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CARDIOLOGY CASEBOOK |
During a junior varsity hockey game, a 15-year-old player was roughly handled and benched by his coach. An irate father watching the game from the stands ran down the stairs and in deep rage and anger struck out at the coach. The player’s father immediately fell over in what appeared to be a faint. He was moved to the sidelines and the coach and a parent of one of the team members, who was a nurse, initiated cardiopulmonary resuscitation. Advanced life support service personnel arrived approximately 7 minutes later and found the patient unresponsive to cardiopulmonary resuscitation. An autopsy performed the following morning revealed coronary atherosclerosis with an occlusive thrombus in the paroxysmal left anterior oblique coronary artery. The family advised that there were no previous cardiac symptoms or history.
QUESTIONS
ANSWERS
1. b. anger
Coronary artery disease (CAD) is the primary cause of morbidity and mortality in people over 50. Fifteen percent of deaths due to CAD occur before age 65. Several modifiable (lifestyle habits, comorbid disease) and nonmodifiable (sex, age, genetics) risk factors are known to predispose an individual to CAD and acute coronary events. These and other classic CV risk factors account for only 50% of the acute CV events. A number of studies have documented the precipitation of ischemia due to coronary artery vasospasm resulting from mental stress in patients with CAD. Emotional or psychological stress, specifically anger or hostility, are significant and independent risk factors in ischemic heart disease and can precipitate an acute myocardial infarction (MI) or lethal arrhythmias.
2. a. anger
b. hostility
Sir William Osler, a noted physician early in the last century, described the typical patient with CAD as one who "works at maximum capacity, is incessantly striving for success in commercial, professional or political life."1 In the past 40 years, extrapolations from epidemiologic studies have supported Osler’s observation. The type A personality behavior pattern was originally applied to those with enhanced aggression, ambition, competitive drive, impatience, or hostility. These were considered personality traits and highly significant CV risk factors, independent of the other classic CV risks. Men with type A personalities have greater increases in plasma epinephrine, norepinephrine, and cortisol levels during performance of mathematic testing for monetary incentive.2
Anger has been referred to as an emotional state that ranges in intensity from mild irritation or annoyance to rage and fury, usually in response to perceived mistreatment or provocation.3 In all of the "sad (depression), glad (manic), or mad (anger mix) cardiacs" the components of anger and hostility are the predictive triggers for acute CV events.1,2 Although most CV risk factors become prevalent at older ages, anger has been shown to play a greater role in the younger population. Anger has the most significant impact on mortality in men with preexisting CAD.3
3. a. True
The risk of MI associated with emotional stress, and specifically anger, is almost half of that attributed to heavy exertion. The feature that distinguishes anger from strenuous activity in precipitating an acute coronary event is that anger can persist for up to 2 hours, whereas heavy exertion is transient and the effects usually last less than 1 hour. Although it is unclear why the CV effects of anger persist, it has been suggested that ruminating over the event that precipitated the anger sustains the mood.4 Personalities that chronically demonstrate "toxic" type A behaviors, such as anger, hostility, or cynicism, may also predispose to recurring bouts of intense anger.
4. e. all of the above
Although the exact mechanisms are unclear, anger can evoke potentially life-threatening conditions in patients with CAD, via distinctive physiological pathways. Emotional stress has been reported preceding MI in about 20% of all cases of MI.4 Anger increases catecholamine discharge, causes elevation of blood pressure and heart rate (increasing myocardial oxygen consumption), potentiates vasospasm, and increases platelet aggregability. Anger increases hemodynamic stress, which may disrupt a vulnerable plaque, triggering hemostasis and vasoconstriction, resulting in occlusive ischemic sequelae (MI, SCD). In the presence of vulnerable arterial plaques, acute coronary events can be triggered by angina.5
Procoagulant states, hyperaggregability, and increased platelet count and reactivity have been found in chronically angry people.4,6 Since ischemia due to emotional stress occurs at lower heart rates and lower blood pressures than ischemia induced by exercise, it is possible that ischemia caused by emotional stress results from both an increase in oxygen demands and a decrease in myocardial blood supply.
5. c. stimulation of the hypothalamus
Various emotional behaviors have been elicited by stimulating specific locations in the hypothalamus. The hypothalamus has been commonly referred to as "the head ganglion of the nervous system."4 The sympathetic activity that follows hypothalamic stimulation has been shown to induce ventricular tachyarrhythmias, which have a tenfold greater incidence of ventricular fibrillation then those that follow coronary artery occlusion.
The role of anger in promoting malignant arrhythmias has not been clarified. Both the central and peripheral nervous systems have been implicated in anger-induced cardiac vulnerability. Activation of the sympathetic nervous system has been extensively implicated in the genesis of malignant arrhythmias. Stimulation of both central and peripheral adrenergic structures, infusion of catecholamines, and behavioral stress can heighten vulnerability in normal myocardium and to a greater degree in ischemic myocardium.
6. a. a narrowed coronary artery
Anger causes vasoconstriction in pathologically narrowed arterial segments but has no effect on vasomotion in normal coronary arteries.3,4 Coronary arteries with intact normal endothelium are resistant to catecholamine-induced constriction and have vasodilatory response following emotional arousal, whereas arteries with impaired endothelium are more reactive.7 In echocardiographic and radionuclide studies, recall of intense anger produced alterations in myocardial perfusion and function related to coronary vasoconstriction and a reduction in left ventricular ejection fraction. In single-vessel CAD, anger-induced myocardial ischemia resulted in a greater reduction in left ventricular ejection fraction than did exercise-induced ischemia.
7. a. True
The emotions of anger and fear are commonly generated during dreaming. The intensity of anger and the subsequent autonomic discharge during dreaming can be as great or greater than anger experienced while awake. Acute MI and SCD have often been linked to dream-stage states of anger. Nearly 36 000 cases of SCD occur during the nocturnal period.
8. a. reducing the risk of arrhythmias
b. reducing platelet aggregation and thrombus formation
c. reducing the hemodynamic response to stress
Regular daily use of aspirin was shown to reduce the risk of CV events by 50% when compared with patients who did not use aspirin routinely. The protective effects of aspirin in CAD are due to the reduction in platelet aggregation and thrombus formation.3 ß-adrenergic blockade helps reduce the hemodynamic response to stress, which can lead to plaque disruption and to a decrease in cardiac work; as a result, oxygen demand is reduced and the thresholds for arrhythmogenesis and for triggering lethal arrhythmias are raised.
Summary
A high level of anger has a powerful effect on the incidence of preventable cardiovascular death. Persuasive clinical evidence indicates that anger evokes physiological responses that are potentially life-threatening in the setting of CAD.
Finally, emotional stress, anger, or worry have a dominant influence on the severity, frequency, and treatment of angina. The natural history of angina is characterized by episodic variations in the frequency and severity of symptoms coincident with periods of emotional stress. When angina is associated with periods of emotional stress or anger, the angina is not usually a result of progressive coronary disease, but rather is due to an increase in oxygen demand. Appreciation of this concept will help to rule out "true" unstable angina due to progressive coronary disease from recurrent angina that results from an increase in oxygen demand related to emotional stress. The former requires aggressive medical or surgical therapy; the latter, a demand-induced angina, responds to ß-adrenergic blockade and a tranquilizer.8
ACKNOWLEDGMENT
Supported in part from a grant from the Applebaum Foundation in loving memory of Joseph Applebaum.
Reprint requests: Louis Lemberg, MD, University of Miami School of Medicine, Division of Cardiology (D-39), P O Box 016960, Miami, Fla 33101.
Shekelle RB, Gale M, Ostfeld AM, Oglesby P. Hostility, risk of coronary heart disease, and mortality. Psychosom Med. 1983;45:109–114.
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