Impact of acute mental stress on sympathetic nerve activity and regional blood flow in advanced heart failure : Implications for 'triggering' adverse cardiac events
Evidence is accumulating that specific "triggers," such as intense psychological stress, may precipitate myocardial infarction and sudden death. Patients with advanced heart failure have increased resting sympathoexcitation, which has been directly related to increased mortality. The impac...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1997-09, Vol.96 (6), p.1835-1842 |
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| creator | MIDDLEKAUFF, H. R NGUYEN, A. H NEGRAO, C. E NITZSCHE, E. U HOH, C. K NATTERSON, B. A HAMILTON, M. A FONAROW, G. C HAGE, A MORIGUCHI, J. D |
| description | Evidence is accumulating that specific "triggers," such as intense psychological stress, may precipitate myocardial infarction and sudden death. Patients with advanced heart failure have increased resting sympathoexcitation, which has been directly related to increased mortality. The impact of triggers on sympathetic nerve activity and regional blood flow in heart failure has not been examined in patients with heart failure.
Twenty-seven patients with heart failure (NYHA functional class III or IV) and 26 age-matched normal control subjects were studied. Muscle sympathetic nerve activity, heart rate, mean arterial pressure, forearm blood flow, and renal blood flow were measured during mental stress testing with mental arithmetic and Stroop color word test. Patients with heart failure had elevated levels of resting muscle sympathetic nerve activity and heart rate. Mental stress significantly increased muscle sympathetic nerve activity and heart rate in both patients with heart failure and control subjects, although the magnitude of increases tended to be blunted in patients with heart failure. Nevertheless, absolute levels of sympathetic activity in patients with heart failure remained significantly higher than levels in control subjects during mental stress. The decrease in renal blood flow in patients with heart failure was similar to that of control subjects, despite greater resting renal vasoconstriction. The increase in forearm blood flow during mental stress testing in patients with heart failure was blunted compared with that of control subjects.
Patients with heart failure do not have augmented muscle sympathetic nerve activity responses to mental stress, despite elevated resting levels of sympathetic activity, but they do have markedly higher absolute levels of sympathetic nerve activity during mental stress as well as at rest. |
| doi_str_mv | 10.1161/01.CIR.96.6.1835 |
| format | Article |
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Twenty-seven patients with heart failure (NYHA functional class III or IV) and 26 age-matched normal control subjects were studied. Muscle sympathetic nerve activity, heart rate, mean arterial pressure, forearm blood flow, and renal blood flow were measured during mental stress testing with mental arithmetic and Stroop color word test. Patients with heart failure had elevated levels of resting muscle sympathetic nerve activity and heart rate. Mental stress significantly increased muscle sympathetic nerve activity and heart rate in both patients with heart failure and control subjects, although the magnitude of increases tended to be blunted in patients with heart failure. Nevertheless, absolute levels of sympathetic activity in patients with heart failure remained significantly higher than levels in control subjects during mental stress. The decrease in renal blood flow in patients with heart failure was similar to that of control subjects, despite greater resting renal vasoconstriction. The increase in forearm blood flow during mental stress testing in patients with heart failure was blunted compared with that of control subjects.
Patients with heart failure do not have augmented muscle sympathetic nerve activity responses to mental stress, despite elevated resting levels of sympathetic activity, but they do have markedly higher absolute levels of sympathetic nerve activity during mental stress as well as at rest.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.96.6.1835</identifier><identifier>PMID: 9323069</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Adult ; Biological and medical sciences ; Blood Pressure ; Cardiology. Vascular system ; Death, Sudden - etiology ; Forearm - blood supply ; Forearm - innervation ; Heart ; Heart Failure - complications ; Heart Failure - mortality ; Heart Failure - psychology ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Heart Rate ; Humans ; Medical sciences ; Middle Aged ; Muscle, Skeletal - blood supply ; Muscle, Skeletal - innervation ; Regional Blood Flow ; Renal Circulation ; Stress, Psychological - complications ; Stress, Psychological - physiopathology ; Sympathetic Nervous System - physiopathology ; Vasoconstriction ; Vasodilation</subject><ispartof>Circulation (New York, N.Y.), 1997-09, Vol.96 (6), p.1835-1842</ispartof><rights>1997 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Sep 16,1997</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c344t-8ff1fe54f7263a31a63b16161d11c18a814ff46e4f79309e45a6b77b57d5a0a23</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=2821643$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9323069$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MIDDLEKAUFF, H. R</creatorcontrib><creatorcontrib>NGUYEN, A. H</creatorcontrib><creatorcontrib>NEGRAO, C. E</creatorcontrib><creatorcontrib>NITZSCHE, E. U</creatorcontrib><creatorcontrib>HOH, C. K</creatorcontrib><creatorcontrib>NATTERSON, B. A</creatorcontrib><creatorcontrib>HAMILTON, M. A</creatorcontrib><creatorcontrib>FONAROW, G. C</creatorcontrib><creatorcontrib>HAGE, A</creatorcontrib><creatorcontrib>MORIGUCHI, J. D</creatorcontrib><title>Impact of acute mental stress on sympathetic nerve activity and regional blood flow in advanced heart failure : Implications for 'triggering' adverse cardiac events</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Evidence is accumulating that specific "triggers," such as intense psychological stress, may precipitate myocardial infarction and sudden death. Patients with advanced heart failure have increased resting sympathoexcitation, which has been directly related to increased mortality. The impact of triggers on sympathetic nerve activity and regional blood flow in heart failure has not been examined in patients with heart failure.
Twenty-seven patients with heart failure (NYHA functional class III or IV) and 26 age-matched normal control subjects were studied. Muscle sympathetic nerve activity, heart rate, mean arterial pressure, forearm blood flow, and renal blood flow were measured during mental stress testing with mental arithmetic and Stroop color word test. Patients with heart failure had elevated levels of resting muscle sympathetic nerve activity and heart rate. Mental stress significantly increased muscle sympathetic nerve activity and heart rate in both patients with heart failure and control subjects, although the magnitude of increases tended to be blunted in patients with heart failure. Nevertheless, absolute levels of sympathetic activity in patients with heart failure remained significantly higher than levels in control subjects during mental stress. The decrease in renal blood flow in patients with heart failure was similar to that of control subjects, despite greater resting renal vasoconstriction. The increase in forearm blood flow during mental stress testing in patients with heart failure was blunted compared with that of control subjects.
Patients with heart failure do not have augmented muscle sympathetic nerve activity responses to mental stress, despite elevated resting levels of sympathetic activity, but they do have markedly higher absolute levels of sympathetic nerve activity during mental stress as well as at rest.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Cardiology. Vascular system</subject><subject>Death, Sudden - etiology</subject><subject>Forearm - blood supply</subject><subject>Forearm - innervation</subject><subject>Heart</subject><subject>Heart Failure - complications</subject><subject>Heart Failure - mortality</subject><subject>Heart Failure - psychology</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Heart Rate</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Muscle, Skeletal - blood supply</subject><subject>Muscle, Skeletal - innervation</subject><subject>Regional Blood Flow</subject><subject>Renal Circulation</subject><subject>Stress, Psychological - complications</subject><subject>Stress, Psychological - physiopathology</subject><subject>Sympathetic Nervous System - physiopathology</subject><subject>Vasoconstriction</subject><subject>Vasodilation</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>eNpdkUGLEzEUx4Moa7d69yIEEffUmpfMZDrepLhaWBBEz-FN5qWbZWZSk0yl38cPasqWPXgK4f1-L-H_Z-wNiDWAho8C1tvdj3Wr13oNG1U_YwuoZbWqatU-ZwshRLtqlJQv2XVKD-WqVVNfsatWSSV0u2B_d-MBbebBcbRzJj7SlHHgKUdKiYeJp1Mh8j1lb_lE8UgFzP7o84nj1PNIex-mYnRDCD13Q_jD_cSxP-Jkqef3hDFzh36YI_FPvLw3eIu5SIm7EPlNjn6_p-in_c1Zo5iIW4y9R8vpWL6TXrEXDodEry_nkv26_fJz-2119_3rbvv5bmVVVeXVxjlwVFeukVqhAtSqKyFp6AEsbHADlXOVpgK0SrRU1ai7punqpq9RoFRL9uFx7yGG3zOlbEafLA0DThTmZIomKwVQwHf_gQ9hjiWFZCRIXcM56CUTj5CNIaVIzhyiHzGeDAhzbs8IMKU902qjzbm9ory97J27kfon4VJXmb-_zDFZHFwsGfv0hMmNBF0p9Q9h9KP-</recordid><startdate>19970916</startdate><enddate>19970916</enddate><creator>MIDDLEKAUFF, H. 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Vascular system</topic><topic>Death, Sudden - etiology</topic><topic>Forearm - blood supply</topic><topic>Forearm - innervation</topic><topic>Heart</topic><topic>Heart Failure - complications</topic><topic>Heart Failure - mortality</topic><topic>Heart Failure - psychology</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Heart Rate</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Muscle, Skeletal - blood supply</topic><topic>Muscle, Skeletal - innervation</topic><topic>Regional Blood Flow</topic><topic>Renal Circulation</topic><topic>Stress, Psychological - complications</topic><topic>Stress, Psychological - physiopathology</topic><topic>Sympathetic Nervous System - physiopathology</topic><topic>Vasoconstriction</topic><topic>Vasodilation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MIDDLEKAUFF, H. R</creatorcontrib><creatorcontrib>NGUYEN, A. H</creatorcontrib><creatorcontrib>NEGRAO, C. E</creatorcontrib><creatorcontrib>NITZSCHE, E. U</creatorcontrib><creatorcontrib>HOH, C. K</creatorcontrib><creatorcontrib>NATTERSON, B. A</creatorcontrib><creatorcontrib>HAMILTON, M. A</creatorcontrib><creatorcontrib>FONAROW, G. C</creatorcontrib><creatorcontrib>HAGE, A</creatorcontrib><creatorcontrib>MORIGUCHI, J. D</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>MIDDLEKAUFF, H. R</au><au>NGUYEN, A. H</au><au>NEGRAO, C. E</au><au>NITZSCHE, E. U</au><au>HOH, C. K</au><au>NATTERSON, B. A</au><au>HAMILTON, M. A</au><au>FONAROW, G. C</au><au>HAGE, A</au><au>MORIGUCHI, J. D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of acute mental stress on sympathetic nerve activity and regional blood flow in advanced heart failure : Implications for 'triggering' adverse cardiac events</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1997-09-16</date><risdate>1997</risdate><volume>96</volume><issue>6</issue><spage>1835</spage><epage>1842</epage><pages>1835-1842</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Evidence is accumulating that specific "triggers," such as intense psychological stress, may precipitate myocardial infarction and sudden death. Patients with advanced heart failure have increased resting sympathoexcitation, which has been directly related to increased mortality. The impact of triggers on sympathetic nerve activity and regional blood flow in heart failure has not been examined in patients with heart failure.
Twenty-seven patients with heart failure (NYHA functional class III or IV) and 26 age-matched normal control subjects were studied. Muscle sympathetic nerve activity, heart rate, mean arterial pressure, forearm blood flow, and renal blood flow were measured during mental stress testing with mental arithmetic and Stroop color word test. Patients with heart failure had elevated levels of resting muscle sympathetic nerve activity and heart rate. Mental stress significantly increased muscle sympathetic nerve activity and heart rate in both patients with heart failure and control subjects, although the magnitude of increases tended to be blunted in patients with heart failure. Nevertheless, absolute levels of sympathetic activity in patients with heart failure remained significantly higher than levels in control subjects during mental stress. The decrease in renal blood flow in patients with heart failure was similar to that of control subjects, despite greater resting renal vasoconstriction. The increase in forearm blood flow during mental stress testing in patients with heart failure was blunted compared with that of control subjects.
Patients with heart failure do not have augmented muscle sympathetic nerve activity responses to mental stress, despite elevated resting levels of sympathetic activity, but they do have markedly higher absolute levels of sympathetic nerve activity during mental stress as well as at rest.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>9323069</pmid><doi>10.1161/01.CIR.96.6.1835</doi><tpages>8</tpages></addata></record> |
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| source | Journals@Ovid Complete - AutoHoldings; MEDLINE; American Heart Association Journals; EZB-FREE-00999 freely available EZB journals |
| subjects | Adult Biological and medical sciences Blood Pressure Cardiology. Vascular system Death, Sudden - etiology Forearm - blood supply Forearm - innervation Heart Heart Failure - complications Heart Failure - mortality Heart Failure - psychology Heart failure, cardiogenic pulmonary edema, cardiac enlargement Heart Rate Humans Medical sciences Middle Aged Muscle, Skeletal - blood supply Muscle, Skeletal - innervation Regional Blood Flow Renal Circulation Stress, Psychological - complications Stress, Psychological - physiopathology Sympathetic Nervous System - physiopathology Vasoconstriction Vasodilation |
| title | Impact of acute mental stress on sympathetic nerve activity and regional blood flow in advanced heart failure : Implications for 'triggering' adverse cardiac events |
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