Among mediating mechanisms of psychogenic cardiovascular disease, which bridges psychiatry and cardiology, sympathetic nervous pathophysiology is a prime mover. Acute mental stress can trigger heart attacks. This truth is contested, but the remarkable increase in non-traumatic sudden death during earthquakes provides one indisputable example. Sympathetic activation occurs preferentially in the cardiac sympathetic outflow. Adverse cardiac events in patients with panic disorder are analogous. Clinical case material includes cardiac arrhythmias, coronary artery spasm and myocardial infarction. Sympathetic nerve recording during panic attacks demonstrates a massive increase in multiunit burst amplitude. Neuronal noradrenaline uptake is reduced in panic disorder patients, magnifying the sympathetic neural signal in the heart. Reduced abundance of NET protein is evident in Western blot analysis of sympathetic nerve proteins accessed via subcutaneous vein biopsy. Major Depressive Disorder (MDD) is a risk factor for coronary heart disease. With noradrenaline isotope dilution methodology a subset (approximately 40%) of MDD patients exhibit extraordinarily high levels of sympathetic activity in the heart; this is normalised during clinical remission. Chronic mental stress is probably a cause of essential hypertension. Opinion here is polarized, no doubt because occupational health litigation dimensions of the subject are so divisive. Supporting biological evidence is: (i) sympathetic activation is commonly present, (ii) noradrenergic brain neurons projecting to the hypothalamus and amygdala are activated, (iii) adrenaline is released as a cotransmitter from sympathetic nerves, (iv) sympathetic nerves (accessed from a subcutaneous forearm vein biopsy) contain PNMT, absent in health, the probable origin of the co-released adrenaline.
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© 2015 Published by Elsevier Inc.