الکتروکورتیکال فرونتال و واکنش های قلبی و عروقی در طول شادی و خشم

The present study investigated electrocortical and cardiovascular reactivity during positive and negative emotion, and examined the relation of asymmetric frontal lobe activation to cardiovascular responses. Participants were 30 healthy, right-handed university students (mean age, 23.9; 60% female; 76% Caucasian). Electroencephalographic (EEG), blood pressure (BP), and heart rate (HR) responses were assessed while subjects engaged in laboratory tasks (personally-relevant recall tasks and film clips) designed to elicit happiness or anger. Happiness-inducing tasks evoked more prominent left than right frontal EEG activation, and greater left frontal EEG activation than anger-inducing tasks. However, anger-inducing tasks were, on average, associated with comparable left and right frontal EEG activation. Irrespective of emotional valence, cardiovascular activation was more pronounced during personally-relevant recall tasks than during the viewing of film clips. During anger recall, both greater left frontal EEG response (r=−0.46, P<0.02) and greater right frontal EEG response (r=−0.45, P<0.02) were correlated significantly with increased HR reactivity during the task. In addition, a right lateralized frontal EEG response during anger-inducing tasks was associated with greater concomitant systolic BP (P<0.03) and diastolic BP (P<0.008) reactivity. Exploratory analyses also indicated that men who displayed a left lateralized frontal EEG response during happiness-inducing tasks showed the greatest concomitant systolic BP and HR reactivity (P's<0.03). These findings suggest that asymmetric frontal EEG responses to emotional arousal may elicit different patterns of cardiovascular reactivity in healthy adults.

Intense emotional arousal is posited to play a role in the onset of acute coronary events such as myocardial infarction and sudden cardiac death (Kamarck and Jennings, 1991, Lane and Jennings, 1995, Mittleman et al., 1995 and Krantz et al., 1996). It is hypothesized that emotions activate regions of the brain that stimulate sympathetic outflow, thus promoting elevations in various cardiovascular parameters. Cardiovascular responses (reactivity) of sufficient magnitude may, in turn, elicit coronary events via myocardial ischemia and a lowered threshold for ventricular arrhythmias (Kamarck and Jennings, 1991). Repeated cardiovascular responses during emotional arousal have also been hypothesized as a link between dispositional psychological traits (e.g. anger, anxiety) and cardiovascular disease (Manuck, 1994 and Rozanski et al., 1999). Although numerous investigations have linked central nervous system (CNS) activation to emotional arousal, and others have related emotional arousal to cardiovascular reactivity (see below), actual brain–heart interconnections remain poorly understood (Armour and Ardell, 1994). Indeed, despite that CNS activation may partially mediate associations between emotion and cardiovascular reactivity, it is unusual for each of these parameters to be examined in conjunction in a single investigation. Yet, such studies are critical first steps in the identification of brain–heart linkages during emotional activation that may ultimately prove to have relevance to the development of cardiovascular disease or the elicitation of acute coronary events. The primary goal of the present study was, therefore, to examine whether laboratory tasks designed to elicit happiness or anger, both of which are emotions that may play a role in eliciting cardiac arrhythmias or sudden cardiac death (Kamarck and Jennings, 1991), evoke concomitant increases in regional cerebral (particularly frontal lobe) and cardiovascular activation in healthy young adults. Evaluating the feasibility of such an investigation in a healthy sample was also deemed an important initial step prior to studying a more pertinent, yet biologically vulnerable, patient population that is prone to cardiac arrhythmias and sudden cardiac death (such as patients with implantable defibrillators). Rationale pertinent to this study's hypotheses regarding patterns of cerebral and cardiovascular responses during positive (happiness) and negative (anger) emotion derives from several different bodies of literature that, to date, have been largely unintegrated (Lane and Schwartz, 1987). These investigations generally use fairly distinct paradigms and methodologies and include studies of emotions and CNS activation; emotions and cardiovascular reactivity; and CNS activation and cardiovascular reactivity. The relation between acute emotional arousal and CNS activation has been examined using electroencephalography (EEG), and results of numerous studies indicate that positive and negative emotions are associated with different patterns of cortical activation. Most studies have demonstrated that left frontal lobe activation is associated with the expression and experience of positive emotions and approach behaviors, whereas activation of the right frontal lobe relates to the experience and expression of negative emotions and withdrawal behaviors (Davidson, 1992, Jones and Fox, 1992, Davidson, 1993, Davidson, 1995 and Hagemann et al., 1998). Happiness and anger were selected for the present investigation as target emotions that were representative of positive and negative valence, respectively, and that were high on the arousal dimension of emotion (Russell, 1997). In addition, as noted above, both emotions may be pertinent to the elicitation of cardiac arrhythmias (Kamarck and Jennings, 1991). In studies of emotion and autonomic responses, it is less clear whether positive and negative emotions produce similar or different patterns of cardiovascular activation. Several investigations have noted differential blood pressure, heart rate (HR), and peripheral vascular resistance responses to positive emotions such as joy or happiness and negative emotions such as anger, fear, and sadness (Schwartz et al., 1981, Ekman et al., 1983 and Sinha et al., 1992). However, other studies have shown similar cardiovascular responses during positive and negative emotion (Cacioppo et al., 1993 and Warner and Strowman, 1994). Although few investigations have directly examined relations between CNS measures and cardiovascular reactivity during emotional activation, several available theoretical models can be used to derive hypotheses regarding such associations. For example, Wittling (1990) has suggested that the right cerebral hemisphere is dominant for the elicitation of autonomic responses. In this regard, some research has shown that damage to the right hemisphere is more likely to result in autonomic dysregulation as compared with left hemisphere damage (Hachinski et al., 1992, Gainotti et al., 1993 and Andersson and Finsett, 1998). However, other investigators have noted that sympathetic outflow can be elicited by activation of multiple cortical and subcortical regions of the brain (Lane and Jennings, 1995). Within cortical regions, activation of the frontal lobes is thought to be particularly important in eliciting sympathetic outflow, cardiovascular reactivity, myocardial instability, and cardiac arrhythmias (Skinner and Reed, 1981, Lane and Schwartz, 1987 and Lane and Jennings, 1995). Lane and Schwartz (1987) suggest that individuals who display the greatest lateralized frontal lobe activity during either positive or negative emotional arousal will experience lateralized sympathetic input to the heart via select stimulation of the stellate ganglion either contralateral or ipsilateral to the activated cerebral hemisphere (Lane and Schwartz, 1987 and Lane and Jennings, 1995). Such an imbalance in sympathetic (particularly left) cardiac input has been shown, in animal models, to be arrhythmogenic (Schwartz, 1984). More directly pertinent to the present investigation, however, distinct patterns of cardiac activation may also result from asymmetric stimulation of the stellate ganglion due to differences in the topographical distribution of the right and left stellate cardiac nerves (Lane and Schwartz, 1987). In this regard, stimulation of the left stellate ganglion has been shown to increase cardiac inotropic activity as reflected in increased myocardial contractility, systolic and mean arterial blood pressure, in addition to increased AV conduction and prolongation of the QT interval; in contrast, stimulation of the right stellate ganglion tends to increase cardiac chronotropic activity as reflected in an increased HR (Lane and Schwartz, 1987 and Wittling, 1995). Although the biological underpinnings of Lane and Schwartz's model are not tested directly in the present investigation, the model suggests specific hypotheses regarding associations between asymmetric cerebral activation and cardiovascular response patterns. Accordingly, the present study examined the hypothesis that the negative emotion of anger asymmetrically activates the right frontal lobe and is associated with increased blood pressure reactivity. Conversely, asymmetric activation of the left frontal lobe during the positive emotion of happiness was expected to be associated with increased HR responses. The potential moderating influence of gender was also examined in exploratory analyses given previously identified gender differences in emotional expression (Brody and Hall, 1993) and cardiovascular reactivity (Stoney et al., 1987).

The present data indicate that cerebral response patterns to emotionally challenging situations may play a role in the magnitude (and patterning) of cardiovascular reactivity. Future research should determine whether such central-autonomic linkages during emotional activation could play a role in eliciting myocardial instability or cardiac arrhythmias in vulnerable populations.