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Myocardial changes in cardiac transplant-associated coronary arteriosclerosis: potential for timely diagnosis
1Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115.
Insights
Graft arteriosclerosis, a major limitation in heart transplants, causes myocardial changes like vacuolization and necrosis. Recognizing these biopsy-detectable lesions may enable early diagnosis and intervention for better patient survival.
Area of Science:
- Cardiovascular Pathology
- Transplantation Medicine
- Cardiac Surgery
Background:
- Graft arteriosclerosis significantly limits long-term survival following heart transplantation.
- Characterizing myocardial pathological changes is crucial for early diagnosis and intervention.
Purpose of the Study:
- To characterize myocardial pathological changes in heart transplant recipients with graft arteriosclerosis.
- To identify biopsy-detectable lesions indicative of graft arteriosclerosis for early diagnosis.
Main Methods:
- Analysis of endomyocardial biopsy specimens and explanted hearts from nine heart transplant recipients.
- Histopathological examination for arterial stenoses, myocardial ischemic lesions, and infarction.
Main Results:
- All nine patients exhibited severe diffuse proliferative arterial stenoses.
- Myocardial ischemic lesions included subendocardial myocyte vacuolization and microfocal coagulation necrosis or scar.
- Five patients had biopsy-identified myocardial abnormalities linked to graft arteriosclerosis.
Conclusions:
- Graft arteriosclerosis causes myocardial changes similar to coronary atherosclerosis, plus unique ischemic lesions.
- Subendocardial myocyte vacuolization and microfocal infarction are key biopsy-detectable findings.
- Early recognition of these myocardial changes can guide therapeutic interventions.
Abstract:
Graft arteriosclerosis is the major limitation to long-term survival after heart transplantation. In this study, myocardial pathologic changes, especially those that might permit early diagnosis, were characterized in endomyocardial biopsy specimens and hearts obtained at retransplantation or autopsy from nine orthotopic heart transplant recipients. All had severe diffuse proliferative arterial stenoses without plaque rupture or coronary thrombi. Eight patients died with and one underwent retransplantation because of graft arteriosclerosis less than 12 months (six patients) or greater than 46 months (three patients) after operation. Six patients had antecedent symptoms of congestive heart failure and six had angiographically demonstrated epicardial coronary artery graft arteriosclerosis; four had both. Myocardial ischemic lesions included subendocardial myocyte vacuolization (seven patients) and microfocal to regional coagulation necrosis and granulation tissue or scar, or both (seven patients). Subendocardial myocyte vacuolization (indicative of sublethal ischemic injury) was diagnosed at prior right ventricular biopsy in two patients and was noted at autopsy in areas accessible to right-sided biopsy in three additional patients. Three patients had pathologic changes diagnostic of acute infarction on right or left ventricular biopsy, or both. Thus, all nine patients had lesions, of which five had biopsy-identified myocardial abnormalities caused by graft arteriosclerosis. It is concluded that graft arteriosclerosis yields not only myocardial pathologic changes similar to those associated with typical coronary atherosclerosis, but also lesions resulting from focal or diffuse ischemia caused by small vessel obstructions. This is manifest as subendocardial myocyte vacuolization or microfocal infarction. Recognition of these biopsy-accessible myocardial changes associated with graft arteriosclerosis may allow early recognition and appropriate therapeutic intervention.