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• Seasonal variation in mortality from myocardial infarction and haemopericardium: a postmortem study
  Richard M Jones
  Published on: 18 April 2016

• Published on: 18 April 2016

  Seasonal variation in mortality from myocardial infarction and haemopericardium: a postmortem study

  • Richard M Jones, Specialist Registrar Forensic Pathology

  Dear Editor,

  I read with interest the recent article by Biedrzycki and Baithun[1] investigating the relationship between myocardial infarction complicated by haemopericardium, and season. The study utilised data collected during Coronial postmortem examinations, carried out over a 5-year period in East London. They concluded that there was indeed a ‘seasonal variation’ for this entity, and that the likelihood of ven...

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  Dear Editor,

  I read with interest the recent article by Biedrzycki and Baithun[1] investigating the relationship between myocardial infarction complicated by haemopericardium, and season. The study utilised data collected during Coronial postmortem examinations, carried out over a 5-year period in East London. They concluded that there was indeed a ‘seasonal variation’ for this entity, and that the likelihood of ventricular rupture after a myocardial infarction is greater in ‘winter’ than ‘summer’.

  It is well established that cardiac events, including arrhythmias, myocardial infarction and sudden cardiac death are multifactorial, and involve complex inter-relationships between anatomical or structural elements, factors such as age and sex, and more transient risks including the time of day, and emotional stress, for example.[2,3]

  The underlying mechanism proposed by the authors to explain their findings is that of ‘an increase in sympathetic tone’ in cold weather. It is unfortunate then that the authors made no attempt to correlate their findings with local meteorological data.

  Months of the year are conveniently grouped into 2 ‘seasons’ - ‘winter’ and ‘summer’. Thus their peak occurrence of haemopericardium in March falls within their ‘winter’ category. An analysis of data based on a more conventional division of the year into 4 seasons may have been more meaningful.

  Despite commenting on the possibility that the study population may not be representative of other areas ‘within London’, there is no analysis of ethnicity. An opportunity has therefore been missed to examine the relationship between ethnicity, fatal myocardial infarction and the development of haemopericardium.

  Other factors that would have been of interest in a Coronial population from an area such as East London (and in particular the London Borough of Tower Hamlets) include indicators of deprivation, which could provide additional information about the underlying risks for fatal cardiac events.

  The development of a haemopericardium as a complication of myocardial infarction reflects the complex interplay between various risk factors, and as such demands a rigorous multivariate analysis for potentially confounding factors. A follow up study by the authors addressing these issues will be eagerly awaited.

  References

  1. Biedrzycki O, Baithun S. Seasonal variation in mortality from myocardial infarction and haemopericardium. A postmortem study. J Clin Pathol. 2006; 59:64-66.

  2. Zipes DP, Wellens HJJ. Sudden cardiac death. Circulation. 1998; 98:2334-2351.

  3. Willich SN, Maclure M, Mittleman M et al. Sudden cardiac death – support for a role of triggering in causation. Circulation. 1993; 87(5): 1442-1450.

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  Conflict of Interest:
  None declared.

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