Vulnerable Plaque: The Pathology of Unstable Coronary Lesions
Vulnerable plagues have been defined as precursors to lesions that rupture. However, coronary thrombosis may occur from other lesions like plaque erosion and calcified nodules, although to a lesser frequency than rupture. Therefore, the definition of vulnerable plaque should be all‐inclusive. Using...
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Veröffentlicht in: | Journal of interventional cardiology 2002-12, Vol.15 (6), p.439-446 |
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description | Vulnerable plagues have been defined as precursors to lesions that rupture. However, coronary thrombosis may occur from other lesions like plaque erosion and calcified nodules, although to a lesser frequency than rupture. Therefore, the definition of vulnerable plaque should be all‐inclusive. Using descriptive terminology, the authors define the precursor lesion of plaque rupture as “thin‐cap fibroatheroma” (TCFA). Morphologically, TCFAs have a necrotic core with an overlying thin fibrous cap (< 65 mm) consisting of collagen type I, which is infiltrated by macrophages. These lesions are most frequent in the coronary tree of patients dying with acme myocardial infarction and least common in those with plaque erosion. TCFAs are more common in patients with high serum total cholesterol (TC) and a high TC to high density cholesterol ratio, in women >50 years, and in those patients with elevated levels of high sensitivity C‐reactive protein. TCFAs are mostly found in the proximal left anterior descending coronary arteries and less commonly in the proximal right or the proximal left circumflex coronary arteries. In TCFAs, necrotic core length is ˜ 2–17 mm (mean 8 mm) and the underlying cross‐sectional luminal narrowing in over 75% of cases is < 75% (< 50% diameter stenosis). The area of the necrotic core in at least 75% of cases is ≤3 mm2. Clinical studies of TCFAs are limited as angiography and intravascular ultrasound (TVUS) catheters cannot precisely identify these lesions. Newer catheters and other techniques are at various stages of development and will play a significant role in the understanding of plaque progression and the development of symptomatic coronary artery disease. |
doi_str_mv | 10.1111/j.1540-8183.2002.tb01087.x |
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However, coronary thrombosis may occur from other lesions like plaque erosion and calcified nodules, although to a lesser frequency than rupture. Therefore, the definition of vulnerable plaque should be all‐inclusive. Using descriptive terminology, the authors define the precursor lesion of plaque rupture as “thin‐cap fibroatheroma” (TCFA). Morphologically, TCFAs have a necrotic core with an overlying thin fibrous cap (< 65 mm) consisting of collagen type I, which is infiltrated by macrophages. These lesions are most frequent in the coronary tree of patients dying with acme myocardial infarction and least common in those with plaque erosion. TCFAs are more common in patients with high serum total cholesterol (TC) and a high TC to high density cholesterol ratio, in women >50 years, and in those patients with elevated levels of high sensitivity C‐reactive protein. TCFAs are mostly found in the proximal left anterior descending coronary arteries and less commonly in the proximal right or the proximal left circumflex coronary arteries. In TCFAs, necrotic core length is ˜ 2–17 mm (mean 8 mm) and the underlying cross‐sectional luminal narrowing in over 75% of cases is < 75% (< 50% diameter stenosis). The area of the necrotic core in at least 75% of cases is ≤3 mm2. Clinical studies of TCFAs are limited as angiography and intravascular ultrasound (TVUS) catheters cannot precisely identify these lesions. Newer catheters and other techniques are at various stages of development and will play a significant role in the understanding of plaque progression and the development of symptomatic coronary artery disease.</description><identifier>ISSN: 0896-4327</identifier><identifier>EISSN: 1540-8183</identifier><identifier>DOI: 10.1111/j.1540-8183.2002.tb01087.x</identifier><identifier>PMID: 12476646</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Calcinosis - pathology ; Coronary Artery Disease - pathology ; Death, Sudden, Cardiac - pathology ; Diagnostic Techniques, Cardiovascular ; Female ; Humans ; Incidence ; Male ; Myocardial Infarction - pathology ; Risk Factors ; Rupture, Spontaneous</subject><ispartof>Journal of interventional cardiology, 2002-12, Vol.15 (6), p.439-446</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3909-262835081076a54a18a8e86a4c5712a5b290fed2303449364a68d6c55a4dbcf83</citedby><cites>FETCH-LOGICAL-c3909-262835081076a54a18a8e86a4c5712a5b290fed2303449364a68d6c55a4dbcf83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12476646$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>VIRMANI, RENU</creatorcontrib><creatorcontrib>BURKE, ALLEN P.</creatorcontrib><creatorcontrib>KOLODGIE, FRANK D.</creatorcontrib><creatorcontrib>FARB, ANDREW</creatorcontrib><title>Vulnerable Plaque: The Pathology of Unstable Coronary Lesions</title><title>Journal of interventional cardiology</title><addtitle>J Interv Cardiol</addtitle><description>Vulnerable plagues have been defined as precursors to lesions that rupture. However, coronary thrombosis may occur from other lesions like plaque erosion and calcified nodules, although to a lesser frequency than rupture. Therefore, the definition of vulnerable plaque should be all‐inclusive. Using descriptive terminology, the authors define the precursor lesion of plaque rupture as “thin‐cap fibroatheroma” (TCFA). Morphologically, TCFAs have a necrotic core with an overlying thin fibrous cap (< 65 mm) consisting of collagen type I, which is infiltrated by macrophages. These lesions are most frequent in the coronary tree of patients dying with acme myocardial infarction and least common in those with plaque erosion. TCFAs are more common in patients with high serum total cholesterol (TC) and a high TC to high density cholesterol ratio, in women >50 years, and in those patients with elevated levels of high sensitivity C‐reactive protein. TCFAs are mostly found in the proximal left anterior descending coronary arteries and less commonly in the proximal right or the proximal left circumflex coronary arteries. In TCFAs, necrotic core length is ˜ 2–17 mm (mean 8 mm) and the underlying cross‐sectional luminal narrowing in over 75% of cases is < 75% (< 50% diameter stenosis). The area of the necrotic core in at least 75% of cases is ≤3 mm2. Clinical studies of TCFAs are limited as angiography and intravascular ultrasound (TVUS) catheters cannot precisely identify these lesions. Newer catheters and other techniques are at various stages of development and will play a significant role in the understanding of plaque progression and the development of symptomatic coronary artery disease.</description><subject>Calcinosis - pathology</subject><subject>Coronary Artery Disease - pathology</subject><subject>Death, Sudden, Cardiac - pathology</subject><subject>Diagnostic Techniques, Cardiovascular</subject><subject>Female</subject><subject>Humans</subject><subject>Incidence</subject><subject>Male</subject><subject>Myocardial Infarction - pathology</subject><subject>Risk Factors</subject><subject>Rupture, Spontaneous</subject><issn>0896-4327</issn><issn>1540-8183</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkF1PwjAUhhujEUT_glm88G6z3-1IjDFE-ZCIGtDLphudDseK64jw7y1C8NrenCZ9zttzHgAuEIyQP1ezCDEKQ4kkiTCEOKoTiKAU0eoANPdPh6AJZcxDSrBogBPnZh6FjOFj0ECYCs4pb4Lr12VRmkonhQmeCv21NO1g_OHvuv6whX1fBzYLJqWrf4mOrWypq3UwNC63pTsFR5kunDnb1RaY3N-NO71wOOr2O7fDMCUxjEPMsSQMSgQF14xqJLU0kmuaMoGwZgmOYWammEBCaUw41VxOecqYptMkzSRpgctt7qKyfkRXq3nuUlMUujR26ZTAQvg1qQfbWzCtrHOVydSiyud-YoWg2shTM7UxpDaG1Eae2slTK998vvtlmczN9K91Z8sDN1vgOy_M-h_RajDqdyiJfUK4TchdbVb7BF19Ki6IYOrtsatennuw9zBASpAfC9mMeA</recordid><startdate>200212</startdate><enddate>200212</enddate><creator>VIRMANI, RENU</creator><creator>BURKE, ALLEN P.</creator><creator>KOLODGIE, FRANK D.</creator><creator>FARB, ANDREW</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200212</creationdate><title>Vulnerable Plaque: The Pathology of Unstable Coronary Lesions</title><author>VIRMANI, RENU ; BURKE, ALLEN P. ; KOLODGIE, FRANK D. ; FARB, ANDREW</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3909-262835081076a54a18a8e86a4c5712a5b290fed2303449364a68d6c55a4dbcf83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Calcinosis - pathology</topic><topic>Coronary Artery Disease - pathology</topic><topic>Death, Sudden, Cardiac - pathology</topic><topic>Diagnostic Techniques, Cardiovascular</topic><topic>Female</topic><topic>Humans</topic><topic>Incidence</topic><topic>Male</topic><topic>Myocardial Infarction - pathology</topic><topic>Risk Factors</topic><topic>Rupture, Spontaneous</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>VIRMANI, RENU</creatorcontrib><creatorcontrib>BURKE, ALLEN P.</creatorcontrib><creatorcontrib>KOLODGIE, FRANK D.</creatorcontrib><creatorcontrib>FARB, ANDREW</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of interventional cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>VIRMANI, RENU</au><au>BURKE, ALLEN P.</au><au>KOLODGIE, FRANK D.</au><au>FARB, ANDREW</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vulnerable Plaque: The Pathology of Unstable Coronary Lesions</atitle><jtitle>Journal of interventional cardiology</jtitle><addtitle>J Interv Cardiol</addtitle><date>2002-12</date><risdate>2002</risdate><volume>15</volume><issue>6</issue><spage>439</spage><epage>446</epage><pages>439-446</pages><issn>0896-4327</issn><eissn>1540-8183</eissn><abstract>Vulnerable plagues have been defined as precursors to lesions that rupture. However, coronary thrombosis may occur from other lesions like plaque erosion and calcified nodules, although to a lesser frequency than rupture. Therefore, the definition of vulnerable plaque should be all‐inclusive. Using descriptive terminology, the authors define the precursor lesion of plaque rupture as “thin‐cap fibroatheroma” (TCFA). Morphologically, TCFAs have a necrotic core with an overlying thin fibrous cap (< 65 mm) consisting of collagen type I, which is infiltrated by macrophages. These lesions are most frequent in the coronary tree of patients dying with acme myocardial infarction and least common in those with plaque erosion. TCFAs are more common in patients with high serum total cholesterol (TC) and a high TC to high density cholesterol ratio, in women >50 years, and in those patients with elevated levels of high sensitivity C‐reactive protein. TCFAs are mostly found in the proximal left anterior descending coronary arteries and less commonly in the proximal right or the proximal left circumflex coronary arteries. In TCFAs, necrotic core length is ˜ 2–17 mm (mean 8 mm) and the underlying cross‐sectional luminal narrowing in over 75% of cases is < 75% (< 50% diameter stenosis). The area of the necrotic core in at least 75% of cases is ≤3 mm2. Clinical studies of TCFAs are limited as angiography and intravascular ultrasound (TVUS) catheters cannot precisely identify these lesions. Newer catheters and other techniques are at various stages of development and will play a significant role in the understanding of plaque progression and the development of symptomatic coronary artery disease.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>12476646</pmid><doi>10.1111/j.1540-8183.2002.tb01087.x</doi><tpages>8</tpages></addata></record> |
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subjects | Calcinosis - pathology Coronary Artery Disease - pathology Death, Sudden, Cardiac - pathology Diagnostic Techniques, Cardiovascular Female Humans Incidence Male Myocardial Infarction - pathology Risk Factors Rupture, Spontaneous |
title | Vulnerable Plaque: The Pathology of Unstable Coronary Lesions |
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