Impact of Mechanical Unloading on Microvasculature and Associated Central Remodeling Features of the Failing Human Heart
Objectives This study investigates alterations in myocardial microvasculature, fibrosis, and hypertrophy before and after mechanical unloading of the failing human heart. Background Recent studies demonstrated the pathophysiologic importance and significant mechanistic links among microvasculature,...
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| Veröffentlicht in: | Journal of the American College of Cardiology 2010-07, Vol.56 (5), p.382-391 |
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| creator | Drakos, Stavros G., MD Kfoury, Abdallah G., MD Hammond, Elizabeth H., MD Reid, Bruce B., MD Revelo, Monica P., MD, PhD Rasmusson, Brad Y., MD Whitehead, Kevin J., MD Salama, Mohamed E., MD Selzman, Craig H., MD Stehlik, Josef, MD Clayson, Stephen E., MD Bristow, Michael R., MD, PhD Renlund, Dale G., MD Li, Dean Y., MD, PhD |
| description | Objectives This study investigates alterations in myocardial microvasculature, fibrosis, and hypertrophy before and after mechanical unloading of the failing human heart. Background Recent studies demonstrated the pathophysiologic importance and significant mechanistic links among microvasculature, fibrosis, and hypertrophy during the cardiac remodeling process. The effect of left ventricular assist device (LVAD) unloading on cardiac endothelium and microvasculature is unknown, and its influence on fibrosis and hypertrophy regression to the point of atrophy is controversial. Methods Hemodynamic data and left ventricular tissue were collected from patients with chronic heart failure at LVAD implant and explant (n = 15) and from normal donors (n = 8). New advances in digital microscopy provided a unique opportunity for comprehensive whole-field, endocardium-to-epicardium evaluation for microvascular density, fibrosis, cardiomyocyte size, and glycogen content. Ultrastructural assessment was done with electron microscopy. Results Hemodynamic data revealed significant pressure unloading with LVAD. This was accompanied by a 33% increase in microvascular density (p = 0.001) and a 36% decrease in microvascular lumen area (p = 0.028). We also identified, in agreement with these findings, ultrastructural and immunohistochemical evidence of endothelial cell activation. In addition, LVAD unloading significantly increased interstitial and total collagen content without any associated structural, ultrastructural, or metabolic cardiomyocyte changes suggestive of hypertrophy regression to the point of atrophy and degeneration. Conclusions The LVAD unloading resulted in increased microvascular density accompanied by increased fibrosis and no evidence of cardiomyocyte atrophy. These new insights into the effects of LVAD unloading on microvasculature and associated key remodeling features might guide future studies of unloading-induced reverse remodeling of the failing human heart. |
| doi_str_mv | 10.1016/j.jacc.2010.04.019 |
| format | Article |
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Background Recent studies demonstrated the pathophysiologic importance and significant mechanistic links among microvasculature, fibrosis, and hypertrophy during the cardiac remodeling process. The effect of left ventricular assist device (LVAD) unloading on cardiac endothelium and microvasculature is unknown, and its influence on fibrosis and hypertrophy regression to the point of atrophy is controversial. Methods Hemodynamic data and left ventricular tissue were collected from patients with chronic heart failure at LVAD implant and explant (n = 15) and from normal donors (n = 8). New advances in digital microscopy provided a unique opportunity for comprehensive whole-field, endocardium-to-epicardium evaluation for microvascular density, fibrosis, cardiomyocyte size, and glycogen content. Ultrastructural assessment was done with electron microscopy. Results Hemodynamic data revealed significant pressure unloading with LVAD. This was accompanied by a 33% increase in microvascular density (p = 0.001) and a 36% decrease in microvascular lumen area (p = 0.028). We also identified, in agreement with these findings, ultrastructural and immunohistochemical evidence of endothelial cell activation. In addition, LVAD unloading significantly increased interstitial and total collagen content without any associated structural, ultrastructural, or metabolic cardiomyocyte changes suggestive of hypertrophy regression to the point of atrophy and degeneration. Conclusions The LVAD unloading resulted in increased microvascular density accompanied by increased fibrosis and no evidence of cardiomyocyte atrophy. These new insights into the effects of LVAD unloading on microvasculature and associated key remodeling features might guide future studies of unloading-induced reverse remodeling of the failing human heart.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/j.jacc.2010.04.019</identifier><identifier>PMID: 20650360</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adolescent ; Adult ; Algorithms ; Cardiology ; Cardiology - methods ; Cardiomegaly - pathology ; Cardiomyocytes ; Cardiomyopathy ; Cardiovascular ; Collagen ; Endothelium - pathology ; Female ; Heart ; heart failure ; Heart Failure - therapy ; Heart rate ; Heart Ventricles - pathology ; Heart-Assist Devices ; Humans ; Hypertrophy ; Internal Medicine ; left ventricular assist device ; Male ; Microcirculation ; Microscopy ; Microscopy, Electron - methods ; microvasculature ; Middle Aged ; Myocardium - pathology ; Patients ; Pulmonary arteries ; remodeling ; Stress, Mechanical ; Studies ; unloading ; Veins & arteries ; Ventricular Remodeling</subject><ispartof>Journal of the American College of Cardiology, 2010-07, Vol.56 (5), p.382-391</ispartof><rights>American College of Cardiology Foundation</rights><rights>2010 American College of Cardiology Foundation</rights><rights>Copyright 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Jul 27, 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c652t-21cb61ffd734c3254dd957fa7fb70f08c571c3dbffd81ddd54e4b2daf07ac8883</citedby><cites>FETCH-LOGICAL-c652t-21cb61ffd734c3254dd957fa7fb70f08c571c3dbffd81ddd54e4b2daf07ac8883</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0735109710019029$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20650360$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Drakos, Stavros G., MD</creatorcontrib><creatorcontrib>Kfoury, Abdallah G., MD</creatorcontrib><creatorcontrib>Hammond, Elizabeth H., MD</creatorcontrib><creatorcontrib>Reid, Bruce B., MD</creatorcontrib><creatorcontrib>Revelo, Monica P., MD, PhD</creatorcontrib><creatorcontrib>Rasmusson, Brad Y., MD</creatorcontrib><creatorcontrib>Whitehead, Kevin J., MD</creatorcontrib><creatorcontrib>Salama, Mohamed E., MD</creatorcontrib><creatorcontrib>Selzman, Craig H., MD</creatorcontrib><creatorcontrib>Stehlik, Josef, MD</creatorcontrib><creatorcontrib>Clayson, Stephen E., MD</creatorcontrib><creatorcontrib>Bristow, Michael R., MD, PhD</creatorcontrib><creatorcontrib>Renlund, Dale G., MD</creatorcontrib><creatorcontrib>Li, Dean Y., MD, PhD</creatorcontrib><title>Impact of Mechanical Unloading on Microvasculature and Associated Central Remodeling Features of the Failing Human Heart</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description>Objectives This study investigates alterations in myocardial microvasculature, fibrosis, and hypertrophy before and after mechanical unloading of the failing human heart. Background Recent studies demonstrated the pathophysiologic importance and significant mechanistic links among microvasculature, fibrosis, and hypertrophy during the cardiac remodeling process. The effect of left ventricular assist device (LVAD) unloading on cardiac endothelium and microvasculature is unknown, and its influence on fibrosis and hypertrophy regression to the point of atrophy is controversial. Methods Hemodynamic data and left ventricular tissue were collected from patients with chronic heart failure at LVAD implant and explant (n = 15) and from normal donors (n = 8). New advances in digital microscopy provided a unique opportunity for comprehensive whole-field, endocardium-to-epicardium evaluation for microvascular density, fibrosis, cardiomyocyte size, and glycogen content. Ultrastructural assessment was done with electron microscopy. Results Hemodynamic data revealed significant pressure unloading with LVAD. This was accompanied by a 33% increase in microvascular density (p = 0.001) and a 36% decrease in microvascular lumen area (p = 0.028). We also identified, in agreement with these findings, ultrastructural and immunohistochemical evidence of endothelial cell activation. In addition, LVAD unloading significantly increased interstitial and total collagen content without any associated structural, ultrastructural, or metabolic cardiomyocyte changes suggestive of hypertrophy regression to the point of atrophy and degeneration. Conclusions The LVAD unloading resulted in increased microvascular density accompanied by increased fibrosis and no evidence of cardiomyocyte atrophy. These new insights into the effects of LVAD unloading on microvasculature and associated key remodeling features might guide future studies of unloading-induced reverse remodeling of the failing human heart.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Algorithms</subject><subject>Cardiology</subject><subject>Cardiology - methods</subject><subject>Cardiomegaly - pathology</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Cardiovascular</subject><subject>Collagen</subject><subject>Endothelium - pathology</subject><subject>Female</subject><subject>Heart</subject><subject>heart failure</subject><subject>Heart Failure - therapy</subject><subject>Heart rate</subject><subject>Heart Ventricles - pathology</subject><subject>Heart-Assist Devices</subject><subject>Humans</subject><subject>Hypertrophy</subject><subject>Internal Medicine</subject><subject>left ventricular assist device</subject><subject>Male</subject><subject>Microcirculation</subject><subject>Microscopy</subject><subject>Microscopy, Electron - methods</subject><subject>microvasculature</subject><subject>Middle Aged</subject><subject>Myocardium - pathology</subject><subject>Patients</subject><subject>Pulmonary arteries</subject><subject>remodeling</subject><subject>Stress, Mechanical</subject><subject>Studies</subject><subject>unloading</subject><subject>Veins & arteries</subject><subject>Ventricular Remodeling</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kkFv1DAQhSMEokvhD3BAkThwyjJ2YjuRUKVqxbKVWiEBPVuOPel6SezFTlb03-N0S4EeOFkaf-9pZt5k2WsCSwKEv98td0rrJYVUgGoJpHmSLQhjdVGyRjzNFiBKVhBoxEn2IsYdAPCaNM-zEwqcQclhkf28GPZKj7nv8ivUW-WsVn1-7XqvjHU3uXf5ldXBH1TUU6_GKWCunMnPY_TaqhFNvkI3hiT6goM32M-qNd6RcbYdt5ivlb2rb6ZBuXyDKowvs2ed6iO-un9Ps-v1x2-rTXH5-dPF6vyy0JzRsaBEt5x0nRFlpUvKKmMaJjolulZAB7VmgujStImoiTGGVVi11KgOhNJ1XZen2dnRdz-1Axp9bFbugx1UuJVeWfnvj7NbeeMPsgRGK1Img3f3BsH_mDCOcrBRY98rh36KUlR1w7ngPJFvH5E7PwWXppOEAaeCAqsSRY9U2mqMAbuHXgjIOVe5k3Oucs5VQiVTrkn05u8pHiS_g0zAhyOAaZcHi0FGbdFpNDagHqXx9v_-Z4_kOgU238J3vMX4Zw4ZqQT5db6s-bAIJDXQpvwFcmrLOg</recordid><startdate>20100727</startdate><enddate>20100727</enddate><creator>Drakos, Stavros G., MD</creator><creator>Kfoury, Abdallah G., MD</creator><creator>Hammond, Elizabeth H., MD</creator><creator>Reid, Bruce B., MD</creator><creator>Revelo, Monica P., MD, PhD</creator><creator>Rasmusson, Brad Y., MD</creator><creator>Whitehead, Kevin J., MD</creator><creator>Salama, Mohamed E., MD</creator><creator>Selzman, Craig H., MD</creator><creator>Stehlik, Josef, MD</creator><creator>Clayson, Stephen E., MD</creator><creator>Bristow, Michael R., MD, PhD</creator><creator>Renlund, Dale G., MD</creator><creator>Li, Dean Y., MD, PhD</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</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>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100727</creationdate><title>Impact of Mechanical Unloading on Microvasculature and Associated Central Remodeling Features of the Failing Human Heart</title><author>Drakos, Stavros G., MD ; Kfoury, Abdallah G., MD ; Hammond, Elizabeth H., MD ; Reid, Bruce B., MD ; Revelo, Monica P., MD, PhD ; Rasmusson, Brad Y., MD ; Whitehead, Kevin J., MD ; Salama, Mohamed E., MD ; Selzman, Craig H., MD ; Stehlik, Josef, MD ; Clayson, Stephen E., MD ; Bristow, Michael R., MD, PhD ; Renlund, Dale G., MD ; Li, Dean Y., MD, PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c652t-21cb61ffd734c3254dd957fa7fb70f08c571c3dbffd81ddd54e4b2daf07ac8883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Algorithms</topic><topic>Cardiology</topic><topic>Cardiology - methods</topic><topic>Cardiomegaly - pathology</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathy</topic><topic>Cardiovascular</topic><topic>Collagen</topic><topic>Endothelium - pathology</topic><topic>Female</topic><topic>Heart</topic><topic>heart failure</topic><topic>Heart Failure - therapy</topic><topic>Heart rate</topic><topic>Heart Ventricles - pathology</topic><topic>Heart-Assist Devices</topic><topic>Humans</topic><topic>Hypertrophy</topic><topic>Internal Medicine</topic><topic>left ventricular assist device</topic><topic>Male</topic><topic>Microcirculation</topic><topic>Microscopy</topic><topic>Microscopy, Electron - methods</topic><topic>microvasculature</topic><topic>Middle Aged</topic><topic>Myocardium - pathology</topic><topic>Patients</topic><topic>Pulmonary arteries</topic><topic>remodeling</topic><topic>Stress, Mechanical</topic><topic>Studies</topic><topic>unloading</topic><topic>Veins & arteries</topic><topic>Ventricular Remodeling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Drakos, Stavros G., MD</creatorcontrib><creatorcontrib>Kfoury, Abdallah G., MD</creatorcontrib><creatorcontrib>Hammond, Elizabeth H., MD</creatorcontrib><creatorcontrib>Reid, Bruce B., MD</creatorcontrib><creatorcontrib>Revelo, Monica P., MD, PhD</creatorcontrib><creatorcontrib>Rasmusson, Brad Y., MD</creatorcontrib><creatorcontrib>Whitehead, Kevin J., MD</creatorcontrib><creatorcontrib>Salama, Mohamed E., MD</creatorcontrib><creatorcontrib>Selzman, Craig H., MD</creatorcontrib><creatorcontrib>Stehlik, Josef, MD</creatorcontrib><creatorcontrib>Clayson, Stephen E., MD</creatorcontrib><creatorcontrib>Bristow, Michael R., MD, PhD</creatorcontrib><creatorcontrib>Renlund, Dale G., MD</creatorcontrib><creatorcontrib>Li, Dean Y., MD, PhD</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of the American College of Cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Drakos, Stavros G., MD</au><au>Kfoury, Abdallah G., MD</au><au>Hammond, Elizabeth H., MD</au><au>Reid, Bruce B., MD</au><au>Revelo, Monica P., MD, PhD</au><au>Rasmusson, Brad Y., MD</au><au>Whitehead, Kevin J., MD</au><au>Salama, Mohamed E., MD</au><au>Selzman, Craig H., MD</au><au>Stehlik, Josef, MD</au><au>Clayson, Stephen E., MD</au><au>Bristow, Michael R., MD, PhD</au><au>Renlund, Dale G., MD</au><au>Li, Dean Y., MD, PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of Mechanical Unloading on Microvasculature and Associated Central Remodeling Features of the Failing Human Heart</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>2010-07-27</date><risdate>2010</risdate><volume>56</volume><issue>5</issue><spage>382</spage><epage>391</epage><pages>382-391</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><abstract>Objectives This study investigates alterations in myocardial microvasculature, fibrosis, and hypertrophy before and after mechanical unloading of the failing human heart. Background Recent studies demonstrated the pathophysiologic importance and significant mechanistic links among microvasculature, fibrosis, and hypertrophy during the cardiac remodeling process. The effect of left ventricular assist device (LVAD) unloading on cardiac endothelium and microvasculature is unknown, and its influence on fibrosis and hypertrophy regression to the point of atrophy is controversial. Methods Hemodynamic data and left ventricular tissue were collected from patients with chronic heart failure at LVAD implant and explant (n = 15) and from normal donors (n = 8). New advances in digital microscopy provided a unique opportunity for comprehensive whole-field, endocardium-to-epicardium evaluation for microvascular density, fibrosis, cardiomyocyte size, and glycogen content. Ultrastructural assessment was done with electron microscopy. Results Hemodynamic data revealed significant pressure unloading with LVAD. This was accompanied by a 33% increase in microvascular density (p = 0.001) and a 36% decrease in microvascular lumen area (p = 0.028). We also identified, in agreement with these findings, ultrastructural and immunohistochemical evidence of endothelial cell activation. In addition, LVAD unloading significantly increased interstitial and total collagen content without any associated structural, ultrastructural, or metabolic cardiomyocyte changes suggestive of hypertrophy regression to the point of atrophy and degeneration. Conclusions The LVAD unloading resulted in increased microvascular density accompanied by increased fibrosis and no evidence of cardiomyocyte atrophy. These new insights into the effects of LVAD unloading on microvasculature and associated key remodeling features might guide future studies of unloading-induced reverse remodeling of the failing human heart.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>20650360</pmid><doi>10.1016/j.jacc.2010.04.019</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescent Adult Algorithms Cardiology Cardiology - methods Cardiomegaly - pathology Cardiomyocytes Cardiomyopathy Cardiovascular Collagen Endothelium - pathology Female Heart heart failure Heart Failure - therapy Heart rate Heart Ventricles - pathology Heart-Assist Devices Humans Hypertrophy Internal Medicine left ventricular assist device Male Microcirculation Microscopy Microscopy, Electron - methods microvasculature Middle Aged Myocardium - pathology Patients Pulmonary arteries remodeling Stress, Mechanical Studies unloading Veins & arteries Ventricular Remodeling |
| title | Impact of Mechanical Unloading on Microvasculature and Associated Central Remodeling Features of the Failing Human Heart |
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