The present study found that the frequency of ventricular ectopy 12 weeks following MI was associated with daily stress levels and state anxiety, such that patients reporting more stress or greater state anxiety experienced more ectopic beats. Trait anxiety, however, was not associated with VPBs. Our findings also demonstrated a temporal relationship between stress and VPBs such that diary-reported stress significantly predicted VPBs in the subsequent hour period. This finding extends previous evidence from prospective studies that have shown that psychological factors such as negative affect, distress, and low social support are associated with ventricular arrhythmias (6
). Moreover, our observations are unique in that they are based upon the assessment of both stress and ventricular ectopy during a typical 24-hour period following MI. Previous studies investigating psychological stress in acute post-MI patients have reported positive associations with VPBs but have either done so in the laboratory setting (2
) or prospectively using personality measures administered during hospitalization (12
Prior research has shown that the frequency of VPBs may be prognostic of subsequent sudden cardiac death (SCD) among post-MI patients (12
) although this relationship is thought to be mediated by LV dysfunction (10
). Previous investigations have also found that ischemia may cause increased rates of arrhythmias through disturbances in ion concentrations, accumulation of arrhythmogenic metabolites, or metabolic changes which disrupt conduction at the cellular level (22
). The current findings suggest that stress also predicts ventricular ectopy and that these effects remain significant after adjusting for the effects of LVEF and extent of CAD. Our findings differ from those reported in previous studies among CHF patients (8
), which demonstrated that the association between psychological stress and ventricular arrhythmias is dependent on cardiac function assessed by LVEF. However, the exclusion criteria for the current study, which precluded patients with LVEF < 30% from participating, prevented an investigation into the mediating role of low LVEF in this sample. This finding that CAD severity may be more strongly associated with VPBs than LVEF is consistent with previous research showing that the relatively higher risk of mortality associated with LV dysfunction may be mediated by CAD severity (23
Approximately 40% of the CHD population experiences repetitive VPBs (1
) and more complex ventricular arrhythmias that constitute repetitive VPBs may only be observable upon more extensive holter monitoring (24
). Patients exhibiting complex ventricular arrhythmias are significantly more likely to have higher frequencies of VPBs and patients with increased frequency of VPBs are more likely to experience complex ventricular arrhythmias, such as ventricular tachycardia (VT) (24
). Furthermore, CHD patients with more complex ventricular ectopy tend to show greater overall levels of VPBs and are at higher risk for mortality, especially in the presence of MI (25
). We found that individuals experiencing repetitive VPBs also experience greater levels of psychological stress, but that state and trait anxiety were not elevated in this subset of patients.
Our finding that state anxiety and stress were associated with total VPBs while trait anxiety was not, conflicts with previous studies demonstrating an association between trait psychological factors and VPBs (11
). It is possible that previous studies showing that trait-level psychological factors were associated with an increased incidence of arrhythmias may have been influenced by state-dependent factors associated with peri-hospitalization events (26
). Previous studies have utilized relatively brief assessment periods (11
) or have relied on group comparison with medical controls (26
). Moreover, the measurement of trait-level psychological constructs such as perceived social support (27
), distress (11
), and depression may have been confounded by state-dependent factors (19
). Experimental studies manipulating state-dependent psychological factors have demonstrated an association between induced states of emotional arousal and increased levels of VPBs (2
), indicating that changes in arousal, not trait levels, may be associated with increased levels of VPBs.
The relationship between stress and anxiety is complex and poorly defined. Because of the inherent difficulty in differentiating between these interrelated constructs, previous metanalyses investigating the relationship between psychological stress and CHD have separated this term into related subcomponents such as phobic anxiety, depression, and hostility (30
). Anxiety has conventionally been construed as a more chronic, anticipatory state of arousal (31
), whereas stress is characterized by an acute psychological reaction to an emotional stimulus (32
). Trait-level anxiety reflects individual differences in the tendency to respond with state anxiety in the anticipation of threatening situations (15
). Although both emotions are characterized by a heightened state of emotional arousal in the face an aversive stimulus, a cognitive appraisal of threat is characteristic of anxiety (32
), whereas stress is characterized by an acute response that is less influenced by cognition (33
). Anxiety and stress may be interrelated in that one might experience anxiety as a symptom following a stressful event, as a cognition in responding to a stressful event, or as an accompanying emotion (34
). More recent definitions of stress have noted that stress can be cognitively mediated, so that the perception of a stressor is influenced by individual differences in appraisal (35
). At a general level, stress may be thought of as a reactive state, whereas anxiety may be thought of as an anticipatory state.
The present findings should be viewed with several limitations in mind. First, our analysis of the relationship between psychosocial factors and VPBs evaluated this relationship over a 24-hour period. Because ECG recordings continued during the night, nocturnal arrhythmias were included in our calculation of VPBs, although diary-reported stress was evaluated only during waking hours. There is some evidence to suggest that the frequency of arrhythmias is significantly lower during sleep compared with waking states among CHD patients (1
) but these findings are inconsistent (36
). In the current sample, the exclusion of nocturnal ectopy did not alter our findings. Additionally, patients who reported stress during their assessment were less likely to be taking beta-blockers as compared to patients who did not report stress (p = .04). A post hoc analysis, however, demonstrated that the relationship between stress and VPBs was not significantly altered after controlling for beta-blocker usage.
The present study may have important implications for the clinical management of post-MI patients. Previous studies of cardiac patients have shown that self-reported levels of anger precipitate implantable cardio-defibrillator (ICD) discharge (20
), but the temporal association between VPB rates and mood has yet to be investigated. Although no patients in the current sample reported palpitations, the possibility of somatic symptoms eliciting stressful diary responses cannot be discounted. Previous studies have reported that male post-MI patients admitted to being aware of irregularities of their heartbeat during holter monitoring when questioned, although their responses were not readily reported (37
). Further research is needed evaluate the relationship between psychosocial factors and ventricular ectopy among ambulatory post-MI patients.
In summary, the present findings suggest that the experience of psychological stressors during daily life may be associated with increased ventricular ectopy in patients with CHD. Although levels of anxiety experienced at the beginning of 24-hour monitoring were also predictive of ventricular ectopy, trait anxiety was not associated with increased amounts of ectopy. These findings underscore the importance of psychological stress during daily life as a risk factor for ventricular ectopy in CHD patients.