Vascular Inflammation

Vascular Inflammation
Vascular inflammation is a pathological process involving the activation and dysfunction of the blood vessel lining (endothelium), characterized by infiltration of inflammatory cells, release of cytokines, and oxidative stress. It plays a central role in the development and progression of atherosclerosis and cardiovascular diseases.
Causes and Mechanisms
- Endothelial Dysfunction: Triggered by risk factors such as hypertension, diabetes, smoking, and dyslipidemia, leading to reduced nitric oxide availability and increased adhesion molecule expression.
- Inflammatory Cell Recruitment: Monocytes and lymphocytes adhere to activated endothelium, migrate into the vessel wall, and perpetuate inflammation.
- Oxidative Stress: Reactive oxygen species promote lipid oxidation and vascular injury.
- Sleep Disturbances: Poor sleep quality, short sleep duration (≤6 hours), and sleep fragmentation are associated with increased vascular inflammation and endothelial activation, independent of traditional risk factors and sleep apnea.
- Sympathetic Activation: Acute sleep deprivation elevates sympathetic tone, increases blood pressure, and promotes endothelial inflammation.
Clinical Implications
- Vascular inflammation contributes to plaque formation, instability, and progression of atherosclerosis, increasing risk for myocardial infarction, stroke, and other cardiovascular events.
- Imaging studies (e.g., FDG PET/MRI) show higher vascular inflammation in individuals with short sleep duration and fragmented sleep, suggesting subclinical atherosclerosis risk.
- Sleep disorders and inadequate sleep are modifiable risk factors for vascular inflammation and cardiovascular disease, emphasizing the importance of sleep assessment in cardiovascular risk management.
Summary Table
Aspect | Details |
---|---|
Definition | Inflammatory activation of blood vessel walls leading to endothelial dysfunction and vascular injury |
Key Mechanisms | Endothelial activation, immune cell infiltration, oxidative stress, reduced nitric oxide |
Risk Factors | Hypertension, diabetes, smoking, dyslipidemia, sleep disturbances, acute sleep deprivation |
Effects | Atherosclerosis progression, increased blood pressure, plaque instability, cardiovascular events |
Sleep and Vascular Inflammation | Short sleep duration (≤6 hours) and sleep fragmentation linked to increased vascular inflammation and carotid wall thickness |
Diagnostic Tools | FDG PET/MRI imaging, biomarkers of endothelial activation (e.g., adhesion molecules, cytokines) |
Management | Addressing traditional risk factors, improving sleep quality, treating sleep disorders, lifestyle changes |
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Key References
- Kundel V, Reid M, Fayad Z, et al. Sleep duration and vascular inflammation using hybrid positron emission tomography/magnetic resonance imaging: results from the Multi-Ethnic Study of Atherosclerosis. J Clin Sleep Med. 2021;17(10):2009–2018.
https://doi.org/10.5664/jcsm.9382
PMC Article - Irwin MR, Olmstead R, Carroll JE. Sleep disturbance, sleep duration, and inflammation: a systematic review and meta-analysis of cohort studies and experimental sleep deprivation. Biol Psychiatry. 2016;80(1):40-52.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403737/ - Covassin N, Singh P. Sleep duration and cardiovascular disease risk: epidemiologic and experimental evidence. Sleep Med Clin. 2016;11(1):81-89.
https://pmc.ncbi.nlm.nih.gov/articles/PMC10757461/ - Sauvet F, Leftheriotis G, Gomez-Merino D, et al. Effect of acute sleep deprivation on vascular function in healthy subjects. J Appl Physiol. 2010;108(1):68-75.
https://doi.org/10.1152/japplphysiol.00851.2009
Full Text - American Heart Association. Sleep Disorders and Heart Health.
https://www.heart.org/en/health-topics/sleep-disorders/sleep-and-heart-health
Vascular inflammation is a key contributor to cardiovascular disease, with emerging evidence highlighting the significant role of sleep disturbances in promoting endothelial dysfunction and inflammatory processes. Improving sleep quality and duration represents a promising target for reducing vascular inflammation and cardiovascular risk.