Folk wisdom has it that both acute and chronic “stress” leads to heart disease.
Scientifically, however, “stress” is difficult to define and measure. Nevertheless, the study of “stress” is being increasingly refined and new data strongly supports the view that it does indeed cause heart disease.
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“Stress” and heart disease
The word “stress” is placed in quotes since until now the concept has not been clearly defined. It is used loosely for all sorts of different situations and in different contexts.
Does the word “stress”, for example, refer to the precipitating event or to the reaction of the target individual or group – or to both? Does the mood, personality or circumstances of the individual play a role and, if so, in what way? Do different stressors have different effects? Can they be measured? And so on.
Three general factors are included in the concept of stress:
that there needs to be a stressor which will vary for different individuals to some extent
that many factors relating to the person (the stressee, so to speak) will determine the nature and intensity of the response
that there are objective physiological and subjective mood effects on the person
Evidence has accumulated on the increased risk associated with the following factors:
Stressors: These include chronic life events: death in the family, divorce, job loss or job strain and many others. If prolonged and severe enough these result in what is called “vital exhaustion” or “burn-out”.
Follow-up of such people shows an increased incidence of coronary artery disease (CAD). Other stressors may be more acute and precipitate an acute coronary or cerebral event (stroke) well before any effects on the underlying atherosclerosis could occur.
Host factors: These are multiple and include chronic mood characteristics (depression or anxiety), personality traits (levels of anger, hostility, impatience, perfectionism and so forth) and such factors as social isolation, low socio-economic status and education. All of these in clinical studies are associated with an increased likelihood of CAD.
Physiological and mood changes: Some of these have been mentioned such as depression and anxiety. Both these moods may be innate and present with little if any marked environmental stress or they may be precipitated by a recognisable stressor.
In addition, there is often an increased heart rate, diminished ability to regulate heart rate in response to demand, increased blood pressure response, increased levels of circulating hormones such as cortisol and adrenalin and changes in cellular and platelet reactivity.
Dysfunctional behaviour patterns, including smoking, lack of exercise, poor eating habits, alcohol abuse and non-compliance with treatment, are also common in predisposed individuals. The precise pattern seen depends on the nature and severity of the stressor and host factors.
The important point to bear in mind is that the ill effects of stress, or stressors, are very much dependent on the reaction of the affected person. The sequence, stressor – susceptible target – poor clinical outcome, can be broken by the deliberate intervention of the person, perhaps with counselling or other forms of treatment.
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