Otros procesos para fabricación de noyos endurecidos en frio Generalidades

The expected features o f this model are: - a. short duration o f effect.

b. strong associations between distress and measures o f underlying disease.

c. reduction o f distress effect when the distress: CHD association is adjusted for, or stratified by, underlying disease.

The confounding on which this model relies may occur either as result o f psychological distress arising in response to physical symptoms or due to measurement issues. Since somatic symptoms are a feature of depression and anxiety, the psychological instrument used may actually detect physical illness. Aetiological studies in depression have attempted to eliminate these issues by excluding those with baseline disease, not analysing events in the first period o f follow-up, or by removing somatic symptoms from depression

scales^’. The associations between depressive symptoms and CHD persist despite these exclusions, which argues against confounding. Similarly, the long-term effects reported in several studies are difficult to reconcile with the confounded model. The effect o f phobic anxiety on fatal CHD might be accounted for by such confounding, with symptoms o f CHD leading to anxiety, but the fact that the effect persisted for 10 years is not supportive.

There are, however, other indications that some element o f confounding remains in the aetiological studies. Several authors have found that it is only an increase in depressive symptoms that is associated with future CHD^^’ Similarly, Ariyo reported stronger associations between mean depression scores over six years of follow-up than for baseline depression scores^^. One obvious explanation for these findings is that depressive symptoms may be a response to subclinical or early disease rather than an aetiological factor, which is consistent with the third model.

Vital exhaustion, although distinct from depression, may be an example o f the third model. Appels argues that this state o f fatigue and mood changes may be a response to the final stage o f chronic stress, with an increase in inflammatory processes^^’ Appels has shown that amongst angioplasty patients, the exhausted/depressed had higher levels o f inflammatory markers^^ and Kop has shown a similar pattern of associations in healthy men^^. They have also shown that the effect o f YE persists for only two years and that it is the fatigue symptoms, rather than depressive symptoms, that are the most important predictors of subsequent CHD events^"^’ Recent opinion about the genesis o f depressive symptoms suggest that dysregulation o f the inflammatory system, resulting in an imbalance in brain cytokines, may cause depressive s y m p t o m s I t could be argued that the increase in inflammatory processes involved in YE leads to progression in an existing atherosclerotic plaque (second acceleration model), but equally an increase in inflammation due to the progression of a plaque prior to an acute CHD event could lead to the symptoms o f YE, such as depression and fatigue (third confounded model). The direction o f causality is a matter o f debate^"^^.

There are other explanations for the findings relating to the duration o f depressive symptoms. Newly depressed mood may operate via different physiological pathways from

predict cancer’ and Barefoot proposed that the depressive symptoms in his study were best considered as chronic characteristics due to the long-lasting effect^^. It could be that new depressed mood acts later in the pathogenesis o f CHD, whereas chronic mood, related to personality and showing a longer-term effect, is an atherogenic risk factor. The two studies where only new depressive symptoms predicted CHD both had a relatively short follow-up time of five years or less, perhaps insufficient to detect an atherogenic effect of chronic symptoms. These potential interactions between the duration o f distress and the extent o f underlying disease have not been examined in the literature.

The effect o f persistence o f anxiety symptoms has not been examined explicitly, although some studies study both state and trait anxiety in the STAI, with no clear pattern o f more positive findings with one or the other.

The issue of confounding between distress symptoms and the severity o f disease is very important for the prognostic studies, where reported effects could be easily explained if a more severe disease status was correlated with depressive symptoms. Most studies controlled for severity o f disease, although in some cases this was crude. Measures used include left ventricular ejection fraction, Killip class and Peel index. Most studies have shown an association between anxiety or depressive symptoms and disease severity, and hence the effect sizes were reduced by adjustment. The possibility o f residual confounding is a concern, since objective measures are unlikely to quantify disease status completely’

but it is unlikely that the strong and consistent effects reported are all due to residual confounding. If self-reported symptoms are used to assess disease severity rather than objective measures, this may lead to over-adjustment^^. Lesperance et al reported that baseline BDI scores were more important prognostically than scores one year after MI, and that, for those with higher initial scores, subsequent improvement made no difference to outcome. He suggests that BDI is measuring a stable facet o f personality’^^.

In summarv. the literature offers some support for the third model, but it is not possible to explain all the reported associations by this mechanism. The inflammatory effect o f an incipient acute CHD event, producing fatigue and depressive symptoms, may account for the syndrome o f vital exhaustion. A similar process may explain the findings related to new depressive symptoms, but there are other possible explanations, such as alternative

pathways operating with transient symptoms accelerating underlying disease. The persistence o f symptoms may be a useful tool to differentiate the effects o f personality or more chronic distress from transient distress, and to explore their respective pathways of action.

II.2.6 Evidence for personality factors or other external psychosocial factors