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Published on: February 14, 2022
Intraplaque hemorrhage in cardiac allograft vasculopathy
C Castellani1, A Angelini, O J de Boer
1Department of Cardiac, Thoracic and Vascular Sciences, University of Padua, Padua, Italy.
Insights
Intraplaque hemorrhage (IPH) is more common in cardiac allograft vasculopathy (CAV) than native atherosclerosis. IPH in CAV is linked to inflammation and microvessel damage, indicating plaque vulnerability.
Area of Science:
- Cardiovascular Pathology
- Transplant Medicine
- Atherosclerosis Research
Background:
- Plaque vulnerability in native coronary atherosclerosis is influenced by hemorrhage, inflammation, and microvessel density.
- Cardiac allograft vasculopathy (CAV) is a significant concern in heart transplant recipients.
- Understanding CAV plaque characteristics is crucial for managing transplant outcomes.
Purpose of the Study:
- To investigate the presence and significance of intraplaque hemorrhage (IPH) in CAV lesions.
- To examine the relationship between IPH, inflammation, and microvessel density in CAV.
- To compare IPH prevalence in CAV versus native coronary artery disease.
Main Methods:
- Analysis of 70 coronary plaques from 12 heart transplant recipients who died from CAV.
- Semi-quantitative assessment of intralesional inflammation, microvessels, and IPH.
- Comparison of CAV plaques with native coronary artery disease (ATS) plaques from the same patients.
Main Results:
- IPH was found in 60% of CAV lesions versus 22.9% of native ATS plaques.
- A strong association was observed between fibrocellular lesions and IPH in CAV (p = 0.0142).
- Microvessels were detected in 74.3% of CAV lesions, with endothelial damage signs in 69.2%.
- IPH was strongly associated with microvessels (p < 0.0001) and inflammation (present in 88.6% of CAV lesions).
- CAV lesions with IPH often contained both fresh and old hemorrhage (57.1%).
Conclusions:
- IPH is a significant feature of CAV, frequently associated with microvessel damage and inflammation.
- The presence of fresh and old hemorrhage suggests ongoing plaque remodeling and progression in CAV.
- IPH contributes to the vulnerability of cardiac allografts, impacting long-term transplant survival.
Abstract:
Plaque hemorrhage, inflammation and microvessel density are key determinants of plaque vulnerability in native coronary atherosclerosis (ATS). This study investigates the role of intraplaque hemorrhage (IPH) and its relation with inflammation and microvessels in cardiac allograft vasculopathy (CAV) in posttransplanted patients. Seventy coronary plaques were obtained from 12 patients who died because of CAV. For each patient we collected both native heart and the allograft, at the time of transplantation and autopsy, respectively. Intralesion inflammation, microvessels and IPH were assessed semi-quantitatively. IPH was observed in 21/35 (60%) CAV lesions and in 8/35 (22.9%) native ATS plaques, with a strong association between fibrocellular lesions and IPH (p = 0.0142). Microvessels were detected in 26/35 (74.3%) of CAV lesions with perivascular leakage as sign of endothelial damage in 18/26 (69.2%). IPH was strongly associated with microvessels (p < 0.0001). Inflammation was present in 31/35 (88.6%) of CAV lesions. CAV IPH+ lesions were characterized by presence of both fresh and old hemorrhage in 12/21 (57.1%). IPH, associated with microvessel damage and inflammation, is an important feature of CAV. Fresh and old intralesion hemorrhage suggests ongoing remodeling processes promoting the lesion progression and vulnerability.
