CARDIOVASCULAR JOURNAL OF AFRICA • Vol 21, No 4, July/August 2010
AFRICA
183
Editorial
The cost of coping: a cardio-neuro-metabolic risk for
black South Africans?
Psychosocial stress is a contributing factor to cardiovascular
disease.
1
An important way of investigating the mechanisms
underlying this association is acute psycho-physiological stress
testing, involving measurement of physiological responses to
laboratory-induced stress. Psycho-physiological stress testing
allows individual differences in responses to standardised stress
to be evaluated and related to psychosocial and cardiovascular
risk factors. Accumulating evidence has demonstrated asso-
ciations of disturbed psycho-physiological responses with sub-
clinical measures of atherosclerosis, hypertension and metabolic
risk.
2-11
The complex pattern of responding to stress is influenced
by individual differences, such as coping style, race and ethnic-
ity, genetic make-up, background stress, and lifestyle habits,
which should be taken into account when interpreting results.
For example, a unique interplay between cardiac and vascular
responses in urban black Africans
2
is thought to contribute
towards a heightened risk of hypertension in this group. Whether
or not psycho-physiological risk markers provide prognostic
information over and above that of established risk markers is not
clear but adapting to or appraisal of an urban environment could
add to heightened responses.
There are, however, marked ethnic differences in cardio-
vascular responses or reactivity (CVR) that may in part be
explained by psychosocial factors. Black Africans
7,8
and African-
Americans
4
normally and when exposed to stressful situations
exhibit exaggerated CVR and a higher risk for the development
of hypertension
1
in comparison to Caucasians. In three separate
regions, including rural and urban black South Africans, results
demonstrated increased vascular responses on exposure to the
handgrip and cold pressor tests in urban participants compared
to their rural counterparts. It is suggested that in urban Africans
the physiological adaptation process is inclined to shift towards
increased vascular responses and prevalence of hypertension. We
might speculate that the individual who experiences emotional–
social–cultural disruption in an urban environment is in a contin-
uous state of hyper-vigilant coping and vascular sympathetic
hyperactivity/overdrive through exaggerated CVR.
Mental and chronic psychosocial stress triggers sympathetic
nervous system (SNS) hyperactivity and has been shown to
be associated with increased vascular responsiveness, pressure
overload, hypertension and myocardial ischaemic risk.
5,7
Also,
increased vascular and plasma renin responses seen in black
African men further increase sympathetic activity through periph-
eral vascular hyper-responsiveness and higher blood pressure.
6,7,9
This change to a high vascular resistance pattern accompanying
hypertension predisposes to the development of left ventricular
hypertrophy. In fact, studies show that African-Americans have
greater left ventricular wall thickness than Caucasians, suggest-
ing that increased peripheral vascular resistance may be due to
structural changes in the vasculature. However, it is not certain
whether this is also true for black Africans.
The concept of coping style or strategies implies that humans
have a differential capacity to adapt to the same environmental
conditions. When attended to and appraised in certain ways, a
coordinated set of responses involving behavioural and physi-
ological systems is triggered.
3
Mainly, two different apprais-
als or stress coping responses may be distinguished: firstly,
defensive problem-solving active coping (high AC), seeking
social support and being-in-control responses, which elicit
fight-or-flight
b
-adrenergic central cardiac responses. Secondly,
avoidance coping (low AC) and loss-of-control responses which
elicit defeat
α
-adrenergic vascular responses and are associated
with pathology.
3
If a coping strategy fails, stress pathology may
develop because of an over-arousal of the sympathetic nervous
system, thereby increasing the risk for related cardiovascular
diseases (CVD).
4
It is difficult to fully elucidate if an enhanced stress response
is dependent on the appraisal of the stressor, and if mental stress
evokes the same stress response pattern in groups of differ-
ent ethnicity. What is however evident from animal studies is
that stress and re-exposure illicit different mono-aminergic
(nor-adrenaline, dopamine and serotonin) responses in corti-
cal and sub-cortical (e.g. hippocampus) brain regions, result-
ing in behavioural changes, and which have their origin in
altered functioning of the hypothalamic–pituitary–adrenal stress
axis. Appraisal or detection of stressful stimuli at conscious
and subconscious levels involves the thalamus, sensory and
prefrontal cortex. Reciprocal connections exist with several
sub-cortical pathways, determining autonomic and emotional
responses through the hypothalamus and amygdala.
5
Defensive
high active coping responses are generated in a reward centre,
i.e. the paraventricular nuclei of the hypothalamus, secreting
vasopressin, involving sub-cortical pathways via central cardiac
b
-adrenergic response patterns.
5
Animal studies indicate that while acute stress significantly
elevates nor-adrenalin levels, especially in the hippocampus, a
significant attenuation is experienced following re-experience.
Interestingly, this does not occur in the frontal cortex, suggest-
ing that subsequent behavioural changes following re-stress are
driven by adrenergic-mediated changes in the hippocampus,
such as deficits in cognition. The latter will compromise stress
coping and stress responsiveness and in this way ultimately
compromise central and peripheral cardiovascular response
mechanisms. Hence a sensitisation of defensive pathways may
occur, with
α
-adrenergic vascular pathways gaining influence.
Consequently, the risk for established essential hypertension in
high-demand situations may increase.
5
