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Evaluating the causal relevance of diverse risk markers: horizontal systematic review

Hannah Kuper1, Amanda Nicholson, Mika Kivimaki

  • 1Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, London WC1E 7HT. hannah.kuper@lshtm.ac.uk

BMJ (Clinical Research Ed.)
|November 7, 2009
PubMed

Insights

This study developed a new method to compare evidence on coronary heart disease risk factors like depression and diabetes. It found inconsistencies between evidence and current guidelines, highlighting areas for future research.

Area of Science:

  • Cardiovascular Disease Epidemiology
  • Systematic Review Methodology
  • Evidence-Based Medicine

Background:

  • Coronary heart disease (CHD) risk assessment relies on diverse markers.
  • Current guidelines may not fully reflect the strength of evidence for all risk markers.
  • A systematic approach is needed to compare evidence quality across different risk factors.

Purpose of the Study:

  • To develop a novel methodology for systematically comparing evidence across various coronary heart disease risk markers.
  • To evaluate the evidence for depression, exercise, C-reactive protein, and type 2 diabetes as CHD risk factors.
  • To compare the synthesized evidence with existing clinical guideline recommendations.

Main Methods:

  • A "horizontal" systematic review was conducted, integrating evidence from observational studies, genetic association studies, and randomized controlled trials.
  • Data were extracted from Medline and guideline searches for four risk markers: depression, exercise, C-reactive protein, and type 2 diabetes.
  • Meta-analyses of observational and genetic studies, alongside available randomized controlled trials, were analyzed.

Main Results:

  • Observational studies indicated significant CHD risk associations for depression (RR 1.9), C-reactive protein (RR 1.6), and type 2 diabetes (RR 2.0-3.0). Exercise showed a potential protective effect (RR 0.7).
  • Mendelian randomization did not support a causal effect for C-reactive protein; such analyses were lacking for depression, exercise, and diabetes.
  • Randomized controlled trials were unavailable for most risk markers concerning CHD incidence, though some benefit was seen for glucose control in diabetic patients. Trials for depression treatment did not reduce further CHD events.

Conclusions:

  • The horizontal systematic review identified strengths and weaknesses in the evidence base for depression, exercise, C-reactive protein, and type 2 diabetes as causes of CHD.
  • The developed methodology can inform the creation of field synopses.
  • This approach can prioritize future guideline development and research efforts in cardiovascular disease risk assessment.
Abstract

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