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In patients after myocardial infarction the risk
potential for letal arrhythmias can be reasonably quantified by measuring one or more of
the following several non-invasive variables such as ventricular ejection fraction,
indices of ischemia, the presence of frequent and sustained asymptomatic arrhythmias, and
signal averaged ECGs. However, because of their rather low positive predictive value, they
offer insufficient help for the identification of patients at such a high risk to justify
truly aggressive strategies.
Prophylactic antiarrhythmia treatment in high risk patients has been and is being
evaluated in several clinical trials. The recent results of EMIAT1
demonstrate that absence of a classic marker of electrical instability such as fequent or
complex premature ventricular beats does not imply a low risk for subsequent cardiac and
arrhythmic mortality; indeed 40% of all deaths occurred among the patients with
"clean" Holters. This suggests that one should look elsewhere for the
identification of useful markers of high and low risk. MADIT2
provided a successful example of identification of high risk patients; however, the
procedure for the selection of patients was complex and, at the end, it appears to have
involved only a small fraction of post-infarction patients3.
These and other considerations suggest that there is still a need for a better
understanding of all the factors that may modulate the vulnerable substrate for lethal
arrhythmias. These factors could then become, together with the substrate itself, a
logical target on which to focus preventive therapies.
Data from multiple studies, including our own, point toward alterations in sympathetic
and parasympathetic activity as being of major importance among the modulating factors
favouring the onset of life-threatening arrhythmias. These alterations may be analyzed by
indirect markers such as the beat-to-beat variability of heart rate (HRV)4 and the reflex chronotropic response to a blood pressure
change, ie baroreflex sensitivity (BRS)5.
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