The Impact of Emotions on Cardiovascular Health
Acute, subacute and chronic stress, when it
constitutes an excessive response to external stimulation and in
connection with psychosocial and behavioral factors, can provoke
cardiovascular symptoms of more or less significant magnitude that may
contribute to the onset of cardiopathy or worsen the prognosis of
concomitant pathologies. Stress is the way in which the organism signals
an alteration that, by interacting with the immune system, can have
serious consequence on the cardiovascular apparatus, and thus lead to
life-threatening disease.
 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.
Which emotions have a pathological effect? And, in
which subjects are they most likely to be manifested? 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 between arterial 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 9 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 emotional states 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,
chronic sense of urgency, hyperactivity, and hostility, showed an
increase in the risk of cardiovascular diseases by a factor of two and a
greater incidence of cerebral atherosclerosis (Stevens, Turner,
Rhodewalt, & Talbot, 1984). Successive studies have uncovered another
personality type, type D or distressed, characterized by a negative
experiencing of social situations and a tendency to inhibit the
expression of emotions (Denollet, Sys, & Brutsaert, 1995). Two Dutch
psychologists, Pedersen and Denollet (2004), have 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 increases 4
times in the presence of depression. Blomhoff and colleagues (2004)
offer evidence that while depression causes negative effects on folic
acid and LDL-cholesterol concentrations. Acute stress determines the
transitory increase of arterial blood pressure; fibrinogen and other
coagulants and such modifications can persist for weeks after the acute
event and explain the increased risk of cardiopathy.
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