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The impact of natural disasters on myocardial infarction
  1. Andrew Steptoe (a.steptoe{at}ucl.ac.uk)
  1. University College London, United Kingdom

    Abstract

    There is substantial evidence that emotional stress can trigger acute cardiac events in vulnerable individuals.1 2 Most research on emotional triggers has involved retrospective interviews with survivors of acute myocardial infarction, asking them about the circumstances surrounding the onset of their illness, but in addition the impact of natural or human disasters has been studied. Investigations of major events such as earthquakes have the advantages that a population-based sampling methodology can be used, that the timing of stimuli can be defined objectively instead of relying on self-report, and that the incidence of cardiac events can be contrasted with levels during nontraumatic comparison periods. The first set of thorough analyses was conducted in the wake of the Northridge earthquake that took place in January 1994 in the Los Angeles area. There was an abrupt increase in sudden cardiac deaths immediately after the earthquake,3 together with a rise in coronary heart disease mortality that were not observed for other cardiovascular diseases or non-cardiac causes.4 Deaths typically occurred among people with advanced coronary atherosclerosis. Acute physiological responses such as autonomic dysfunction and inflammatory, neuroendocrine and platelet activation, coupled with disruption of vulnerable plaque, may be responsible for the onset of acute infarction in these circumstances.5 One study of survivors of acute myocardial infarction measured the physiological responses to a standardised mental stress test in patients whose cardiac event had apparently been triggered by emotional stress, in comparison with those who reported no stress before their infarction.6 The emotional trigger group showed more prolonged blood pressure responses to standardised stress, together with heightened blood platelet activation, suggesting that they had a particular proclivity to respond with physiological responses that might contribute to cardiac vulnerability.

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