CENTER ON BEHAVIORAL MEDICINE
Psychoneuroendocrine: Related Papers
graciously given by the author to reproduce this paper
The Impact of Emotions on Cardiopathy
Mark R. Zuccolo
Since antiquity, the link between heart and emotions, and indeed the placing of the heart as the center of all feelings by poets and artists and above all by popular culture, has been well established. "It breaks my heart" is only one of the common phrases that indicate a broad acceptance of the relationship between emotions and the heart. The scientific understanding of this relationship dates from the first half of the nineteenth century, with the publication of a text by William that speculated on the neurological etiology of heart palpitations (Rhodri, 2005). By the end of the 1800's cardiac disturbances came to be viewed as having a neurasthenic component. In 1910, Osler asserted that patients suffering from angina pectoris often appeared to be sad and that these patients were individuals "whose heart always worked at maximum rhythm" (quoted in Januzzi, Stern, & Pasternak, 2000, p. 1914). Current research has shown that various psychosocial factors contribute to the development of cardiovascular diseases (Frasure-Smith & Lesperance, 2005), that there is a close association between personality and cardiovascular disease, and that the relationship between psychosocial factors and personality is synergic and linear, that is, the closer these factors are associated and the more they are important in determining the onset and course of cardiovascular disease (Graves & Miller, 2003). Psychosocial factors include emotions such as depression, anxiety, hostility, and anger and external stress-provoking factors such as job loss, relationship problems, low socioeconomic level, low level of social support and caregiver stress.
Emotions precede or follow endogenous or exogenous events that trigger the activation of a response mediated by subjective perception, behavior, and physiological variations. Somatic alterations vary based on personality, perception of the stimulus that may be mitigated or enhanced by previous experiences, automatic reactions of the central nervous system and endocrine secretions. The emotions that appear to be more significant in cardiopathy are anger, fear, and hostility. Tugade and Frederickson (2002) have illustrated that in patients with prevailing optimism there is a more rapid recovery of baseline cardiac frequency after a stress stimulus. Other researchers (Beck & Servatius, 2003; Firdaus, 2002; Larson, 2002) have shown a greater production of cytokine in patients with positive affect. Steptoe & Wardle (2004) conducted a study on 116 men and 100 women in London of ages between 45 and 59 years without evidence of prior hypertension or coronary disease. Their data show a correlation among arterial blood pressure, concentration of cortisol in saliva, degree of optimism on a five-level scale, stress levels and blood fibrinogen. The levels of cortisol appear to be inversely proportional to the degree of optimism; cardiac frequency also appears inversely correlated to optimism, but such association is significant only in male subjects; the production of fibrinogen after acute stress is smaller for the subjects with greater degree of optimism. This study offers evidence of the remarkable impact of stress on the body. Cortisol is a hormone related to the onset of diabetes, hypertension, and autoimmune pathologies; its concentration is elevated in patients affected by depression, and it contributes to the increase of cardiovascular risk. Fibrinogen is also a factor in cardiovascular risk, inasmuch as it increases the blood viscosity and it stimulates the proliferation of lipoproteins and platelet aggregation.
Chronic stress alters an individual’s vitality and flexibility causing fatigue, inability to adapt, and rapid exhaustion of coping resources (Robles, Glaser, & Kiecolt-Glaser, 2005). Job-related stress, stress in one’s primary relationship, insufficient rest, sleep disturbances, and low socioeconomic status can contribute to pessimism, sadness, anxiety, and depression. These events are mediated by the excessive and chronic stimulation of the sympathetic nervous system and the hypothalamic-pituitary axis with consequent increase in the levels of cortisol and norepinephrine in the blood stream and an increase of cardiac frequency at rest. These events influence cardiac functioning in numerous ways: they activate endothelial dysfunction (Miller, Freedland, Carney, Stetler, & Banks, 2003), they cause a chronic inflammatory state, as evidenced by the increase of protein C and interleukin (Ladwig, Marten-Mittag, Deisenhofer, Hofmann, Schapperer, Weyerbrock, Erazo, & Schmitt, 2002). These markers of inflammation are found to be more elevated in patients suffering from depression, who also exhibit greater progression of cerebral atherosclerosis, in terms of intimal arterial thickening and carotidal plaque (Friedman & Rosenman, 1959).
In outlining the effects of
on the body it is also necessary to consider the personality profile of
the individual. Early studies by Friedman and Rosenman (1959) provided
evidence that type A personality, characterized by aggressiveness,
sense of urgency, hyperactivity, and hostility, showed an increase in
risk of cardiovascular diseases by a factor of two and a greater
of cerebral atherosclerosis. Successive studies have uncovered another
personality type, type D or distressed, characterized by a negative
of social situations and a tendency to inhibit the expression of
(Denollet, Sys, & Brutsaert, 1995; Stevens, Turner, Rhodewalt,
Talbot, 1984). Two Dutch psychologists, Pedersen and Denollet (2004),
provided further evidence of the connection between type D personality
and disease. Their study of 319 patients with coronary disease who were
followed for five years has shown that type D personality increases the
risk of cardiopathy (infarct of the myocardium) and that this risk
4 times in the presence of depression. Blomhoff and colleagues (2004)
evidence that depression causes negative effects on folic acid and
concentrations; that cute stress determines the transitory increase of
arterial blood pressure; and that such modifications can persist for
after the acute event and explain the increased risk of cardiopathy.
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