Description Module

Description Module

The Description Module contains narrative descriptions of the clinical trial, including a brief summary and detailed description. These descriptions provide important information about the study's purpose, methodology, and key details in language accessible to both researchers and the general public.

Description Module path is as follows:

Study -> Protocol Section -> Description Module

Description Module


Ignite Creation Date: 2025-12-24 @ 6:55 PM
Ignite Modification Date: 2025-12-24 @ 6:55 PM
NCT ID: NCT01176357
Brief Summary: Coronary artery disease (CAD), the most common type of heart disease, is caused by hardening of the arteries, or atherosclerosis that is an inflammatory process in which immune mechanisms interact with metabolic risk factors to initiate, propagate, and activate lesions in the arterial trees. Epidemiological studies have found that increased cardiovascular risks are associated with increased levels of inflammatory cytokines (eg, interleukin-6 \[IL-6\] and tumor necrosis factor-alpha\[TNF-alpha\]) or their hepatic product, C-reactive protein (CRP). Higher expression of interleukin-Ibeta(IL-1beta),IL-6, monocyte chemotactic protein-1 (MCP-1), and TNF-alpha were observed in epicardial adipose tissues in patients with CAD. These findings suggested that the pericoronary tissues could be a source of inflammatory mediators or act as paracrine that lead to vascular inflammation on CAD pathogenesis. However, adiponectin, a kind of adipocytokine, produced and secreted exclusively by adipose tissue, has been reported to have a variety of anti-inflammatory functions against atherosclerosis, resulting in risk reduction for incidence of CAD events. It remains unclear whether adiponectin and inflammatory mediators in mediastinal adipose tissue contribute to CAD. We therefore aim to analyze the expression of adiponectin and inflammatory mediators in mediastinal adipose tissue between patients with CAD and with valve diseases, and to correlate these parameters with clinical atherosclerotic risks, medications (statins or antiplatelet), and blood sugar.
Study: NCT01176357
Study Brief:
Protocol Section: NCT01176357