Reduced systolic wave generation and increased peripheral wave reflection in chronic heart failure
1 International Centre for Circulatory Health, and 2 Department of Bioengineering, Faculty of Engineering, Saint Mary's Hospital and Imperial College, London, United Kingdom Submitted 6 October 2006 ; accepted in final form 23 March 2007 In human heart failure the role of wave generation by the...
Saved in:
Published in | American journal of physiology. Heart and circulatory physiology Vol. 293; no. 1; pp. H557 - H562 |
---|---|
Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
American Physiological Society
01.07.2007
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | 1 International Centre for Circulatory Health, and 2 Department of Bioengineering, Faculty of Engineering, Saint Mary's Hospital and Imperial College, London, United Kingdom
Submitted 6 October 2006
; accepted in final form 23 March 2007
In human heart failure the role of wave generation by the ventricle and wave reflection by the vasculature is contentious. The aim of this study was to compare wave generation and reflection in normal subjects with patients with stable compensated heart failure. Twenty-nine normal subjects and 67 patients with heart failure (New York Heart Association class II or III) were studied by noninvasive techniques applied to the common carotid artery. Data were analyzed by wave intensity analysis to determine the nature and direction of waves during the cardiac cycle. The energy carried by an early systolic forward compression wave (S wave) generated by the left ventricle and responsible for acceleration of flow in systole was significantly reduced in subjects with heart failure ( P < 0.001), and the timing of the peak of this wave was delayed. In contrast, reflection of this wave was increased in subjects with heart failure ( P < 0.001), but the timing of reflections with respect to the S wave was unchanged. The energy of an expansion wave generated by the heart in protodiastole was unaffected by heart failure. The carotid artery wave speed and the augmentation index did not significantly differ between subjects with heart failure compared with normal individuals. The ability of the left ventricle to generate a forward compression wave is markedly impaired in heart failure. Increased wave reflection serves to maintain systolic blood pressure but also places an additional load on cardiac function in heart failure.
cardiac function; blood pressure
Address for reprint requests and other correspondence: A. D. Hughes, Clinical Pharmacology, National Heart and Lung Div., Faculty of Medicine, Imperial College London, QEQM Wing, St. Mary's Hospital, S. Wharf Rd., London W2 1NY, UK (e-mail: a.hughes{at}imperial.ac.uk ) |
---|---|
AbstractList | 1 International Centre for Circulatory Health, and 2 Department of Bioengineering, Faculty of Engineering, Saint Mary's Hospital and Imperial College, London, United Kingdom
Submitted 6 October 2006
; accepted in final form 23 March 2007
In human heart failure the role of wave generation by the ventricle and wave reflection by the vasculature is contentious. The aim of this study was to compare wave generation and reflection in normal subjects with patients with stable compensated heart failure. Twenty-nine normal subjects and 67 patients with heart failure (New York Heart Association class II or III) were studied by noninvasive techniques applied to the common carotid artery. Data were analyzed by wave intensity analysis to determine the nature and direction of waves during the cardiac cycle. The energy carried by an early systolic forward compression wave (S wave) generated by the left ventricle and responsible for acceleration of flow in systole was significantly reduced in subjects with heart failure ( P < 0.001), and the timing of the peak of this wave was delayed. In contrast, reflection of this wave was increased in subjects with heart failure ( P < 0.001), but the timing of reflections with respect to the S wave was unchanged. The energy of an expansion wave generated by the heart in protodiastole was unaffected by heart failure. The carotid artery wave speed and the augmentation index did not significantly differ between subjects with heart failure compared with normal individuals. The ability of the left ventricle to generate a forward compression wave is markedly impaired in heart failure. Increased wave reflection serves to maintain systolic blood pressure but also places an additional load on cardiac function in heart failure.
cardiac function; blood pressure
Address for reprint requests and other correspondence: A. D. Hughes, Clinical Pharmacology, National Heart and Lung Div., Faculty of Medicine, Imperial College London, QEQM Wing, St. Mary's Hospital, S. Wharf Rd., London W2 1NY, UK (e-mail: a.hughes{at}imperial.ac.uk ) In human heart failure the role of wave generation by the ventricle and wave reflection by the vasculature is contentious. The aim of this study was to compare wave generation and reflection in normal subjects with patients with stable compensated heart failure. Twenty-nine normal subjects and 67 patients with heart failure (New York Heart Association class II or III) were studied by noninvasive techniques applied to the common carotid artery. Data were analyzed by wave intensity analysis to determine the nature and direction of waves during the cardiac cycle. The energy carried by an early systolic forward compression wave (S wave) generated by the left ventricle and responsible for acceleration of flow in systole was significantly reduced in subjects with heart failure (P < 0.001), and the timing of the peak of this wave was delayed. In contrast, reflection of this wave was increased in subjects with heart failure (P < 0.001), but the timing of reflections with respect to the S wave was unchanged. The energy of an expansion wave generated by the heart in protodiastole was unaffected by heart failure. The carotid artery wave speed and the augmentation index did not significantly differ between subjects with heart failure compared with normal individuals. The ability of the left ventricle to generate a forward compression wave is markedly impaired in heart failure. Increased wave reflection serves to maintain systolic blood pressure but also places an additional load on cardiac function in heart failure. In human heart failure the role of wave generation by the ventricle and wave reflection by the vasculature is contentious. The aim of this study was to compare wave generation and reflection in normal subjects with patients with stable compensated heart failure. Twenty-nine normal subjects and 67 patients with heart failure (New York Heart Association class II or III) were studied by noninvasive techniques applied to the common carotid artery. Data were analyzed by wave intensity analysis to determine the nature and direction of waves during the cardiac cycle. The energy carried by an early systolic forward compression wave (S wave) generated by the left ventricle and responsible for acceleration of flow in systole was significantly reduced in subjects with heart failure (P < 0.00 1), and the timing of the peak of this wave was delayed. In contrast, reflection of this wave was increased in subjects with heart failure (P < 0.00 1), but the timing of reflections with respect to the S wave was unchanged. The energy of an expansion wave generated by the heart in protodiastole was unaffected by heart failure. The carotid artery wave speed and the augmentation index did not significantly differ between subjects with heart failure compared with normal individuals. The ability of the left ventricle to generate a forward compression wave is markedly impaired in heart failure. Increased wave reflection serves to maintain systolic blood pressure but also places an additional load on cardiac function in heart failure. [PUBLICATION ABSTRACT] In human heart failure the role of wave generation by the ventricle and wave reflection by the vasculature is contentious. The aim of this study was to compare wave generation and reflection in normal subjects with patients with stable compensated heart failure. Twenty-nine normal subjects and 67 patients with heart failure (New York Heart Association class II or III) were studied by noninvasive techniques applied to the common carotid artery. Data were analyzed by wave intensity analysis to determine the nature and direction of waves during the cardiac cycle. The energy carried by an early systolic forward compression wave (S wave) generated by the left ventricle and responsible for acceleration of flow in systole was significantly reduced in subjects with heart failure (P < 0.001), and the timing of the peak of this wave was delayed. In contrast, reflection of this wave was increased in subjects with heart failure (P < 0.001), but the timing of reflections with respect to the S wave was unchanged. The energy of an expansion wave generated by the heart in protodiastole was unaffected by heart failure. The carotid artery wave speed and the augmentation index did not significantly differ between subjects with heart failure compared with normal individuals. The ability of the left ventricle to generate a forward compression wave is markedly impaired in heart failure. Increased wave reflection serves to maintain systolic blood pressure but also places an additional load on cardiac function in heart failure.In human heart failure the role of wave generation by the ventricle and wave reflection by the vasculature is contentious. The aim of this study was to compare wave generation and reflection in normal subjects with patients with stable compensated heart failure. Twenty-nine normal subjects and 67 patients with heart failure (New York Heart Association class II or III) were studied by noninvasive techniques applied to the common carotid artery. Data were analyzed by wave intensity analysis to determine the nature and direction of waves during the cardiac cycle. The energy carried by an early systolic forward compression wave (S wave) generated by the left ventricle and responsible for acceleration of flow in systole was significantly reduced in subjects with heart failure (P < 0.001), and the timing of the peak of this wave was delayed. In contrast, reflection of this wave was increased in subjects with heart failure (P < 0.001), but the timing of reflections with respect to the S wave was unchanged. The energy of an expansion wave generated by the heart in protodiastole was unaffected by heart failure. The carotid artery wave speed and the augmentation index did not significantly differ between subjects with heart failure compared with normal individuals. The ability of the left ventricle to generate a forward compression wave is markedly impaired in heart failure. Increased wave reflection serves to maintain systolic blood pressure but also places an additional load on cardiac function in heart failure. |
Author | Foale, Rodney Mayet, Jamil Hughes, Alun D Curtis, Stephanie L Zambanini, Andrew McG Thom, Simon A Parker, Kim H |
Author_xml | – sequence: 1 fullname: Curtis, Stephanie L – sequence: 2 fullname: Zambanini, Andrew – sequence: 3 fullname: Mayet, Jamil – sequence: 4 fullname: McG Thom, Simon A – sequence: 5 fullname: Foale, Rodney – sequence: 6 fullname: Parker, Kim H – sequence: 7 fullname: Hughes, Alun D |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17400718$$D View this record in MEDLINE/PubMed |
BookMark | eNp9kc1q3DAUhUVIaSZJnyBQTBfdeaofS7K7K6FpCoFAmL2Q5euxBo3kSnaTefsqM_mBQLPSQt93dXXOKTr2wQNCFwQvCeH0m96MA-g4LTHBDV9SjMURWuQbWhLOmmO0wEywUhDGT9BpShuMMZeCfUQnRFYYS1IvUHsH3WygK9IuTcFZU9zrv1CswUPUkw2-0L4rrDcRdMrYCNHmZ6N2BzBC78DsQesLM8Tg84z9XkWvrZsjnKMPvXYJPj2dZ2h19XN1eV3e3P76ffnjpjRVLaayNcJI3EGvW5C16ZmutCSaN3npjouW1ZUmhAgKBLeGEhBVwzXWuO65qDA7Q18PY8cY_syQJrW1yYBz2kOYk5JYYlLTKoNf3oCbMEefV1OUNoLXTNIMfX6C5nYLnRqj3eq4U8_JZaA5ACaGlHIMythpn9gU878VweqxJfXcktq3pB5byi57476Mf9daHqzBrod7G0GNwy7Z4MJ69yrQhimirjmXWfj-f-Fqdm4FD9OL-SqqsevZP_MSvus |
CODEN | AJPPDI |
CitedBy_id | crossref_primary_10_1161_JAHA_122_027666 crossref_primary_10_1038_jhh_2008_47 crossref_primary_10_1007_s00246_021_02544_x crossref_primary_10_1007_s00404_022_06517_0 crossref_primary_10_1097_HJH_0000000000000854 crossref_primary_10_1097_HJH_0000000000001623 crossref_primary_10_1536_ihj_14_159 crossref_primary_10_1038_ajh_2011_60 crossref_primary_10_1177_1753944707086935 crossref_primary_10_2991_artres_k_191224_157 crossref_primary_10_1371_journal_pone_0179938 crossref_primary_10_1016_j_clinthera_2009_12_011 crossref_primary_10_1111_j_1475_097X_2010_00943_x crossref_primary_10_1007_s11517_008_0388_x crossref_primary_10_1016_j_atherosclerosis_2013_01_015 crossref_primary_10_1016_j_ultrasmedbio_2022_09_016 crossref_primary_10_1097_HJH_0b013e32835ed884 crossref_primary_10_1155_2013_920605 crossref_primary_10_3389_fbioe_2021_737055 crossref_primary_10_1007_s10439_014_1087_4 crossref_primary_10_1111_1471_0528_17061 crossref_primary_10_1016_j_athplu_2021_07_020 crossref_primary_10_1016_j_jbiomech_2011_05_016 crossref_primary_10_1016_j_ultrasmedbio_2008_08_013 crossref_primary_10_1016_j_artres_2008_02_002 crossref_primary_10_7133_jca_52_235 crossref_primary_10_1097_MAT_0000000000000361 crossref_primary_10_1016_j_jbiomech_2013_10_007 crossref_primary_10_1088_1361_6579_aafcc4 crossref_primary_10_1007_s00129_020_04612_4 crossref_primary_10_14814_phy2_15731 crossref_primary_10_1016_j_artres_2013_03_001 crossref_primary_10_1038_ajh_2011_26 crossref_primary_10_1152_ajpheart_00349_2023 crossref_primary_10_1111_joim_12715 crossref_primary_10_36628_ijhf_2020_0029 crossref_primary_10_1002_uog_24854 crossref_primary_10_1093_eurjhf_hfs124 crossref_primary_10_3389_fphys_2020_578701 crossref_primary_10_1002_uog_27521 crossref_primary_10_1016_j_cardfail_2019_03_005 crossref_primary_10_1016_j_atherosclerosis_2013_08_032 crossref_primary_10_1097_MBP_0b013e32832941ce crossref_primary_10_1177_20480040221092893 crossref_primary_10_3389_fphys_2014_00101 crossref_primary_10_1007_s44200_024_00058_4 crossref_primary_10_1093_ehjci_jez227 crossref_primary_10_1093_europace_eur028 crossref_primary_10_3389_fcvm_2019_00169 crossref_primary_10_1371_journal_pone_0023106 crossref_primary_10_1111_j_1751_7133_2008_07210_x crossref_primary_10_1093_ckj_sfae172 crossref_primary_10_1152_japplphysiol_00863_2010 crossref_primary_10_1007_s00380_016_0914_y crossref_primary_10_1002_uog_20121 crossref_primary_10_1016_j_ultrasmedbio_2016_12_018 crossref_primary_10_1111_aor_12288 crossref_primary_10_1093_eurheartj_ehy346 crossref_primary_10_1111_j_1475_097X_2009_00856_x crossref_primary_10_1016_j_bspc_2013_01_003 crossref_primary_10_1152_ajpheart_00219_2024 crossref_primary_10_1016_j_ajog_2024_08_039 crossref_primary_10_3390_jcm12062321 crossref_primary_10_1088_1361_6579_aa8de3 crossref_primary_10_1097_HJH_0b013e328342ca56 crossref_primary_10_1002_uog_24913 crossref_primary_10_1002_uog_24914 crossref_primary_10_1177_0954411920926094 |
Cites_doi | 10.1093/cvr/27.11.1902 10.1016/S1071-9164(03)00585-2 10.1016/S0021-9290(01)00076-8 10.1115/1.2891191 10.1161/01.CIR.92.11.3212 10.1016/0735-1097(92)90198-V 10.1152/ajpheart.00636.2003 10.1161/01.CIR.80.6.1652 10.1161/01.CIR.84.6.2418 10.1152/jappl.1971.30.4.593 10.1007/BF01747827 10.1161/01.CIR.75.4.711 10.1161/01.CIR.95.7.1827 10.1152/ajpheart.1996.271.6.H2399 10.1016/j.jacc.2006.04.094 10.1161/01.CIR.58.3.460 10.1161/hy1201.098298 10.1093/cvr/26.3.265 10.1093/oxfordjournals.eurheartj.a061690 10.1016/S0021-9290(02)00449-9 10.1259/0007-1285-69-818-172 10.1007/BF02058593 10.1097/00004872-200106000-00007 10.1016/0002-9149(85)90387-X 10.1161/hy1201.096539 10.1007/BF03257237 10.1093/eurheartj/13.suppl_E.113 10.1016/S0894-7317(89)80014-8 10.1007/BF02820867 10.1016/S0008-6363(96)00241-6 |
ContentType | Journal Article |
Copyright | Copyright American Physiological Society Jul 2007 |
Copyright_xml | – notice: Copyright American Physiological Society Jul 2007 |
DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7QP 7QR 7TS 7U7 8FD C1K FR3 P64 7X8 |
DOI | 10.1152/ajpheart.01095.2006 |
DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Calcium & Calcified Tissue Abstracts Chemoreception Abstracts Physical Education Index Toxicology Abstracts Technology Research Database Environmental Sciences and Pollution Management Engineering Research Database Biotechnology and BioEngineering Abstracts MEDLINE - Academic |
DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Technology Research Database Toxicology Abstracts Chemoreception Abstracts Engineering Research Database Calcium & Calcified Tissue Abstracts Physical Education Index Biotechnology and BioEngineering Abstracts Environmental Sciences and Pollution Management MEDLINE - Academic |
DatabaseTitleList | MEDLINE Technology Research Database CrossRef MEDLINE - Academic |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine Anatomy & Physiology |
EISSN | 1522-1539 |
EndPage | H562 |
ExternalDocumentID | 1303829031 17400718 10_1152_ajpheart_01095_2006 ajpheart_293_1_H557 |
Genre | Research Support, Non-U.S. Gov't Journal Article Feature |
GroupedDBID | - 02 23M 2WC 39C 4.4 53G 5GY 5VS 8M5 ABFLS ABPTK ACIWK ACPRK ADACO ADBBV AENEX AFFNX AFRAH ALMA_UNASSIGNED_HOLDINGS BAWUL BKOMP C1A DIK DL E3Z EBS EJD F5P GX1 H13 KQ8 O0- OK1 P2P PQEST PQQKQ RAP RHF RHI RPL UKR WH7 WOQ --- 3O- 6J9 AAFWJ AAYXX ABJNI ACBEA BKKCC BTFSW CITATION EMOBN ITBOX RPRKH TR2 W8F XSW YSK YYP ~02 CGR CUY CVF ECM EIF NPM 7QP 7QR 7TS 7U7 8FD C1K FR3 P64 7X8 |
ID | FETCH-LOGICAL-c486t-bc6c70defabe78cf3a4a71a59057d56b384a11162e10bc21e6495a0a08f56403 |
ISSN | 0363-6135 |
IngestDate | Thu Jul 10 23:06:55 EDT 2025 Mon Jun 30 16:46:58 EDT 2025 Thu Apr 03 07:02:44 EDT 2025 Tue Jul 01 04:20:09 EDT 2025 Thu Apr 24 23:05:40 EDT 2025 Mon May 06 11:41:34 EDT 2019 Tue Jan 05 18:11:22 EST 2021 |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 1 |
Language | English |
LinkModel | OpenURL |
MergedId | FETCHMERGED-LOGICAL-c486t-bc6c70defabe78cf3a4a71a59057d56b384a11162e10bc21e6495a0a08f56403 |
Notes | SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 |
PMID | 17400718 |
PQID | 229658372 |
PQPubID | 48261 |
ParticipantIDs | proquest_miscellaneous_70701824 crossref_citationtrail_10_1152_ajpheart_01095_2006 highwire_physiology_ajpheart_293_1_H557 pubmed_primary_17400718 proquest_journals_229658372 crossref_primary_10_1152_ajpheart_01095_2006 |
ProviderPackageCode | CITATION AAYXX |
PublicationCentury | 2000 |
PublicationDate | 20070701 2007-07-00 2007-Jul |
PublicationDateYYYYMMDD | 2007-07-01 |
PublicationDate_xml | – month: 07 year: 2007 text: 20070701 day: 01 |
PublicationDecade | 2000 |
PublicationPlace | United States |
PublicationPlace_xml | – name: United States – name: Bethesda |
PublicationTitle | American journal of physiology. Heart and circulatory physiology |
PublicationTitleAlternate | Am J Physiol Heart Circ Physiol |
PublicationYear | 2007 |
Publisher | American Physiological Society |
Publisher_xml | – name: American Physiological Society |
References | R21 R20 R23 R22 R25 R24 R27 R26 R29 R28 R1 R2 R3 R4 R5 R6 R7 R8 R9 R30 R10 R32 R31 R12 R11 R33 R14 R13 R16 R15 R18 R17 R19 |
References_xml | – ident: R6 doi: 10.1093/cvr/27.11.1902 – ident: R19 doi: 10.1016/S1071-9164(03)00585-2 – ident: R11 doi: 10.1016/S0021-9290(01)00076-8 – ident: R23 doi: 10.1115/1.2891191 – ident: R26 doi: 10.1161/01.CIR.92.11.3212 – ident: R9 doi: 10.1016/0735-1097(92)90198-V – ident: R32 doi: 10.1152/ajpheart.00636.2003 – ident: R10 doi: 10.1161/01.CIR.80.6.1652 – ident: R1 doi: 10.1161/01.CIR.84.6.2418 – ident: R28 doi: 10.1152/jappl.1971.30.4.593 – ident: R12 doi: 10.1007/BF01747827 – ident: R15 doi: 10.1161/01.CIR.75.4.711 – ident: R3 doi: 10.1161/01.CIR.95.7.1827 – ident: R8 doi: 10.1152/ajpheart.1996.271.6.H2399 – ident: R21 doi: 10.1016/j.jacc.2006.04.094 – ident: R25 doi: 10.1161/01.CIR.58.3.460 – ident: R33 – ident: R18 doi: 10.1161/hy1201.098298 – ident: R13 doi: 10.1093/cvr/26.3.265 – ident: R17 doi: 10.1093/oxfordjournals.eurheartj.a061690 – ident: R20 – ident: R29 doi: 10.1016/S0021-9290(02)00449-9 – ident: R5 doi: 10.1259/0007-1285-69-818-172 – ident: R24 doi: 10.1007/BF02058593 – ident: R31 doi: 10.1097/00004872-200106000-00007 – ident: R4 doi: 10.1016/0002-9149(85)90387-X – ident: R7 doi: 10.1161/hy1201.096539 – ident: R22 doi: 10.1007/BF03257237 – ident: R14 doi: 10.1093/eurheartj/13.suppl_E.113 – ident: R27 doi: 10.1016/S0894-7317(89)80014-8 – ident: R2 – ident: R16 doi: 10.1007/BF02820867 – ident: R30 doi: 10.1016/S0008-6363(96)00241-6 |
SSID | ssj0005763 |
Score | 2.1655684 |
Snippet | 1 International Centre for Circulatory Health, and 2 Department of Bioengineering, Faculty of Engineering, Saint Mary's Hospital and Imperial College, London,... In human heart failure the role of wave generation by the ventricle and wave reflection by the vasculature is contentious. The aim of this study was to compare... |
SourceID | proquest pubmed crossref highwire |
SourceType | Aggregation Database Index Database Enrichment Source Publisher |
StartPage | H557 |
SubjectTerms | Aged Blood Flow Velocity Blood pressure Cardiac Output, Low - complications Cardiac Output, Low - physiopathology Cardiology Cardiovascular system Comparative analysis Female Heart failure Humans Male Middle Aged Myocardial Contraction Stroke Volume Systole Ventricular Dysfunction, Left - etiology Ventricular Dysfunction, Left - physiopathology |
Title | Reduced systolic wave generation and increased peripheral wave reflection in chronic heart failure |
URI | http://ajpheart.physiology.org/cgi/content/abstract/293/1/H557 https://www.ncbi.nlm.nih.gov/pubmed/17400718 https://www.proquest.com/docview/229658372 https://www.proquest.com/docview/70701824 |
Volume | 293 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9QwELaqIiEuCFoeS3n4gOCwpCSO89hjhVoqaItAqVRxsWyvUxVt02qbFVr-Kn-GGT-SrCgVcIlWie2NPV_GM57xZ0JeTg2bSsVkpHidR5zJLFKTuoxUEssUpssJdwmyR_n-Mf9wkp2srf0cZC0tWrWtf1y7r-R_pAr3QK64S_YfJNs1CjfgN8gXriBhuP6VjL8g7ypYjEjHjPy-4-94ltCpZZJuQ57xWYOG4RUUQ1JjyyIwcwVhcpwZHbIdtaPJRdNx3o5reTbzZCMdSW0I7gzYJuzCiF2Z38YdTXOXr67P5pjeauP3fYku3LHAE6C7FDPc4z7ulqC_ynMFd-xBU8NsS7tovvSRE1yUGWa02LYAdA2ouUP9fmUlo-iyXtvB5gFU_eHFLEx99upAL2LoGawQFww3Xm-DTw3KezJU7MydvbiCYKem9zPHiv37_JEhH638dmnHehvjhpmNT_XTZUgROPok9o4PDkS1e1KtPnXOFdgGGKTGPf63GPgwqIQ_fu6p7MHRS0MgHXvjKbHgDd5e8_-rZlOgsv6zW2TNo-oeuev9GrrjQHqfrJlmg2zuNACC8yV9RbvRXm6Q24c-oWOTKA9hGiBMEZm0hzAFPNEOwrSHsCvYQxgKUQ9hartFPYQfkGpvt3q3H_ljPyLNy7yNlM51EU9NLZUpSl2nkssikdkEhmya5SotuYQZOmcmiZVmicnByZexjMs6y3mcPiTrzUVjHhNaaD3hqki44ZznXIFvBqYJ40aWqanjfERYGFShPSU-nswyE9Y1zpgIkhBWEnhmK1R601W6dIwwNxdPg7RE_8UJXGCqADFdFQCrSAQCU1xO6xF5fV2trv2-9IhsBQgI__lfCcaQ0ykt2Ii86J7CvIHBQNmYi8WVKGCuT0rGR-SRw03fmYKj41E-ubHlLXKn_4afkvV2vjDPwD5v1XOL81_Y8_Aj |
linkProvider | Colorado Alliance of Research Libraries |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Reduced+systolic+wave+generation+and+increased+peripheral+wave+reflection+in+chronic+heart+failure&rft.jtitle=American+journal+of+physiology.+Heart+and+circulatory+physiology&rft.au=Curtis%2C+Stephanie+L&rft.au=Zambanini%2C+Andrew&rft.au=Mayet%2C+Jamil&rft.au=Thom%2C+Simon+A+McG&rft.date=2007-07-01&rft.pub=American+Physiological+Society&rft.issn=0363-6135&rft.eissn=1522-1539&rft.volume=293&rft.issue=1&rft.spage=H557&rft_id=info:doi/10.1152%2Fajpheart.01095.2006&rft.externalDBID=NO_FULL_TEXT&rft.externalDocID=1303829031 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0363-6135&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0363-6135&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0363-6135&client=summon |