Comparing the clinical and prognostic impact of proximal versus nonproximal lesions in dominant right coronary artery ST-elevation myocardial infarction.

ST-segment elevation myocardial infarction cardiogenic shock percutaneous coronary intervention proximal lesion location right ventricular marginal artery thrombolytic therapy

Journal

Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions
ISSN: 1522-726X
Titre abrégé: Catheter Cardiovasc Interv
Pays: United States
ID NLM: 100884139

Informations de publication

Date de publication:
01 04 2021
Historique:
revised: 22 07 2020
received: 12 05 2020
accepted: 17 08 2020
pubmed: 2 9 2020
medline: 21 9 2021
entrez: 2 9 2020
Statut: ppublish

Résumé

To evaluate the prognostic significance of culprit lesion location in dominant right coronary artery (RCA) ST-elevation myocardial infarction (STEMI). In RCA STEMI, proximal culprit lesions have been shown to have higher rates of acute complications such as bradycardia and cardiogenic shock (CS) but data on mortality is limited. We retrospectively identified and analyzed data from consecutive patients with a dominant RCA STEMI who underwent either primary or rescue percutaneous coronary intervention (PCI) between January 2003 and December 2016. We compared the rates of sustained ventricular tachycardia (VT), CS, intra-aortic balloon pump (IABP), temporary cardiac pacing (TCP) and death between culprit lesions located proximal and distal to the origin of the last right ventricular (RV) marginal artery >1 mm in diameter. The 939 patients were included; 599 (63.7%) had a proximal lesion and 340 (36.3%) had a nonproximal lesion. The 801 (85.3%) underwent primary PCI and 138 (14.7%) underwent rescue PCI. There was no difference in first medical contact to balloon or fibrinolysis times between the groups; p = .98 and .71. There was no significant difference in the rate of sustained VT (3.0%vs. 3.2%, p = .85) but proximal lesions were more likely to develop CS (10.9%vs. 5.8%, p = .01), require IABP (7.3%vs.2.9%, p < .01) and TCP (6.3%vs. 2.6%, p = .01). Thirty-day mortality was higher for proximal lesions (5.0%vs. 0.9%, p < .01) particularly for those with CS (35.3%vs. 10.0%, p = .05). Culprit lesions located proximal to the origin of the last RV marginal artery had a higher rate of acute complications such as CS and mortality.

Sections du résumé

OBJECTIVE
To evaluate the prognostic significance of culprit lesion location in dominant right coronary artery (RCA) ST-elevation myocardial infarction (STEMI).
BACKGROUND
In RCA STEMI, proximal culprit lesions have been shown to have higher rates of acute complications such as bradycardia and cardiogenic shock (CS) but data on mortality is limited.
METHODS
We retrospectively identified and analyzed data from consecutive patients with a dominant RCA STEMI who underwent either primary or rescue percutaneous coronary intervention (PCI) between January 2003 and December 2016. We compared the rates of sustained ventricular tachycardia (VT), CS, intra-aortic balloon pump (IABP), temporary cardiac pacing (TCP) and death between culprit lesions located proximal and distal to the origin of the last right ventricular (RV) marginal artery >1 mm in diameter.
RESULTS
The 939 patients were included; 599 (63.7%) had a proximal lesion and 340 (36.3%) had a nonproximal lesion. The 801 (85.3%) underwent primary PCI and 138 (14.7%) underwent rescue PCI. There was no difference in first medical contact to balloon or fibrinolysis times between the groups; p = .98 and .71. There was no significant difference in the rate of sustained VT (3.0%vs. 3.2%, p = .85) but proximal lesions were more likely to develop CS (10.9%vs. 5.8%, p = .01), require IABP (7.3%vs.2.9%, p < .01) and TCP (6.3%vs. 2.6%, p = .01). Thirty-day mortality was higher for proximal lesions (5.0%vs. 0.9%, p < .01) particularly for those with CS (35.3%vs. 10.0%, p = .05).
CONCLUSION
Culprit lesions located proximal to the origin of the last RV marginal artery had a higher rate of acute complications such as CS and mortality.

Identifiants

pubmed: 32870605
doi: 10.1002/ccd.29245
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

E646-E652

Informations de copyright

© 2021 Wiley Periodicals LLC.

Références

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Auteurs

Giuseppe Femia (G)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.
Faculty of Medicine and Health, Sydney Medical School, The University of Sydney, Sydney, Australia.

Amir Faour (A)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.
South Western Sydney Clinical School, University of New South Wales Medicine, Liverpool, New South Wales, Australia.

Joseph Assad (J)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.
South Western Sydney Clinical School, University of New South Wales Medicine, Liverpool, New South Wales, Australia.

Lokesh Sharma (L)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.

Hanan Idris (H)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.

Oliver Gibbs (O)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.
South Western Sydney Clinical School, University of New South Wales Medicine, Liverpool, New South Wales, Australia.

Patrick Pender (P)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.

Dominic Leung (D)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.
South Western Sydney Clinical School, University of New South Wales Medicine, Liverpool, New South Wales, Australia.

Andrew Hopkins (A)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.

Rohan Rajaratnam (R)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.
South Western Sydney Clinical School, University of New South Wales Medicine, Liverpool, New South Wales, Australia.

Craig P Juergens (C)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.
South Western Sydney Clinical School, University of New South Wales Medicine, Liverpool, New South Wales, Australia.

Christian Mussap (C)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.
South Western Sydney Clinical School, University of New South Wales Medicine, Liverpool, New South Wales, Australia.

John K French (J)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.
South Western Sydney Clinical School, University of New South Wales Medicine, Liverpool, New South Wales, Australia.

Sidney Lo (S)

Department of Cardiology, Liverpool Hospital, Liverpool, New South Wales, Australia.

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