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Updated: Sep 27, 2025
Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Pathophysiological evaluations of initial plaque development after heart transplantation via serial multimodality
Tatsuya Shiraki1, Yasuhiro Ichibori2, Tomohito Ohtani1
1Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita, Japan.
Insights
Progression of coronary allograft vasculopathy after heart transplantation is linked to fibrous plaque growth. Elevated serum interleukin-31 levels may predict this intimal fibrous proliferation within one year post-transplant.
Area of Science:
- Cardiology
- Immunology
- Transplantation Medicine
Background:
- Coronary allograft vasculopathy (CAV) is a major cause of graft failure after heart transplantation.
- The morphological characteristics of de novo and donor-transmitted plaques in CAV are not fully understood.
- The association between serum T-lymphocyte cytokine levels and CAV progression remains unclear.
Purpose of the Study:
- To investigate the morphological features of de novo and donor-transmitted plaques in CAV.
- To determine the relationship between serum cytokine levels and plaque progression within one year post-heart transplantation.
- To explore the role of specific cytokines in the development and progression of CAV.
Main Methods:
- Retrospective analysis of 40 heart transplant recipients with prospectively maintained data.
- Serial optical coherence tomography and intravascular ultrasound at 8 weeks and 12 months post-transplantation.
- Serum cytokine measurements and correlation analysis with plaque burden changes based on morphology.
Main Results:
- De novo plaques showed significantly higher plaque burden increase compared to donor-transmitted plaques.
- Fibrous morphology was predominant in de novo plaques, contributing to progression.
- Baseline serum interleukin-31 levels correlated significantly with fibrous plaque proliferation, even under immunosuppression.
Conclusions:
- Intimal fibrous proliferation is a key factor in the progression of both de novo and donor-transmitted plaques in CAV.
- Serum interleukin-31 may play a role in promoting intimal fibrous proliferation within the first year after heart transplantation.
- Further research into interleukin-31's role could inform targeted therapies for CAV prevention and management.
Background:
Detailed morphological characteristics of de novo and donor-transmitted plaques and the association of serum T-lymphocyte cytokine levels with plaque progression of coronary allograft vasculopathy within 1 year after heart transplantation are unknown.
Methods:
In this retrospective analysis of data in a prospectively maintained database, 40 heart transplant recipients were included. We performed serial 3 vessel optical coherence tomography and intravascular ultrasound analyses, at the 8 week (baseline) and 12 month post-transplantation follow-ups, and serum cytokine measurements (n = 23). The correlation between serum cytokines and Δplaque burden (between baseline and follow-up) was evaluated depending on plaque morphology.
Results:
Thirteen de novo plaques (maximum intimal thickness ≥0.5 mm at the 12 month follow-up without plaques at baseline) were identified in 8 recipients, and 31 donor-transmitted plaques (maximum intimal thickness ≥0.5 mm at baseline) were detected in 17 recipients. Compared with donor-transmitted plaques, the Δplaque burden in the de novo plaques, with mainly fibrous morphology, was high (38.8% [29.6%-41.2%] vs 8.7% [1.33%-13.6%], p < 0.001). Stratification of the morphology of donor-transmitted plaques revealed that the Δplaque burden in fibrous plaques (10.6% [7.0%-18.0%]) was similar to that in fibroatheroma (10.3% [8.7%-23.8%]). Serum interleukin-31 levels at baseline correlated with fibrous plaque proliferation (r = 0.73, p = 0.007) even under immunosuppressive conditions, whereas other cytokines (interleukin-1β, interleukin-17, and interferon-gamma) were mostly undetectable.
Conclusions:
Intimal fibrous proliferation contributed to the progression of donor-transmitted and de novo plaques. Serum interleukin-31 levels at baseline may contribute to intimal fibrous proliferation within 1 year after heart transplantation.
