Autonomic dysfunction is a strong correlate of morbidity and mortality in cardiovascular disease. While increased sympathetic stimulation drives many adverse events in coronary artery disease and heart failure, beta-adrenergic blockade is associated with improved outcomes. Similarly, diminished parasympathetic tone is also associated with adverse outcomes in cardiovascular disease, suggesting a key role for this limb of the autonomic system in maintenance of cardiac homeostasis.
The mechanism of parasympathetic protection, however, is not clearly understood. Although an antiarrhythmic mechanism appears intuitive, such a mechanism has not been corroborated by animal studies. Recently, Tracey and colleagues provided new insight by demonstrating that parasympathetic stimulation in mice and in human macrophages results in a decreased release of mediators of systemic inflammation. Given the importance of inflammation in atherosclerosis and adverse remodeling in congestive heart failure, it is possible that parasympathetic tone assuages atherogenesis and deleterious cardiac remodeling by directly inhibiting inflammation.