Autopsy of myocardial infarction: Difference between revisions

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Revision as of 10:41, 19 December 2019

Author: Mikael Häggström [note 1]

Autopsy

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))

Coronary arteries

File:Coronary vessels, with annotated arteries.svg

Make longitudinal (or transverse cuts at 3 mm intervals[1]) 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.

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.[1]

Myocardium

File:Histological features of myocardial infarction at different stages.jpg
Histological features of MI at different stages, without reperfusion;
(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.[1]

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]
  • Glycogen Depletion, as seen with a PAS Stain
  • Possibly waviness of fibers at border
4 – 12 hours
  • Sometimes dark mottling
  • Initiation of coagulation necrosis
  • Edema
  • Hemorrhage
12 – 24 hours
  • Dark mottling
  • Ongoing coagulation necrosis
  • Karyopyknosis
  • Hypereosinophilia of myocytes
  • Contraction band necrosis in margins
  • Beginning of neutrophil infiltration
1 – 3 days
  • Infarct center becomes yellow-tan
  • Continued coagulation necrosis
  • Loss of nuclei and striations
  • Increased infiltration of neutrophils to interstitium
3 – 7 days
  • Hyperemia at border
  • Softening yellow-tan center
  • Beginning of disintegration of dead muscle fibers
  • Apoptosis of neutrophils
  • Beginning of macrophage removal of dead cells at border
7 – 10 days
  • Maximally soft and yellow-tan
  • Red-tan margins
  • Increased phagocytosis of dead cells at border
  • Beginning of granulation tissue formation at margins
10 – 14 days
  • Red-gray and depressed borders
  • Mature granulation tissue with type I collagen[2]
2 – 8 weeks
  • Gray-white granulation tissue
  • Increased collagen deposition
  • Decreased cellularity
More than 2 months Completed scarring[notes 3] Dense collagenous scar formed[notes 3]
If not else specified in boxes, then reference is nr [3]

Notes

  1. 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.
  2. 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. 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.
  1. 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.

Main page

References

  1. 1.0 1.1 1.2 1.3 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:10.1007/s00428-019-02662-1. ISSN 0945-6317. 
  2. 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
  3. 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