Contributed by Michael A. Nalesnik, M.D.
PATIENT HISTORY:
Per referral letter, the patient is a middle aged male who received a heart transplant for idiopathic cardiomyopathy. In the interim years, the patient has done well, including nine endomyocardial biopsies negative for rejection. The last biopsy was obtained that included an immunofluorescent study for humoral rejection using immunofluorescent labeling. The latter was negative for immune mediated vascular rejection.

Most recently, the patient developed symptomatology that clinically was felt to possibly represent chronic rejection. Cyclosporin levels have been stable and well maintained. The patient was scheduled to be evaluated with a coronary arteriogram, however, before that study could be initiated, the patient was emergently admitted over a weekend, subsequently developing and succumbing to cardiogenic shock. Review of outside material.


Final Diagnosis (Case 3)

ALLOGRAFT HEART, POST MORTEM -
  1. CHRONIC REJECTION WITH CORONARY ARTERITIS (see comment).
  2. SMALL SUBACUTE TO CHRONIC INFARCT.

Comment:
The overall change, ie, patchy fibrosis, small lymphocytic inflammation, coronary atherosclerosis and vascular inflammation, is compatible with an established chronic rejection process. Although the significance of inflammatory cells within vessels is controversial, this is a recognized component of chronic rejection and the nature of inflammation in this case suggests that it is an extension of this process, rather than a separate acute rejection episode event.

Previous Biopsies on this Patient:
None

TPIS Related Resources:
Heart Allograft Rejection Grading
Heart Transplant Topics


Gross Description:


The specimen consists of six (6) consult slides. No autopsy report is enclosed with these slides.


Microscopic Description:


The myocardium is involved with multiple small foci of chronic inflammatory cells. These are generally well demarcated and, in some areas, are associated with areas of previous myocyte dropout. The infiltrate is predominantly perivascular and is unaccompanied by any significant eosinophilic infiltrate. Also noted is inflammation involving both intramyocardial and extramyocardial branches of coronary arteries. The latter are characterized by a circumferential intimal atherosclerotic thickening with significant numbers of chronic inflammatory cells and a moderately prominent endothelialitis. Focal thrombosis is also noted in a small intramyocardial branch. One section shows a small subendocardial infarct with mummification of myocytes.


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