cardiology
ISSN: 1558-3597
Titre abrégé: J Am Coll Cardiol
Pays: United States
ID NLM: 8301365

Informations de publication

Date de publication:
23 05 2023
Historique:
received: 02 02 2023
revised: 23 02 2023
accepted: 10 03 2023
medline: 19 5 2023
pubmed: 18 5 2023
entrez: 17 5 2023
Statut: ppublish

Résumé

Takotsubo syndrome (TTS) is a reversible form of heart failure with incompletely understood pathophysiology. This study analyzed altered cardiac hemodynamics during TTS to elucidate underlying disease mechanisms. Left ventricular (LV) pressure-volume loops were recorded in 24 consecutive patients with TTS and a control population of 20 participants without cardiovascular diseases. TTS was associated with impaired LV contractility (end-systolic elastance 1.74 mm Hg/mL vs 2.35 mm Hg/mL [P = 0.024]; maximal rate of change in systolic pressure over time 1,533 mm Hg/s vs 1,763 mm Hg/s [P = 0.031]; end-systolic volume at a pressure of 150 mm Hg, 77.3 mL vs 46.4 mL [P = 0.002]); and a shortened systolic period (286 ms vs 343 ms [P < 0.001]). In response, the pressure-volume diagram was shifted rightward with significantly increased LV end-diastolic (P = 0.031) and end-systolic (P < 0.001) volumes, which preserved LV stroke volume (P = 0.370) despite a lower LV ejection fraction (P < 0.001). Diastolic function was characterized by prolonged active relaxation (relaxation constant 69.5 ms vs 45.9 ms [P < 0.001]; minimal rate of change in diastolic pressure -1,457 mm Hg/s vs -2,192 mm Hg/s [P < 0.001]), whereas diastolic stiffness (1/compliance) was not affected during TTS (end-diastolic volume at a pressure of 15 mm Hg, 96.7 mL vs 109.0 mL [P = 0.942]). Mechanical efficiency was significantly reduced in TTS (P < 0.001) considering reduced stroke work (P = 0.001), increased potential energy (P = 0.036), and a similar total pressure-volume area compared with that of control subjects (P = 0.357). TTS is characterized by reduced cardiac contractility, a shortened systolic period, inefficient energetics, and prolonged active relaxation but unaltered diastolic passive stiffness. These findings may suggest decreased phosphorylation of myofilament proteins, which represents a potential therapeutic target in TTS. (Optimized Characterization of Takotsubo Syndrome by Obtaining Pressure Volume Loops [OCTOPUS]; NCT03726528).

Sections du résumé

BACKGROUND
Takotsubo syndrome (TTS) is a reversible form of heart failure with incompletely understood pathophysiology.
OBJECTIVES
This study analyzed altered cardiac hemodynamics during TTS to elucidate underlying disease mechanisms.
METHODS
Left ventricular (LV) pressure-volume loops were recorded in 24 consecutive patients with TTS and a control population of 20 participants without cardiovascular diseases.
RESULTS
TTS was associated with impaired LV contractility (end-systolic elastance 1.74 mm Hg/mL vs 2.35 mm Hg/mL [P = 0.024]; maximal rate of change in systolic pressure over time 1,533 mm Hg/s vs 1,763 mm Hg/s [P = 0.031]; end-systolic volume at a pressure of 150 mm Hg, 77.3 mL vs 46.4 mL [P = 0.002]); and a shortened systolic period (286 ms vs 343 ms [P < 0.001]). In response, the pressure-volume diagram was shifted rightward with significantly increased LV end-diastolic (P = 0.031) and end-systolic (P < 0.001) volumes, which preserved LV stroke volume (P = 0.370) despite a lower LV ejection fraction (P < 0.001). Diastolic function was characterized by prolonged active relaxation (relaxation constant 69.5 ms vs 45.9 ms [P < 0.001]; minimal rate of change in diastolic pressure -1,457 mm Hg/s vs -2,192 mm Hg/s [P < 0.001]), whereas diastolic stiffness (1/compliance) was not affected during TTS (end-diastolic volume at a pressure of 15 mm Hg, 96.7 mL vs 109.0 mL [P = 0.942]). Mechanical efficiency was significantly reduced in TTS (P < 0.001) considering reduced stroke work (P = 0.001), increased potential energy (P = 0.036), and a similar total pressure-volume area compared with that of control subjects (P = 0.357).
CONCLUSIONS
TTS is characterized by reduced cardiac contractility, a shortened systolic period, inefficient energetics, and prolonged active relaxation but unaltered diastolic passive stiffness. These findings may suggest decreased phosphorylation of myofilament proteins, which represents a potential therapeutic target in TTS. (Optimized Characterization of Takotsubo Syndrome by Obtaining Pressure Volume Loops [OCTOPUS]; NCT03726528).

Identifiants

pubmed: 37197841
pii: S0735-1097(23)05152-5
doi: 10.1016/j.jacc.2023.03.398
pii:
doi:

Banques de données

ClinicalTrials.gov
['NCT03726528']

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1979-1991

Commentaires et corrections

Type : CommentIn
Type : CommentIn
Type : CommentIn

Informations de copyright

Copyright © 2023 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Thomas Stiermaier (T)

Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Hamburg-Kiel-Lübeck, Lübeck, Germany. Electronic address: thomas.stiermaier@uksh.de.

Jan-Christian Reil (JC)

Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany; Department of General and Interventional Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum, Bad Oeynhausen, Germany. Electronic address: janchristian.reil@gmail.com.

Vasco Sequeira (V)

Comprehensive Heart Failure Center (CHFC), University Clinic Würzburg, Würzburg, Germany.

Elias Rawish (E)

Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Hamburg-Kiel-Lübeck, Lübeck, Germany.

Matthias Mezger (M)

Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.

Toni Pätz (T)

Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.

Christina Paitazoglou (C)

Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.

Tobias Schmidt (T)

Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.

Christian Frerker (C)

Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.

Paul Steendijk (P)

Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.

Gert-Hinrich Reil (GH)

Department of Cardiology, University Hospital Oldenburg, Oldenburg, Germany.

Ingo Eitel (I)

Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Hamburg-Kiel-Lübeck, Lübeck, Germany.

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