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Updated: Jun 1, 2026
An Immunological Model for Heterotopic Heart and Cardiac Muscle Cell Transplantation in Rats
Published on: May 8, 2020
Diverse morphologic manifestations of cardiac allograft vasculopathy: a pathologic study of 64 allograft hearts
Wei-hui Lu1, Kathy Palatnik, Gregory A Fishbein
1Department of Pathology and Laboratory Medicine, Division of Anatomic Pathology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA.
Insights
Cardiac allograft vasculopathy (CAV) is a complex disease affecting transplanted hearts, characterized by intimal hyperplasia, atherosclerosis, and inflammation in coronary arteries of both adults and children. Understanding these varied lesions is crucial for developing effective therapies to improve long-term transplant success.
Area of Science:
- Cardiovascular Pathology
- Transplantation Medicine
- Immunology
Background:
- Cardiac allograft vasculopathy (CAV) significantly limits long-term cardiac transplant success.
- Previous studies have described CAV lesions but lacked detailed pathology from a large retransplantation cohort.
Purpose of the Study:
- To delineate the pathological features of cardiac allograft vasculopathy (CAV) in explanted hearts from patients undergoing retransplantation due to CAV.
- To analyze the types and severity of vascular lesions in both adult and pediatric cardiac allograft recipients.
Main Methods:
- Retrospective review of archival records and microscopic sections from 64 explanted hearts (54 adults, 10 children) undergoing retransplantation for CAV.
- Categorization of vascular lesions including intimal fibromuscular hyperplasia, atherosclerosis, and inflammation.
- Estimation of luminal narrowing from gross and microscopic examination.
Main Results:
- 75% of hearts showed evidence of acute cellular rejection.
- Intramyocardial arteries primarily exhibited intimal fibromuscular hyperplasia and inflammation.
- Epicardial coronary arteries in all hearts displayed narrowing, with lesions comprising intimal fibromuscular hyperplasia, atherosclerosis, and/or inflammation affecting multiple vascular layers.
- Severe luminal narrowing (>75%) was observed in major coronary arteries (LAD, LCx, RCA) and smaller branches.
- Atheromas were present in both adult and pediatric recipients, indicating they are not exclusively pre-transplant lesions.
Conclusions:
- Cardiac allograft vasculopathy (CAV) is a complex disorder with diverse pathological manifestations, including intimal fibromuscular hyperplasia, atherosclerosis, and inflammation (vasculitis).
- These lesions affect both large and small epicardial coronary arteries in adult and pediatric transplant recipients.
- Effective therapeutic strategies for CAV must address the multifaceted nature of these vascular lesions.
Background:
Cardiac allograft vasculopathy (CAV) is a major limitation to the long-term success of cardiac transplantation. Although there are published descriptions of the lesions, there have been no studies delineating the pathology of CAV in a large series of patients who underwent retransplantation for CAV.
Methods:
We reviewed archival records and microscopic sections of surgically explanted hearts from 64 patients who underwent cardiac retransplantation: 54 adults (18 to 70 years old) and 10 children (3 to 15 years old). Vascular lesions were categorized as showing intimal fibromuscular hyperplasia, atherosclerosis and/or inflammation. The degree of luminal narrowing was estimated from gross descriptions and microscopic sections.
Results:
In total, 75% of hearts had evidence of acute cellular rejection, mostly mild. Intramyocardial arteries showed primarily intimal fibromuscular hyperplasia and inflammation with no atheromas present. Large and branch epicardial coronary arteries were narrowed in at least one artery of all hearts. Lesions in the epicardial coronary arteries were composed of intimal fibromuscular hyperplasia, atherosclerosis and/or inflammation affecting one or more vascular layers (intima, media and adventitia). Severe CAV with >75% luminal narrowing was seen in the LAD in 17% of hearts, the LCx in 17% and the RCA in 22% of hearts. Two hearts had severe narrowing of the left main coronary artery. Nineteen arteries had luminal thrombi. All hearts had narrowing of smaller epicardial branch coronary arteries that was often severe. Atheromas were present in arteries of adults and children; thus, not all atheromas could be considered pre-existing prior to transplantation. Both arteries and veins showed intimal hyperplasia and inflammation.
Conclusions:
CAV is a pathologically multifaceted disorder that affects large and small epicardial coronary arteries of adults and children, with different types of lesions: intimal fibromuscular hyperplasia; atherosclerosis; and/or inflammation (vasculitis). Therapies to address this disease must take into account the protean nature of the vascular lesions.
