Thrombosis and Acute Coronary-Artery Lesions in Sudden Cardiac Ischemic Death

Davies, Michael John; Thomas, Anthony

doi:10.1056/nejm198405033101801

Cited by 1,694Acute Myocardial Infarction ResearchCoronary Interventions and DiagnosticsCardiac electrophysiology and arrhythmias

Thrombosis and Acute Coronary-Artery Lesions in Sudden Cardiac Ischemic Death

Davies, Michael John, Thomas, Anthony·1984·New England Journal of Medicine

DOI 10.1056/nejm198405033101801

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Abstract

The nature of the pathologic lesion in sudden cardiac ischemic death is in dispute. Among 100 subjects who died of ischemic heart disease in less than six hours, coronary thrombi were found in 74. There was no difference in incidence between those who died in less than 15 minutes, those who died in 15 to 60 minutes, and those who died after one hour. Among 26 cases without an intraluminal thrombus, plaque fissuring was found in 21; thus, in only 5 cases was no acute arterial lesion demonstrated. No intraluminal thrombi were found in age-matched controls. Forty-eight of the 74 thrombi were found at sites of preexisting high-grade stenosis; 14 were found at points of previous stenosis of less than 50 per cent of the diameter of the lumen. Forty-seven per cent of the thrombi were found in the right coronary artery. Only 30 per cent were found in the left anterior descending coronary artery. The pathologic process in sudden ischemic death involves a rapidly evolving coronary-artery lesion in which plaque fissuring and resultant thrombus formation are present. These findings have implications for the prevention of sudden cardiac death by antithrombotic therapy.

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The integrity of the fibrous cap, comprising mostly αSMA-positive cells and associated ECM, is critical to stabilise and protect plaques from rupture.
“detailed post-mortem analyses of culprit plaques in sudden cardiac death established that the integrity of the fibrous cap, comprising mostly α SMA-positive cells and associated extracellular matrix (ECM), is critical to stabilise and protect plaques from rupture, a major cause of the clinical sequalae of atherosclerosis 142,163,168 .”
From Vascular smooth muscle cells in atherosclerosis (2019) · cites this paper as [163]

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Authors: Davies, M. J., & Thomas, A.
Affiliations: St George's, University of London (GB)
ORCID: Davies, Michael John
Venue: New England Journal of Medicine
Publisher: Massachusetts Medical Society
Published: 1984-05-03
Volume: 310
Issue: 18
Pages: 1137-1140
ISSN: 0028-4793 (ISSN-L)
1533-4406
DOI: 10.1056/nejm198405033101801
OpenAlex: W2327467387
Cited by: 1,694
References: 24
Citations by year: 2026: 7 · 2025: 26 · 2024: 14 · 2023: 16 · 2022: 20 · 2021: 27 · 2020: 29 · 2019: 32 · 2018: 20 · 2017: 30 · 2016: 39 · 2015: 42 · 2014: 38 · 2013: 53 · 2012: 51
FWCI: 40.83
Type: journal article
Language: en
Open access: closed
Locations: New England Journal of Medicine (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Acute Myocardial Infarction Research
Health Sciences › Medicine › Surgery › Coronary Interventions and Diagnostics
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Keywords: sudden cardiac death, coronary thrombus, coronary artery stenosis, right coronary artery, left anterior descending artery, ischemic heart disease, antithrombotic therapy, sudden cardiac death prevention
MeSH terms: Aged, Coronary Disease, Coronary Vessels, Death, Sudden, Female, Humans, Male, Myocardial Infarction, Thrombosis, Time Factors

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Thrombosis and Acute Coronary-Artery Lesions in Sudden Cardiac Ischemic Death

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