| Autor: |
DeConne TM; Section of Gerontology and Geriatric Medicine, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States., Buzkova P; Department of Biostatistics, University of Washington, Seattle, Washington, United States., Pewowaruk R; Ryan Pewowaruk Research Consulting, Madison, Wisconsin, United States., Delaney JA; Department of Medicine, University of Washington, Seattle, Washington, United States.; Department of Epidemiology, University of Washington, Seattle, Washington, United States., Psaty BM; Cardiovascular Health Research Unit, Departments of Medicine, Epidemiology, and Health Systems and Population Health, University of Washington, Seattle, Washington, United States., Tracy RP; Department of Pathology and Laboratory Medicine, University of Vermont Larner College of Medicine, Burlington, Vermont, United States., Doyle MF; Department of Pathology and Laboratory Medicine, University of Vermont Larner College of Medicine, Burlington, Vermont, United States., Sitlani CM; Department of Medicine, University of Washington, Seattle, Washington, United States., Landay AL; Division of Geriatrics, Department of Internal Medicine, University of Texas Medical Branch at Galveston, Texas, United States., Huber SA; Department of Pathology and Laboratory Medicine, University of Vermont Larner College of Medicine, Burlington, Vermont, United States., Hughes TM; Section of Gerontology and Geriatric Medicine, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States., Bertoni AG; Division of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States., Gepner AD; Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, United States.; William S. Middleton Memorial Veterans Hospital and Clinics, Madison, Wisconsin, United States., Ding J; Section of Gerontology and Geriatric Medicine, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States., Olson NC; Department of Pathology and Laboratory Medicine, University of Vermont Larner College of Medicine, Burlington, Vermont, United States. |
| Abstrakt: |
Arterial stiffness measured by total pulse wave velocity (T-PWV) is associated with an increased risk of multiple age-related diseases. T-PWV can be described by structural (S-PWV) and load-dependent (LD-PWV) arterial stiffening. T-cells have been implicated in arterial remodeling, arterial stiffness, and hypertension in humans and animals; however, it is unknown whether T-cells are risk factors for T-PWV or its components. Therefore, we evaluated the cross-sectional associations of peripheral T-cell subpopulations with T-PWV, S-PWV, and LD-PWV. Peripheral blood T-cells were characterized using flow cytometry, and carotid artery stiffness was measured using B-mode ultrasound to calculate T-PWV at the baseline examination in a participant subset of the Multi-Ethnic Study of Atherosclerosis (MESA, n = 1,984). A participant-specific exponential model was used to calculate S-PWV and LD-PWV based on elastic modulus and blood pressure gradients. The associations between five primary ( P -significance < 0.01) and 25 exploratory ( P -significance < 0.05) immune cell subpopulations, per 1-SD increment, and arterial stiffness measures were assessed using adjusted linear regression models. For the primary analysis, higher CD4 + CD28 - CD57 + , but not CD8 + CD28 - CD57 + , T-cells were associated with higher LD-PWV (β = 0.04 m/s, P < 0.01) after adjusting for covariates. None of the remaining T-cell subpopulations in the primary analysis were associated with T-PWV or S-PWV. For the exploratory analysis, several memory and differentiated/senescence-associated CD4 + and CD8 + T-cell subpopulations were associated with greater T-PWV, S-PWV, and LD-PWV after adjusting for covariates. In conclusion, we highlight novel associations in humans between CD4 + and CD8 + memory and differentiated/senescence-associated T-cell subpopulations and measures of arterial stiffness in MESA. These results warrant longitudinal, prospective studies that examine changes in T-cell subpopulations and arterial stiffness in humans. NEW & NOTEWORTHY We investigated associations between T-cells and novel measures of structural and load-dependent arterial stiffness in a large multiethnic cohort. The primary analysis revealed that pro-inflammatory, senescence-associated CD4 + CD28 - CD57 + T-cells were associated with higher load-dependent arterial stiffness. An exploratory analysis revealed that multiple pro-inflammatory CD4 + and CD8 + T-cell subpopulations were associated with both higher structural and load-dependent arterial stiffness. These results suggest that pro-inflammatory T-cells may contribute to arterial stiffness through both arterial remodeling and elevated blood pressure. |
