1. In searching for biological evidence that essential hypertension is caused by chronic mental stress, a disputed proposition, parallels are noted with panic disorder, which provides an explicit clinical model of recurring stress responses. 2. There is clinical comorbidity; panic disorder prevalence is increased threefold in essential hypertension. Plasma cortisol is elevated in both. 3. In panic disorder and essential hypertension, but not in health, single sympathetic nerve fibres commonly fire repeatedly within an individual cardiac cycle; this appears to be a signature of stress exposure. For both conditions, adrenaline cotransmission is present in sympathetic nerves. 4. Tissue nerve growth factor is increased in both (nerve growth factor is a stress reactant). There is induction of the adrenaline synthesizing enzyme, phenylethanolamine-N-methyltransferase, in sympathetic nerves, an explicit indicator of mental stress exposure. 5. The question of whether chronic mental stress causes high blood pressure, still hotly debated, has been reviewed by an Australian Government body, the Specialist Medical Review Council. Despite the challenging medicolegal implications, the Council determined that stress is one proven cause of hypertension, this ruling being published in the 27 March 2002 Australian Government Gazette. This judgement was reached after consideration of the epidemiological evidence, but in particular after review of the specific elements of the neural pathophysiology of essential hypertension, described above.

Introduction: Patients who are anxious or depressed after an acute cardiac event are at increased risk of a subsequent event and premature death. It is therefore important to identify these patients early in order to initiate supportive or even preventive measures. In the present study, we report on the prevalence of anxiety and depression during the first 12 months after an acute cardiac event, and the patient characteristics predictive of increased anxiety and depression risk in early and late convalescence. Methods: We recruited a sample of 911 patients with acute myocardial infarction (AMI), acute coronary syndrome (ACS), and/or unstable angina (UA), and/or undergoing coronary artery bypass graft surgery (CABGS). Patients completed the Hospital Anxiety and Depression Scale (HADS) close to the time of their event, and again during early (2-4 months post-event) and late (6-12 months post-event) convalescence. Using HADS-A and HADS-D cutoffs of 8+, prevalence rates for anxiety, depression, and comorbid anxiety and depression were determined for each timepoint. Chi-square tests and odds ratios were used to identify baseline patient characteristics associated with increased anxiety and depression risk over 12 months. Results: Anxiety rates were 43, 28, and 27% at the time of the event, early, and late convalescence. Depression rates were 22, 17, and 15%, respectively. Factors consistently associated with increased anxiety and depression risk were history of depression, financial strain, poor self-rated health, low socioeconomic status, younger age (<55 years), and smoking. Obesity, diabetes, and social isolation (living alone or being unpartnered) were identified as important albeit less significant risk factors. Neither sex nor event type were predictive of anxiety or depression. Conclusion: This large patient sample provided the opportunity to identify rates of anxiety and depression during the 12 months after a cardiac event and key patient characteristics for increased risk. These risk factors are easily identifiable at the time of the event, and could be used to guide the targeting of support programs for patients at risk.

Defective neuronal reuptake of noradrenaline, by augmenting the sympathetic neural signal in the heart, might have a dual effect, sensitizing the heart such as to lead to symptom development (and thus perhaps causing panic disorder) and, second, potentially contributing to adverse cardiac events in established PD.