Pub Date : 1996-01-01DOI: 10.3109/9781420019292-43
P. Guerrieri, P. Montemaggi, B. Huth, C. Roedel, Stephan Mose, H. Hricak, O. Akin, H. Vargas, D. Indelicato, R. Sagerman, Lydia T. Komarnicky-Kocher, A. Dragun, Brandon J. Fisher, L. Daugherty, D. Michalski, M. Huq, B. Hasson, Lindsay G. Jensen, L. Mell, Filip T. Troicki
{"title":"Fibrohistiocytic tumors.","authors":"P. Guerrieri, P. Montemaggi, B. Huth, C. Roedel, Stephan Mose, H. Hricak, O. Akin, H. Vargas, D. Indelicato, R. Sagerman, Lydia T. Komarnicky-Kocher, A. Dragun, Brandon J. Fisher, L. Daugherty, D. Michalski, M. Huq, B. Hasson, Lindsay G. Jensen, L. Mell, Filip T. Troicki","doi":"10.3109/9781420019292-43","DOIUrl":"https://doi.org/10.3109/9781420019292-43","url":null,"abstract":"","PeriodicalId":76185,"journal":{"name":"Monographs in pathology","volume":"38 1","pages":"162-80"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69464796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Atherosclerotic plaques: natural and unnatural history.","authors":"W D Edwards","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76185,"journal":{"name":"Monographs in pathology","volume":"37 ","pages":"12-46"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18608326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pathologic considerations in replacement heart valves and other cardiovascular prosthetic devices.","authors":"F J Schoen","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76185,"journal":{"name":"Monographs in pathology","volume":"37 ","pages":"194-222"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18608331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Myocardial infarction is a dynamic process that begins with the transition from reversible to irreversible ischemic injury and culminates in the replacement of dead myocardium by a fibrous scar. Many biochemical and metabolic changes have been observed early after the onset of ischemia, but the precise cause of the transition to irreversibility has not been elucidated. However, disruption of the plasmalemma of the sarcolemma is an early event, the presence of which indicates that the ischemic myocytes are dead. Not all ischemic myocytes become irreversibly injured simultaneously in experimental infarction in the canine heart; rather, myocytes die in a transmural wavefront of cell death proceeding from the subendocardial to the subepicardial myocardium with the subendocardial layer dying first and the subepicardial layer last. About 6 hours of ischemia are required to complete the wave-front. During the reversible phase of ischemic injury, reperfusion salvages all ischemic myocytes in all layers, but once lethal injury begins to develop, reperfusion salvages reversibly injured myocytes that are located chiefly in the subepicardial and midmyocardial layers and thereby limits the transmural extent of infarction. The gradual evolution of cell death in experimental acute ischemia provides a basis for limitation of infarct size by reperfusion with arterial blood in man. Many functions of myocardium subjected to reversible episodes of ischemia return to the control condition a few seconds or minutes after the onset of reperfusion. Others, such as repletion of the adenine nucleotide pool, require hours to days to repair. Reversibly injured myocardium exhibits reduced contractile efficiency, termed stunning, which is a form of reperfusion injury. Stunning is reversible; it disappears after hours or days of reperfusion. Finally, reversibly injured myocardium develops adaptive changes that protect it against subsequent episodes of ischemia. One such change, termed ischemic preconditioning, persists for 1-2 hours and serves to delay the development of cell death if the tissue is subjected to a new prolonged episode of ischemia. Another, heat shock protein synthesis, does not appear until the tissue has been reperfused for 12-24 hours; it also protects the myocardium against subsequent ischemic injury. The molecular mechanisms underlying stunning, ischemic preconditioning, and heat shock protein synthesis remain to be established.
{"title":"Myocardial ischemia and reperfusion.","authors":"R B Jennings, C Steenbergen, K A Reimer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Myocardial infarction is a dynamic process that begins with the transition from reversible to irreversible ischemic injury and culminates in the replacement of dead myocardium by a fibrous scar. Many biochemical and metabolic changes have been observed early after the onset of ischemia, but the precise cause of the transition to irreversibility has not been elucidated. However, disruption of the plasmalemma of the sarcolemma is an early event, the presence of which indicates that the ischemic myocytes are dead. Not all ischemic myocytes become irreversibly injured simultaneously in experimental infarction in the canine heart; rather, myocytes die in a transmural wavefront of cell death proceeding from the subendocardial to the subepicardial myocardium with the subendocardial layer dying first and the subepicardial layer last. About 6 hours of ischemia are required to complete the wave-front. During the reversible phase of ischemic injury, reperfusion salvages all ischemic myocytes in all layers, but once lethal injury begins to develop, reperfusion salvages reversibly injured myocytes that are located chiefly in the subepicardial and midmyocardial layers and thereby limits the transmural extent of infarction. The gradual evolution of cell death in experimental acute ischemia provides a basis for limitation of infarct size by reperfusion with arterial blood in man. Many functions of myocardium subjected to reversible episodes of ischemia return to the control condition a few seconds or minutes after the onset of reperfusion. Others, such as repletion of the adenine nucleotide pool, require hours to days to repair. Reversibly injured myocardium exhibits reduced contractile efficiency, termed stunning, which is a form of reperfusion injury. Stunning is reversible; it disappears after hours or days of reperfusion. Finally, reversibly injured myocardium develops adaptive changes that protect it against subsequent episodes of ischemia. One such change, termed ischemic preconditioning, persists for 1-2 hours and serves to delay the development of cell death if the tissue is subjected to a new prolonged episode of ischemia. Another, heat shock protein synthesis, does not appear until the tissue has been reperfused for 12-24 hours; it also protects the myocardium against subsequent ischemic injury. The molecular mechanisms underlying stunning, ischemic preconditioning, and heat shock protein synthesis remain to be established.</p>","PeriodicalId":76185,"journal":{"name":"Monographs in pathology","volume":"37 ","pages":"47-80"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18608332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Diagnostic vascular pathology: still the old fashion way.","authors":"J T Lie","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76185,"journal":{"name":"Monographs in pathology","volume":"37 ","pages":"129-43"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18608327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Do we have a magic yardstick that will establish whether SCD of the patient is definitely caused by the presence of an underlying abnormality? We are afraid that in most cases of cardiac disease the cause of death is at best probable, or even presumed. It has always been that circumstantial evidence has helped us establish that the cause of death is related to the anatomic abnormality. Even the presence of severe coronary artery disease in a patient who dies suddenly, especially in the absence of a thrombus, cannot be stated categorically to be the cause and effect. With the knowledge we have today, establishing cause and effect are difficult in most cases of SCD.
{"title":"Problems in forensic cardiovascular pathology.","authors":"R Virmani, A P Burke, A Farb, J Smialek","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Do we have a magic yardstick that will establish whether SCD of the patient is definitely caused by the presence of an underlying abnormality? We are afraid that in most cases of cardiac disease the cause of death is at best probable, or even presumed. It has always been that circumstantial evidence has helped us establish that the cause of death is related to the anatomic abnormality. Even the presence of severe coronary artery disease in a patient who dies suddenly, especially in the absence of a thrombus, cannot be stated categorically to be the cause and effect. With the knowledge we have today, establishing cause and effect are difficult in most cases of SCD.</p>","PeriodicalId":76185,"journal":{"name":"Monographs in pathology","volume":"37 ","pages":"173-93"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18608330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Update on the pathobiology of vasculitis.","authors":"J C Jennette, R J Falk","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76185,"journal":{"name":"Monographs in pathology","volume":"37 ","pages":"156-72"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18608329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Atherogenesis: current concepts.","authors":"M A Gimbrone","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76185,"journal":{"name":"Monographs in pathology","volume":"37 ","pages":"1-11"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18608324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Surgical pathology of the heart: endomyocardial biopsy, valvular heart disease, and cardiac tumors.","authors":"H D Tazelaar","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76185,"journal":{"name":"Monographs in pathology","volume":"37 ","pages":"81-107"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18608333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pathology of human cardiac transplantation.","authors":"M E Billingham","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76185,"journal":{"name":"Monographs in pathology","volume":"37 ","pages":"108-28"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18608325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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