Emotionally charged events are associated with an increased risk of sudden cardiac death (SCD). In this study we assessed RR and QT variability index (QTVI) at baseline during anger recall test (AR). We calculated QTVI from a 5-min ECG recording and from a 10-beats segment around the presumed maximum sympathetic activation in thirty post-myocardial infarction patients under β-blocker therapy and 10 controls underwent. In all groups, the low-frequency component of RR and SBP increased during AR. In all recordings, the QTVI calculated on a 5-min ECG recording and the Q T V I 1 0 b e a t s were higher in patients than in controls (P < 0.05). The QTVI during AR remained unchanged from baseline within each group. Conversely, during AR, the Q T V I 1 0 b e a t s in controls diminished significantly (P < 0.05) from baseline whereas in patients remained unchanged. The inability to buffer an acute stress-induced increase in sympathetic activity could explain why events charged with acute stress are associated with an increased risk of ventricular arrhythmias in this setting of patients and support the role of cognitive behavior stress management strategies. 1. Introduction Sudden, unexpected events with a high emotional content [1, 2], such as, earthquakes [3–6], terrorist attacks [6–9], sports matches [10, 11], sexual activities [12, 13], or episodes of anger [14, 15] can lead to malignant ventricular arrhythmias and hence to sudden cardiac death (SCD), mainly in patients with structural heart disease. The body reacts to these stressful circumstances by increasing sympathetic nervous activity and reducing vagal control of heart rate and blood pressure [16], such imbalance known to be a trigger for malignant ventricular arrhythmias [1, 2, 17]. Several Authors suggest that stressful events, such as, those experimentally induced through an anger recall test (AR), might lead also to a significant worsening in myocardial repolarization dispersion, another phenomenon thought to be a potential striking of lethal arrhythmias [18–20]. Moreover, evidence about a possible relationship between autonomic nervous system (ANS) activity and myocardial repolarization dispersion comes from a recent experimental study showing that the QT variability index (QTVI), marker of temporal dispersion in myocardial repolarization [21–24], tends to increase in a manner directly proportional to the increased sympathetic nerve activity [25]. However, stress-induced events typically cause nonuniform, short-lasting changes in ANS activity and, most likely, in myocardial repolarization
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