[The autonomic nervous system in myocardial infarction].
The occurrence of alterations in the autonomic control of cardiovascular function has long been known. Nevertheless, only in the last 15 years with the development and utilization of techniques such as heart rate variability and baroreflex analysis, unforeseeable amounts of information have been collected. The appraisal of alterations in the autonomic control mechanisms in the acute and post-acute phase of myocardial infarction has not only confirmed the presence of an increased sympathetic and of a reduced vagal modulation in most of post-myocardial infarction patients. It has also allowed the clinically relevant identification of those patients with an increased arrhythmic and total cardiac mortality. Most the high-risk patients are indeed characterized by a marked reduction in heart rate variability that can be detected using different methodologies. For example, with time-domain analysis of heart rate variability, it has been shown that an SDNN < 70 ms identifies patients at risk. By using spectral analysis, it has been possible to realize that the loss or marked attenuation of those rhythmical components that reflect autonomic modulation is also a characteristic of the high-risk patients. A decreased responsiveness of the sinus node to autonomic inputs may also explain the reduction in baroreflex sensitivity that characterizes patients with an increased arrhythmic mortality. In conclusion, the appraisal in each patient of the extent of the alterations in the autonomic control mechanism is nowadays a critical component of the clinical assessment not only for risk stratification but also in order to guide the prescription of new pharmacological and non-pharmacological therapies.
Lombardi
F
F
Dipartimento di Medicina, Chirurgia e Odontoiatria, Università degli Studi Ospedale San Paolo, Via A. di Rudinì 8 20142 Milano. Federico.Lombardi@unimi.it
Colombo
A
A
Belletti
S
S
Tarricone
D
D
D001341:Autonomic Nervous System / Q000503:physiopathology*; D006339:Heart Rate; D006801:Humans; D009203:Myocardial Infarction / Q000503:physiopathology*; D011311:Pressoreceptors / Q000503:physiopathology