Nguyen-Duong H.
Univ. Ulm, D-89079 Ulm. Email: hoang.nguyen-duong@gmx.de
Heart rate variability (HRV), defined as the variation in the time interval between successive heartbeats, is caused by both competing branches of the autonomic nervous system (ANS) sending opposing signals synchronously to the heart. When the ANS is in balance, the myocardium is constantly instructed to beat slower by the parasympathetic nervous system and faster by the sympathetic nervous system. A reduced HRV indicates an increased risk of sudden cardiac death and increased mortality. Traditionally, coronary artery disease (CAD) is associated with atherosclerotic plaques damaging epicardial arteries; however, new evidence suggests that many, if not most, patients with chronic CAD have patent or unoccluded epicardial arteries. In addition to plaques, other risk factors may play a role in the epicardial coronary arteries, such as: 1. coronary spasms; 2. rhythmic contractions induced in vascular smooth muscle cells (SMC) by pacemakers; 3. reduced bioavailability of nitric oxide (NO) as a marker of endothelial cell dysfunction; and 4. an arhythmicity of the downstream precapillary arteriolar “vasomotion”. Reduced production of NO, which is processed as a signal by the adjacent SMCs, leads to reduced coronary dilatation. Complete stenoses result unavoidably if contractions of the epicardial arteries triggered by activation of muscarinic M3 receptors are superimposed on rhythms induced by vascular pacemakers. In contrast to the generally prevailing opinion that activation of the sympathetic nervous system is the main trigger for coronary spasm, the hypothesis presented here posits that a shift in the autonomic balance in favor of the parasympathetic nervous system is responsible for the acute triggering of myocardial ischemia. The use of NO donors (including isosorbide dinitrate, nitroglycerin), which actually causally correct the endothelial dysfunction, as well as an adequate administration of Mg ions, can be viewed as the most effective therapy.