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Plasma adiponectin levels and risk of myocardial infarction in men

  • 0Department of Nutrition, Harvard School of Public Health, Channing Laboratory, Boston, Mass 02115, USA. tpischon@hsph.harvard.edu
Jama +

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April 15, 2004

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April 15, 2004

View abstract on PubMed

Summary

This summary is machine-generated.

Higher adiponectin (a peptide hormone) levels in men are linked to a significantly lower risk of myocardial infarction (MI). This association remains strong even after accounting for various health factors and risk indicators.

Area Of Science

  • Cardiovascular Disease Research
  • Endocrinology
  • Metabolic Syndrome Studies

Background

  • Adiponectin, an adipocyte-derived peptide, plays a role in insulin sensitivity and lipid metabolism.
  • Emerging evidence suggests adiponectin's involvement in atherosclerosis and coronary heart disease (CHD) pathogenesis.

Purpose Of The Study

  • To prospectively investigate the association between plasma adiponectin concentrations and the risk of myocardial infarction (MI).

Main Methods

  • A nested case-control study was conducted using 18,225 male participants from the Health Professionals Follow-up Study (1993-1995).
  • Participants were aged 40-75 and free of cardiovascular disease at baseline.
  • Over 6 years, 266 men developed nonfatal MI or fatal CHD; controls were matched for age, blood draw date, and smoking status.

Main Results

  • Men in the highest quintile of adiponectin levels had a significantly reduced risk of MI (RR, 0.39; 95% CI, 0.23-0.64).
  • This inverse relationship persisted after adjusting for traditional cardiovascular risk factors, including BMI, physical activity, and diabetes history.
  • The association was only modestly attenuated by adjustment for lipid levels, remaining independent of inflammation and glycemic control.

Conclusions

  • Elevated plasma adiponectin concentrations are associated with a lower risk of myocardial infarction in men.
  • The protective effect of adiponectin is partly mediated by lipid profiles but is largely independent of inflammatory markers and glycemic status.

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