Psychogenic Cardiovascular Disease: Underlying Autonomic Nervous Mechanisms

Background: Although the mediating mechanisms of psychogenic heart disease, which bridges the boundary between psychiatry and cardiology are unclear, sympathetic nervous pathophysiology seems to be a prime mover. Sympathetic nervous activation in acute human anxiety occurs preferentially in the cardiac sympathetic outflow, where it can trigger ventricular arrhythmias and sudden death.

Observations and interpretation: Panic disorder is associated with increased cardiac risk. Clinical case material includes recurrent emergency room attendances with ECG ischaemia, arrhythmias and coronary artery spasm. During panic attacks the sympathetic co-transmitter, neuropeptide Y (NPY), is released from the heart, an intriguing finding given that NPY can cause coronary spasm.

In depressive illness, the level of sympathetic nervous activity is bimodally distributed, in 35% of patients being extremely high, to the level seen in cardiac failure, where it is a proven lethality factor. It is probable that in depressive illness also, high cardiac sympathetic tone contributes to heart risk.

Most disputed is whether chronic mental stress causes hypertension, although this receives support in a ruling by a Governmental body, the Specialist Medical Review Council. The judgement reached, that mental stress is one proven cause of hypertension, was based in particular on the neural pathophysiology of essential hypertension: (i) sympathetic activation is commonly present, (ii) noradrenergic brain neurons are activated, (iii) adrenaline is released as a co-transmitter in the sympathetic nerves of hypertensive patients, and (iv) tissue nerve growth factor is over-expressed, all being confirmed experimentally as mental stress biomarkers.