RT-27
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Role of baroreflex sensitivity in the identification of post-MI patients candidates to implantable cardioverter defibrillator
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Maria Teresa La Rovere, Andrea Mortara, Marco Gnemmi, Peter J. Schwartz*.
Centro Medico Montescano, Fondazione “Salvatore Maugeri” IRCCS, Montescano, *Dipartimento di Cardiologia, Universita di Pavia e Policlinico S. Matteo IRCCS, Pavia, Italy
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Introduction
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Following the results of MADIT1 showing that in a well defined
population of patients at increased risk the prophylactic use of the ICD significantly improves survival,
other populations need to be defined who may benefit of this therapeutic option2. Accordingly, primary
prevention trials have been recently launched3,4. However, in
MADIT-II3 and SCD-HeFT4 risk
stratification is based only on severely depressed left ventricular function and clinical symptoms of heart
failure.
Although there is a growing awareness that the autonomic nervous system (particularly its imbalances
characterized by an increase in sympathetic and/or a decrease in vagal activity) plays an important role
in the chain of events leading to cardiovascular mortality5, measures of autonomic control have not yet
entered in the process of risk stratification on a routine basis.
Increased sympathetic activity links several important risk factors for coronary artery disease, and the
deleterious effects of the circadian surge in sympathetic activity on platelet aggregability and on
vasoconstriction have been recognised to account for the increased incidence of myo-cardial infarction
and sudden death6.
Myocardial infarction can affect the function of the autonomic nervous system which through its
sympathetic and parasympathetic outflows and their complex influences can modify cardiac
electrophysiology thus playing a role in the development of life-threatening arrhythmias7. As the
arterial baroreflex is an important control mechanism regulating vagal and sympathetic activity, the
measure of the sensitivity of the arterial baroreflex (BRS) does inform on the sympatho-vagal balance
to the heart. The underlying pathophysiology implies that a reduced BRS has to be interpreted as the
result of a decresased capability to activate vagal reflexes thus limiting the antifibrillatory effect of
vagal activity. Clinical data support previous experimental observations8. In the study by Mitrani et
al9 patients with previously implanted cardioverter defibrillators had induction of ventricular fibrillation
(VF) both in the control state and after infusion of phenylephrine which by activation of the
baroreceptors produces a reflex increase in vagal activity. It was observed that in the majority of
patients who had a vagal response (identified from the increase in sinus cycle length) following
phenylephrine injection there was an increase in the energy required to induce VF, while this was
observed in only 20% of patients who did not show signs of vagal activation.
Two distinct aspects of the value of BRS will be considered: a) the role of baroreceptors in the
hemodynamic outcome of sustained ventricular arrhythmias and b) the role of the analysis of
baroreceptive responses in risk stratification.
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