Review
Emotional triggering of cardiac events

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Abstract

Psychological factors may contribute not only to the evolution of coronary atherosclerosis and long-term risk of coronary heart disease, but also to the triggering of acute cardiac events in patients with advanced atherosclerosis. Evidence for emotional triggering of cardiac events derives both from population-based studies of hospital admissions and sudden deaths following major traumas such as earthquakes and terrorist incidents, and from individually based interview studies with survivors of acute coronary syndromes (ACS). The latter indicate that acute anger, stress and depression or sadness may trigger ACS within a few hours in vulnerable individuals. The psychobiological processes underlying emotional triggering may include stress-induced haemodynamic responses, autonomic dysfunction and parasympathetic withdrawal, neuroendocrine activation, inflammatory responses involving cytokines and chemokines, and prothrombotic responses, notably platelet activation. These factors in turn promote coronary plaque disruption, myocardial ischaemia, cardiac dysrhythmia and thrombus formation. The implications of these findings for patient care and ACS prevention are outlined.

Introduction

Cardiovascular disease is one of the main causes of serious illness, and a major cause of death and reduced quality of life. The costs of cardiovascular disease, including healthcare costs, the price of unpaid care and loss of earnings, were estimated at €169 billion in 2003 (Leal et al., 2006). Coronary heart disease (CHD) is the largest single cause of death in Europe, accounting for 21% of male and 22% of female deaths (Allender et al., 2008). It is also the leading cause of death in people aged less than 75 years (20% male and 19% female deaths). However, death rates have been declining for the past three decades in many countries, due primarily to improvements in risk factor profile, and also to increased survival following acute coronary events. This means that the prevalence of diagnosed CHD in the population has been rising. Recent figures from the USA indicate that 6.5% of the population have a history of heart attack (myocardial infarction) or angina pectoris (Anon., 2007).

There is an extensive literature relating psychosocial factors with the development of CHD (Everson-Rose and Lewis, 2005, Kuper et al., 2005). The condition underlying CHD is coronary atherosclerosis, a progressive process of arterial wall thickening due to lipid deposition, inflammation and smooth muscle infiltration (Hansson, 2005). The psychosocial factors implicated in both atherosclerosis and CHD include low socioeconomic status (SES), chronic stress exposure, particularly in the work place, and aspects of the social environment such as social isolation and low social support. In addition, emotional factors including depression, anxiety, anger and hostility are thought to contribute to the development of CHD (Suls and Bunde, 2005, Steptoe, 2006). This research has been primarily concerned with long-term aetiology, and with demonstrating that exposure to psychosocial risk factors promotes accelerated atherosclerosis and higher rates of CHD incidence. There is, however, another way in which emotional factors might contribute to cardiovascular disease, and this is through the stimulation of acute cardiac events such as myocardial infarction (MI), unstable angina, or sudden cardiac death. Such cardiac events typically occur in people with advance coronary atherosclerosis. The emotional factors involved in these situations are not necessarily the same as those implicated in long-term aetiology, since they act over a much shorter time scale. The purpose of this review is to summarize the evidence for emotional triggering of cardiac events, and to outline the psychophysiological processes that stimulate the pathological responses underlying acute coronary syndromes (ACS, comprising myocardial infarction and unstable angina) or sudden cardiac death.

Section snippets

Acute cardiac events

It used to be thought that acute MI occurred as the end product of a passive process of lipid accumulation in the coronary artery wall, when the vessel walls became so thick that the artery was completely blocked. However, it is now recognized that atherosclerosis is an active inflammatory disease in which the accumulation of oxidized lipoprotein, macrophageous foam cells and smooth muscle cell proliferation leads to the development of fibrous plaque (Steptoe and Brydon, 2007). The key

Methods of studying emotional triggers

It is difficult to study emotional triggering of cardiac events prospectively, since the occurrence of acute MI or sudden cardiac death cannot be anticipated in advance. Studies of emotional triggering are therefore typically retrospective, and involve two broad strategies. The first is to study the impact of emotionally stressful events such as natural disasters, terrorist attacks, industrial disasters and sporting events on admissions for ACS or the occurrence of sudden cardiac death. The

Earthquakes

Earthquakes are devastating and very stressful experiences, and their effects on acute cardiac events have been studied in several countries (Bhattacharyya and Steptoe, 2007). Unfortunately, results have not been completely consistent. The most thorough analyses were carried out in the aftermath of the Northridge Earthquake that took place in the Los Angeles area in January 1994. A postal survey of more than 100 hospitals showed that admissions for acute MI increased from 149 in the week before

Individual emotional triggers

The first large scale project to evaluate emotional triggers in individuals was the Multicenter Investigation of Limitation of Infarct Size (MILIS) study, which involved 849 patients interviewed within 18 h of acute MI. 18% reported emotional upset in the period immediately before symptom onset (Tofler et al., 1990). In the Triggers and Mechanisms of Myocardial Infarction (TRIMM) study, 35% of patients reported either emotional upset or stress within the hours before acute MI (Willich et al.,

Psychobiological processes underlying acute triggering

Psychological stress elicits a range of physiological responses that are potentially relevant to the triggering of ACS. Some of these responses occur both in healthy individuals and in patients with advanced coronary atherosclerosis, while others are present only in people with diseased coronary vessels. Fig. 2 outlines five categories of physiological response to acute stress, and the possible effects that these might have in people with advanced coronary artery disease.

First is the widely

Psychophysiological studies of triggering

Fig. 2 summarizes the processes that potentially underlie emotional triggering of cardiac events, but direct evidence is difficult to obtain. Since ACS are unpredictable, there have been few studies that have been able to measure physiological responses at the time of cardiac events. However, in one study, an earthquake happened to occur as 15 patients with suspected coronary artery disease were undergoing Holter monitoring (Lin et al., 2001). Spectral analysis of R–R intervals showed a marked

Clinical implications

There are important clinical implications to understanding the role of emotional stimuli as triggers of ACS that have been considered comprehensively by Tofler and Muller (2006). They have argued that clinical strategies for reducing risk of triggering should complement the management of long-term risk factors. Vulnerability to emotional triggering may place certain types of patient at high risk when they are exposed to interpersonal situations that elicit strong negative emotions. If such

Conclusions

Studies involving a range of different methodologies provide convergent evidence supporting the role of emotional stimuli in the acute triggering of ACS. Emotional triggering appears to be more common in people of lower SES. The pathophysiological processes underlying emotional triggering remained to be fully elucidated, but include processes that may promote plaque rupture, together with a prothrombotic vascular environment that encourages thrombus formation, and neuroendocrine and autonomic

Acknowledgements

The research described in this article was supported by the British Heart Foundation, and the Medical Research Council.

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