Nonculprit Lesion Progression in Patients With ST Elevation Myocardial Infarction After Primary Percutaneous Coronary Intervention

The majority of cardiovascular events in patients with ST elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary interventions (PPCI) arise from the progression of nonculprit lesions (NCL) during the long-term follow-up period. However, the clinical and angiographic factors...

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Veröffentlicht in:International Heart Journal 2014, Vol.55(1), pp.48-52
Hauptverfasser: Wang, Jian, Liu, Jing-hua, Zhu, Xiao-ling, Zhang, Ming, Wang, Shao-ping, Zheng, Ze
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container_start_page 48
container_title International Heart Journal
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creator Wang, Jian
Liu, Jing-hua
Zhu, Xiao-ling
Zhang, Ming
Wang, Shao-ping
Zheng, Ze
description The majority of cardiovascular events in patients with ST elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary interventions (PPCI) arise from the progression of nonculprit lesions (NCL) during the long-term follow-up period. However, the clinical and angiographic factors related to the progression of nonculprit lesions are unknown. The purpose of the study was to investigate the clinical and angiographic factors related to the progression of nonculprit lesions of patients with STEMI undergoing PPCI. A total of 492 patients with STEMI who underwent PPCI from January 2006 to December 2009 were enrolled. All patients underwent PPCI as a treatment for the culprit lesion. The clinical and angiographic follow-up was performed at 12 months. Primary endpoint: Clinically driven nonculprit lesion PCI. The levels of serum catecholamines [epinephrine (E), norepinephrine (NE)] and C-reactive protein (CRP) were assayed, and the clinical and angiographic features were also analyzed. The clinical and angiographic follow-up was performed in 492 patients, and 45 patients underwent clinically driven nonculprit lesions PCI (study group). A total of 447 patients were free of additional PCI (control group). There were significant differences in the level of catecholamines (E (621.48 ± 79.31) pg/mL versus (268.14 ± 73.26) pg/mL, P < 0.0001), NE (6212.43 ± 822.41) pg/mL versus (3218.34 ± 614.16) pg/mL, P < 0.0001), CRP (3.29 ± 1.31) mg/dL versus (2.51 ± 1.14) mg/dL, P < 0.0001, cTnI peak value (27.27 ± 4.02) ng/mL versus (16.12 ± 3.23) ng/mL, P < 0.0001), thrombotic lesion rate ((62.22% versus 23.04%), P < 0.0001), ≥ 2 vessel lesions rate (80.00% versus 46.09%), P < 0.0001), culprit lesion length ((33.2 ± 2.9 versus 28.1 ± 3.1), P = 0.013), and complex lesion rate ((57.78% versus 36.02%), P = 0.006) between the two groups. Correlation analysis between nonculprit lesion stenosis degree and serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, and complex lesion rate showed that there were significant correlations between serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, complex lesion rate, and nonculprit lesion stenosis degree. The correlation coefficients were 0.95, 0.97, 0.83, 0.90, 0.81, 0.84, 0.95, and 0.96, respectively, and P < 0.0001, P < 0.0001, P = 0.01, P = 0.01, P = 0.01, P = 0.01, P < 0.0001, and P < 0.0001,
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However, the clinical and angiographic factors related to the progression of nonculprit lesions are unknown. The purpose of the study was to investigate the clinical and angiographic factors related to the progression of nonculprit lesions of patients with STEMI undergoing PPCI. A total of 492 patients with STEMI who underwent PPCI from January 2006 to December 2009 were enrolled. All patients underwent PPCI as a treatment for the culprit lesion. The clinical and angiographic follow-up was performed at 12 months. Primary endpoint: Clinically driven nonculprit lesion PCI. The levels of serum catecholamines [epinephrine (E), norepinephrine (NE)] and C-reactive protein (CRP) were assayed, and the clinical and angiographic features were also analyzed. The clinical and angiographic follow-up was performed in 492 patients, and 45 patients underwent clinically driven nonculprit lesions PCI (study group). A total of 447 patients were free of additional PCI (control group). There were significant differences in the level of catecholamines (E (621.48 ± 79.31) pg/mL versus (268.14 ± 73.26) pg/mL, P < 0.0001), NE (6212.43 ± 822.41) pg/mL versus (3218.34 ± 614.16) pg/mL, P < 0.0001), CRP (3.29 ± 1.31) mg/dL versus (2.51 ± 1.14) mg/dL, P < 0.0001, cTnI peak value (27.27 ± 4.02) ng/mL versus (16.12 ± 3.23) ng/mL, P < 0.0001), thrombotic lesion rate ((62.22% versus 23.04%), P < 0.0001), ≥ 2 vessel lesions rate (80.00% versus 46.09%), P < 0.0001), culprit lesion length ((33.2 ± 2.9 versus 28.1 ± 3.1), P = 0.013), and complex lesion rate ((57.78% versus 36.02%), P = 0.006) between the two groups. Correlation analysis between nonculprit lesion stenosis degree and serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, and complex lesion rate showed that there were significant correlations between serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, complex lesion rate, and nonculprit lesion stenosis degree. The correlation coefficients were 0.95, 0.97, 0.83, 0.90, 0.81, 0.84, 0.95, and 0.96, respectively, and P < 0.0001, P < 0.0001, P = 0.01, P = 0.01, P = 0.01, P = 0.01, P < 0.0001, and P < 0.0001, respectively. Recurrent PCI was mainly due to nonculprit lesion progression in patients with STEMI after primary PCI. Complex nonculprit lesions may be prone to for additional PCI. Chronic inflammation and sustained stress may be involved in the progression of nonculprit lesions in patients with STEMI.]]></description><identifier>ISSN: 1349-2365</identifier><identifier>EISSN: 1349-3299</identifier><identifier>DOI: 10.1536/ihj.13-081</identifier><identifier>PMID: 24463926</identifier><language>eng</language><publisher>Japan: International Heart Journal Association</publisher><subject>Adult ; Aged ; Aged, 80 and over ; China - epidemiology ; Complex nonculprit lesion ; Disease Progression ; Female ; Follow-Up Studies ; Humans ; Incidence ; Infl ammation ; Male ; Middle Aged ; Myocardial Infarction - surgery ; Percutaneous Coronary Intervention - statistics &amp; numerical data ; Postoperative Complications - epidemiology ; Postoperative Complications - surgery ; Recurrence ; Recurrent percutaneous coronary intervention ; Reoperation - statistics &amp; numerical data ; Stress</subject><ispartof>International Heart Journal, 2014, Vol.55(1), pp.48-52</ispartof><rights>2014 by the International Heart Journal Association</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c437t-9d1c9d5b85925b0d72680737f06a5558feca9d0a282e59faf82a3d847b045fa13</citedby><cites>FETCH-LOGICAL-c437t-9d1c9d5b85925b0d72680737f06a5558feca9d0a282e59faf82a3d847b045fa13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24463926$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Jian</creatorcontrib><creatorcontrib>Liu, Jing-hua</creatorcontrib><creatorcontrib>Zhu, Xiao-ling</creatorcontrib><creatorcontrib>Zhang, Ming</creatorcontrib><creatorcontrib>Wang, Shao-ping</creatorcontrib><creatorcontrib>Zheng, Ze</creatorcontrib><title>Nonculprit Lesion Progression in Patients With ST Elevation Myocardial Infarction After Primary Percutaneous Coronary Intervention</title><title>International Heart Journal</title><addtitle>Int. Heart J.</addtitle><description><![CDATA[The majority of cardiovascular events in patients with ST elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary interventions (PPCI) arise from the progression of nonculprit lesions (NCL) during the long-term follow-up period. However, the clinical and angiographic factors related to the progression of nonculprit lesions are unknown. The purpose of the study was to investigate the clinical and angiographic factors related to the progression of nonculprit lesions of patients with STEMI undergoing PPCI. A total of 492 patients with STEMI who underwent PPCI from January 2006 to December 2009 were enrolled. All patients underwent PPCI as a treatment for the culprit lesion. The clinical and angiographic follow-up was performed at 12 months. Primary endpoint: Clinically driven nonculprit lesion PCI. The levels of serum catecholamines [epinephrine (E), norepinephrine (NE)] and C-reactive protein (CRP) were assayed, and the clinical and angiographic features were also analyzed. The clinical and angiographic follow-up was performed in 492 patients, and 45 patients underwent clinically driven nonculprit lesions PCI (study group). A total of 447 patients were free of additional PCI (control group). There were significant differences in the level of catecholamines (E (621.48 ± 79.31) pg/mL versus (268.14 ± 73.26) pg/mL, P < 0.0001), NE (6212.43 ± 822.41) pg/mL versus (3218.34 ± 614.16) pg/mL, P < 0.0001), CRP (3.29 ± 1.31) mg/dL versus (2.51 ± 1.14) mg/dL, P < 0.0001, cTnI peak value (27.27 ± 4.02) ng/mL versus (16.12 ± 3.23) ng/mL, P < 0.0001), thrombotic lesion rate ((62.22% versus 23.04%), P < 0.0001), ≥ 2 vessel lesions rate (80.00% versus 46.09%), P < 0.0001), culprit lesion length ((33.2 ± 2.9 versus 28.1 ± 3.1), P = 0.013), and complex lesion rate ((57.78% versus 36.02%), P = 0.006) between the two groups. Correlation analysis between nonculprit lesion stenosis degree and serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, and complex lesion rate showed that there were significant correlations between serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, complex lesion rate, and nonculprit lesion stenosis degree. The correlation coefficients were 0.95, 0.97, 0.83, 0.90, 0.81, 0.84, 0.95, and 0.96, respectively, and P < 0.0001, P < 0.0001, P = 0.01, P = 0.01, P = 0.01, P = 0.01, P < 0.0001, and P < 0.0001, respectively. Recurrent PCI was mainly due to nonculprit lesion progression in patients with STEMI after primary PCI. Complex nonculprit lesions may be prone to for additional PCI. Chronic inflammation and sustained stress may be involved in the progression of nonculprit lesions in patients with STEMI.]]></description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>China - epidemiology</subject><subject>Complex nonculprit lesion</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Humans</subject><subject>Incidence</subject><subject>Infl ammation</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - surgery</subject><subject>Percutaneous Coronary Intervention - statistics &amp; numerical data</subject><subject>Postoperative Complications - epidemiology</subject><subject>Postoperative Complications - surgery</subject><subject>Recurrence</subject><subject>Recurrent percutaneous coronary intervention</subject><subject>Reoperation - statistics &amp; numerical data</subject><subject>Stress</subject><issn>1349-2365</issn><issn>1349-3299</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kF9PwjAUxRujEURf_ABmzybD_lm39U1CUElQScT4uJSuhZKxkrYj4dVPbtmQl3tvz_3dk-YAcI_gEFGSPun1ZohIDHN0AfqIJCwmmLHL04xJSnvgxrkNhAmiMLsGPZwkKWE47YPfD1OLptpZ7aOZdNrU0dyalZWunXV4cq9l7V30o_06-lpEk0rugxa27wcjuC01r6JprbgVrTpSXtrgorfcHqK5tKLxvJamcdHYWFMf1WkdmH2wDQe34Erxysm7Ux-A75fJYvwWzz5fp-PRLBYJyXzMSiRYSZc5ZZguYZnhNIcZyRRMOaU0V1JwVkKOcywpU1zlmJMyT7IlTKjiiAzAY-crrHHOSlXsuj8WCBbHIIsQZIFIEYIM8EMH75rlVpZn9D-5ADx3wMZ5vpJngFuvRSVbL0oL1JbW87wSa24LWZM_cNeIuQ</recordid><startdate>2014</startdate><enddate>2014</enddate><creator>Wang, Jian</creator><creator>Liu, Jing-hua</creator><creator>Zhu, Xiao-ling</creator><creator>Zhang, Ming</creator><creator>Wang, Shao-ping</creator><creator>Zheng, Ze</creator><general>International Heart Journal Association</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>2014</creationdate><title>Nonculprit Lesion Progression in Patients With ST Elevation Myocardial Infarction After Primary Percutaneous Coronary Intervention</title><author>Wang, Jian ; Liu, Jing-hua ; Zhu, Xiao-ling ; Zhang, Ming ; Wang, Shao-ping ; Zheng, Ze</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c437t-9d1c9d5b85925b0d72680737f06a5558feca9d0a282e59faf82a3d847b045fa13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>China - epidemiology</topic><topic>Complex nonculprit lesion</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Humans</topic><topic>Incidence</topic><topic>Infl ammation</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - surgery</topic><topic>Percutaneous Coronary Intervention - statistics &amp; numerical data</topic><topic>Postoperative Complications - epidemiology</topic><topic>Postoperative Complications - surgery</topic><topic>Recurrence</topic><topic>Recurrent percutaneous coronary intervention</topic><topic>Reoperation - statistics &amp; numerical data</topic><topic>Stress</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Jian</creatorcontrib><creatorcontrib>Liu, Jing-hua</creatorcontrib><creatorcontrib>Zhu, Xiao-ling</creatorcontrib><creatorcontrib>Zhang, Ming</creatorcontrib><creatorcontrib>Wang, Shao-ping</creatorcontrib><creatorcontrib>Zheng, Ze</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>International Heart Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Jian</au><au>Liu, Jing-hua</au><au>Zhu, Xiao-ling</au><au>Zhang, Ming</au><au>Wang, Shao-ping</au><au>Zheng, Ze</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nonculprit Lesion Progression in Patients With ST Elevation Myocardial Infarction After Primary Percutaneous Coronary Intervention</atitle><jtitle>International Heart Journal</jtitle><addtitle>Int. Heart J.</addtitle><date>2014</date><risdate>2014</risdate><volume>55</volume><issue>1</issue><spage>48</spage><epage>52</epage><pages>48-52</pages><issn>1349-2365</issn><eissn>1349-3299</eissn><abstract><![CDATA[The majority of cardiovascular events in patients with ST elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary interventions (PPCI) arise from the progression of nonculprit lesions (NCL) during the long-term follow-up period. However, the clinical and angiographic factors related to the progression of nonculprit lesions are unknown. The purpose of the study was to investigate the clinical and angiographic factors related to the progression of nonculprit lesions of patients with STEMI undergoing PPCI. A total of 492 patients with STEMI who underwent PPCI from January 2006 to December 2009 were enrolled. All patients underwent PPCI as a treatment for the culprit lesion. The clinical and angiographic follow-up was performed at 12 months. Primary endpoint: Clinically driven nonculprit lesion PCI. The levels of serum catecholamines [epinephrine (E), norepinephrine (NE)] and C-reactive protein (CRP) were assayed, and the clinical and angiographic features were also analyzed. The clinical and angiographic follow-up was performed in 492 patients, and 45 patients underwent clinically driven nonculprit lesions PCI (study group). A total of 447 patients were free of additional PCI (control group). There were significant differences in the level of catecholamines (E (621.48 ± 79.31) pg/mL versus (268.14 ± 73.26) pg/mL, P < 0.0001), NE (6212.43 ± 822.41) pg/mL versus (3218.34 ± 614.16) pg/mL, P < 0.0001), CRP (3.29 ± 1.31) mg/dL versus (2.51 ± 1.14) mg/dL, P < 0.0001, cTnI peak value (27.27 ± 4.02) ng/mL versus (16.12 ± 3.23) ng/mL, P < 0.0001), thrombotic lesion rate ((62.22% versus 23.04%), P < 0.0001), ≥ 2 vessel lesions rate (80.00% versus 46.09%), P < 0.0001), culprit lesion length ((33.2 ± 2.9 versus 28.1 ± 3.1), P = 0.013), and complex lesion rate ((57.78% versus 36.02%), P = 0.006) between the two groups. Correlation analysis between nonculprit lesion stenosis degree and serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, and complex lesion rate showed that there were significant correlations between serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, complex lesion rate, and nonculprit lesion stenosis degree. The correlation coefficients were 0.95, 0.97, 0.83, 0.90, 0.81, 0.84, 0.95, and 0.96, respectively, and P < 0.0001, P < 0.0001, P = 0.01, P = 0.01, P = 0.01, P = 0.01, P < 0.0001, and P < 0.0001, respectively. Recurrent PCI was mainly due to nonculprit lesion progression in patients with STEMI after primary PCI. Complex nonculprit lesions may be prone to for additional PCI. Chronic inflammation and sustained stress may be involved in the progression of nonculprit lesions in patients with STEMI.]]></abstract><cop>Japan</cop><pub>International Heart Journal Association</pub><pmid>24463926</pmid><doi>10.1536/ihj.13-081</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record>
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subjects Adult
Aged
Aged, 80 and over
China - epidemiology
Complex nonculprit lesion
Disease Progression
Female
Follow-Up Studies
Humans
Incidence
Infl ammation
Male
Middle Aged
Myocardial Infarction - surgery
Percutaneous Coronary Intervention - statistics & numerical data
Postoperative Complications - epidemiology
Postoperative Complications - surgery
Recurrence
Recurrent percutaneous coronary intervention
Reoperation - statistics & numerical data
Stress
title Nonculprit Lesion Progression in Patients With ST Elevation Myocardial Infarction After Primary Percutaneous Coronary Intervention
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