Early detection of vascular inflammation would allow deployment of targeted strategies for the prevention or treatment of multiple disease states. Because vascular inflammation is not detectable with commonly used imaging modalities, we hypothesized that phenotypic changes in perivascular adipose tissue (PVAT) induced by vascular inflammation could be quantified using a new computerized tomography (CT) angiography methodology. We show that inflamed human vessels release cytokines that prevent lipid accumulation in PVAT-derived preadipocytes in vitro, ex vivo, and in vivo. We developed a three-dimensional PVAT analysis method and studied CT images of human adipose tissue explants from 453 patients undergoing cardiac surgery, relating the ex vivo images with in vivo CT scan information on the biology of the explants. We developed an imaging metric, the CT fat attenuation index (FAI), that describes adipocyte lipid content and size. The FAI has excellent sensitivity and specificity for detecting tissue inflammation as assessed by tissue uptake of 18F-fluorodeoxyglucose in positron emission tomography. In a validation cohort of 273 subjects, the FAI gradient around human coronary arteries identified early subclinical coronary artery disease in vivo, as well as detected dynamic changes of PVAT in response to variations of vascular inflammation, and inflamed, vulnerable atherosclerotic plaques during acute coronary syndromes. Our study revealed that human vessels exert paracrine effects on the surrounding PVAT, affecting local intracellular lipid accumulation in preadipocytes, which can be monitored using a CT imaging approach. This methodology can be implemented in clinical practice to noninvasively detect plaque instability in the human coronary vasculature.
ED is associated with increased inflammatory and endothelial-prothrombotic activation in men with or without CAD. ED confers an incremental unfavourable impact on the circulating levels of these markers/mediators when combined with CAD. These findings have implications for increased cardiovascular risk in ED patients.
Coronary calcification has long been known to occur as a part of the atherosclerotic process, although whether it is a marker of plaque stability or instability is still a topic of considerable debate. Coronary calcification is an active process resembling bone formation within the vessel wall and, with the advances in CT technology of the past decade, can be easily quantified and expressed as a coronary artery calcium (CAC) score. The extent of calcium is thought to reflect the total coronary atherosclerotic burden, which has generated interest in using CAC as a marker of risk of cardiovascular events. The current consensus is that large amounts of CAC identify a highly vulnerable patient rather than a vulnerable plaque or vulnerable vessel. Indeed, CAC has incremental prognostic value beyond traditional risk factors in various subsets of the population. Furthermore, whereas the presence of CAC is associated with increased risk, a zero CAC score predicts excellent short-term to mid-term prognosis, even in high-risk patients. The advent of CT angiography has perhaps clouded the importance of CAC as a long-term marker of risk, as opposed to the presence of luminal stenoses that are associated with a more immediate risk of events.
The present study shows, for the first time, that when smoking and caffeine intake are combined, they interact and exert a synergistic, unfavorable effect on aortic stiffness and wave reflections on both an acute and chronic basis.
Our study shows for the first time that consumption of dark chocolate acutely decreases wave reflections, that it does not affect aortic stiffness, and that it may exert a beneficial effect on endothelial function in healthy adults. Chocolate consumption may exert a protective effect on the cardiovascular system; further studies are warranted to assess any long-term effects.
Green tea consumption has an acute beneficial effect on endothelial function, assessed with FMD of the brachial artery, in healthy individuals. This may be involved in the beneficial effect of tea on cardiovascular risk.
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