Evidence map›Paper›PMID 40049585›Full record

ArticleEuropean heart journal2025

The Australian-New Zealand spontaneous coronary artery dissection cohort study: predictors of major adverse cardiovascular events and recurrence.

Quan M Dang, Peter J Psaltis, Sonya Burgess, Jaya Chandrasekhar, Swati Mukherjee, Leonard Kritharides, Nigel Jepson, Sarah Fairley, Abdul Ihdayhid, Jamie Layland and 15 more

Abstract readMulticenter Study
In one paragraph

Article in European heart journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed.

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  14. Spontaneous Coronary Artery Dissection Clinical Review: Current State of Evidence and Challenges Ahead.The International journal of angiology : official publication of the International College of Angiology, Inc · 2025
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

25 authors.

Quan M DangWestmead Applied Research Centre, University of Sydney, Sydney, Australia.ORCID 0000-0003-0309-1289
Peter J PsaltisAdelaide Medical School, The University of Adelaide, Adelaide, Australia.ORCID 0000-0003-0222-5468
Sonya BurgessUniversity of Sydney, Sydney, Australia.ORCID 0000-0001-5262-3064
Jaya ChandrasekharDepartment of Cardiology, Box Hill Hospital, Melbourne, Australia.
Swati MukherjeeDepartment of Cardiology, Cabrini Hospital, Melbourne, Australia.ORCID 0009-0001-4791-2328
Leonard KritharidesANZAC Medical Research Institute, Sydney, Australia.ORCID 0000-0001-5818-8024
Nigel JepsonDepartment of Cardiology, Prince of Wales Hospital, Sydney, Australia.
Sarah FairleyDepartment of Cardiology, Wellington Hospital, Wellington, New Zealand.
Abdul IhdayhidDepartment of Cardiology, Fiona Stanley Hospital, Perth, Australia.ORCID 0000-0003-0501-0980
Jamie LaylandDepartment of Cardiology, Frankston Hospital, Melbourne, Australia.
Richard SzirtDepartment of Cardiology, St George Hospital, Sydney, Australia.
Seif El-JackCardiovascular Unit, North Shore Hospital, Waitemata, New Zealand.
Aniket PuriDepartment of Cardiology, Christchurch Hospital, Christchurch, New Zealand.
Esther DavisVictorian Heart Institute, Monash University, Melbourne, Australia.
Imran ShiekhDepartment of Cardiology, Royal Perth Hospital, Perth, Australia.
Ruth ArnoldOrange Base Hospital, Orange, Australia.
Monique WattsDepartment of Cardiology, Alfred Hospital, Melbourne, Australia.
Jessica A MaratheANZAC Medical Research Institute, Sydney, Australia.
Rohan BhagwandeenCardiology Department, John Hunter Hospital, Newcastle, Australia.ORCID 0009-0001-2163-5393
Edwina Wing-LunUniversity of Sydney, Sydney, Australia.ORCID 0000-0001-8301-9249
Ravinay BhindiDepartment of Cardiology, Royal North Shore Hospital, Sydney, Australia.
Tom FordThe University of Newcastle Central Coast Clinical School, Gosford, Australia.ORCID 0000-0003-4009-6652
Sidney LoDepartment of Cardiology, Liverpool Hospital, Sydney, Australia.
Simone MarschnerWestmead Applied Research Centre, University of Sydney, Sydney, Australia.ORCID 0000-0002-5484-9144
Sarah ZamanWestmead Applied Research Centre, University of Sydney, Sydney, Australia.ORCID 0000-0001-6289-583X

Funding

CSANZ-Bayer Young Investigator GrantNational Heart Foundation FLF 106656New South Wales Cardiovascular Research Elite Post-doctoral GrantNew South Wales Health Cardiovascular Research Elite Post-doctoral GrantUniversity of SydneyWellcome Trust 102627
6 · The paper itself

Abstract

BACKGROUND AND

aimsSpontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of acute coronary syndrome (ACS). Recent data suggest a harmful association of dual antiplatelet therapy compared with single antiplatelet therapy following SCAD. This study investigated independent predictors of major adverse cardiovascular events (MACEs) and recurrence in patients with SCAD.

methodsThis multicentre cohort study involving 23 Australian and New Zealand sites included patients aged ≥18 years with an ACS due to SCAD confirmed on core laboratory adjudication. Multivariable Cox proportional hazard models analysed predictors for the primary MACE outcome.

resultsAmong 586 patients, 505 (150 prospective, 355 retrospective) with SCAD confirmed by core laboratory adjudication, mean age was 52.2 ± 10.6 years, 88.6% were female, and 74.5% were Caucasian. At long-term follow-up (median 21 months), MACE and SCAD recurrence occurred in 8.6% and 3.6% of patients, respectively. Oral anticoagulation on discharge [adjusted hazard ratio (aHR) 3.8, 95% confidence interval (CI) 1.6-9.3, P = .003], ticagrelor combined with aspirin (aHR 1.8, 95% CI 1.04-3.2, P = .037), fibromuscular dysplasia (aHR 2.2, 95% CI 1.05-4.5, P = .037), and history of stroke (aHR 3.8, 95% CI 1.2-12.2, P = .03) were independently associated with higher MACE. Fibromuscular dysplasia (aHR 3.9, 95% CI 1.5-26.5, P = .01), ticagrelor combined with aspirin (aHR 2.6, 95% CI 2.1-5.3, P = .01), and history of stroke (aHR 6.2, 95% CI 1.8-9.5, P = .01) were also associated with higher SCAD recurrence.

conclusionsThe findings support the hypothesis that SCAD is primarily caused by intramural bleeding, with a harmful association of more potent antiplatelet therapy and anticoagulation with adverse cardiovascular outcomes.

Indexed as

Acute Coronary SyndromeCoronary Vessel AnomaliesVascular DiseasesAdultAgedAnticoagulantsAspirinAustraliaFemaleHumansMaleMiddle AgedNew ZealandPlatelet Aggregation InhibitorsProspective StudiesRecurrenceAnticoagulantsAspirinPlatelet Aggregation InhibitorsTicagrelorAcute coronary syndromeAnticoagulationFibromuscular dysplasiaMajor adverse cardiovascular eventMyocardial infarctionRecurrenceSpontaneous coronary artery dissectionTicagrelor

Identifiers

PMID40049585
PMCPMC12127729

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.