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By Matthew M. Burg and Ph. DAaron Soufer, Rachel Lampert, Matthew M. Burg and Ph. D

Abstract

www.molmed.org Molecular Medicine Rationale: In CAD, endothelin-1 (ET-1) is released by activated macrophages and UNCORRECTED PROOF thereby contributes to coronary plaque rupture and triggered cardiac events. The multifactorial regulation of ET-1 includes stimulated release by cytokines and autonomic factors. Laboratory stress provokes alteration in autonomic tone and prolonged ET-1 mediated endothelial dysfunction. Objectives: To determine the autonomic contribution to an increase in ET-1 in response to laboratory stress in patients with CAD. Methods: Patients (n=88) with chronic stable CAD instrumented with hemodynamic monitor, digital ECG monitor, and indwelling catheter for blood sampling completed a laboratory protocol that included initial rest (30min), baseline (BL: 10-min), and anger recall stress (AR: 8-min). Change from BL to AR was determined for: 1) parasympathetic activity (by spectral analysis of ECG); 2) sympathetic activity (by circulating catecholamines); and 3) ET-1. Results: AR provoked increases from BL in catecholamines, and a decrease i

Year: 2011
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