Increased arterial stiffness in resistant hypertension is associated with inflammatory biomarkers

Barbaro, Natália R.; Fontana, Vanessa; Modolo, Rodrigo; Faria, Ana Paula de; Sabbatini, A.; Fonseca, Francisco A.H.; Anhê, Gabriel Forato; Moreno, Heitor

doi:10.3109/08037051.2014.940710

Cited by 87 publications

(64 citation statements)

References 36 publications

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“…Furthermore, these markers are also increased with the deterioration of renal function [38] . Thus, our results, emphasize the possibility of a common pathophysiologic mechanism affecting renal dysfunction, anemia and AS deterioration: inflammation and endothelial dysfunction may play a prominent role in the interrelation of these entities [37,39] . The cross sectional design, which does not allow to establish cause-effect relationships as well as the small number of patients involved are potential limitations of our study.…”

Section: Resultssupporting

confidence: 65%

Albuminuria as a marker of arterial stiffness in chronic kidney disease patients

Kalaitzidis

Karasavvidou

Tatsioni

et al. 2015

WJN

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Section: Resultssupporting

confidence: 65%

Albuminuria as a marker of arterial stiffness in chronic kidney disease patients

Kalaitzidis

Karasavvidou

Tatsioni

et al. 2015

WJN

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“…19 Both RH and HTN patients present higher levels of inflammatory cytokines and their levels are related to TOD. 6 MCP-1 is a proinflammatory cytokine with potent chemoattractant activity for monocytes and macrophages. 5 The recruitment and activation of monocytes in rat models appear to be involved with hypertension and TOD process 20 by increasing oxidative stress in the vascular wall.…”

Section: Discussionmentioning

confidence: 99%

“…5,6 Several inflammatory mediators are enhanced in hypertensive subjects, 7 including monocyte chemoattractant protein-1 (MCP-1). 8 MCP-1, also known as CCL2, can be produced by different cells and is responsible for migration of monocytes and macrophages cells to the tissue, 9 exacerbating the local damage.…”

Section: Introductionmentioning

confidence: 99%

MCP-1 Levels are Associated with Cardiac Remodeling but not with Resistant Hypertension

Ritter¹,

Faria²,

Sabbatini³

et al. 2017

Arquivos Brasileiros De Cardiologia

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BackgroundHypertension 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.ObjectiveThis 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.MethodsWe 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.ResultsWe 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.ConclusionSince 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.

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“…3, 4 The pathophysiology of RHTN is poorly understood although several suggested mechanisms include (1) hyperactivity of both sympathetic and renin-angiotensin-aldosterone systems; 5, 6 (2) arterial stiffness; 7,8 (3) cardiac hypertrophy; 9 and (4) inflammation. 10 With regards to the last, hypertension and target organ damage are linked to increased levels of circulating inflammatory biomarkers, 11 which may regulate cell adhesion molecules (CAM). 12 CAM include intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) -which belong to the immunoglobulin superfamily, and the RHTN of the University of Campinas (UNICAMP, Campinas, Brazil) and 112 mild-moderate hypertension (HTN) patients from Hypertension Clinic of Valinhos (Valinhos, Brazil).…”

Section: Subjectsmentioning

confidence: 99%

Deregulation of Soluble Adhesion Molecules in Resistant Hypertension and Its Role in Cardiovascular Remodeling

Faria

Ritter

Sabbatini

et al. 2016

Circ J

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Background: Resistant hypertension (RHTN) and target organ damage are linked to increased inflammatory biomarkers, which may regulate adhesion molecules, such as intracellular adhesion molecule-1 (ICAM-1); vascular cell adhesion molecule-1 (VCAM-1); and the platelet (P-selectin) and endothelial (E-selectin) selectins. We investigated a previously unknown relationship between soluble P-selectin (sP-selectin), E-selectin (sE-selectin), ICAM-1 (sICAM-1) and VCAM-1 (sVCAM-1) with RHTN and target organ damage. Methods and Results:We included 110 subjects diagnosed for true RHTN and 112 mild-moderate hypertensive (HTN) patients. Blood pressure parameters, pulse wave velocity and left ventricular mass index (LVMI) were measured. Adhesion molecules were measured on ELISA. Both sP-selectin and sE-selectin were increased; in contrast, sICAM-1 was reduced in RHTN compared with HTN patients, while similar sVCAM-1 was noted in the groups. sPselectin and sVCAM-1 were elevated in the presence of arterial stiffness (sP-selectin: 104±47 vs. 89±45 ng/ml, P<0.05; sVCAM-1: 1,189±411 vs. 1,060±412 ng/ml, P<0.05) and cardiac hypertrophy (sP-selectin: 105±51 vs. 88±43 ng/ml, P<0.05; sVCAM-1: 1,170±433 vs. 1,040±383 ng/ml, P<0.05) in all HTN patients. sP-selectin was associated with target organ damage after adjustment for age and BP. Apart from potential confounders, sE-selectin was a significant indicator of RHTN. Conclusions:The adhesion molecule sP-selectin plays a role in cardiovascular damage, and sE-selectin in resistance to antihypertensive therapy. (Circ J 2016; 80: 1196 -1201

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Increased arterial stiffness in resistant hypertension is associated with inflammatory biomarkers

Abstract: RHTN subjects have higher levels of inflammatory cytokines (TNF-α, IL-1β and IL-10) as well as increased arterial stiffness, and detectable IL-1β levels are associated arterial stiffness. These findings suggest that inflammation plays a possible role in the pathophysiology of RHTN.

Cited by 87 publications

References 36 publications

Albuminuria as a marker of arterial stiffness in chronic kidney disease patients

Albuminuria as a marker of arterial stiffness in chronic kidney disease patients

MCP-1 Levels are Associated with Cardiac Remodeling but not with Resistant Hypertension

Deregulation of Soluble Adhesion Molecules in Resistant Hypertension and Its Role in Cardiovascular Remodeling

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