Coronary microvascular dysfunction in Takotsubo syndrome and associations with left ventricular function.

Cardiovascular magnetic resonance imaging Coronary flow reserve Coronary microvascular dysfunction Index of microcirculatory resistance Ischaemia and no obstructive coronary arteries Takotsubo syndrome

Journal

ESC heart failure
ISSN: 2055-5822
Titre abrégé: ESC Heart Fail
Pays: England
ID NLM: 101669191

Informations de publication

Date de publication:
08 2023
Historique:
revised: 30 03 2023
received: 20 12 2022
accepted: 24 04 2023
medline: 31 7 2023
pubmed: 23 5 2023
entrez: 23 5 2023
Statut: ppublish

Résumé

Coronary microvascular dysfunction (CMD) has been proposed as an important pathophysiological mechanism in Takotsubo syndrome (TTS). Our aims were (i) to evaluate and compare levels of CMD in patients with TTS and patients with ischaemia and no obstructive coronary arteries (INOCA) and (ii) to investigate associations between CMD and clinical parameters, left ventricular function, and coronary atherosclerosis in TTS. We conducted a prospective study of 27 female TTS patients and an equally sized, age- and gender-matched, cohort of INOCA patients. Coronary microvascular function was quantified invasively using the index of microcirculatory resistance (IMR), coronary flow reserve (CFR), and resistive reserve ratio (RRR). CMD was defined as IMR ≥ 25 and/or CFR ≤ 2. In the TTS patients, left ventricular function was assessed with echocardiography and cardiovascular magnetic resonance (CMR) imaging, and coronary atherosclerosis was visualized with intravascular ultrasound with near-infrared spectroscopy (IVUS-NIRS). The incidence of CMD was higher in the TTS patients than in the INOCA cohort (78% vs. 44%, P = 0.01), with higher IMR (30 vs. 14, P = 0.002), lower CFR (1.8 vs. 2.8, P = 0.009), and lower RRR (2.1 vs. 3.5, P = 0.003). In apical compared with midventricular TTS, IMR was numerically higher (50 vs. 28, P = 0.20), whereas CFR and RRR were lower (1.5 vs. 2.5, P = 0.003 and 1.6 vs. 2.7, P = 0.01, respectively). Global longitudinal strain and global circumferential strain, assessed with CMR imaging, were more impaired in apical than in midventricular TTS (-11 vs. -14, P < 0.001 and -12 vs. -15, P = 0.049, respectively). In the TTS patients, CFR and RRR correlated with echocardiography-derived (R Coronary microvascular dysfunction is common in patients with TTS and more frequent than in patients with INOCA. CMD in TTS is more severe in the apical compared with the midventricular phenotype of the syndrome, is associated with left ventricular function, but is unrelated to coronary atherosclerosis. Our results support the notion of CMD as a key mediator in TTS.

Identifiants

pubmed: 37218383
doi: 10.1002/ehf2.14394
pmc: PMC10375085
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

2395-2405

Informations de copyright

© 2023 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.

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Auteurs

Christina Ekenbäck (C)

Karolinska Institutet, Department of Clinical Sciences, Danderyd Hospital, Division of Cardiovascular Medicine, Stockholm, Sweden.
Department of Cardiology and Physiology, Danderyd Hospital, Stockholm, Sweden.

Jannike Nickander (J)

Department of Clinical Physiology, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.

Fadi Jokhaji (F)

Department of Cardiology and Physiology, Danderyd Hospital, Stockholm, Sweden.

Per Tornvall (P)

Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden.

Henrik Engblom (H)

Department of Clinical Physiology, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
Department of Clinical Physiology, Skåne University Hospital and Lund University, Lund, Sweden.

Jonas Spaak (J)

Karolinska Institutet, Department of Clinical Sciences, Danderyd Hospital, Division of Cardiovascular Medicine, Stockholm, Sweden.
Department of Cardiology and Physiology, Danderyd Hospital, Stockholm, Sweden.

Jonas Persson (J)

Karolinska Institutet, Department of Clinical Sciences, Danderyd Hospital, Division of Cardiovascular Medicine, Stockholm, Sweden.
Department of Cardiology and Physiology, Danderyd Hospital, Stockholm, Sweden.

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