Korean J Leg Med.  2018 Aug;42(3):92-97. 10.7580/kjlm.2018.42.3.92.

Acute Myocardial Infarction due to Cardiac Allograft Vasculopathy: An Autopsy Report

• Kim MY
• Kim JH
• Park MJ
• Lee SD

• KMID: 2419459
• DOI: http://doi.org/10.7580/kjlm.2018.42.3.92

Abstract

After the Organ Transplant Act was enforced in 2000, the criteria for the diagnosis of brain death have been legalized, and cardiac transplantation has become a promising treatment choice for patients with chronic heart disease. Even though more than hundreds of cases have been accumulated in the national registry and the survival rates are increasing, the compliance of long-term survivors may decrease paradoxically, which can hinder the efforts to enhance the quality of the registry. The patients who are lost from the doctor's surveillance and die outside hospitals should be appropriately examined to determine the cause of death so that the influence of their medical condition, if any, on their death could be revealed. Here, we report an autopsy case of a patient who died of a complication of chronic rejection after cardiac transplantation.

Keyword

Heart transplantation; Graft rejection; Coronary vessels; Cause of death; Myocardial infarction

MeSH Terms

Allografts*
Autopsy*
Brain Death
Cause of Death
Compliance
Coronary Vessels
Diagnosis
Graft Rejection
Heart Diseases
Heart Transplantation
Humans
Myocardial Infarction*
Survival Rate
Survivors
Transplants

Figure

• 

  Fig. 1. Gross findings of formalin-fixed heart and coronary arteries of the deceased. (A) The heart is enlarged and the entire epicardium is adhered to the pericardial sac. (B) Cross section of the lateral wall of left ventricle shows focal discoloration which implies ischemic necrosis. (C) In the serial section of major coronary arteries, the lumens are narrowed due to diffuse concentric wall thickening (left circumflex artery).

• 

  Fig. 2. Microscopic findings of cardiac allograft vasculopathy and related myocardial infarction. (A) The cross-section of the coronary artery shows intimal hyperplasia with inflammatory cell infiltration (Masson-Trichrome stain, ×100). Intraluminal thrombosis (B, H&E stain, ×40) and arteritis (C, H&E stain, ×200) observed in subcoronary branches. (D) The ischemic area shows extensive myocyte necrosis and karyorrhexis (H&E stain, ×400).

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  Fig. 3. Microscopic findings of acute cellular rejection. Dense infiltration of mixed inflammatory cells is observed in myocardial interstitium, which is mainly composed of lymphocytes and monocytes, accompanied by myocyte injury and intramyocardial vasculitis (A, H&E stain, ×100; B, H&E stain, ×400).

• 

  Fig. 4. Microscopic findings of antibody-mediated rejection. Some myocardial capillaries are positively stained with C4d stain (×400).

Reference

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