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Anger and Heart Disease
The concept of anger as a risk factor for cardiovascular disease originated from the idea that certain behavior patterns were found more commonly among cardiac patients. At the end of the 19th century, Sir William Osler (1892), considered the father of modern medicine, noticed certain characteristics of patients with heart disease:
In the worry and strain of modern life, arterial degeneration is not only very common but develops at a relatively early age. For this, I believe that the high pressure at which men live, and the habit of working the machine to its maximum capacity are responsible [for coronary disease].
In the mid-20th century, the Type A “coronaryprone behavior” was defined by Friedman and Rosenman (1959/1974). Typical characteristics of the Type A behavior included competitiveness, excessive drive or achievement-striving, enhanced sense of time urgency, enhanced aggressiveness, ambitiousness, intense concentration and alertness, and high levels of “free-floating hostility.” In 1978, this stereotype later became known as the Framingham Type A behavior. Additional descriptors for this type included pressed for time, preoccupied with work, stretched by work, uncertain/dissatisfied about your performance, eating too quickly, strong need to excel, upset when waiting, hard-driving and competitive, bossy or dominating.
However, there were conflicting studies for and against the “Type A hypothesis” as a true risk factor for heart disease. With further investigation, the anger-hostility complex was identified as the “toxic element.” According to the Structured Interview personality test, people with this complex had the potential for hostility, anger directed outward, competitiveness, anger experience, vigorous answers, irritation at waiting in lines, and explosive voice modulations. A special hostility scale was developed by Cook and Medley in 1954 as part of the Minnesota Multiphasic Personality Inventory, and included traits such as cynicism, angry feelings, and aggressive responding to provocation. Investigations over the past couple decades have focused on anger-hostility as the potentially important risk factor for heart disease.
Epidemiological Evidence
Commonly recognized components of anger include anger-out (expression, nonneurotic hostility), anger-in (suppression, neurotic hostility), and anger experience. Although studies have shown mixed results, anger-in, or the suppression of anger, competes with anger-out, or the full-blown expression of anger, as the main predictor for coronary artery disease risk. The Cook-Medley Hostility (Ho) Scale has been the most frequently used quantitative measure for anger and hostility, and high Ho scores have been related to cardiovascular disease in many studies. Other frequently used measurement tools for anger and hostility include the Spielberger Multidimensional Anger Inventory, the Framingham Anger Scale, Hostility scales of the Buss-Durkee Inventory, and subscales of various other personality tests.
Cross-sectional studies have shown that episodes of anger may “trigger” heart attacks. In the ONSET study, the risk of myocardial infarction was found to be elevated only during the first 2 hours after an outburst of anger. Several studies have demonstrated an ill effect of mental stress or anger on cardiovascular physiologic responses, such as increased blood pressure and heart rates, lower heart function, and coronary vasoconstriction.
Many prospective cohort studies have shown that anger or hostility leads to an increased risk of developing subsequent cardiovascular disease, particularly coronary heart disease, hypertension, and stroke. This relationship has been seen in the Framingham Heart Study, the Western Collaborative Group Study, Normative Aging Study, Finnish men, Danish men and women, the Caerphilly Study, the Atherosclerosis Risk in Communities (ARIC) Study, the Johns Hopkins Precursors Study, and various student populations. This risk may be conferred in a doseresponse manner. A recent report suggested that anger experienced in younger populations may increase risk for premature heart disease.
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