Atherosclerotic plaques constitute the primary cause of heart attack and stroke. However, we still lack a clear identification of the plaques. Here, we evaluate the feasibility of scanning acoustic microscopy (SAM) and time-resolved fluorescence spectroscopy (TRFS) in atherosclerotic plaque characterization. We perform dual-modality microscopic imaging of the human carotid atherosclerotic plaques. We first show that the acoustic impedance values are statistically higher in calcified regions compared with the collagen-rich areas. We then use CdTe/CdS quantum dots for imaging the atherosclerotic plaques by TRFS and show that fluorescence lifetime values of the quantum dots in collagen-rich areas are notably different from the ones in calcified areas. In summary, both modalities are successful in differentiating the calcified regions from the collagen-rich areas within the plaques indicating that these techniques are confirmatory and may be combined to characterize atherosclerotic plaques in the future.
Atherosclerosis is the underlying factor in the premature death of millions of humans annually. The cause of death is often a result of the rupture of an atherosclerotic plaque followed by the discharge of the associated molecular debris into the vessel lumen which occludes the artery leading to ischemia of downstream tissue and to morbidity or mortality of the individual. This is most serious when it occurs in the heart (heart attack) or brain (stroke).
Introduction: The involvement of thyroid hormone in cardiovascular disease remains debated. The aim of our research was to ascertain whether thyroid hormone sensitivity indices are related to carotid plaque (CAP) risk in the general population.
Methods: We recruited 5,360 participants for health examinations to explore the correlation between thyroid hormone sensitivity indices and CAP risk.
Background: Atherosclerosis involves the buildup of macrophage-derived foam cells in the arterial intima. Facilitating the egress of these cells from plaques can significantly slow disease progression. The transmembrane receptor Unc5b, a vascular-specific axon guidance receptor, is upregulated in foam cells, and inhibits their migration from the plaques.
Rheumatology Unit, First Department of Propaedeutic Internal Medicine, Joint Academic Rheumatology Program, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Objective: Cardiovascular disease is a leading cause of mortality in Systemic Lupus Erythematosus (SLE). We assessed atherosclerotic plaque progression and incident cardiovascular events in SLE patients over a 10-year follow-up.
Methods: We prospectively analyzed 738 carotid ultrasound measurements (413 in SLE patients and 325 in age/sex-matched healthy controls [HC]) to assess new plaque development from baseline to 3-, 7-, and 10-year follow-up.
Objective: Excess cholesterol loading on arterial macrophages is linked to foam cell formation, atherosclerosis and cardiovascular risk in rheumatoid arthritis (RA). However, the effect of changes in cholesterol loading on coronary plaque trajectory and the impact of RA therapies on this relationship are unknown. We investigated the association between variations in cholesterol loading capacity (CLC) over time and atherosclerosis progression.
