Generalised anxiety disorder (GAD) is associated with a near doubling of the risk of adverse outcomes following myocardial infarction (MI), a Dutch naturalised cohort study has found.

A total of 438 patients were recruited following an MI. At three months follow-up, ICD-10 GAD and ICD-10 depressive episode were identified using a standardised diagnostic interview (Composite International Diagnostic Interview). Participants were then followed up over an average of 5.7 years. An adverse outcome was defined as death from any cause or readmission with a cardiovascular event.

After adjustment for age and gender, the hazard ratio for adverse events was 1.94 for those with GAD (95% CI: 1.14-3.30). Additional adjustment for depression and severity of cardiac disease did not affect the results.

The wide confidence interval reflects the small number of patients with GAD. As a result, it was only possible to adjust for a limited number of potential confounders. For example, the increased risk associated with GAD may have been partly due to the fact that GAD is commonly associated with chronic physical health problems (14% of diabetes patients have GAD)1.

A number of psychobiological mechanisms could explain the increased risk, including autonomic imbalance, inflammatory processes, platelet activation and lifestyle factors. However, a prospective cohort study of 1,017 outpatients with stable coronary heart disease (CHD) found that, whereas the association between depression and cardiovascular events could be largely explained by physical inactivity, the association between GAD and cardiovascular events was unexplained.2

If both anxiety and depression independently increase the risk of adverse outcomes in CHD patients, it is illogical to screen for depression alone.

I would suggest that we use the two question screen for GAD, see below:3

• During the past four weeks, have you been bothered by feeling worried, tense or anxious most of the time?

• Are you frequently tense, irritable and having trouble sleeping?

This should be followed either by a HADS or a GAD-7 questionnaire. These are screening, not diagnostic, tools: to make a diagnosis of GAD, the symptoms must have been present for at least six months and should not be experienced only during the course of a depressive illness.

However, screening can only be justified if there is an effective intervention. As far as I am aware, there have been no trials to assess whether treatment of GAD improves CHD outcomes. Nor is there any evidence that recognition and treatment of depression after MI results in improved outcomes: the ENRICHD trial found that CBT improved depression but did not increase event-free survival;4 the SADHART trial was not designed to assess the effects of treatment on cardiovascular prognosis;5 and the MIND-IT trial found that antidepressant treatment had no effect on either long-term depression or cardiac prognosis.6

Dr Phillip Bland