ST elevation myocardial infarction histopathology: Difference between revisions
Jump to navigation
Jump to search
Ochuko Ajari (talk | contribs) No edit summary |
No edit summary |
||
| Line 4: | Line 4: | ||
==Overview== | ==Overview== | ||
[[Anatomical pathology|Histopathological]] examination of the heart may reveal infarction at autopsy. Under the microscope, myocardial infarction presents as a circumscribed area of ischemic, | [[Anatomical pathology|Histopathological]] examination of the [[heart]] may reveal [[infarction]] at autopsy. Under the [[microscope]], myocardial infarction presents as a circumscribed area of [[ischemic]], [[coagulative necrosis]] ([[cell]] death). On [[gross examination]], the [[infarct]] is not identifiable within the first 12 hours.<ref name="rubin546">{{cite book | coauthors = Emanuel Rubin, Fred Gorstein, Raphael Rubin, Roland Schwarting, David Strayer | title = Rubin's Pathology - Clinicopathological Foundations of Medicine | publisher = Lippincott Williams & Wilkins | date = 2001 | location = Maryland | pages = p. 546 | id = ISBN 0-7817-4733-3 }}</ref> | ||
==Histopathology== | ==Histopathology== | ||
===Wavy | ===Wavy fiber phase=== | ||
Although earlier changes can be discerned using [[electron microscopy]], one of the earliest changes under a normal microscope are so-called ''wavy fibers''.<ref name="pmid782705">{{cite journal |author=Eichbaum FW |title='Wavy' myocardial fibers in spontaneous and experimental adrenergic cardiopathies |journal=Cardiology |volume=60 |issue=6 |pages=358–65 |year=1975 |pmid=782705 |doi= |url=}}</ref>Thin wavy myocytes are (the earliest light microscopic finding of acute myocardial infarction) visible as early as one hour following the onset of infarction. <ref name="pmid4359735">{{cite journal |author=Bouchardy B, Majno G |title=Histopathology of early myocardial infarcts. A new approach |journal=Am. J. Pathol. |volume=74 |issue=2 |pages=301–30 |year=1974 |month=February |pmid=4359735 |pmc=1910768 |doi= |url=}}</ref> | Although earlier changes can be discerned using [[electron microscopy]], one of the earliest changes under a normal [[microscope]] are so-called ''wavy fibers''.<ref name="pmid782705">{{cite journal |author=Eichbaum FW |title='Wavy' myocardial fibers in spontaneous and experimental adrenergic cardiopathies |journal=Cardiology |volume=60 |issue=6 |pages=358–65 |year=1975 |pmid=782705 |doi= |url=}}</ref>Thin wavy [[myocytes]] are (the earliest light microscopic finding of acute myocardial infarction) visible as early as one hour following the onset of [[infarction]]. <ref name="pmid4359735">{{cite journal |author=Bouchardy B, Majno G |title=Histopathology of early myocardial infarcts. A new approach |journal=Am. J. Pathol. |volume=74 |issue=2 |pages=301–30 |year=1974 |month=February |pmid=4359735 |pmc=1910768 |doi= |url=}}</ref> | ||
===Eosinophilic | ===Eosinophilic phase with loss of cell nucleus=== | ||
Subsequently, the myocyte [[cytoplasm]] becomes more [[eosinophilic]] (pink) and the cells lose their transversal striations, with typical changes and eventually loss of the [[cell nucleus]].<ref name=histopathologyIndia>S Roy. [http://www.histopathology-india.net/Heart5.htm Myocardial infarction]. Retrieved November 28, 2006.</ref> | Subsequently, the [[myocyte]] [[cytoplasm]] becomes more [[eosinophilic]] (pink) and the cells lose their transversal striations, with typical changes and eventually loss of the [[cell nucleus]].<ref name="histopathologyIndia">S Roy. [http://www.histopathology-india.net/Heart5.htm Myocardial infarction]. Retrieved November 28, 2006.</ref> | ||
===Coagulation | ===Coagulation necrosis=== | ||
Coagulation necrosis, characterized by hypereosinophilia and nuclear [[pyknosis]], followed by karyorrhexis, karyolysis, total loss of nuclei and loss of cytoplasmic cross-striations, is generally first visible in the period from 4-12 hours following infarction.<ref>Schoen FJ. The heart. Chapter 12 in Robbins Pathologic Basis of Disease, fifth edition, 1994, Cotran RS, Kumar V, Schoen FJ, eds., Philadelphia, W.B.Saunders, pp.517-582</ref>. Necrotic myocytes may retain their striations for a long time.<ref name="pmid657859">{{cite journal |author=Fishbein MC, Maclean D, Maroko PR |title=The histopathologic evolution of myocardial infarction |journal=Chest |volume=73 |issue=6 |pages=843–9 |year=1978 |month=June |pmid=657859 |doi= |url=http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=657859}}</ref> | [[Coagulation necrosis]], characterized by [[hypereosinophilia]] and [[nuclear]] [[pyknosis]], followed by [[karyorrhexis]], [[karyolysis]], total loss of [[nuclei]] and loss of [[cytoplasmic]] cross-striations, is generally first visible in the period from 4-12 hours following [[infarction]].<ref>Schoen FJ. The heart. Chapter 12 in Robbins Pathologic Basis of Disease, fifth edition, 1994, Cotran RS, Kumar V, Schoen FJ, eds., Philadelphia, W.B.Saunders, pp.517-582</ref>. [[Necrotic]] [[myocytes]] may retain their striations for a long time.<ref name="pmid657859">{{cite journal |author=Fishbein MC, Maclean D, Maroko PR |title=The histopathologic evolution of myocardial infarction |journal=Chest |volume=73 |issue=6 |pages=843–9 |year=1978 |month=June |pmid=657859 |doi= |url=http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=657859}}</ref> | ||
Neutrophilic infiltration (acute inflammation), edema and hemorrhage are also first visible at 4-12 hours but generally closer to 12 hours. The interstitium at the margin of the infarcted area is initially infiltrated with [[neutrophil]]s, then with [[lymphocyte]]s and [[macrophage]]s, who [[phagocytosis|phagocytose]] (eat) the myocyte debris. The necrotic area is surrounded and progressively invaded by [[granulation tissue]], which will replace the infarct with a fibrous ([[collagen]]ous) [[scar]] (which are typical steps in [[wound healing]]). The interstitial space (the space between cells outside of blood vessels) may be infiltrated with [[red blood cell]]s.<ref name=rubin546/> | [[Neutrophilia|Neutrophilic]] infiltration (acute [[inflammation]]), [[edema]] and [[hemorrhage]] are also first visible at 4-12 hours but generally closer to 12 hours. The [[interstitium]] at the margin of the [[Infarction|infarcted]] area is initially infiltrated with [[neutrophil]]s, then with [[lymphocyte]]s and [[macrophage]]s, who [[phagocytosis|phagocytose]] (eat) the [[myocyte]] debris. The [[necrotic]] area is surrounded and progressively invaded by [[granulation tissue]], which will replace the [[infarct]] with a [[fibrous]] ([[collagen]]ous) [[scar]] (which are typical steps in [[wound healing]]). The [[interstitial]] space (the space between cells outside of [[blood vessels]]) may be infiltrated with [[red blood cell]]s.<ref name="rubin546" /> | ||
Acute inflammation is generally present in a narrow band of the periphery at 24 hours, in a broad band of the periphery at 48 hours and tends to be maximal around 72 hours, with extensive basophilic debris from degenerating neutrophils.<ref name="pmid657859">{{cite journal |author=Fishbein MC, Maclean D, Maroko PR |title=The histopathologic evolution of myocardial infarction |journal=Chest |volume=73 |issue=6 |pages=843–9 |year=1978 |month=June |pmid=657859 |doi= |url=http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=657859}}</ref> | Acute [[inflammation]] is generally present in a narrow band of the periphery at 24 hours, in a broad band of the periphery at 48 hours and tends to be maximal around 72 hours, with extensive [[basophilic]] debris from degenerating [[neutrophils]].<ref name="pmid657859">{{cite journal |author=Fishbein MC, Maclean D, Maroko PR |title=The histopathologic evolution of myocardial infarction |journal=Chest |volume=73 |issue=6 |pages=843–9 |year=1978 |month=June |pmid=657859 |doi= |url=http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=657859}}</ref> | ||
Infiltration by macrophages, lymphocytes, eosinophils, fibroblasts and capillaries begins around the periphery at 3-10 days. Contraction band necrosis, characterized by hypereosinophilic transverse bands of precipitated myofibrils in dead myocytes is usually seen at the edge of an infarct or with reperfusion (e.g. with thrombolytic therapy).<ref>Reichenbach D, Cowan MJ. Healing of myocardial infarction with and without reperfusion. Chapter 5, in Cardiovascular Pathology, 1991, Virmani R, Atkinson JB, Fenoglio JJ, eds., Philadelphia, W.B.Saunders, pp. 86-98.</ref> | Infiltration by [[macrophages]], [[lymphocytes]], [[eosinophils]], [[fibroblasts]] and [[capillaries]] begins around the periphery at 3-10 days. Contraction band [[necrosis]], characterized by [[Hypereosinophilia|hypereosinophilic]] transverse bands of precipitated [[myofibrils]] in dead [[myocytes]] is usually seen at the edge of an [[infarct]] or with [[reperfusion]] (e.g. with [[thrombolytic therapy]]).<ref>Reichenbach D, Cowan MJ. Healing of myocardial infarction with and without reperfusion. Chapter 5, in Cardiovascular Pathology, 1991, Virmani R, Atkinson JB, Fenoglio JJ, eds., Philadelphia, W.B.Saunders, pp. 86-98.</ref> | ||
Reperfusion of an infarct is also associated with more hemorrhage, less acute inflammation, less limitation of the acute inflammation to the periphery in the first few days, reactive stromal cells, more macrophage infiltration earlier and a more patchy distribution of necrosis, especially around the periphery.<ref>Reichenbach D, Cowan MJ. Healing of myocardial infarction with and without reperfusion. Chapter 5, in Cardiovascular Pathology, 1991, Virmani R, Atkinson JB, Fenoglio JJ, eds., Philadelphia, W.B.Saunders, pp. 86-98.</ref> | [[Reperfusion]] of an [[infarct]] is also associated with more [[hemorrhage]], less acute [[inflammation]], less limitation of the acute [[inflammation]] to the periphery in the first few days, reactive [[stromal cells]], more [[macrophage]] infiltration earlier and a more patchy distribution of [[necrosis]], especially around the periphery.<ref>Reichenbach D, Cowan MJ. Healing of myocardial infarction with and without reperfusion. Chapter 5, in Cardiovascular Pathology, 1991, Virmani R, Atkinson JB, Fenoglio JJ, eds., Philadelphia, W.B.Saunders, pp. 86-98.</ref> | ||
These features can be recognized in cases where the perfusion was not restored; reperfused infarcts can have other hallmarks, such as contraction band necrosis.<ref name="pmid2182247">{{cite journal |author=Fishbein MC |title=Reperfusion injury |journal=Clin Cardiol |volume=13 |issue=3 |pages=213–7 |year=1990 |month=March |pmid=2182247 |doi= |url=}}</ref> | These features can be recognized in cases where the perfusion was not restored; reperfused [[Infarct|infarcts]] can have other hallmarks, such as contraction band [[necrosis]].<ref name="pmid2182247">{{cite journal |author=Fishbein MC |title=Reperfusion injury |journal=Clin Cardiol |volume=13 |issue=3 |pages=213–7 |year=1990 |month=March |pmid=2182247 |doi= |url=}}</ref> | ||
Summary of | Summary of time from onset and morphologic findings: | ||
*1 - 3 hours: Wavy myocardial fibers | *1 - 3 hours: Wavy [[myocardial]] fibers | ||
*2 - 3 hours: Staining defect with tetrazolium or basic fuchsin dye | *2 - 3 hours: Staining defect with tetrazolium or basic fuchsin dye | ||
*4 - 12 hours: Coagulation necrosis with loss of cross striations, contraction bands, edema, hemorrhage, and early neutrophilic infiltrate | *4 - 12 hours: [[Coagulation necrosis]] with loss of cross striations, contraction bands, [[edema]], [[hemorrhage]], and early [[Neutrophilia|neutrophilic]] infiltrate | ||
*18 - 24 hours: Continuing coagulation necrosis, pyknosis of nuclei, and marginal contraction bands | *18 - 24 hours: Continuing [[coagulation necrosis]], [[pyknosis]] of [[nuclei]], and marginal contraction bands | ||
*24 - 72 hours: Total loss of nuclei and striations along with heavy neutrophilic infiltrate | *24 - 72 hours: Total loss of [[nuclei]] and striations along with heavy [[Neutrophilia|neutrophilic]] infiltrate | ||
*3 - 7 days: Macrophage and mononuclear infiltration begin, fibrovascular response begins | *3 - 7 days: [[Macrophage]] and [[Mononuclear cells|mononuclear]] infiltration begin, fibrovascular response begins | ||
*10 - 21 days: Fibrovascular response with prominent granulation tissue | *10 - 21 days: Fibrovascular response with prominent [[granulation tissue]] | ||
*7 weeks: Fibrosis | *7 weeks: [[Fibrosis]] | ||
===Images=== | ===Images=== | ||
| Line 42: | Line 42: | ||
{| align="center" | {| align="center" | ||
! | ! | ||
|-valign="top" | |- valign="top" | ||
| [[Image:Image15380.jpg|left|thumb|400px|Acute Myocardial infarction with PMNs]] | | [[Image:Image15380.jpg|left|thumb|400px|Acute Myocardial infarction with PMNs]] | ||
| Line 50: | Line 50: | ||
{| align="center" | {| align="center" | ||
! | ! | ||
|-valign="top" | |- valign="top" | ||
| [[Image:Image916.JPG|left|thumb|400px|H&E, medium magnification view of healing infarct.]] | | [[Image:Image916.JPG|left|thumb|400px|H&E, medium magnification view of healing infarct.]] | ||
| Line 58: | Line 58: | ||
{| align="center" | {| align="center" | ||
! | ! | ||
|-valign="top" | |- valign="top" | ||
| [[Image:Image15644.jpg|left|thumb|400px|Myocardial infarction, subacute, granulation tissue.]] | | [[Image:Image15644.jpg|left|thumb|400px|Myocardial infarction, subacute, granulation tissue.]] | ||
| Line 66: | Line 66: | ||
{| align="center" | {| align="center" | ||
! | ! | ||
|-valign="top" | |- valign="top" | ||
| [[Image:Image15646.jpg|left|thumb|400px|Myocardial infarction, mural thrombus]] | | [[Image:Image15646.jpg|left|thumb|400px|Myocardial infarction, mural thrombus]] | ||
| [[Image:Image15882.jpg|left|thumb|400px|Acute myocardial infarction, ischemic fibers demonstrated by aldehyde fuchsin stain]] | | [[Image:Image15882.jpg|left|thumb|400px|Acute myocardial infarction, ischemic fibers demonstrated by aldehyde fuchsin stain]] | ||
|} | |} | ||
<br clear="left"/> | <br clear="left" /> | ||
==Virtual Microscopic Images== | ==Virtual Microscopic Images== | ||
Revision as of 13:29, 29 September 2017
|
ST Elevation Myocardial Infarction Microchapters |
|
Differentiating ST elevation myocardial infarction from other Diseases |
|
Diagnosis |
|
Treatment |
|
|
Case Studies |
|
ST elevation myocardial infarction histopathology On the Web |
|
ST elevation myocardial infarction histopathology in the news |
|
Directions to Hospitals Treating ST elevation myocardial infarction |
|
Risk calculators and risk factors for ST elevation myocardial infarction histopathology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
Histopathological examination of the heart may reveal infarction at autopsy. Under the microscope, myocardial infarction presents as a circumscribed area of ischemic, coagulative necrosis (cell death). On gross examination, the infarct is not identifiable within the first 12 hours.[1]
Histopathology
Wavy fiber phase
Although earlier changes can be discerned using electron microscopy, one of the earliest changes under a normal microscope are so-called wavy fibers.[2]Thin wavy myocytes are (the earliest light microscopic finding of acute myocardial infarction) visible as early as one hour following the onset of infarction. [3]
Eosinophilic phase with loss of cell nucleus
Subsequently, the myocyte cytoplasm becomes more eosinophilic (pink) and the cells lose their transversal striations, with typical changes and eventually loss of the cell nucleus.[4]
Coagulation necrosis
Coagulation necrosis, characterized by hypereosinophilia and nuclear pyknosis, followed by karyorrhexis, karyolysis, total loss of nuclei and loss of cytoplasmic cross-striations, is generally first visible in the period from 4-12 hours following infarction.[5]. Necrotic myocytes may retain their striations for a long time.[6]
Neutrophilic infiltration (acute inflammation), edema and hemorrhage are also first visible at 4-12 hours but generally closer to 12 hours. The interstitium at the margin of the infarcted area is initially infiltrated with neutrophils, then with lymphocytes and macrophages, who phagocytose (eat) the myocyte debris. The necrotic area is surrounded and progressively invaded by granulation tissue, which will replace the infarct with a fibrous (collagenous) scar (which are typical steps in wound healing). The interstitial space (the space between cells outside of blood vessels) may be infiltrated with red blood cells.[1]
Acute inflammation is generally present in a narrow band of the periphery at 24 hours, in a broad band of the periphery at 48 hours and tends to be maximal around 72 hours, with extensive basophilic debris from degenerating neutrophils.[6]
Infiltration by macrophages, lymphocytes, eosinophils, fibroblasts and capillaries begins around the periphery at 3-10 days. Contraction band necrosis, characterized by hypereosinophilic transverse bands of precipitated myofibrils in dead myocytes is usually seen at the edge of an infarct or with reperfusion (e.g. with thrombolytic therapy).[7]
Reperfusion of an infarct is also associated with more hemorrhage, less acute inflammation, less limitation of the acute inflammation to the periphery in the first few days, reactive stromal cells, more macrophage infiltration earlier and a more patchy distribution of necrosis, especially around the periphery.[8]
These features can be recognized in cases where the perfusion was not restored; reperfused infarcts can have other hallmarks, such as contraction band necrosis.[9]
Summary of time from onset and morphologic findings:
- 1 - 3 hours: Wavy myocardial fibers
- 2 - 3 hours: Staining defect with tetrazolium or basic fuchsin dye
- 4 - 12 hours: Coagulation necrosis with loss of cross striations, contraction bands, edema, hemorrhage, and early neutrophilic infiltrate
- 18 - 24 hours: Continuing coagulation necrosis, pyknosis of nuclei, and marginal contraction bands
- 24 - 72 hours: Total loss of nuclei and striations along with heavy neutrophilic infiltrate
- 3 - 7 days: Macrophage and mononuclear infiltration begin, fibrovascular response begins
- 10 - 21 days: Fibrovascular response with prominent granulation tissue
- 7 weeks: Fibrosis
Images
 |
 |
 |
 |
 |
 |
 |
 |
Virtual Microscopic Images
References
- ↑ 1.0 1.1 Rubin's Pathology - Clinicopathological Foundations of Medicine. Maryland: Lippincott Williams & Wilkins. 2001. pp. p. 546. ISBN 0-7817-4733-3. Unknown parameter
|coauthors=ignored (help) - ↑ Eichbaum FW (1975). "'Wavy' myocardial fibers in spontaneous and experimental adrenergic cardiopathies". Cardiology. 60 (6): 358–65. PMID 782705.
- ↑ Bouchardy B, Majno G (1974). "Histopathology of early myocardial infarcts. A new approach". Am. J. Pathol. 74 (2): 301–30. PMC 1910768. PMID 4359735. Unknown parameter
|month=ignored (help) - ↑ S Roy. Myocardial infarction. Retrieved November 28, 2006.
- ↑ Schoen FJ. The heart. Chapter 12 in Robbins Pathologic Basis of Disease, fifth edition, 1994, Cotran RS, Kumar V, Schoen FJ, eds., Philadelphia, W.B.Saunders, pp.517-582
- ↑ 6.0 6.1 Fishbein MC, Maclean D, Maroko PR (1978). "The histopathologic evolution of myocardial infarction". Chest. 73 (6): 843–9. PMID 657859. Unknown parameter
|month=ignored (help) - ↑ Reichenbach D, Cowan MJ. Healing of myocardial infarction with and without reperfusion. Chapter 5, in Cardiovascular Pathology, 1991, Virmani R, Atkinson JB, Fenoglio JJ, eds., Philadelphia, W.B.Saunders, pp. 86-98.
- ↑ Reichenbach D, Cowan MJ. Healing of myocardial infarction with and without reperfusion. Chapter 5, in Cardiovascular Pathology, 1991, Virmani R, Atkinson JB, Fenoglio JJ, eds., Philadelphia, W.B.Saunders, pp. 86-98.
- ↑ Fishbein MC (1990). "Reperfusion injury". Clin Cardiol. 13 (3): 213–7. PMID 2182247. Unknown parameter
|month=ignored (help)