Autopsy of myocardial infarction

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Author: Mikael Häggström [note 1]
Heart autopsy in possible 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.

On this resource, the following formatting is used for comprehensiveness:

  • Minimal depth
  • (Moderate depth)
  • ((Comprehensive))
Other legend

<< Decision needed between alternatives separated by / signs >>
{{Common findings / In case of findings}}
Organs or important regions are in bold in the report example, but does not need to be in an actual report.

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.
Valve circumferences are measured at the basal ring (bottom in image).
  • (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)

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

Coronary vessels, with annotated arteries.svg

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. Further information: Arteries

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]

Microscopy of the myocardium

By individual parameters

Myocardial histologic parameters (HE staining)[2][3] Earliest manifestation[2] Full development[2] Decrease/disappearance[2] Image
Streched/wavy fibres 0.5–4 h[3] Histopathology of myofiber waviness in myocardial infarction.jpg
Coagulative necrosis: cytoplasmic hypereosinophilia 1–3 h 1–3 days; cytoplasmic hypereosinophilia and loss of striations > 3 days: disintegration Histopathology of coagulative necrosis of cardiomyocytes.jpg
Interstitial edema 4–12 h Histopathology of interstitial edema in myocardial infarction.jpg
Coagulative necrosis: ‘nuclear changes’ 12–24 (pyknosis, karyorrhexis) 1–3 days (loss of nuclei) Depends on size of infarction Histopathology of myocardial infarction with loss of nuclei.jpg
Neutrophil infiltration 12–24 h 1–3 days 5–7 days Histopathology of neutrophil infiltration in myocardial infarction.jpg
Neutrophil karyorrhexis 1.5–2 days 3–5 days Histopathology of myocardial infarction with karyorrhexis and few lymphocytes.jpg
Macrophages and lymphocytes 3–5 days 5–10 days (including ‘siderophages’) 10 days to 2 months Histopathology of macrophages and lymphocyte infiltration with early removal of necrotic debris in myocardial infarction.jpg
Vessel/endothelial sprouts* 5–10 days 10 days–4 weeks 4 weeks: disappearance of capillaries; some large dilated vessels persist Histopathology of granulation tissue with formation of microvessels in myocardial infarction.jpg
Fibroblast and young collagen* 5–10 days 2–4 weeks After 4 weeks; depends on size of infarction; Histopathology of fibroblast proliferation and early collagen deposition in myocardial infarction.jpg
Dense fibrosis
Further information: Myocardial fibrosis
4 weeks 2–3 months No Histopathology of dense fibrous scar replacing myocyte loss in myocardial infarction.jpg
  • Some authors summarize the vascular and early fibrotic changes as ‘granulation tissue’, which is maximal at 2–3 weeks


Time Gross examination Histopathology
(light microscopy)
0 - 0.5 hours None[note 4] None[note 4]
0.5 – 4 hours None[note 5]
  • 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[4]
2 – 8 weeks
  • Gray-white granulation tissue
  • Increased collagen deposition
  • Decreased cellularity
More than 2 months Completed scarring[note 6] Dense collagenous scar formed[note 6]
If not else specified in boxes, then reference is nr [5]


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


  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.
  2. The right ventricle can alternatively be cut in circumferential slices along with the left ventricle.
  3. 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.)
  4. 4.0 4.1 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.
  5. 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.
  6. 6.0 6.1 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.

Main page


  1. 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:10.1016/S0025-6196(12)64946-5. 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
    ". Pulmonary Medicine 2012: 1–6. doi:10.1155/2012/617531. ISSN 2090-1836. 
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 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. 
  3. 3.0 3.1 Page 547 in: Kumar, Vinay (2021). Robbins & Cotran pathologic basis of disease . Philadelphia, Pa: Elsevier. ISBN 978-0-323-60993-7. OCLC 1161987164. 
  4. 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
  5. 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