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• Systemic inflammation and fatal versus non-fatal coronary events
  Carr J. Smith
  Published on: 16 June 2011
• Systemic inflammation sometimes displays paradoxical outcomes
  Carr J Smith
  Published on: 16 June 2011

• Published on: 16 June 2011

  Systemic inflammation and fatal versus non-fatal coronary events

  • Carr J. Smith, medical researcher

  In a group of middle-aged, hypercholesterolic men with no prior history of diabetes or CVD, Logue et al. (2011) recently report that obesity is associated with fatal coronary heart disease (CHD), but not non -fatal CHD independently of traditional CVD risk factors. The authors hypothesize that since excessive adipose tissue is known to secrete inflammatory mediators, that increased systemic inflammation might be making t...

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  In a group of middle-aged, hypercholesterolic men with no prior history of diabetes or CVD, Logue et al. (2011) recently report that obesity is associated with fatal coronary heart disease (CHD), but not non -fatal CHD independently of traditional CVD risk factors. The authors hypothesize that since excessive adipose tissue is known to secrete inflammatory mediators, that increased systemic inflammation might be making these obese subjects more prone to adverse coronary events. Although logical, there may be a potential confounder in the study as the authors note that "There were lower proportions of current smokers and higher proportions of ex-smokers in higher than lower BMI categories." Current smoking to a much greater extent than past smoking is associated with systemic inflammation and a pro-coagulative state (CJ Smith and TH Fischer, Atherosclerosis 2001, 158: 257-267.) Although smokers form thrombus more easily than nonsmokers, smokers survive their first heart attack better than nonsmokers [Jaatun et al. (2004) Am J Cardiology; Mueller et al. (1992)Circulation]. This is presumably because the smoker presents with MI at an earlier stage of CVD. If obese subjects were experiencing MI due to systemic inflammation, they too might be expected to display an advantage in surviving, rather than dying from the first MI.

  Sincerely, Carr J. Smith, Ph.D. Visiting Scholar, UNC Chapel Hill Dept. of Pathology

  Conflict of Interest:

  None declared

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  Conflict of Interest:
  None declared.

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• Published on: 16 June 2011

  Systemic inflammation sometimes displays paradoxical outcomes

  • Carr J Smith, experimental pathologist

  To the editor: The very interesting study by Logue et al. (2011) on a group of middle- aged, hypercholesterolic men with no prior history of diabetes or CVD, recently reported that obesity is associated with fatal coronary heart disease (CHD), but not non -fatal CHD independently of traditional CVD risk factors. The authors hypothesize that since excessive adipose tissue is known to secrete inflammatory mediators, that in...

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  To the editor: The very interesting study by Logue et al. (2011) on a group of middle- aged, hypercholesterolic men with no prior history of diabetes or CVD, recently reported that obesity is associated with fatal coronary heart disease (CHD), but not non -fatal CHD independently of traditional CVD risk factors. The authors hypothesize that since excessive adipose tissue is known to secrete inflammatory mediators, that increased systemic inflammation might be making these obese subjects more prone to fatal adverse coronary events. Although mechanistically very plausible, there may be a potential confounder in the study as the authors noted that, "There were lower proportions of current smokers and higher proportions of ex-smokers in higher than lower BMI categories." Whether reduced smoking in the heaviest members of the studied cohort suggests that this group quit smoking at a higher rate due to cardiac or other health-related symptoms is not reported. Current smoking to a much greater extent than past smoking is associated with systemic inflammation and a pro- coagulative state (1). Although smokers form occlusive thrombus more readily than nonsmokers, smokers paradoxically survive their first heart attack better than nonsmokers (2). This is presumably because the smoker presents with MI at an earlier stage of CVD and thereby represents a "less sick" patient (3). If obese subjects were experiencing MI due to systemic inflammation-induced hypercoagulability, they too might be expected to present with MI at an earlier stage of CVD and display an advantage in surviving, rather than dying from the first MI. Additional clinical and pathological factors might be interacting with increased systemic inflammation in increasing the risk of fatal CVD events in these obese subjects.

  Correspondence: Carr J. Smith, Ph.D., Visiting Scholar, UNC Chapel Hill Dept. of Pathology, 1012 Bartlett Circle, Hillsborough NC 27278, carrjsmith@yahoo.com.

  1. Smith CJ, Fischer TH. Particulate and vapor phase constituents of cigarette mainstream smoke and risk of myocardial infarction. Atherosclerosis 2001; 158: 257 2. Jaatun HJ, Sutradhar SC, Dickstein K. Comparison of mortality rates after acute myocardial infarction in smokers versus non-smokers. Am J Cardiol 2004; 94: 632-636. 3. Mueller HS, Cohen LS, Braunwald E et al. Predictors of early morbidity and mortality after thrombolytic therapy of acute myocardial infarction. Analyses of patient subgroups in the Thrombolysis in Mycardial Infarction (TIMI) trial, phase II. Circulation 1992; 85: 1254-1264.

  Conflict of Interest:

  None declared

  Conflict of Interest:

  None declared

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  Conflict of Interest:
  None declared.

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