Evidence of multifocal activity of coronary disease in patients with acute myocardial infarction
Destabilization of the fibrous cap facilitates plaque rupture, thrombus formation, and myocardial infarction. Because systemic stimuli, such as lipoproteins, infectious agents, and autoantigens, may incite this reaction, one may wonder whether disruption mechanisms are only local or systemic and inf...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1997-08, Vol.96 (4), p.1145-1151 |
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| container_title | Circulation (New York, N.Y.) |
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| creator | GUAZZI, M. D BUSSOTTI, M GRANCINI, L DE CESARE, N GUAZZI, M PERA, I. L LOALDI, A |
| description | Destabilization of the fibrous cap facilitates plaque rupture, thrombus formation, and myocardial infarction. Because systemic stimuli, such as lipoproteins, infectious agents, and autoantigens, may incite this reaction, one may wonder whether disruption mechanisms are only local or systemic and infarction is caused by an arbitrary plaque event or by a systemic, acute activity of the coronary disease.
Early (3 to 5 days) and late (1 month) peri-infarction coronary angiographic data in 23 patients with first infarction were compared with that in 23 similar patients, with angiography performed because of stable angina and repeated after 1 month before angioplasty. Nonculprit lesion changes at the narrowest point defined progression or regression when exceeding 0.27 mm. In patients with recent infarction we found that 16 had progression, 4 had regression, 1 had both, 2 were steady (values in patients with stable angina being 2 [P |
| doi_str_mv | 10.1161/01.CIR.96.4.1145 |
| format | Article |
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Early (3 to 5 days) and late (1 month) peri-infarction coronary angiographic data in 23 patients with first infarction were compared with that in 23 similar patients, with angiography performed because of stable angina and repeated after 1 month before angioplasty. Nonculprit lesion changes at the narrowest point defined progression or regression when exceeding 0.27 mm. In patients with recent infarction we found that 16 had progression, 4 had regression, 1 had both, 2 were steady (values in patients with stable angina being 2 [P<.0011, 1 [NS], 0 [NS], and 20 [P<.001]); 27 lesions were infarct related; 17 of the 45 nonculprit lesions progressed and 5 regressed (values in stable angina being 2 [P<.001] and 1 [P<.05] out of 78); minimal diameter reduction of progressing stenoses averaged 0.39 mm; lumen increase of regressing lesions averaged 0.30 mm; 3 patients developed interim rest angina associated with progression of a nonculprit lesion.
A greater proportion of subjects and lesions with progression or regression (in infarction versus stable angina) supports the hypothesis that infarction is a hallmark of systemic coronary disease activity. Changes might vary according to the "maturation" stage of an atheroma, and maximal expression would be at the level of the offending plaque. Shrinkage, thrombolysis, or vascular remodeling would determine the residual plaque morphology.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.96.4.1145</identifier><identifier>PMID: 9286942</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Analysis of Variance ; Angina Pectoris - diagnostic imaging ; Angina Pectoris - physiopathology ; Biological and medical sciences ; Cardiology. Vascular system ; Case-Control Studies ; Coronary Angiography ; Coronary Artery Disease - complications ; Coronary Artery Disease - physiopathology ; Coronary heart disease ; Disease Progression ; Female ; Heart ; Humans ; Male ; Medical sciences ; Middle Aged ; Myocardial Infarction - diagnostic imaging ; Myocardial Infarction - etiology ; Myocardial Infarction - physiopathology ; Prospective Studies</subject><ispartof>Circulation (New York, N.Y.), 1997-08, Vol.96 (4), p.1145-1151</ispartof><rights>1997 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Aug 19, 1997</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-571265cd58618c9d738e3d85b387c05098dfc711e75849f014f25644c607d3bb3</citedby><cites>FETCH-LOGICAL-c391t-571265cd58618c9d738e3d85b387c05098dfc711e75849f014f25644c607d3bb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2793190$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9286942$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GUAZZI, M. D</creatorcontrib><creatorcontrib>BUSSOTTI, M</creatorcontrib><creatorcontrib>GRANCINI, L</creatorcontrib><creatorcontrib>DE CESARE, N</creatorcontrib><creatorcontrib>GUAZZI, M</creatorcontrib><creatorcontrib>PERA, I. L</creatorcontrib><creatorcontrib>LOALDI, A</creatorcontrib><title>Evidence of multifocal activity of coronary disease in patients with acute myocardial infarction</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Destabilization of the fibrous cap facilitates plaque rupture, thrombus formation, and myocardial infarction. Because systemic stimuli, such as lipoproteins, infectious agents, and autoantigens, may incite this reaction, one may wonder whether disruption mechanisms are only local or systemic and infarction is caused by an arbitrary plaque event or by a systemic, acute activity of the coronary disease.
Early (3 to 5 days) and late (1 month) peri-infarction coronary angiographic data in 23 patients with first infarction were compared with that in 23 similar patients, with angiography performed because of stable angina and repeated after 1 month before angioplasty. Nonculprit lesion changes at the narrowest point defined progression or regression when exceeding 0.27 mm. In patients with recent infarction we found that 16 had progression, 4 had regression, 1 had both, 2 were steady (values in patients with stable angina being 2 [P<.0011, 1 [NS], 0 [NS], and 20 [P<.001]); 27 lesions were infarct related; 17 of the 45 nonculprit lesions progressed and 5 regressed (values in stable angina being 2 [P<.001] and 1 [P<.05] out of 78); minimal diameter reduction of progressing stenoses averaged 0.39 mm; lumen increase of regressing lesions averaged 0.30 mm; 3 patients developed interim rest angina associated with progression of a nonculprit lesion.
A greater proportion of subjects and lesions with progression or regression (in infarction versus stable angina) supports the hypothesis that infarction is a hallmark of systemic coronary disease activity. Changes might vary according to the "maturation" stage of an atheroma, and maximal expression would be at the level of the offending plaque. Shrinkage, thrombolysis, or vascular remodeling would determine the residual plaque morphology.</description><subject>Analysis of Variance</subject><subject>Angina Pectoris - diagnostic imaging</subject><subject>Angina Pectoris - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Case-Control Studies</subject><subject>Coronary Angiography</subject><subject>Coronary Artery Disease - complications</subject><subject>Coronary Artery Disease - physiopathology</subject><subject>Coronary heart disease</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Heart</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - diagnostic imaging</subject><subject>Myocardial Infarction - etiology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Prospective Studies</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkE2LFDEQhoMo6-zq3YvQiOytx1Q-O0cZVl1YEETPMZMPzNKdjEl6l_n3ZthhD55Cqp63qngQegd4CyDgE4bt7vbHVokt6wXGX6ANcMJGxql6iTYYYzVKSshrdFnrff8KKvkFulBkEoqRDfp98xCdT9YPOQzLOrcYsjXzYGyLD7EdT2WbS06mHAcXqzfVDzENB9OiT60Oj7H96fTa_LAce7S42OMxBVP6iJzeoFfBzNW_Pb9X6NeXm5-7b-Pd96-3u893o6UK2sglEMGt45OAySon6eSpm_ieTtJijtXkgpUAXvKJqYCBBcIFY1Zg6eh-T6_Q9dPcQ8l_V1-bXmK1fp5N8nmtWioiQGLawQ__gfd5LanfpgmQvpeC6hB-gmzJtRYf9KHEpTvQgPXJvMagu3mthGb6ZL5H3p_nrvvFu-fAWXXvfzz3Te2GQzHJxvqMEan6Ykz_ARXPiuA</recordid><startdate>19970819</startdate><enddate>19970819</enddate><creator>GUAZZI, M. D</creator><creator>BUSSOTTI, M</creator><creator>GRANCINI, L</creator><creator>DE CESARE, N</creator><creator>GUAZZI, M</creator><creator>PERA, I. L</creator><creator>LOALDI, A</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</general><scope>IQODW</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>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>19970819</creationdate><title>Evidence of multifocal activity of coronary disease in patients with acute myocardial infarction</title><author>GUAZZI, M. D ; BUSSOTTI, M ; GRANCINI, L ; DE CESARE, N ; GUAZZI, M ; PERA, I. L ; LOALDI, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-571265cd58618c9d738e3d85b387c05098dfc711e75849f014f25644c607d3bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Analysis of Variance</topic><topic>Angina Pectoris - diagnostic imaging</topic><topic>Angina Pectoris - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Case-Control Studies</topic><topic>Coronary Angiography</topic><topic>Coronary Artery Disease - complications</topic><topic>Coronary Artery Disease - physiopathology</topic><topic>Coronary heart disease</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Heart</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - diagnostic imaging</topic><topic>Myocardial Infarction - etiology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Prospective Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GUAZZI, M. D</creatorcontrib><creatorcontrib>BUSSOTTI, M</creatorcontrib><creatorcontrib>GRANCINI, L</creatorcontrib><creatorcontrib>DE CESARE, N</creatorcontrib><creatorcontrib>GUAZZI, M</creatorcontrib><creatorcontrib>PERA, I. L</creatorcontrib><creatorcontrib>LOALDI, A</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GUAZZI, M. D</au><au>BUSSOTTI, M</au><au>GRANCINI, L</au><au>DE CESARE, N</au><au>GUAZZI, M</au><au>PERA, I. L</au><au>LOALDI, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evidence of multifocal activity of coronary disease in patients with acute myocardial infarction</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1997-08-19</date><risdate>1997</risdate><volume>96</volume><issue>4</issue><spage>1145</spage><epage>1151</epage><pages>1145-1151</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Destabilization of the fibrous cap facilitates plaque rupture, thrombus formation, and myocardial infarction. Because systemic stimuli, such as lipoproteins, infectious agents, and autoantigens, may incite this reaction, one may wonder whether disruption mechanisms are only local or systemic and infarction is caused by an arbitrary plaque event or by a systemic, acute activity of the coronary disease.
Early (3 to 5 days) and late (1 month) peri-infarction coronary angiographic data in 23 patients with first infarction were compared with that in 23 similar patients, with angiography performed because of stable angina and repeated after 1 month before angioplasty. Nonculprit lesion changes at the narrowest point defined progression or regression when exceeding 0.27 mm. In patients with recent infarction we found that 16 had progression, 4 had regression, 1 had both, 2 were steady (values in patients with stable angina being 2 [P<.0011, 1 [NS], 0 [NS], and 20 [P<.001]); 27 lesions were infarct related; 17 of the 45 nonculprit lesions progressed and 5 regressed (values in stable angina being 2 [P<.001] and 1 [P<.05] out of 78); minimal diameter reduction of progressing stenoses averaged 0.39 mm; lumen increase of regressing lesions averaged 0.30 mm; 3 patients developed interim rest angina associated with progression of a nonculprit lesion.
A greater proportion of subjects and lesions with progression or regression (in infarction versus stable angina) supports the hypothesis that infarction is a hallmark of systemic coronary disease activity. Changes might vary according to the "maturation" stage of an atheroma, and maximal expression would be at the level of the offending plaque. Shrinkage, thrombolysis, or vascular remodeling would determine the residual plaque morphology.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>9286942</pmid><doi>10.1161/01.CIR.96.4.1145</doi><tpages>7</tpages></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 1997-08, Vol.96 (4), p.1145-1151 |
| issn | 0009-7322 1524-4539 |
| language | eng |
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| source | Journals@Ovid Ovid Autoload; MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Analysis of Variance Angina Pectoris - diagnostic imaging Angina Pectoris - physiopathology Biological and medical sciences Cardiology. Vascular system Case-Control Studies Coronary Angiography Coronary Artery Disease - complications Coronary Artery Disease - physiopathology Coronary heart disease Disease Progression Female Heart Humans Male Medical sciences Middle Aged Myocardial Infarction - diagnostic imaging Myocardial Infarction - etiology Myocardial Infarction - physiopathology Prospective Studies |
| title | Evidence of multifocal activity of coronary disease in patients with acute myocardial infarction |
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