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Published on: January 28, 2020
Circulating progenitor cells are associated with plaque progression and long-term outcomes in heart transplant
Ilke Ozcan1, Takumi Toya1,2, Michel T Corban1
1Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.
Insights
Higher levels of CD34+CD133+ circulating progenitor cells (CPCs) are linked to reduced cardiac allograft vasculopathy (CAV) progression and major adverse cardiac events (MACEs) post-heart transplant. Conversely, elevated osteocalcin-expressing CPCs correlate with increased MACE risk.
Area of Science:
- Cardiovascular Research
- Transplantation Immunology
- Cell Biology
Background:
- Circulating progenitor cells (CPCs) are crucial for vascular repair and plaque stability.
- Osteocalcin (OC)-expressing CPCs have been implicated in unstable plaques and adverse cardiovascular outcomes.
- The specific role of CPCs in cardiac allograft vasculopathy (CAV) remains unclear.
Purpose of the Study:
- To investigate the association between CPCs and CAV progression after heart transplantation.
- To determine the contribution of CPCs to major adverse cardiac events (MACEs) in heart transplant recipients.
Main Methods:
- A cohort of 80 heart transplant patients was studied.
- Peripheral blood CPCs (CD34+, CD133+, OC+) were quantified via flow cytometry.
- CAV progression was assessed using intravascular ultrasound (IVUS); MACEs were recorded over a median follow-up of 8 years.
Main Results:
- Elevated CD34+CD133+ CPCs were associated with a decreased risk of CAV progression (OR 0.58, P=0.01) and MACEs (HR 0.79, P=0.05).
- Higher counts of OC+ cells correlated with an increased risk of MACEs (HR 1.26, P=0.02).
- Intravascular ultrasound (IVUS) was used to measure CAV progression.
Conclusions:
- Lower levels of CD34+CD133+ CPCs are linked to plaque progression and adverse outcomes in heart transplant recipients.
- Higher circulating OC+ cell levels are associated with adverse long-term outcomes.
- CPCs may ameliorate transplant vasculopathy, while OC expression might drive progression.
Aims:
Circulating progenitor cells (CPCs) play a role in vascular repair and plaque stability, while osteocalcin (OC) expressing CPCs have been linked to unstable plaque and adverse cardiovascular outcomes. However, their role in cardiac allograft vasculopathy (CAV) has not been elucidated. This cohort study aimed to investigate the contribution of CPCs on CAV progression and cardiovascular events after heart transplantation.
Methods And Results:
A total of 80 heart transplant patients (mean age 55 ± 14 years, 72% male) undergoing annual intravascular ultrasound (IVUS) had fresh CPCs marked by CD34, CD133, and OC counted in peripheral blood using flow cytometry, on the same day as baseline IVUS. CAV progression was assessed by IVUS as the change (Δ) in plaque volume divided by segment length (PV/SL), adjusted for the time between IVUS measurements [median 3.0, interquartile range (2.8-3.1) years] and was defined as ΔPV/SL that is above the median ΔPV/SL of study population. Major adverse cardiac events (MACEs) were defined as any incident of revascularization, myocardial infarction, heart failure admission, re-transplantation, stroke, and death. Patients with higher CD34+CD133+ CPCs had a decreased risk of CAV progression [odds ratio 0.58, 95% confidence interval (CI) (0.37-0.92), P = 0.01] and MACE [hazard ratio (HR) 0.79, 95% CI (0.66-0.99), P = 0.05] during a median (interquartile range) follow-up of 8.0 years (7.2-8.3). Contrarily, higher OC+ cell counts were associated with an increased risk of MACE [HR 1.26, 95% CI (1.03-1.57), P = 0.02].
Conclusions:
Lower levels of CD34+CD133+ CPCs are associated with plaque progression and adverse long-term outcomes in patients who underwent allograft heart transplantation. In contrast, higher circulating OC+ levels are associated with adverse long-term outcomes. Thus, CPCs might play a role in amelioration of transplant vasculopathy, while OC expression by these cells might play a role in progression.
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