title: MCP-1 Levels are Associated with Cardiac Remodeling but not with Resistant Hypertension.
abstract: Hypertension is a chronic, low-grade inflammation process associated with the release of cytokines and development of target organ damage. Deregulated monocyte chemoattractant protein-1 (MCP-1) levels have been associated with high blood pressure and cardiovascular complications; however, the mechanisms involved are complex and not fully understood.
  
  
  
  This study aimed to compare the levels of MCP-1 in patients with resistant (RH) versus mild-to-moderate (HTN) hypertension and their association with the presence or absence of left ventricular hypertrophy (LVH) in all hypertensive subjects.
  
  
  
  We enrolled 256 hypertensive subjects: 120 RH and 136 HTN, investigating the relationship between circulating MCP-1 levels and blood pressure, biochemical data, hematologic profile, and cardiac damage within the RH and HTN groups. Plasma MCP-1 levels were measured by ELISA and LVH was assessed by echocardiography.
  
  
  
  We found no difference in MCP-1 levels between RH and HTN subjects. On the other hand, we encountered lower MCP-1 levels in patients with LVH (105 pg/mL [100 - 260 pg/mL] versus 136 pg/mL (100 - 200 pg/mL), p = 0.005, respectively] compared with those without LVH. A logistic regression model adjusted for body mass index (BMI), age, race, aldosterone levels, and presence of diabetes and RH demonstrated that median levels of MCP-1 (2.55 pg/mL [1.22 - 5.2 pg/mL], p = 0.01) were independently associated with LVH in the entire hypertensive population.
  
  
  
  Since MCP-1 levels were similar in both RH and HTN subjects and decreased in hypertensive patients with existing LVH, our study suggests a possible downregulation in MCP-1 levels in hypertensive individuals with LVH, regardless of hypertension strata.
authors.affiliation: Universidade Estadual de Campinas (UNICAMP), Campinas, SP - Brazil.
authors.forename: Alessandra Mileni Versuti
authors.initials: AMV
authors.lastname: Ritter
authors.affiliation: Universidade Estadual de Campinas (UNICAMP), Campinas, SP - Brazil.
authors.forename: Ana Paula Cabral de
authors.initials: APC
authors.lastname: Faria
authors.affiliation: Universidade Estadual de Campinas (UNICAMP), Campinas, SP - Brazil.
authors.forename: Andrea
authors.initials: A
authors.lastname: Sabbatini
authors.affiliation: Universidade Estadual de Campinas (UNICAMP), Campinas, SP - Brazil.
authors.forename: Nathalia Batista
authors.initials: NB
authors.lastname: Corrêa
authors.affiliation: Universidade Estadual de Campinas (UNICAMP), Campinas, SP - Brazil.
authors.forename: Veridiana
authors.initials: V
authors.lastname: Brunelli
authors.affiliation: Universidade Estadual de Campinas (UNICAMP), Campinas, SP - Brazil.
authors.forename: Rodrigo
authors.initials: R
authors.lastname: Modolo
authors.affiliation: Universidade Estadual de Campinas (UNICAMP), Campinas, SP - Brazil.
authors.forename: Heitor
authors.initials: H
authors.lastname: Moreno
mesh_terms: D000368:Aged; D018660:Blood Pressure Monitoring, Ambulatory; D018932:Chemokine CCL2 / Q000032:analysis*; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D018932:Chemokine CCL2