Stable versus unstable atherosclerosis: Clinical aspects☆,☆☆,★
Section snippets
Plaque vulnerability
The risk of plaque disruption depends more on plaque type than on plaque size; lipid-rich and soft plaques are more vulnerable and prone to rupture than are collagen-rich and hard plaques.3 Furthermore, they are highly thrombogenic after disruption because of high content of tissue factor.4 Pathoanatomic studies have identified 3 major determinants of a plaque’s vulnerability to rupture (Figure 1): (1) the size of the lipid-rich core; (2) inflammation with plaque degradation; and (3) lack of
Plaque disruption
Rupture of vulnerable plaques occurs frequently. Autopsy data indicate that 9% of healthy persons harbor disrupted plaques (without superimposed thrombosis) in their coronary arteries, which increases to 22% in persons with diabetes or hypertension.35 In fatal coronary artery disease, more than one disrupted plaque, with or without superimposed thrombosis, usually is present in the coronary arteries.13, 36
Disruption of the plaque surface occurs most often where the cap is thinnest and most
Plaque thrombosis
The most feared consequence of coronary plaque disruption is thrombotic occlusion of the artery. Approximately 75% of thrombi responsible for acute coronary syndromes are precipitated by plaque disruption, whereby the highly thrombogenic gruel is exposed to the flowing blood. In the remaining 25%, superficial plaque erosion without frank disruption (ie, no deep injury) is usually present.2 Most disrupted plaques are resealed by a small mural thrombus, and only sometimes does a major luminal
Clinical manifestations
Plaque disruption itself is asymptomatic, and the associated rapid plaque growth is usually clinically silent. However, rupture-related hemorrhage into the plaque, luminal thrombosis, and/or vasospasm may cause sudden flow obstruction, giving rise to an acute coronary syndrome. The culprit lesion is frequently “dynamic,” causing intermittent flow obstruction, and the clinical presentation and the outcome depend on the severity and duration of myocardial ischemia.1, 40 A nonocclusive or
Conclusions
For event-free survival in patients with coronary atherosclerosis, we must focus on plaque composition and vulnerability to rupture and plaque thrombogenicity rather than on plaque size and stenosis severity. There appear to be 3 major determinants of a plaque’s vulnerability to rupture: (1) the size of the lipid-rich core, (2) inflammation with plaque degradation, and (3) lack of SMCs with impaired healing. Lipid accumulation, macrophage infiltration, and lack of SMCs destabilize plaques,
References (40)
- et al.
Hemodynamic shear force in rupture of coronary arterial atherosclerotic plaques
Am J Cardiol
(1990) - et al.
Evidence that the death of macrophage foam cells contributes to the lipid core of atheroma
Atherosclerosis
(1995) - et al.
Chronic infections and coronary heart disease: is there a link?
Lancet
(1997) - et al.
The mechanisms by which infectious agents may contribute to atherosclerosis and its clinical manifestations
Trends Cardiovasc Med
(1998) - et al.
Increased incidence of Chlamydia species within the coronary arteries of patients with symptomatic atherosclerotic versus other forms of cardiovascular disease
J Am Coll Cardiol
(1996) - et al.
C-reactive protein is a potent predictor of mortality independently of and in combination with troponin T in acute coronary syndromes: a TIMI 11A substudy
J Am Coll Cardiol
(1998) - et al.
Collagen types I and III, collagen content, GAGs and mechanical strength of human atherosclerotic plaque caps: span-wise variations
Atherosclerosis
(1992) - et al.
Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaques
Lancet
(1989) - et al.
The pathogenesis of coronary artery disease and the acute coronary syndromes
N Eng J Med
(1992) Coronary thrombosis: pathogenesis and clinical manifestations
Am J Cardiol
(1991)
Coronary plaque disruption
Circulation
Tissue factor modulates the thrombogenicity of human atherosclerotic plaque
Circulation
Molecular bases of the acute coronary syndromes
Circulation
Vulnerable plaque: relation of characteristics to degree of stenosis in human coronary arteries
Circulation
Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content
Br Heart J
Evidence for apoptosis in advanced human atheroma
Am J Pathol
Apoptosis is abundant in human atherosclerotic lesions, especially in inflammatory cells (macrophages and T cells), and may contribute to the accumulation of gruel and plaque instability
Am J Pathol
Immune responses in atherosclerosis
Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis: characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi
Br Heart J
Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology
Circulation
Cited by (82)
The histological characteristics and virtual histology findings of the tissues obtained by a distal protection device during endovascular therapy for peripheral artery disease
2017, Journal of CardiologyCitation Excerpt :VH-IVUS technology has been shown to have between 80% and 92% accuracy in vitro and 87–97% accuracy in vivo [17] when used to identify the four different types of atherosclerotic tissue (fibrosis, fibrofatty, dense calcium, and necrotic core) in the coronary artery. The vulnerability of plaque to rupture is typically characterized by the presence of NC, which is a region of the fibroatheroma that is largely devoid of viable cells and which consists of cellular debris and cholesterol clefts, a thin fibrous cap, and macrophage infiltration [18]. An NC was observed in 19.7–35% and 18.1–32% of the patients with acute coronary syndrome (ACS) and stable angina pectoris (SAP), respectively [19,20].
Deteriorated clinical outcome in coronary artery disease patients with a high prevalence of Porphyromonas gingivalis infection
2016, IJC Metabolic and EndocrineCitation Excerpt :However, coronary CTA is useful to identify the morphology of coronary plaque, even in asymptomatic patients with CAD. In the pathological dynamics of atherosclerosis in the coronary arterial wall, some triggers caused by inflammation within atheromatous plaque leads to its destabilization, causing acute coronary syndrome [12]. On the other hand, dental plaque bacteria can also contribute to this destabilization [13], because the periodontopathic bacteria in the oral cavity can invade internal systems, passing through the damaged periodontal tissue.
Differential identification of atypical pneumonia pathogens in aorta and internal mammary artery related to ankle brachial index and walking distance
2013, Journal of Surgical ResearchCitation Excerpt :Inflammation may contribute to the weakening of atherosclerotic plaque, and thrombus can easily develop on the lipid content that becomes apparent due to the tearing of the fibrosis sheath of the plaque. Thrombus development is related to acute peripheral artery ischemia, unstable angina, acute myocardial infarction, and sudden death [6,20]. Microbiological determinants such as CP, CMV, and Helicobacter pylori (HP), which are found at different stages of these pathogenic mechanisms, may increase the development of inflammation and atherosclerosis.
Association of tissue plasminogen activator and plasminogen activator inhibitor polymorphism with myocardial infarction: A meta-analysis
2012, Thrombosis ResearchCitation Excerpt :The PAI-1 is located on chromosome 7q21.3-q22 and spans approximately 12.2 kb with nine exons and eight introns. Higher levels of PAI-1 protein have been found in patients with MI compared to healthy/normal individuals [9]. In PAI-1 a single nucleotide 4 G/5 G insertion/deletion polymorphism (rs1799768) is located at position − 675 bp in the promoter sequence.
Histologic characterization of mobile and nonmobile carotid plaques detected with ultrasound imaging
2011, Journal of Vascular Surgery
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Reprint requests: Prof Erling Falk, Department of Cardiology, Research Unit, Aarhus University Hospital (Skejby), DK-8200 Aarhus N, Denmark. E-mail: [email protected]
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Am Heart J 1999;138:S421-S425.
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0002-8703/99/$8.00 + 0 4/0/101757