Vulnerable Plaques and Patients: Improving Prediction of Future Coronary Events

Ambrose, John A.; Srikanth, Sundararajan

doi:10.1016/j.amjmed.2009.07.019

Cited by 33 publications

(24 citation statements)

References 40 publications

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“…25,26 The vulnerability of a plaque for rupture depends on its lipid composition, fibrous cap, degradation of extracellular matrix proteins, recruitment of inflammatory cells, and intraplaque hemorrhage. 26 It was …”

Section: Smoking Plaque Vulnerability and Thrombosismentioning

confidence: 99%

“…[30][31][32][33] Intraplaque inflammation and intraplaque neovascularization lead to intraplaque hemorrhage and subsequent necrotic core enlargement. 26 Furthermore, CSE was found to cause an increased sympathetic activity leading to a rise in blood pressure, pulse rate, and vasospasm, which might create a high-mechanical stress zone near a vulnerable plaque. 34 All these together are likely to cause plaque instability that contributes toward plaque rupture.…”

Section: Arterioscler Thromb Vasc Biolmentioning

confidence: 99%

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Mechanisms of Coronary Thrombosis in Cigarette Smoke Exposure

Barua

Ambrose

2013

ATVB

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126

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Abstract-Acute rupture or erosion of a coronary atheromatous plaque and subsequent coronary artery thrombosis cause the majority of sudden cardiac deaths and myocardial infarctions. Cigarette smoking is a major risk factor for acute coronary thrombosis. Indeed, a majority of sudden cardiac deaths attributable to acute thrombosis are in cigarette smokers. Both active and passive cigarette smoke exposure seem to increase the risk of coronary thrombosis and myocardial infarctions. Cigarette smoke exposure seems to alter the hemostatic process via multiple mechanisms, which include alteration of the function of endothelial cells, platelets, fibrinogen, and coagulation factors. This creates an imbalance of antithrombotic/ prothrombotic factors and profibrinolytic/antifibrinolytic factors that support the initiation and propagation of thrombosis.

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Section: Smoking Plaque Vulnerability and Thrombosismentioning

confidence: 99%

Section: Arterioscler Thromb Vasc Biolmentioning

confidence: 99%

Mechanisms of Coronary Thrombosis in Cigarette Smoke Exposure

Barua

Ambrose

2013

ATVB

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200

126

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“…Disintegration of the endothelium at the site of ulceration/destruction of the fibrous cap of unstable atherosclerotic plaque or vulnerable atherosclerotic plaque liable to ulceration/destruction triggers thrombus formation on the surface of the atherosclerotic plaque resulting in artery occlusion and myocardial infarction [1,4,11]. The critical stage in the development of atherosclerotic focus [7,13] is the formation of unstable plague with thin/thinned or locally thinned cap, local destruction of the endothelium, infl ammatory infi ltration, and loose lipid core (sometimes with foci of necrosis and calcifi cation) [5,8,9,14].…”

mentioning

confidence: 99%

Activity of the Inflammatory Process in Different Types of Unstable Atherosclerotic Plaques

Ragino¹,

Chernyavski

Polonskaya³

et al. 2012

Bull Exp Biol Med

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Inflammatory biomarkers and chemoattractants characteristic and important for different types (lipid; inflammatory erosive; degenerative necrotic) of unstable plaques in coronary arteries were identified and studied in male patients with coronary atherosclerosis without acute coronary syndrome we studied. Among the three types of unstable plaques, elevated concentrations of IL-1β, IL-6, IL-8, IL-18 and monocyte chemotactic protein-1 were characteristic of not only inflammatory erosive type, but also lipid type compared with degenerative necrotic type. Thus, intensification of the inflammatory process plays an important role in the development of not only inflammatory and destructive, but also of lipid type of unstable atherosclerotic plaques.

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“…High-risk vulnerable atherosclerotic plaques are characterized by lesions with a prominent lipid-rich necrotic core, thin fibrous cap and active plaque inflammation [3][4][5]12]. The infiltration of inflammatory cells together with an abundant plexus of neovessels are considered the histological hallmarks of plaque inflammatory activity, and therefore, it is of clinical relevance to develop and validate non-invasive techniques able to assess these features [4,8].…”

Section: Discussionmentioning

confidence: 99%

“…In recent years, it has become clear that sudden clinical events do not necessarily correlate with the degree of luminal obstruction caused by lesions, but rather with plaque composition [3]. Atherosclerotic plaques consist of accumulated lipids, cells, cellular debris, calcium and other elements in the tunica intima of the vessel wall.…”

mentioning

confidence: 99%

Dynamic contrast enhanced (DCE) magnetic resonance imaging (MRI) of atherosclerotic plaque angiogenesis

et al. 2010

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Atherosclerosis is a progressive systemic disease of the large arteries characterized by the formation of plaques in the vessel wall. Despite our knowledge of its pathogenesis, many vulnerable plaques still remain undiagnosed while in their asymptomatic phase and manifest for the first time with dramatic clinical events, such as stroke or myocardial infarction. In recent years, it is becoming clearer that sudden clinical events do not necessarily correlate with the degree of luminal obstruction caused by lesions, but rather with plaque composition. In particular, the degree of plaque inflammation is important in the pathogenesis of atherosclerosis and is considered a good marker of high-risk/vulnerable plaques. The presence of inflammatory infiltrate and plaque neovascularization are both histological hallmarks of atherosclerotic plaque inflammation. Therefore, plaque angiogenesis represents an attractive target to try and identify asymptomatic high-risk lesions. Dynamic contrast enhanced (DCE) magnetic resonance imaging (MRI) is a technique that has been used extensively in the past to study the vascularity of tumors and its changes following therapeutic intervention. Recently, delayed and dynamic contrast enhanced (CE) MRI have been proposed as non-invasive tools to study the extent of plaque neovascularization in animals and patients with atherosclerosis. In this review, we will provide a brief introduction on DCE-MRI acquisition and analysis techniques. We will follow this with a description of contrast enhanced MR methods for the detection and quantification of neovasculature in atherosclerosis, with an emphasis on DCE-MRI. Finally, we will examine the current limitations and challenges faced by DCE-MRI and briefly discuss its future applications in the context of atherosclerosis.

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Vulnerable Plaques and Patients: Improving Prediction of Future Coronary Events

Cited by 33 publications

References 40 publications

Mechanisms of Coronary Thrombosis in Cigarette Smoke Exposure

Mechanisms of Coronary Thrombosis in Cigarette Smoke Exposure

Activity of the Inflammatory Process in Different Types of Unstable Atherosclerotic Plaques

Dynamic contrast enhanced (DCE) magnetic resonance imaging (MRI) of atherosclerotic plaque angiogenesis

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