Anybody would be distressed and frightened during a heart attack, but that fear, usually fear of death, is associated with biological changes, including worsening inflammation, which in itself raises the risk of death, London researchers reported in the European Heart Journal. The biological changes linked to fear and distress undermine the patient’s outcome during the weeks that follow the heart attack.

ACS (acute coronary syndrome) occurs when there is blockage of the coronary arteries, caused either by a heart attack (myocardial infarction) or unstable angina. Symptoms may include shortness of breath, sweating, chest pain, nausea and vomiting. Patients have a significant risk of subsequent heart problems and poor quality of life.

In this study, the scientists wanted to determine whether an intense emotional response – extreme fear and distress – was associated with systemic inflammation, this can be gauged by measuring levels of tumor necrosis factor alpha (TNF alpha), types of cell signaling molecules. They also wanted to know whether the fear and distress and TNF Alpha correlated with worse biological function three weeks later (and worse prognosis)?

The study involved 208 individuals who had been diagnosed with ACS between June 2007 and October 2008 – they had all been admitted to St. George’s Hospital, London. Their levels of TNF alpha were measured and levels of distress and fear of dying were assessed 2-3 days after being hospitalized. Three to four weeks after hospitalization the researchers visited them at home and recorded their HRV (heart rate variability) and levels of cortisol, a stress hormone. Low HRV is a predictor of future cardiac problems, while low cortisol levels can result in poor inflammation control.

Professor Andrew Steptoe, Head of the Department of Epidemiology and Public Health and British Heart Foundation Professor of Psychology at University College London (UK), explained:

“We found that, first of all, fear of dying is quite common among patients suffering a heart attack; it was experienced by one in five patients. Although survival rates have improved tremendously over the last few decades, many patients remain quite frightened during the experience.

Secondly, fear of dying is not just an emotional response, but is linked into the biological changes that go on during acute cardiac events. Large inflammatory responses are known to be damaging to the heart, and to increase the risk of longer-term cardiac problems such as having another heart attack. We found that, when compared with a low fear of dying, intense fear was associated with a four-fold increased risk of showing large inflammatory responses, measured by raised levels of TNF alpha. Interestingly, this was independent of demographic and clinical factors such as the severity of the cardiac event.

Thirdly, fear of dying and inflammatory responses in turn predicted biological changes in the weeks following an acute cardiac event, namely reduced heart rate variability and alterations in the output of the hormone cortisol. These processes may contribute to poor outcomes in the longer term.”

Distress levels were unrelated to previous heart attack experiences, the researchers wrote. However, their findings suggested that heightened distress might be triggered by worse and more painful ACS symptoms, and then made even worse if patients are on their own and of low income.

The authors said they are not sure what processes underlie the link between intense emotional responses and elevated TNG alpha levels.

They wrote:

“However, they may be connected as manifestations of an integrated biological and emotional response to severe injury to the heart.”

Prof Steptoe said:

“This is an observational study, so we do not know whether helping people overcome their fears would improve the clinical outlook, or whether reducing the levels of acute inflammation would have beneficial emotional effects, but these are possibilities. At the immediate clinical level, we would recommend that doctors talk to patients more about their emotional experience when having a heart attack, rather than just concentrating on the physical outcomes. The two are closely linked, and better information and reassurance could be of great benefit.

Care for patients with acute heart disease has improved greatly over recent decades, but we are still concerned about people who recover in the short-term, but remain at risk for repeat heart attacks or other cardiovascular problems. This research is an illustration of how closely emotional, behavioural and biological responses are integrated. Patients’ emotional responses are relevant to how they react biologically, and vice versa.”

Susanne Pedersen, Professor of Cardiac Psychology at the University of Tilburg, The Netherlands, and team say Prof Steptoe’s findings are “seminal” (decisive, determining).

They wrote:

“(They) point towards an avenue worthwhile pursuing for the fields of translational cardiovascular medicine and behavioral cardiology.

(conclusion) In order to optimize the management and care of CHD [coronary heart disease] patients, we need to acknowledge that emotions carry independent additional risk, with particular subsets of patients dying prematurely due to their psychological vulnerability. Physiological mechanisms may provide part of the answer to the vicious cycle linking emotions to incident CHD and its progression.

Behavioral mechanisms should not be forgotten, as there is an urgent need for more effective lifestyle management in these patients, due to increases in the prevalence of obesity and diabetes, and no change in the proportion of patients who smoke, despite an increase in the prescription of cardioprotective drugs. The issue of inadequate lifestyle management is unlikely to be resolved without attending to the emotions of our patients, as emotions such as depression play a pivotal role in compliance and adherence. This suggests that the ‘one size fits all approach’ to intervention in CHD patients is unlikely to work and that a personalized medicine approach is warranted.”

“Fear of dying and inflammation following acute coronary syndrome”
Andrew Steptoe1, Gerard J. Molloy, Nadine Messerli-Bürgy, Anna Wikman, Gemma Randall, Linda Perkins-Porras and Juan Carlos Kaski
Eur Heart J (2011) doi: 10.1093/eurheartj/ehr132

Written by Christian Nordqvist