In prehypertension leukocytosis is associated with body mass index but not with blood pressure or incident hypertension

Stevo Julius, Brent M. Egan, Niko A. Kaciroti, Shawna D. Nesbitt, Andrew K. Chen

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background: Previous studies reported increased white blood cell counts (WBCCs), an inflammatory marker, in hypertension, prehypertension and metabolic syndrome. Evidence suggests that inflammation precedes blood pressure (BP) elevation and may contribute to incident hypertension. Angiotensin receptor blockers (ARBs) may reduce inflammation. We analyzed WBCC trends in TRial Of Preventing HYpertension (TROPHY) to determine if this inflammatory marker predicted incident hypertension in prehypertensive individuals and whether randomized assignment to the ARB candesartan (391 individuals) for 2 years, lowered WBCC compared with placebo-treated controls (381 individuals). Methods: A new analysis of TROPHY trial data. Results: In the total population, baseline BMI correlated with WBCC (r=0.185, P<0.0001), neutrophils (r=0.135, P<0.001) and lymphocytes (r=0.204, P<0.0001). Baseline triglycerides also correlated significantly with inflammatory markers. Despite a wide range of home BP (HBP) values, HBP did not correlate with baseline WBCC counts. After 2 years, candesartan decreased placebo corrected HBP by-5.5/-2.5 mmHg, (P<0.0001), but WBCC, neutrophil and lymphocyte counts were not different in placebo and in candesartan groups. Baseline WBCC, neutrophils and lymphocyte counts did not predict incident hypertension in the placebo group. Conclusion: In TROPHY, candesartan lowered BP but did not alter WBCC. Baseline WBCC did not predict incident hypertension. Our findings do not support the hypothesis that inflammation contributes to incident hypertension or that ARB treatment suppresses inflammation. The significant independent association of WBCC with baseline BMI and triglycerides is consistent with the evidence that obesity and insulin resistance are associated with inflammation. The findings highlight the importance of effective lifestyle modification in prehypertension to reduce inflammatory cardio-metabolic risk and suppress transition to hypertension.

Original languageEnglish (US)
Pages (from-to)251-259
Number of pages9
JournalJournal of Hypertension
Volume32
Issue number2
DOIs
StatePublished - Feb 2014

Fingerprint

Prehypertension
Leukocytosis
Leukocyte Count
Body Mass Index
Blood Pressure
Hypertension
Angiotensin Receptor Antagonists
Inflammation
Placebos
Neutrophils
Lymphocyte Count
Triglycerides
Homing Behavior
Insulin Resistance
Life Style
Obesity

Keywords

  • inflammation
  • leukocytes
  • prehypertension
  • treatment with angiotensin receptor blocker

ASJC Scopus subject areas

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

In prehypertension leukocytosis is associated with body mass index but not with blood pressure or incident hypertension. / Julius, Stevo; Egan, Brent M.; Kaciroti, Niko A.; Nesbitt, Shawna D.; Chen, Andrew K.

In: Journal of Hypertension, Vol. 32, No. 2, 02.2014, p. 251-259.

Research output: Contribution to journalArticle

Julius, Stevo ; Egan, Brent M. ; Kaciroti, Niko A. ; Nesbitt, Shawna D. ; Chen, Andrew K. / In prehypertension leukocytosis is associated with body mass index but not with blood pressure or incident hypertension. In: Journal of Hypertension. 2014 ; Vol. 32, No. 2. pp. 251-259.
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abstract = "Background: Previous studies reported increased white blood cell counts (WBCCs), an inflammatory marker, in hypertension, prehypertension and metabolic syndrome. Evidence suggests that inflammation precedes blood pressure (BP) elevation and may contribute to incident hypertension. Angiotensin receptor blockers (ARBs) may reduce inflammation. We analyzed WBCC trends in TRial Of Preventing HYpertension (TROPHY) to determine if this inflammatory marker predicted incident hypertension in prehypertensive individuals and whether randomized assignment to the ARB candesartan (391 individuals) for 2 years, lowered WBCC compared with placebo-treated controls (381 individuals). Methods: A new analysis of TROPHY trial data. Results: In the total population, baseline BMI correlated with WBCC (r=0.185, P<0.0001), neutrophils (r=0.135, P<0.001) and lymphocytes (r=0.204, P<0.0001). Baseline triglycerides also correlated significantly with inflammatory markers. Despite a wide range of home BP (HBP) values, HBP did not correlate with baseline WBCC counts. After 2 years, candesartan decreased placebo corrected HBP by-5.5/-2.5 mmHg, (P<0.0001), but WBCC, neutrophil and lymphocyte counts were not different in placebo and in candesartan groups. Baseline WBCC, neutrophils and lymphocyte counts did not predict incident hypertension in the placebo group. Conclusion: In TROPHY, candesartan lowered BP but did not alter WBCC. Baseline WBCC did not predict incident hypertension. Our findings do not support the hypothesis that inflammation contributes to incident hypertension or that ARB treatment suppresses inflammation. The significant independent association of WBCC with baseline BMI and triglycerides is consistent with the evidence that obesity and insulin resistance are associated with inflammation. The findings highlight the importance of effective lifestyle modification in prehypertension to reduce inflammatory cardio-metabolic risk and suppress transition to hypertension.",
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