Allograft Vasculopathy: The Achilles' Heel of Heart Transplantation
Cardiac allograft vasculopathy (CAV) remains the Achilles' heel of long-term survival after heart transplantation. Almost one-third of patients develop CAV by 5 years post-transplant and 1 in 8 deaths beyond a year are due to CAV. Abnormal vascular fibroproliferation in CAV occurs as a result o...
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| Veröffentlicht in: | Journal of the American College of Cardiology 2016-07, Vol.68 (1), p.80-91 |
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| container_title | Journal of the American College of Cardiology |
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| creator | Chih, Sharon Chong, Aun Yeong Mielniczuk, Lisa M Bhatt, Deepak L Beanlands, Rob S B |
| description | Cardiac allograft vasculopathy (CAV) remains the Achilles' heel of long-term survival after heart transplantation. Almost one-third of patients develop CAV by 5 years post-transplant and 1 in 8 deaths beyond a year are due to CAV. Abnormal vascular fibroproliferation in CAV occurs as a result of coronary endothelial inflammation, injury, and dysfunction triggered by immune and nonimmune insults. Surveillance methods for CAV have significant limitations, particularly for detecting early disease. Areas of investigation include myocardial and coronary blood flow quantification, and intracoronary imaging to detect early changes in the vessel wall and high-risk plaques. Treatment approaches continue to evolve, but prevention remains the focus. Newer mammalian target of rapamycin inhibitors can significantly delay the progression of CAV; however, their optimal use remains to be established. Further investigation is needed to understand the complex pathophysiology of CAV, improve surveillance techniques, and develop therapies to prevent and slow disease progression. |
| doi_str_mv | 10.1016/j.jacc.2016.04.033 |
| format | Article |
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Almost one-third of patients develop CAV by 5 years post-transplant and 1 in 8 deaths beyond a year are due to CAV. Abnormal vascular fibroproliferation in CAV occurs as a result of coronary endothelial inflammation, injury, and dysfunction triggered by immune and nonimmune insults. Surveillance methods for CAV have significant limitations, particularly for detecting early disease. Areas of investigation include myocardial and coronary blood flow quantification, and intracoronary imaging to detect early changes in the vessel wall and high-risk plaques. Treatment approaches continue to evolve, but prevention remains the focus. Newer mammalian target of rapamycin inhibitors can significantly delay the progression of CAV; however, their optimal use remains to be established. Further investigation is needed to understand the complex pathophysiology of CAV, improve surveillance techniques, and develop therapies to prevent and slow disease progression.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/j.jacc.2016.04.033</identifier><identifier>PMID: 27364054</identifier><language>eng</language><publisher>United States: Elsevier Limited</publisher><subject>Allografts ; Cardiology ; Cardiovascular disease ; Cell adhesion & migration ; Cell growth ; Cytokines ; Cytomegalovirus ; Flow velocity ; Gangrene ; Heart ; Heart Transplantation ; Humans ; Infections ; Ischemia ; Medical imaging ; Mortality ; Nitric oxide ; Postoperative Complications - diagnosis ; Postoperative Complications - etiology ; Postoperative Complications - therapy ; Rodents ; Smooth muscle ; Surveillance ; Transplants & implants ; Tumor necrosis factor-TNF ; Vascular Diseases - diagnosis ; Vascular Diseases - etiology ; Vascular Diseases - therapy ; Vascular endothelial growth factor</subject><ispartof>Journal of the American College of Cardiology, 2016-07, Vol.68 (1), p.80-91</ispartof><rights>Copyright © 2016 American College of Cardiology Foundation. 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Almost one-third of patients develop CAV by 5 years post-transplant and 1 in 8 deaths beyond a year are due to CAV. Abnormal vascular fibroproliferation in CAV occurs as a result of coronary endothelial inflammation, injury, and dysfunction triggered by immune and nonimmune insults. Surveillance methods for CAV have significant limitations, particularly for detecting early disease. Areas of investigation include myocardial and coronary blood flow quantification, and intracoronary imaging to detect early changes in the vessel wall and high-risk plaques. Treatment approaches continue to evolve, but prevention remains the focus. Newer mammalian target of rapamycin inhibitors can significantly delay the progression of CAV; however, their optimal use remains to be established. Further investigation is needed to understand the complex pathophysiology of CAV, improve surveillance techniques, and develop therapies to prevent and slow disease progression.</description><subject>Allografts</subject><subject>Cardiology</subject><subject>Cardiovascular disease</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cytokines</subject><subject>Cytomegalovirus</subject><subject>Flow velocity</subject><subject>Gangrene</subject><subject>Heart</subject><subject>Heart Transplantation</subject><subject>Humans</subject><subject>Infections</subject><subject>Ischemia</subject><subject>Medical imaging</subject><subject>Mortality</subject><subject>Nitric oxide</subject><subject>Postoperative Complications - diagnosis</subject><subject>Postoperative Complications - etiology</subject><subject>Postoperative Complications - therapy</subject><subject>Rodents</subject><subject>Smooth muscle</subject><subject>Surveillance</subject><subject>Transplants & implants</subject><subject>Tumor necrosis factor-TNF</subject><subject>Vascular Diseases - diagnosis</subject><subject>Vascular Diseases - etiology</subject><subject>Vascular Diseases - therapy</subject><subject>Vascular endothelial growth factor</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE1Lw0AQhhdRbK3-AQ8S8KCXxP3IfnkLRa1Q8FK9hslmYxO2Scwmh_57t1gvnrzMMwwPLzOD0DXBCcFEPDRJA8YkNPQJThPM2AmaE85VzLiWp2iOJeMxwVrO0IX3DcZYKKLP0YxKJlLM0zlaZs51nwNUY_QB3kyu62Hc7h-jzdZGmdnWzll_F62sdVFXBcIwRpsBWt87aEcY6669RGcVOG-vjlyg9-enzXIVr99eXpfZOu6ppGMM3JQkJUKUAVJZkFUBoZTC6LIwhZKsKIXmShuuyzASFGgKwDUYCpKzBbr_ye2H7muyfsx3tTfWhUVsN_mcKKyEUorg_6gkpUKyNKi3f9Smm4Y2HHKwKKVCq0PgzdGaip0t836odzDs899Psm9gwnUn</recordid><startdate>20160705</startdate><enddate>20160705</enddate><creator>Chih, Sharon</creator><creator>Chong, Aun Yeong</creator><creator>Mielniczuk, Lisa M</creator><creator>Bhatt, Deepak L</creator><creator>Beanlands, Rob S B</creator><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20160705</creationdate><title>Allograft Vasculopathy: The Achilles' Heel of Heart Transplantation</title><author>Chih, Sharon ; Chong, Aun Yeong ; Mielniczuk, Lisa M ; Bhatt, Deepak L ; Beanlands, Rob S B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p272t-a5cd14166dd1478ea7fbaa7fd6c9dbcb873bd69589c59d9db62a24aa59ac2a753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Allografts</topic><topic>Cardiology</topic><topic>Cardiovascular disease</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Cytokines</topic><topic>Cytomegalovirus</topic><topic>Flow velocity</topic><topic>Gangrene</topic><topic>Heart</topic><topic>Heart Transplantation</topic><topic>Humans</topic><topic>Infections</topic><topic>Ischemia</topic><topic>Medical imaging</topic><topic>Mortality</topic><topic>Nitric oxide</topic><topic>Postoperative Complications - diagnosis</topic><topic>Postoperative Complications - etiology</topic><topic>Postoperative Complications - therapy</topic><topic>Rodents</topic><topic>Smooth muscle</topic><topic>Surveillance</topic><topic>Transplants & implants</topic><topic>Tumor necrosis factor-TNF</topic><topic>Vascular Diseases - diagnosis</topic><topic>Vascular Diseases - etiology</topic><topic>Vascular Diseases - therapy</topic><topic>Vascular endothelial growth factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chih, Sharon</creatorcontrib><creatorcontrib>Chong, Aun Yeong</creatorcontrib><creatorcontrib>Mielniczuk, Lisa M</creatorcontrib><creatorcontrib>Bhatt, Deepak L</creatorcontrib><creatorcontrib>Beanlands, Rob S B</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of the American College of Cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chih, Sharon</au><au>Chong, Aun Yeong</au><au>Mielniczuk, Lisa M</au><au>Bhatt, Deepak L</au><au>Beanlands, Rob S B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Allograft Vasculopathy: The Achilles' Heel of Heart Transplantation</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>2016-07-05</date><risdate>2016</risdate><volume>68</volume><issue>1</issue><spage>80</spage><epage>91</epage><pages>80-91</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><abstract>Cardiac allograft vasculopathy (CAV) remains the Achilles' heel of long-term survival after heart transplantation. Almost one-third of patients develop CAV by 5 years post-transplant and 1 in 8 deaths beyond a year are due to CAV. Abnormal vascular fibroproliferation in CAV occurs as a result of coronary endothelial inflammation, injury, and dysfunction triggered by immune and nonimmune insults. Surveillance methods for CAV have significant limitations, particularly for detecting early disease. Areas of investigation include myocardial and coronary blood flow quantification, and intracoronary imaging to detect early changes in the vessel wall and high-risk plaques. Treatment approaches continue to evolve, but prevention remains the focus. Newer mammalian target of rapamycin inhibitors can significantly delay the progression of CAV; however, their optimal use remains to be established. Further investigation is needed to understand the complex pathophysiology of CAV, improve surveillance techniques, and develop therapies to prevent and slow disease progression.</abstract><cop>United States</cop><pub>Elsevier Limited</pub><pmid>27364054</pmid><doi>10.1016/j.jacc.2016.04.033</doi><tpages>12</tpages></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Allografts Cardiology Cardiovascular disease Cell adhesion & migration Cell growth Cytokines Cytomegalovirus Flow velocity Gangrene Heart Heart Transplantation Humans Infections Ischemia Medical imaging Mortality Nitric oxide Postoperative Complications - diagnosis Postoperative Complications - etiology Postoperative Complications - therapy Rodents Smooth muscle Surveillance Transplants & implants Tumor necrosis factor-TNF Vascular Diseases - diagnosis Vascular Diseases - etiology Vascular Diseases - therapy Vascular endothelial growth factor |
| title | Allograft Vasculopathy: The Achilles' Heel of Heart Transplantation |
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