- About EAS
Kitagawa et al examined the role of epicardial adipose tissue (EAT) in the development of coronary artery disease (CAD). They performed computed tomography in 45 patients prior to cardiac surgery, to assess: visceral adipose tissue area, EAT volume, coronary calcium scores and the presence of non-calcified coronary plaque (NCP) on CT angiography as well as assessing inflammation and neoangiogenesis. Their results show a significant association of EAT inflammation and neovascularization with the presence of moderate coronary calcification and the presence of NCPs. In his invited commentary Paolo Raggi pointed that the novelty of this article is in the description of an association between inflammation and neovascularisation in the adipose tissue contained in the pericardial sac. Although this research has its limitations, Paolo Raggi is certain that the paper by Kitagawa et al contributes to further our understanding of atherogenesis and the connection between EAT and CAD.
The potential mechanisms underlying the incidence of cardiac events in chronic methamphetamine (METH) users are investigated by Gao et al using an ApoE-/- mouse model. They found that in this situation METH promoted atherogenesis, increased plasma, aortic and myocardial neuropeptide Y expression and also that inflammation and reactive oxygen species production were increased in the mouse macrophages in vitro. The discussion paper “Speed kills in more ways than one: Methamphetamine and atherosclerosis” by Rye et al, while commending this study, also warns that this mouse model may not fully represent what is happening in humans in light of the observation that the appetites of METH treated mice was enhanced and not diminished. However, they feel that Gao et al’s study should stimulate investigation of the atherosclerotic burden in chronic METH users.
A systematic review and meta-analysis of epidemiological studies was performed by Barkas et al in order to establish whether individuals with familial hypercholesterolemia (FH) had an increased incidence of cerebrovascular disease (ischemic stroke or transient ischemic attack). The main conclusion of this study was that patients with FH were at higher risk of cerebrovascular disease in the pre-statin era and that this risk was significantly reduced after the introduction of statin therapy.
Boesen et al conducted a systematic literature review to determine the reported effects of carotid atherosclerosis on local vessel wall elasticity and stiffness, using measures derived from ultrasound and magnetic resonance imaging. Analysis of the 50 studies that assessed some measure of carotid arterial elasticity or stiffness in patients with carotid plaque shows that regardless of which metric was used for carotid elasticity; decreased carotid elasticity (or increased carotid stiffness) is associated with the presence of atherosclerotic plaque, the degree of atherosclerosis and stroke risk.
Papers in this issue include: