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Circulation. 2007;116:II_801

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(Circulation. 2007;116:II_801.)
© 2007 American Heart Association, Inc.


Epidemiology: Inflammation and Inflammatory Markers

Abstract 3538: The Relationship Between Inflammation, Obesity, and Risk for Hypertension in the Multi-Ethnic Study of Atherosclerosis (MESA)

Susan G Lakoski1; Mary Cushman2; David Siscovick3; Roger S Blumenthal4; Gregory Burke5; Walter Palmas6; David Herrington7

1 Wake Forest Univ Sch of Medicine, Winston Salem, NC
2 Univ of Vermont, Burlington, VT
3 Univ of Washington, Seattle, WA
4 Johns Hopkins Univ, Baltimore, MD
5 Wake Forest Univ Sch of Medicine, Winston Salem, NC
6 Columbia Univ, New York, NY
7 Wake Forest Univ Sch of Medicine, Winston Salem, NC

It has been suggested that inflammation is important in the etiology of hypertension and that this may be most relevant among obese persons. To study this, we examined the relationship between inflammation markers, obesity, and risk for hypertension in the Multi-Ethnic Study of Atherosclerosis (MESA).

Methods: Hypertension, defined as a blood pressure ≥140/90 mmHg or a history of hypertension and use of blood pressure medications, was determined at baseline and two subsequent exams over 5 years. Among 3543 non-hypertensives at baseline, 714 individuals developed incident hypertension by Exam 3. Serum C-reactive protein (CRP) and interleukin-6 (IL-6) concentrations were measured at Exam 1 and were analyzed as categorical variables in relation to incident hypertension. After excluding those on hypertensive medications, the relationship between systolic (SBP) or diastolic blood pressure (DBP) over 5 years and Exam 1 log-transformed CRP and IL-6 concentrations were assessed.

Results: There was an increased risk of incident hypertension (OR 2.1; 95% CI: 1.70–2.70) comparing the highest to lowest CRP quartile (>3.69 vs. <0.71 mg/L). This risk was attenuated after adjusting for body mass index (BMI) (OR 1.5; 95% CI: 1.20–1.98) or BMI and additional covariates (OR 1.3; 95% CI: 0.95–1.74). A similar pattern was observed comparing the highest and lowest IL-6 quartile (>1.69 vs. <0.68 pg/mL); analogous odds ratios were 2.8 (95% CI: 2.21–3.75) 2.2 (95% CI: 1.65–2.89) and 1.4 (95% CI: 1.05–1.97), respectively. These findings were similar for each gender and ethnic group, though they were less robust in Chinese. In univariable models, CRP and IL-6 were significantly associated with change in SBP (p=0.006 and p=0.03, respectively). The association between change in SBP and CRP or IL-6 concentration was not present in individuals with BMI <27 compared to those with a BMI ≥ 27 (both p-value for interaction = 0.02). CRP and IL-6 were not associated with change in DBP in univariable models (p=0.5 and p=0.7).

Conclusion: In MESA, the relationship between inflammation markers and risk for hypertension in middle-aged adults is modest, and partly explained by obesity. In addition, the relationship between inflammation markers and change in SBP is limited to those with higher BMI.





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