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Lewis A. Conner Memorial Lecture. Mechanisms leading to myocardial infarction: insights from studies of vascular biology.
Abstract
Myocardial infarction is the most frequent cause of mortality in the United States as well as in most western countries. In this review, the processes leading to myocardial infarction are described based on the most recent studies of vascular biology; in addition, evolving strategies for prevention are outlined. The following was specifically discussed. (1) Five phases of the progression of coronary atherosclerosis (phases 1 to 5) and eight morphologically different lesions (types I, II, III, IV, Va, Vb, Vc, and VI) in the various phases are defined. (2) The present understanding of the pathogenesis of each of the phases of progression and of the various lesion types preceding myocardial infarction is described; particular emphasis is placed on the physical, structural, cellular, and chemical characteristics of the "vulnerable or unstable plaques" prone to disruption (types IV and Va lesions). (3) The fate of plaque disruption (type VI lesion) in the genesis of the various coronary syndromes and especially acute myocardial infarction is defined; particular emphasis is placed on the combination of plaque disruption and a high thrombogenic risk profile--local factors (ie, degree of plaque disruption, exposure of lipid-macrophage-rich plaque, etc) and systemic factors (ie, catecholamines, RAS, fibrinogen, etc)--in the genesis of myocardial infarction. (4) Strategies of regression or stabilization of "vulnerable or unstable plaques" for prevention of myocardial infarction are presented within the context of recent favorable experience with risk factor modification and lipid-modifying angiographic trials, beta-blockade and angiotensin-converting enzyme inhibition, antithrombotic strategies, and the possible role of estrogens. The recent past has been very fruitful in yielding a better understanding of the processes leading to myocardial infarction, and the near future appears very promising in terms of preventing the number 1 killer in the western world.
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“However, therapies for lowering the concentration of homocysteine through vitamin supplementation did not result in the suppression of events292, 293).”
From Japan Atherosclerosis Society (JAS) guidelines for prevention of atherosclerotic cardiovascular diseases 2017 (2018) · cites this paper as [293]
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Metadata
- Authors
- Fuster, V
- Affiliations
- Mount Sinai Hospital (US)
- Corresponding author
- Fuster, V
- ORCID
- Fuster, V
- Venue
- Circulation
- Published
- 1994-10
- Volume
- 90
- Issue
- 4
- Pages
- 2126-2146
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2110185147
- Cited by
- 848
- References
- 240
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 7 · 2023: 11 · 2022: 9 · 2021: 4 · 2020: 14 · 2019: 6 · 2018: 5 · 2017: 12 · 2016: 19 · 2015: 16 · 2014: 19 · 2013: 24 · 2012: 18
- FWCI
- 16.36
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Coronary Interventions and Diagnostics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Acute Myocardial Infarction Research
- Keywords
- myocardial infarction, coronary artery disease, vulnerable plaque, plaque disruption, lesion type, plaque regression, thrombosis, coronary syndrome, risk factor control, lipid therapy, beta-adrenergic blockade, angiotensin-converting enzyme inhibition, antithrombotic therapy, estrogen, vascular biology
- MeSH terms
- Coronary Artery Disease, Coronary Thrombosis, Coronary Vessels, Humans, Myocardial Infarction, Lipid Metabolism
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