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Abstract: TH-PO460

Serum Magnesium Levels and Subsequent Risk of Peripheral Artery Disease

Session Information

Category: Hypertension and CVD

  • 1401 Hypertension and CVD: Epidemiology, Risk Factors, and Prevention

Authors

  • Menez, Steven, Johns Hopkins Medicine, Baltimore, Maryland, United States
  • Ding, Ning, Johns Hopkins University, Baltimore, Maryland, United States
  • Grams, Morgan, Johns Hopkins University, Baltimore, Maryland, United States
  • Lutsey, Pamela L., University of Minnesota, Minneapolis, Minnesota, United States
  • Selvin, Elizabeth, Johns Hopkins University, Baltimore, Maryland, United States
  • Coresh, Josef, Welch Center for Prevention, Epidemiology & Clinical Research, Baltimore, Maryland, United States
  • Jaar, Bernard G., Johns Hopkins University and Nephrology Center of Maryland, Baltimore, Maryland, United States
  • Matsushita, Kunihiro, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States
Background

Hypomagnesemia has been associated with increased risk of several cardiovascular phenotypes presumably through its interaction with calcium and phosphate, but its relation to peripheral artery disease (PAD) is not well established. Magnesium (Mg) homeostasis is tightly regulated by the kidney, and thus the relationship between Mg and PAD may be weaker in CKD.

Methods

Using data from the Atherosclerosis Risk in Communities (ARIC) Study, we investigated the association of serum Mg with incident PAD in 14,293 participants free of prevalent PAD at baseline (mean age 54.6 years [SD 5.7], 26.2% black, 1.2% with GFR<60 mL/min/1.73m2, 9.5% with DM). We used multivariable Cox models to quantify the association of Mg (< vs. ≥ the median value of 1.6 mEq/L) with incident PAD accounting for potential confounders. We further evaluated these associations, stratified by GFR above and below 60 mL/min/1.73m2.

Results

Over a median follow-up time of 25.9 years, a total of 620 cases of incident PAD were observed. In fully adjusted models, the association between higher Mg and PAD was significant (HR=0.80, 95% CI: 0.67 – 0.95) (Table). Modeled continuously, the risk of PAD decreased significantly with every 0.1 mEq/L increase in Mg (HR 0.49, 95% CI: 0.30 – 0.82). In stratified analysis, this association persisted for participants with GFR above 60 mL/min/1.73m2 but not for those with GFR<60. The interaction between Mg and GFR for PAD risk was significant (p=0.01). Among other electrolytes, higher calcium trended towards lower risk of PAD (HR=0.86, 95% CI: 0.72 – 1.01).

Conclusion

Higher serum Mg is independently associated with a lower hazard of incident PAD, though this association was not seen in individuals with reduced GFR. Our results suggest potential contribution of low serum Mg levels in the development of PAD independent of other calcium-phosphate metabolism.

Multivariable Cox Proportional Hazards Models for Incident PAD
 OVERALL (N=14,293)GFR<60 (N=167)GFR≥60 (N=14,126)
VariableHRPHRPHRP
Serum Mg0.80 (0.67, 0.95)0.011.48 (0.65, 3.39)0.350.79 (0.66, 0.94)0.01
Serum Ca0.86 (0.72, 1.01)0.070.84 (0.33, 2.19)0.730.90 (0.75, 1.07)0.23
Serum P1.09 (0.92, 1.29)0.320.74 (0.29, 1.88)0.531.09 (0.91, 1.29)0.36

Adjusted for age, sex, race, education, smoking status, drinking status, HTN, DM, prevalent coronary heart disease, total cholesterol, HDL cholesterol, serum electrolytes (potassium, calcium, phosphate), and eGFR.

Funding

  • Other NIH Support