Early infarct expansion: Structural or functional?
With the onset of ischemia, the length of myocardial segments increases rapidly, distorting ventricular geometry. Permanent stretching and thinning of infarcted zones have been termed infarct expansion. Although these changes are noted within minutes in vivo, infarct expansion may not be seen for da...
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| Veröffentlicht in: | Journal of the American College of Cardiology 1985-10, Vol.6 (4), p.839-844 |
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| creator | Erlebacher, Jay A. Richter, Richard C. Alonso, Daniel R. Devereux, Richard B. Gay, William A. |
| description | With the onset of ischemia, the length of myocardial segments increases rapidly, distorting ventricular geometry. Permanent stretching and thinning of infarcted zones have been termed infarct expansion. Although these changes are noted within minutes in vivo, infarct expansion may not be seen for days in postmortem preparations. The apparent postmortem reversal of early infarct expansion suggests that early expansion may be a functional phenomenon, reversible in the early hours of infarction. Alternatively, reversal of expansion may be a postmortem artifact, concealing the importance of underlying structural abnormalities.
Myocardial infarction was produced in five dogs by occluding the left anterior descending coronary artery. Ultrasound sonomicrometers were used to measure myocardial segment end-diastolic length in the infarct and normal zones. After 3 hours of ischemia, the heart was arrested in diastole and biopsy specimens were taken from the normal and infarct zones. Sarcomere length was measured from electron photomicrographs, and myofiber width was measured from light photomicrographs. After 3 hours of ischemia, infarct zone segment length had increased significantly more than normal zone length (116 ± 11 [SD] versus 103 ± 4% of control length, p < 0.05), whereas 2 minutes after cardiac arrest, both the infarct and normal zones returned to preischemic segment length, demonstrating apparent reversibility of early infarct expansion. However, histologic study revealed that the infarct zone myofibers were significantly thinner than normal zone myofibers (7.9 ± 0.3 versus 9.4 ± 0.3 ) μm, p < 0.001) and sarcomere length in the infarct zone was significantly longer than that in the normal zone (1.9 ± 0.2 versus 1.5 ± 0.2 μm, p |
| doi_str_mv | 10.1016/S0735-1097(85)80492-7 |
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Myocardial infarction was produced in five dogs by occluding the left anterior descending coronary artery. Ultrasound sonomicrometers were used to measure myocardial segment end-diastolic length in the infarct and normal zones. After 3 hours of ischemia, the heart was arrested in diastole and biopsy specimens were taken from the normal and infarct zones. Sarcomere length was measured from electron photomicrographs, and myofiber width was measured from light photomicrographs. After 3 hours of ischemia, infarct zone segment length had increased significantly more than normal zone length (116 ± 11 [SD] versus 103 ± 4% of control length, p < 0.05), whereas 2 minutes after cardiac arrest, both the infarct and normal zones returned to preischemic segment length, demonstrating apparent reversibility of early infarct expansion. However, histologic study revealed that the infarct zone myofibers were significantly thinner than normal zone myofibers (7.9 ± 0.3 versus 9.4 ± 0.3 ) μm, p < 0.001) and sarcomere length in the infarct zone was significantly longer than that in the normal zone (1.9 ± 0.2 versus 1.5 ± 0.2 μm, p<0.005). Wavy myofibers were seen in all infarct zones, but not in the normal zones.
These data suggest that systolic stretching of ischemic zone segments during ischemia results in sarcomere stretching, myofiber thinning and segment lengthening. The apparent normalization of infarct zone segment length seen postmortem may be caused by elastic retraction which causes waviness of abnormally thinned and stretched myofibers. Thus, early infarct expansion is associated with interrelated structural abnormalities. The absence of expansion in postmortem specimens that demonstrated expansion in vivo should be considered a postmortem artifact.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/S0735-1097(85)80492-7</identifier><identifier>PMID: 4031298</identifier><identifier>CODEN: JACCDI</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Coronary heart disease ; Diastole ; Dogs ; Female ; Heart ; Male ; Medical sciences ; Myocardial Infarction - pathology ; Myocardial Infarction - physiopathology</subject><ispartof>Journal of the American College of Cardiology, 1985-10, Vol.6 (4), p.839-844</ispartof><rights>1985 American College of Cardiology Foundation</rights><rights>1986 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-9a72c6b410f0de72ebf1a9bddf42a083593699b67bee25459fb77fbcbcea35063</citedby><cites>FETCH-LOGICAL-c455t-9a72c6b410f0de72ebf1a9bddf42a083593699b67bee25459fb77fbcbcea35063</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0735-1097(85)80492-7$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8391695$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/4031298$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Erlebacher, Jay A.</creatorcontrib><creatorcontrib>Richter, Richard C.</creatorcontrib><creatorcontrib>Alonso, Daniel R.</creatorcontrib><creatorcontrib>Devereux, Richard B.</creatorcontrib><creatorcontrib>Gay, William A.</creatorcontrib><title>Early infarct expansion: Structural or functional?</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description>With the onset of ischemia, the length of myocardial segments increases rapidly, distorting ventricular geometry. Permanent stretching and thinning of infarcted zones have been termed infarct expansion. Although these changes are noted within minutes in vivo, infarct expansion may not be seen for days in postmortem preparations. The apparent postmortem reversal of early infarct expansion suggests that early expansion may be a functional phenomenon, reversible in the early hours of infarction. Alternatively, reversal of expansion may be a postmortem artifact, concealing the importance of underlying structural abnormalities.
Myocardial infarction was produced in five dogs by occluding the left anterior descending coronary artery. Ultrasound sonomicrometers were used to measure myocardial segment end-diastolic length in the infarct and normal zones. After 3 hours of ischemia, the heart was arrested in diastole and biopsy specimens were taken from the normal and infarct zones. Sarcomere length was measured from electron photomicrographs, and myofiber width was measured from light photomicrographs. After 3 hours of ischemia, infarct zone segment length had increased significantly more than normal zone length (116 ± 11 [SD] versus 103 ± 4% of control length, p < 0.05), whereas 2 minutes after cardiac arrest, both the infarct and normal zones returned to preischemic segment length, demonstrating apparent reversibility of early infarct expansion. However, histologic study revealed that the infarct zone myofibers were significantly thinner than normal zone myofibers (7.9 ± 0.3 versus 9.4 ± 0.3 ) μm, p < 0.001) and sarcomere length in the infarct zone was significantly longer than that in the normal zone (1.9 ± 0.2 versus 1.5 ± 0.2 μm, p<0.005). Wavy myofibers were seen in all infarct zones, but not in the normal zones.
These data suggest that systolic stretching of ischemic zone segments during ischemia results in sarcomere stretching, myofiber thinning and segment lengthening. The apparent normalization of infarct zone segment length seen postmortem may be caused by elastic retraction which causes waviness of abnormally thinned and stretched myofibers. Thus, early infarct expansion is associated with interrelated structural abnormalities. The absence of expansion in postmortem specimens that demonstrated expansion in vivo should be considered a postmortem artifact.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Coronary heart disease</subject><subject>Diastole</subject><subject>Dogs</subject><subject>Female</subject><subject>Heart</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - physiopathology</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1985</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1LwzAUwIMoc07_hEEPInqoJmnTJF6GjPkBAw_Tc0jSF4h07Uxacf-93VZ29fTgvd_7-iE0JfieYFI8rDDPWEqw5LeC3QmcS5ryEzQmjIk0Y5KfovEROUcXMX5hjAtB5AiNcpwRKsUY0YUO1TbxtdPBtgn8bnQdfVM_Jqs2dLbtgq6SJiSuq23b53U1u0RnTlcRroY4QZ_Pi4_5a7p8f3mbPy1TmzPWplJzaguTE-xwCZyCcURLU5YupxqL_sKskNIU3ABQljPpDOfOWGNBZwwX2QTdHOZuQvPdQWzV2kcLVaVraLqoeEH7ZzjrQXYAbWhiDODUJvi1DltFsNq5UntXaidCCab2rhTv-6bDgs6soTx2DXL6-vVQ19HqygVdWx-PmMgkKeRu_eyAQS_jx0NQ0XqoLZQ-gG1V2fh_DvkD4QKFnQ</recordid><startdate>198510</startdate><enddate>198510</enddate><creator>Erlebacher, Jay A.</creator><creator>Richter, Richard C.</creator><creator>Alonso, Daniel R.</creator><creator>Devereux, Richard B.</creator><creator>Gay, William A.</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</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>7X8</scope></search><sort><creationdate>198510</creationdate><title>Early infarct expansion: Structural or functional?</title><author>Erlebacher, Jay A. ; Richter, Richard C. ; Alonso, Daniel R. ; Devereux, Richard B. ; Gay, William A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-9a72c6b410f0de72ebf1a9bddf42a083593699b67bee25459fb77fbcbcea35063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1985</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Coronary heart disease</topic><topic>Diastole</topic><topic>Dogs</topic><topic>Female</topic><topic>Heart</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Erlebacher, Jay A.</creatorcontrib><creatorcontrib>Richter, Richard C.</creatorcontrib><creatorcontrib>Alonso, Daniel R.</creatorcontrib><creatorcontrib>Devereux, Richard B.</creatorcontrib><creatorcontrib>Gay, William A.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>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>Erlebacher, Jay A.</au><au>Richter, Richard C.</au><au>Alonso, Daniel R.</au><au>Devereux, Richard B.</au><au>Gay, William A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Early infarct expansion: Structural or functional?</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>1985-10</date><risdate>1985</risdate><volume>6</volume><issue>4</issue><spage>839</spage><epage>844</epage><pages>839-844</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><coden>JACCDI</coden><abstract>With the onset of ischemia, the length of myocardial segments increases rapidly, distorting ventricular geometry. Permanent stretching and thinning of infarcted zones have been termed infarct expansion. Although these changes are noted within minutes in vivo, infarct expansion may not be seen for days in postmortem preparations. The apparent postmortem reversal of early infarct expansion suggests that early expansion may be a functional phenomenon, reversible in the early hours of infarction. Alternatively, reversal of expansion may be a postmortem artifact, concealing the importance of underlying structural abnormalities.
Myocardial infarction was produced in five dogs by occluding the left anterior descending coronary artery. Ultrasound sonomicrometers were used to measure myocardial segment end-diastolic length in the infarct and normal zones. After 3 hours of ischemia, the heart was arrested in diastole and biopsy specimens were taken from the normal and infarct zones. Sarcomere length was measured from electron photomicrographs, and myofiber width was measured from light photomicrographs. After 3 hours of ischemia, infarct zone segment length had increased significantly more than normal zone length (116 ± 11 [SD] versus 103 ± 4% of control length, p < 0.05), whereas 2 minutes after cardiac arrest, both the infarct and normal zones returned to preischemic segment length, demonstrating apparent reversibility of early infarct expansion. However, histologic study revealed that the infarct zone myofibers were significantly thinner than normal zone myofibers (7.9 ± 0.3 versus 9.4 ± 0.3 ) μm, p < 0.001) and sarcomere length in the infarct zone was significantly longer than that in the normal zone (1.9 ± 0.2 versus 1.5 ± 0.2 μm, p<0.005). Wavy myofibers were seen in all infarct zones, but not in the normal zones.
These data suggest that systolic stretching of ischemic zone segments during ischemia results in sarcomere stretching, myofiber thinning and segment lengthening. The apparent normalization of infarct zone segment length seen postmortem may be caused by elastic retraction which causes waviness of abnormally thinned and stretched myofibers. Thus, early infarct expansion is associated with interrelated structural abnormalities. The absence of expansion in postmortem specimens that demonstrated expansion in vivo should be considered a postmortem artifact.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>4031298</pmid><doi>10.1016/S0735-1097(85)80492-7</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Cardiology. Vascular system Coronary heart disease Diastole Dogs Female Heart Male Medical sciences Myocardial Infarction - pathology Myocardial Infarction - physiopathology |
| title | Early infarct expansion: Structural or functional? |
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