Heart-brain medicine is dedicated to furthering our understanding of the interaction between
the body‚ neurologic and cardiovascular systems. As discussed previously,1 the advent of subspecialization in health care delivery has led to significant advances in the care of patients
with acute disease or acute exacerbations of chronic disease. While these advances have led
to improved outcomes, we were reminded several times this past year how difficult it is to further improve outcomes using the “silo”-based,
highly subspecialized approach that has yielded results in the past.
The 2007 Bakken Heart-Brain Summit, held last June in Cleveland, further demonstrated real progress in our understanding of the importance of heart-brain interactions in health and disease.
A series of presentations ‚éØ highlighted by the Bakken Lecture given by Peter Shapiro, MD, an investigator with the SADHART trial‚ reviewed the effect of psychiatric disorders on the incidence
of cardiovascular disease and its consequences. These presentations by leaders in the field
(many of which are summarized in the pages that follow) offer irrefutable evidence of the following:
-Patients with depression and heart disease have worse outcomes than patients with heart disease without depression
-Patients with depression have decreased vagal tone
-Patients with coronary artery disease (CAD) can be safely treated with and respond to antidepressants.
These data were complemented by a keynote presentation by Kevin Tracey, MD, whose elegant work over the past many years has demonstrated a link between vagal tone and inflammation. His most recent data have shown that the vagus has direct input into the inflammatory state of macrophages in the spleen. The effect is mediated via vagal innervation of the spleen and the subunit of the nicotinic receptor expressed on the cell surface of the resident macrophages. The relevance of vagally mediated modulation of systemic inflammation has been shown in sepsis and more recently by our group in left ventricular remodeling following acute myocardial infarction.