Evolution of left ventricular function among subjects with ST-elevation myocardial infarction after percutaneous coronary intervention.


Journal

BMC cardiovascular disorders
ISSN: 1471-2261
Titre abrégé: BMC Cardiovasc Disord
Pays: England
ID NLM: 100968539

Informations de publication

Date de publication:
29 06 2020
Historique:
received: 26 02 2020
accepted: 19 05 2020
entrez: 1 7 2020
pubmed: 1 7 2020
medline: 12 1 2021
Statut: epublish

Résumé

Atrioventricular plane displacement (AVPD) reflects longitudinal left ventricular (LV) systolic function, and wall thickening (WT) regional radial LV function. The temporal evolution of these measures after STEMI with CMR has not been evaluated. We aimed to investigate how AVPD and WT are affected globally and regionally from the sub-acute to the chronic phase after ST-elevation myocardial infarction (STEMI). Healthy volunteers without cardiovascular disease and medication (controls, n = 20) and patients from the CHILL-MI study ( NCT01379261 ) prospectively underwent magnetic resonance imaging (MRI) 2-6 days and 6 months after STEMI (n = 77). CHILL-MI randomized STEMI-patients to cooling therapy initiated before reperfusion or standard of care. AVPD was measured at six points in three long axis cine images and wall thickening in short axis cine images. Infarction was quantified using late gadolinium enhancement (LGE) and used to define infarct and remote segments. There were no difference in AVPD either at acute or chronic phase (p = 0.90 and p = 0.40) or WT (p = 0.85 and p = 0.99) between patients randomized to cooling therapy and standard of care. Therefore, the results are presented for the pooled cohort. Global AVPD was decreased in both the sub-acute (12 ± 2 mm, p < 0.001) and the chronic phase (13 ± 2 mm, p < 0.001) compared to controls (15 ± 2 mm) with a partial recovery of AVPD (p < 0.001) in the chronic phase. Patients with left anterior descending (LAD) and right coronary artery (RCA) infarcts had decreased AVPD in the chronic phase in both infarcted and remote segments. Mean WT was decreased in patients with LAD infarction both in the sub-acute and the chronic phase in both infarcted and remote segments. The decrease in WT in patients with RCA and left circumflex (LCx) infarcts was more affected in the infarcted segments, especially in the chronic phase. AVPD was a global rather than regional marker of cardiac function in this STEMI study and this may explain the prognostic importance of local measurements of mitral annular plane systolic excursion (MAPSE). The decrease in WT in remote myocardium even in the chronic phase needs to be taken into consideration when combining functional measurements with infarct quantification for diagnosis of post-ischemic stunning and hibernation.

Sections du résumé

BACKGROUND
Atrioventricular plane displacement (AVPD) reflects longitudinal left ventricular (LV) systolic function, and wall thickening (WT) regional radial LV function. The temporal evolution of these measures after STEMI with CMR has not been evaluated. We aimed to investigate how AVPD and WT are affected globally and regionally from the sub-acute to the chronic phase after ST-elevation myocardial infarction (STEMI).
METHODS
Healthy volunteers without cardiovascular disease and medication (controls, n = 20) and patients from the CHILL-MI study ( NCT01379261 ) prospectively underwent magnetic resonance imaging (MRI) 2-6 days and 6 months after STEMI (n = 77). CHILL-MI randomized STEMI-patients to cooling therapy initiated before reperfusion or standard of care. AVPD was measured at six points in three long axis cine images and wall thickening in short axis cine images. Infarction was quantified using late gadolinium enhancement (LGE) and used to define infarct and remote segments.
RESULTS
There were no difference in AVPD either at acute or chronic phase (p = 0.90 and p = 0.40) or WT (p = 0.85 and p = 0.99) between patients randomized to cooling therapy and standard of care. Therefore, the results are presented for the pooled cohort. Global AVPD was decreased in both the sub-acute (12 ± 2 mm, p < 0.001) and the chronic phase (13 ± 2 mm, p < 0.001) compared to controls (15 ± 2 mm) with a partial recovery of AVPD (p < 0.001) in the chronic phase. Patients with left anterior descending (LAD) and right coronary artery (RCA) infarcts had decreased AVPD in the chronic phase in both infarcted and remote segments. Mean WT was decreased in patients with LAD infarction both in the sub-acute and the chronic phase in both infarcted and remote segments. The decrease in WT in patients with RCA and left circumflex (LCx) infarcts was more affected in the infarcted segments, especially in the chronic phase.
CONCLUSION
AVPD was a global rather than regional marker of cardiac function in this STEMI study and this may explain the prognostic importance of local measurements of mitral annular plane systolic excursion (MAPSE). The decrease in WT in remote myocardium even in the chronic phase needs to be taken into consideration when combining functional measurements with infarct quantification for diagnosis of post-ischemic stunning and hibernation.

Identifiants

pubmed: 32600336
doi: 10.1186/s12872-020-01540-y
pii: 10.1186/s12872-020-01540-y
pmc: PMC7322852
doi:

Types de publication

Journal Article Multicenter Study Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

309

Subventions

Organisme : Vetenskapsrådet
ID : Vetenskapsrådet
Pays : International
Organisme : Hjärt-Lungfonden
ID : Hjärt-Lungfonden
Pays : International
Organisme : Knut och Alice Wallenbergs Stiftelse
ID : Wallenberg Molecular Medicine
Pays : International
Organisme : Philips
ID : CHILL-MI
Pays : International
Organisme : Lunds Universitet
ID : ALF
Pays : International

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Auteurs

Ulrika Pahlm (U)

Clinical Physiology, Department of Clinical Sciences Lund, Lund University, Skane University Hospital, Lund, Sweden.
Department of Emergency Medicine, Skane University Hospital, Lund, Sweden.

Ellen Ostenfeld (E)

Clinical Physiology, Department of Clinical Sciences Lund, Lund University, Skane University Hospital, Lund, Sweden.

Felicia Seemann (F)

Clinical Physiology, Department of Clinical Sciences Lund, Lund University, Skane University Hospital, Lund, Sweden.
Department of Biomedical Engineering, Faculty of Engineering, Lund University, Lund, Sweden.

Henrik Engblom (H)

Clinical Physiology, Department of Clinical Sciences Lund, Lund University, Skane University Hospital, Lund, Sweden.

David Erlinge (D)

Cardiology, Department of Clinical Sciences Lund, Lund University, Skane University Hospital, Lund, Sweden.

Einar Heiberg (E)

Clinical Physiology, Department of Clinical Sciences Lund, Lund University, Skane University Hospital, Lund, Sweden.
Wallenberg Center for Molecular Medicine, Lund University, Lund, Sweden.

Håkan Arheden (H)

Clinical Physiology, Department of Clinical Sciences Lund, Lund University, Skane University Hospital, Lund, Sweden.

Marcus Carlsson (M)

Clinical Physiology, Department of Clinical Sciences Lund, Lund University, Skane University Hospital, Lund, Sweden. marcus.carlsson@med.lu.se.

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