Autopsy of myocardial infarction: Difference between revisions
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Autopsy in possible myocardial infarction: | Autopsy in possible myocardial infarction: | ||
{{Autopsy - comprehensiveness}} | |||
{{Heart - standard autopsy cutting|coronary note=''More details in section below''|header= | |||
==Autopsy cutting checklist== | |||
}} | |||
==Coronary arteries== | |||
[[File:Coronary vessels, with annotated arteries.svg|thumb]] | [[File:Coronary vessels, with annotated arteries.svg|thumb]] | ||
Make longitudinal <font color="red">(or transverse cuts at 3 mm intervals<ref name="MichaudBasso2019">{{cite journal|last1=Michaud|first1=Katarzyna|last2=Basso|first2=Cristina|last3=d’Amati|first3=Giulia|last4=Giordano|first4=Carla|last5=Kholová|first5=Ivana|last6=Preston|first6=Stephen D.|last7=Rizzo|first7=Stefania|last8=Sabatasso|first8=Sara|last9=Sheppard|first9=Mary N.|last10=Vink|first10=Aryan|last11=van der Wal|first11=Allard C.|title=Diagnosis of myocardial infarction at autopsy: AECVP reappraisal in the light of the current clinical classification|journal=Virchows Archiv|year=2019|issn=0945-6317|doi=10.1007/s00428-019-02662-1}} | Make longitudinal <font color="red">(or transverse cuts at 3 mm intervals<ref name="MichaudBasso2019">{{cite journal|last1=Michaud|first1=Katarzyna|last2=Basso|first2=Cristina|last3=d’Amati|first3=Giulia|last4=Giordano|first4=Carla|last5=Kholová|first5=Ivana|last6=Preston|first6=Stephen D.|last7=Rizzo|first7=Stefania|last8=Sabatasso|first8=Sara|last9=Sheppard|first9=Mary N.|last10=Vink|first10=Aryan|last11=van der Wal|first11=Allard C.|title=Diagnosis of myocardial infarction at autopsy: AECVP reappraisal in the light of the current clinical classification|journal=Virchows Archiv|year=2019|issn=0945-6317|doi=10.1007/s00428-019-02662-1}} | ||
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The presence of a totally occlusive thrombotic mass confers a diagnosis of likely sudden cardiac death death even in the absence of microscopically visible necrosis.<ref name="MichaudBasso2019"/> | The presence of a totally occlusive thrombotic mass confers a diagnosis of likely sudden cardiac death death even in the absence of microscopically visible necrosis.<ref name="MichaudBasso2019"/> | ||
==Myocardium== | |||
[[File:Histological features of myocardial infarction at different stages.jpg|thumb|400px|Histological features of MI at different stages, without reperfusion; <br>(a) myofiber waviness <br>(b) interstitial oedema<br>(c) hypereosinophilia and coagulative necrosis of cardiomyocytes <br>(d) heavy granulocyte infiltration with karyorrhexis <br>(e) macrophages and lymphocyte infiltration with early removal of necrotic debris <br>(f) granulation tissue with formation of microvessels <br>(g) fibroblast proliferation and early collagen deposition <br>(h) dense fibrous scar replacing myocyte loss <br>All sections are stained with haematoxylin and eosin.<ref name="MichaudBasso2019"/>]] | [[File:Histological features of myocardial infarction at different stages.jpg|thumb|400px|Histological features of MI at different stages, without reperfusion; <br>(a) myofiber waviness <br>(b) interstitial oedema<br>(c) hypereosinophilia and coagulative necrosis of cardiomyocytes <br>(d) heavy granulocyte infiltration with karyorrhexis <br>(e) macrophages and lymphocyte infiltration with early removal of necrotic debris <br>(f) granulation tissue with formation of microvessels <br>(g) fibroblast proliferation and early collagen deposition <br>(h) dense fibrous scar replacing myocyte loss <br>All sections are stained with haematoxylin and eosin.<ref name="MichaudBasso2019"/>]] | ||
Revision as of 10:55, 19 December 2019
Author:
Mikael Häggström [note 1]
Autopsy in possible myocardial infarction:
Comprehensiveness
Factors supporting a relatively more comprehensive autopsy and/or report, particularly in the inclusion of negated findings:
- Lack of explanation from existing evidence. On the other hand, for example, upon finding an obvious aortic rupture, the rest of the autopsy is less relevant and may be relatively short.
- Double-reading: If your report is likely to undergo double reading by another pathologist before sign-out, it needs to be more detailed, because the doctor who will do the double-reading then knows that you have looked at those locations.
- Highly suspected locations, such as given from the referral.
On this resource, the following formatting is used for comprehensiveness:
- Minimal depth
- (Moderate depth)
- ((Comprehensive))
Autopsy cutting checklist
- Remove the parietal pericardium
- Separate the heart from the from lungs by cutting through the major vessels. The pulmonary artery should be cut first and the lumen inspected for any pulmonary embolism.
- Weigh the heart.
- Dissect the coronary vessels. More details in section below Further information: Arteries
- On the right side of the heart, dissect in the direction of blood flow: Superior vena cava > right atrium > tricuspid valve > right ventricle. Look for thromboses or patent foramen ovale.[note 2]
- Dissect the atrial appendages, to exclude thromboses.
- Dissect the left ventricle, such as into circumferential slices from the apex to the base.[note 3] Inspect (and measure) the left ventricular wall thickness.
- (Measure the circumferences of the four valves. Cutoffs for valve dilatation:[1]
- Mitral valve: circumference greater than 9.9 cm in males and 9.1 cm in females
- Aortic valve: circumference greater than 8.5 cm in males and 7.9 cm in females
- Tricuspid valve: circumference greater than 11.8 cm in males and 11.1 cm in females
- Pulmonic valve: circumference greater than 7.5 cm in males and 7.4 cm in females)
Coronary arteries
Make longitudinal (or transverse cuts at 3 mm intervals[2]) through:
- The right coronary artery.
- (The right marginal artery)
- The left coronary and circumflex artery.
- The left anterior descending artery.
- (The left marginal artery)
- (The left diagonal branch)
- Any vessel grafts to the heart
Estimate the percentage of any significant stenosis or occlusion.
-
Plaque at different percentages of atherosclerotic stenosis.[2]
The presence of a totally occlusive thrombotic mass confers a diagnosis of likely sudden cardiac death death even in the absence of microscopically visible necrosis.[2]
Myocardium
(a) myofiber waviness
(b) interstitial oedema
(c) hypereosinophilia and coagulative necrosis of cardiomyocytes
(d) heavy granulocyte infiltration with karyorrhexis
(e) macrophages and lymphocyte infiltration with early removal of necrotic debris
(f) granulation tissue with formation of microvessels
(g) fibroblast proliferation and early collagen deposition
(h) dense fibrous scar replacing myocyte loss
All sections are stained with haematoxylin and eosin.[2]
Look for areas of fibrosis or hemorrhage. Sample tissue from suspected areas.
| Time | Gross examination | Histopathology (light microscopy) |
|---|---|---|
| 0 - 0.5 hours | None[notes 1] | None[notes 1] |
| 0.5 – 4 hours | None[notes 2] |
|
| 4 – 12 hours |
|
|
| 12 – 24 hours |
|
|
| 1 – 3 days |
|
|
| 3 – 7 days |
|
|
| 7 – 10 days |
|
|
| 10 – 14 days |
|
|
| 2 – 8 weeks |
|
|
| More than 2 months | Completed scarring[notes 3] | Dense collagenous scar formed[notes 3] |
| If not else specified in boxes, then reference is nr [4] | ||
Classify the topographic distribution of any myocardial infarction, if possible:
Notes
- ↑ 1.0 1.1 For the first ~30 minutes no change at all can be seen by gross examination or by light microscopy in histopathology. However, in electron microscopy relaxed myofibrils, as well as glycogen loss and mitochondrial swelling can be observered.
- ↑ It is often possible, however, to highlight the area of necrosis that first becomes apparent after 2 to 3 hours by immersion of tissue slices in a solution of triphenyltetrazolium chloride. This dye imparts a brick-red color to intact, noninfarcted myocardium where the dehydrogenase activity is preserved. Because dehydrogenases are depleted in the area of ischemic necrosis (i.e., they leak out through the damaged cell membranes), an infarcted area is revealed as an unstained pale zone. Instead of a triphenyltetrazolium chloride dye, a LDH (lactate dehydrogenase) dye can also be used to visualize an area of necrosis.
- ↑ 3.0 3.1 Once scarring is completed, there is yet no common method of discerning the actual age of the infarct, since e.g. a scar that is four months old looks identical to a scar that is ten years old.
- ↑ For a full list of contributors, see article history. Creators of images are attributed at the image description pages, seen by clicking on the images. See Patholines:Authorship for details.
- ↑ The right ventricle can alternatively be cut in circumferential slices along with the left ventricle.
- ↑ An alternative approach is to cut the left ventricle through a cut along the left lateral margin, followed by an anterior cut from the apex to the aortic root, freeing the anterior wall. Then cut through the plane of the myocardium of the anterior and posterior myocardial wall, as well as the septum, for any signs of infarction. (Dissect one or more papillary muscles for infarction.)
Main page
References
- ↑ Kitzman, Dalane W.; Scholz, David G.; Hagen, Philip T.; Ilstrup, Duane M.; Edwards, William D. (1988). "Age-Related Changes in Normal Human Hearts During the First 10 Decades of Life. Part II (Maturity): A Quantitative Anatomic Study of 765 Specimens From Subjects 20 to 99 Years Old
". Mayo Clinic Proceedings 63 (2): 137–146. doi:. ISSN 00256196.
- Griffith, Christopher C.; Raval, Jay S.; Nichols, Larry (2012). "Intravascular Talcosis due to Intravenous Drug Use Is an Underrecognized Cause of Pulmonary Hypertension
- ↑ 2.0 2.1 2.2 2.3 Michaud, Katarzyna; Basso, Cristina; d’Amati, Giulia; Giordano, Carla; Kholová, Ivana; Preston, Stephen D.; Rizzo, Stefania; Sabatasso, Sara; et al. (2019). "Diagnosis of myocardial infarction at autopsy: AECVP reappraisal in the light of the current clinical classification
". Virchows Archiv. doi:. ISSN 0945-6317.
- This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/)
- ↑ Bishop JE, Greenbaum R, Gibson DG, Yacoub M, Laurent GJ. Enhanced deposition of predominantly type I collagen in myocardial disease. J Mol Cell Cardiol. 1990;22:1157–1165
- ↑ Table 11-2 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. Robbins Basic Pathology . Philadelphia: Saunders. ISBN 1-4160-2973-7. 8th edition.
Image sources