Autopsy of myocardial infarction
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.
In this page, the following signs and text coloring are used for comprehensiveness:
- Minimal depth
- (Moderate depth)
Autopsy cutting checklist
- Remove the parietal pericardium
- Separate the heart from the from lungs by cutting through the major vessels
- Dissect the coronary vessels.More details in section below.
- 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.
- Dissect the atrial appendages, to exclude thromboses.
- Dissect the left ventricle, such as into circumferential slices from the apex to the base.[notes 2] Inspect (and measure) the left ventricular wall thickness.
Look for areas of fibrosis (Further information: Myocardial fibrosis ) or hemorrhage. Sample tissue from suspected areas, at least in cases where a diagnosis cannot be made from gross examination alone.
Gross processing of coronary arteries
Make longitudinal (or transverse cuts at 3 mm intervals) 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.
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.
Microscopy of the myocardium
By individual parameters
|Myocardial histologic parameters (HE staining)||Earliest manifestation||Full development||Decrease/disappearance||Image|
|Streched/wavy fibres||1–2 h|
|Coagulative necrosis: cytoplasmic hypereosinophilia||1–3 h||1–3 days; cytoplasmic hypereosinophilia and loss of striations||> 3 days: disintegration|
|Interstitial edema||4–12 h|
|Coagulative necrosis: ‘nuclear changes’||12–24 (pyknosis, karyorrhexis)||1–3 days (loss of nuclei)||Depends on size of infarction|
|Neutrophil infiltration||12–24 h||1–3 days||5–7 days|
|Neutrophil karyorrhexis||1.5–2 days||3–5 days|
|Macrophages and lymphocytes||3–5 days||5–10 days (including ‘siderophages’)||10 days to 2 months|
|Vessel/endothelial sprouts*||5–10 days||10 days–4 weeks||4 weeks: disappearance of capillaries; some large dilated vessels persist|
|Fibroblast and young collagen*||5–10 days||2–4 weeks||After 4 weeks; depends on size of infarction;|
Further information: Myocardial fibrosis
|4 weeks||2–3 months||No|
- Some authors summarize the vascular and early fibrotic changes as ‘granulation tissue’, which is maximal at 2–3 weeks
|Time||Gross examination||Histopathology |
|0 - 0.5 hours||None[notes 3]||None[notes 3]|
|0.5 – 4 hours||None[notes 4]||
|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 5]||Dense collagenous scar formed[notes 5]|
|If not else specified in boxes, then reference is nr |
Classify the topographic distribution of any myocardial infarction, if possible:
Example of a normal report:
- In the myocardium, there is no evidence of fresh lesion. (The myocardium has normal texture and a homogeneous reddish brown color. No inflammation or scarring.)
- See also: General notes on reporting
- 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.
- 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.)
- 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.
- 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.
- 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.
- 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.