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4.3. Cardiovascular Pathogenesis
~ a psychoneuroendocrinological understanding
To the Heart of the Matter
Research into CV pathogenesis in PNE, has concluded that CV illness is intimately associated with
psychological disturbances, especially depression, anxiety and psychosocial pressures. (Purcell &
Mulcahy 1994); (Hemingway and Marmot 1999); (Kiecolt-Glaser et al. 2002). The passive stress
response, which is characteristic of depression, (Nielsen 1989), is characterised by high HPA, and
subsequently high CRF activity. Previously, in section 4.1.1.2., it was discussed how CRF
influenced the activity of the LC by reducing sympathetic vasomotor activity, reducing
parasympathetic vagal stimulation of the SA and AV nodes of the heart, and via the TS, inhibiting
parasympathetic feedback from the circulatory baro- and chemoreceptors (see appendix VI: fig. 4.).
In addition, there is reason to suppose that there is an astable reinforcing ‘feed-forward’ mechanism
between the LC and the AN in response to stressors, which could be a potential source of
HPA/ANS dysregulation. The CV pathological consequences of these activities are multi-factorial
(see appendicies; VI: fig. 4. & VIII: fig. 6.), but there is a commonality in disease aetiology,
characterised by disturbances/dysregulation of the mechanisms that mediate CV regulatory activity.
The implicated pathological processes have been identified by; Musselman et al. (1996);
Musselman et al. (1998); Carney et al. (1995); Carney et al. (1988); Fuster et al. (1992) and Sloan
et al. (1999). These authors discuss the following aspects in CV pathological mechanisms:
Blood pressure & Heart rate -variability
Ventricular instability
Platelet reactivity
Glucocorticoid induced pathology:
- Increased circulatory cholesterol
- Increased circulatory triglycerides
The data suggests that these factors can result in degenerative processes, which can ultimately cause
CV illness, and that the mediating factors in the development of these degenerative processes are
intimately related to disturbances in the HPA and ANS activity.
Heart rate variability (HRV) is a normal physiological compensatory process that regulates changes
in CV hydrostatic dynamics (see appendix IX: table 4.). Reduced HRV is one of the mechanisms by
which disturbances of ANS activity can contribute to a CV pathological scenario. The implication
of decreased HRV in CV illness has been confirmed by; Krittayaphong et al. (1997) and Thornton
& Hallas (1999). Clinical studies have showed that decreased HRV is an indicator of mortality in
post MI patients (Krittayaphong et al. 1997). Furthermore, depressed patients with CV disease have
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