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A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
B lymphocytes and hyperglycemia synergistically exacerbate coronary in-stent restenosis
Insights
In-stent restenosis (ISR) is linked to higher B cell levels and non-HDL cholesterol. High B cell percentages and hyperglycemia interact to promote ISR development.
Area of Science:
- Cardiology
- Immunology
- Metabolic Syndrome
Background:
- Lymphocytes are implicated in coronary artery disease (CAD).
- Limited clinical data exists on the association between lymphocyte subsets and in-stent restenosis (ISR).
Purpose of the Study:
- To investigate the relationship between lymphocyte subsets and ISR.
- To identify clinical risk factors associated with ISR.
Main Methods:
- 812 patients were divided into ISR (N=237) and non-ISR (N=575) groups.
- Plasma levels of B cells, CD4+ T cells, CD8+ T cells, NK cells, and immunoglobulins were measured.
- Statistical analyses, including logistic regression and restricted cubic spline curves, were performed.
Main Results:
- ISR group showed higher B-cell percentage, B-cell counts, non-HDL cholesterol, and diabetes proportion.
- B-cell percentage, diabetes, and non-HDL cholesterol were independent risk factors for ISR.
- High B-cell percentage and hyperglycemia showed synergistic effects in promoting ISR.
Conclusions:
- B cells, non-HDL cholesterol, and diabetes are key factors in ISR development.
- Elevated B-cell percentage and hyperglycemia interact to exacerbate ISR.
- Understanding these associations can inform ISR prevention and treatment strategies.
Background:
Lymphocytes are tightly associated with coronary artery disease (CAD). However, there is a lack of clinical evidence that lymphocyte subsets are associated with in-stent restenosis (ISR). The aim of this clinical research was to elucidate the association between these.
Methods:
A total of 812 patients were enrolled in the study, and they were categorized into the non-ISR group (N = 575) and the ISR group (N = 237). For each patient, the counts and percentage of CD4+T cell, CD8+T cell, NK cell and B cell in plasma were determined, as well asimmunoglobulin A (IgA), IgG and IgM.
Results:
Compared with non-ISR group, ISR group had higher levels of B-cell% (P = 0.011), B-cell (P = 0.010), non-HDL (P = 0.006), and higher proportion of diabetes (P = 0.002). B cell% (OR 1.033, 95 %CI:1.002-1.065, P = 0.039), diabetes (OR 1.556, 95 %CI:1.134-2.134, P = 0.006), non high density lipoprotein cholesterol (non-HDL-C) (OR 1.210, 95 %CI:1.026-1.428, P = 0.024) were independent risk factors for ISR. The RCS curves showes both B cell% (P for nonlinear = 0.415; P for overall = 0.035) and non-HDL-C (P for nonlinear = 0.168; P for overall = 0.024) showed a linear upward trend consistent with ISR. Subgroup analyses suggested that high B cell% (B cell%≥12) promotes the hazardous effects of diabetes on ISR (P for interaction = 0.042), while chronic hyperglycaemia (HbA1c%≥6.6) exacerbates the ISR promoting effects of B cells(P for interaction = 0.04).
Conclusion:
B cells, non-HDL-C, and diabetes are closely associated with the development of ISR, and high B cell% and Hyperglycemia reciprocally promote ISR.
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