Inflammation and Vascular Responses to Acute Mental Stress: Implications for the Triggering of Myocardial Infarction

Nicola      J. Paine; Jos      A. Bosch; Jet      J.C.S. Veldhuijzen Van Zanten

doi:10.2174/138161212799504713

Abstract

There is evidence that mental stress can trigger myocardial infarction. Even though the underlying mechanisms remain to be determined, both inflammation and vascular responses to mental stress have been implicated as contributing factors. This review explores the effects of inflammation on the vascular responses to mental stress. First, the associations between inflammation and resting vascular function are discussed. It is known that increases in inflammation are associated with endothelial dysfunction, with a reduction in nitric oxide a common pathway through which inflammation can influence endothelial function. Second, the effects of mental stress on vascular responses are reviewed. There is ample evidence that in healthy participants, mental stress induces increases in forearm blood flow, which is impaired in those at risk for cardiovascular disease. Even though several mechanisms are discussed, there is evidence that nitric oxide plays an important role in stress-induced vasodilation. Finally, the influences of inflammation on the vascular responses are described. It is hypothesised that inflammation can alter vascular responses to mental stress, most likely due to lower levels of nitric oxide as a result of the inflammation. This poorer vascular response is thought to be an underlying factor through which mental stress can trigger myocardial infarction.

Keywords: Inflammation, vascular responses, mental stress, myocardial infarction, endothelial dysfunction, stress-induced vasodilation, nitric oxide, cardiovascular disease (CVD), C-reactive protein (CRP), rheumatoid arthritis