Hypertension and vascular calcification

Rattazzi, Marcello; Bertacco, Elisa; Puato, Massimo; Faggin, Elisabetta; Pauletto, Paolo

doi:10.1097/hjh.0b013e328356c257

Cited by 61 publications

(52 citation statements)

References 94 publications

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“…22, 24 Elastin degradation, as may occur from adverse central hemodynamics, leads to medial calcium deposition in animal models 25 and medial calcification may lead to further destruction of elastin. 13 While our CT technique, due to the lack of spatial resolution needed, cannot differentiate between intimal and medial coronary artery calcification, histopathology studies have shown that the overwhelming majority of calcification in subjects without known renal disease can be found in the intima of the coronary arteries.…”

Section: Discussionmentioning

confidence: 99%

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Cross-Sectional Relations of Arterial Stiffness, Pressure Pulsatility, Wave Reflection, and Arterial Calcification

Tsao

Pencina

Massaro

et al. 2014

ATVB

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Objective Arterial hemodynamics and vascular calcification are associated with increased risk for CVD, but their inter-relations remain unclear. We sought to examine the associations of arterial stiffness, pressure pulsatility, and wave reflection with arterial calcification in individuals free of prevalent cardiovascular disease (CVD). Approach and Results Framingham Heart Study Third Generation and Offspring Cohort participants free of CVD underwent applanation tonometry to measure arterial stiffness, pressure pulsatility, and wave reflection, including carotid-femoral pulse wave velocity (CFPWV), central pulse pressure (CPP), forward wave amplitude, and augmentation index (AI). Participants in each cohort (n=1905, 45±6 years and n=1015, 65±9 years, respectively) underwent multi-detector computed tomography to assess presence and quantity of thoracic (TAC) and abdominal (AAC) aortic calcification and coronary artery calcification (CAC). In multivariable-adjusted models, both higher CFPWV and CPP were associated with greater TAC and AAC, whereas higher AI was associated with AAC. Among the tonometry measures, CFPWV was the strongest correlate of all calcification measures in multivariable-adjusted models (odds ratio [OR] per SD for TAC 2.69 (95%CI 2.17-3.35), AAC 1.47 (95%CI 1.26-1.73), and CAC 1.48 (95%CI 1.28-1.72), all p<0.001, respectively). We observed stronger relations of CFPWV, CPP, and forward wave amplitude with nearly all continuous calcification measures in the younger Third Generation Cohort as compared with the Offspring Cohort. Conclusions In community-dwelling individuals without prevalent CVD, abnormal central arterial hemodynamics were positively associated with vascular calcification, and were observed at younger ages than previously recognized. The mechanisms of these associations may be bidirectional and deserve further study.

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Section: Discussionmentioning

confidence: 99%

“…21 However, recent evidence suggests that vascular remodeling in the presence of increased stiffness may contribute to medial and intimal calcification. 22 …”

Section: Introductionmentioning

confidence: 99%

Cross-Sectional Relations of Arterial Stiffness, Pressure Pulsatility, Wave Reflection, and Arterial Calcification

Tsao

Pencina

Massaro

et al. 2014

ATVB

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“…We have summarized these as follows: i) both elastin fragment generation and the deposition of collagen fibers have been linked to remodeling of the arterial wall in hypertension. These changes contribute to the reduction of the elasticity of the vessel associated with extracellular matrix composition and vascular cell phenotype variation (26). ii) The chronic form of heart failure and progressive cardiac dysfunction is constituted by myocardial remodeling.…”

Section: Discussionmentioning

confidence: 99%

Effect of apelin on the cardiac hemodynamics in hypertensive rats with heart failure

Hui

Han

et al. 2014

International Journal of Molecular Medicine

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It is known that apelin has definite protective effects on various cardiovascular diseases; however, the mechanism through which hypertension with heart failure (H-HF) is affected by pyroglutamylated apelin-13 (Pyr-AP13) remain unclear. Thus, in the present study, we investigated the effects of apelin on the cardiac hemodynamics in rats with hypertension and heart failure. In our study, cardiac function, dimensions and histological determination of the fibrosis of rats with two-kidney, one-clip induced hypertension and sham-operated rats were assessed using an echocardiography system and Masson’s trichrome. The infusion of either 5% glucose injection (GS) alone or 5% GS containing Pyr-AP13 as a dose, time-matched design on the cardiac hemodynamics in H-HF rats and sham-operated rats was recorded. For the determination of the effects of potential related proteins on cardiac hemodynamics in the H-HF rats, the animals were divided into 5 groups: i) the sham-operated group (n=8); ii) H-HF (n=8); iii) H-HF with infusion of 0.1 μg dose of Pyr-AP13 (n=8) or 5% glucose (GS) (n=8); iv) H-HF with infusion of 1 μg dose of Pyr-AP13 (n=8) or 5% GS (n=8); and v) H-HF with infusion of 10 μg dose of Pyr-AP13 (n=8) or 5% GS (n=8). The concentration of cyclic adenosine 3′,5′-monophosphate (cAMP) was determined by ELISA. The expression of membrane and cytosolic proteins was evaluated by western blot analysis. Significant cardiac and perivascular fibrosis was observed in the H-HF rats. Following the infusion of Pyr-AP13, the systolic and diastolic function was significantly improved in the cardiac hemodynamic parameters in the H-HF rats treated with Pyr-AP13. The apelin receptor (APJ), which was activated by the exogenous infusion of Pyr-AP13, was partially recycled from the cytoplasm back to the plasma membrane; however, membrane APJ was eventually downregulated in the H-HF rats treated with Pyr-AP13 compared with the sham-operated group rats. Our findings suggested that a complex was formed after Pyr-AP13 combined with cellular membrane APJ receptor. However, the endogenous downregulation of the APJ receptor results in benefits from the exogenous administration of apelin.

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“…Hypertension is an independent and strong predictor of vascular calcification4, which is accompanied with immune cell infiltration in the blood vessels, including monocytes/macrophages, lymphocytes, granulocytes56. Among these, monocytes/macrophages activation, including pro-inflammatory “classical” activation profile (M1) and anti-inflammatory “alternative” activation profile (M2), was involved in the hypertension-related vascular disease789.…”

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confidence: 99%

Osteopontin regulates macrophage activation and osteoclast formation in hypertensive patients with vascular calcification

Ruan

et al. 2017

Sci Rep

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Vascular calcification (VC) is a highly regulated ectopic mineral deposition process involving immune cell infiltration in the vasculatures, which has been recognized to be promoted by hypertension. The matricellular glycoprotein osteopontin (OPN) is strongly induced in myeloid cells as a potential inflammatory mediator of vascular injury. This study aims to examine whether OPN is involved in the regulation of macrophage activation and osteoclast formation in hypertensive subjects with VC. We firstly found an increased proportion of CD11c+CD163- pro-inflammatory peripheral monocytes in hypertensive subjects with VC compared to those without VC by flow cytometric analysis. Primary cultured macrophages from hypertensive subjects with VC also showed altered expression profile of inflammatory factors and higher serum OPN level. Exogenous OPN promoted the differentiation of peripheral monocytes into an alternative, anti-inflammatory phenotype, and inhibited macrophage-to-osteoclast differentiation from these VC patients. In addition, calcified vessels showed increased osteoclasts accumulation accompanied with decreased macrophages infiltration in the of hypertensive subjects. Taken together, these demonstrated that OPN exerts an important role in the monocytes/macrophage phenotypic differentiation from hypertensive patients with VC, which includes reducing inflammatory factor expression and attenuating osteoclast formation.

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Hypertension and vascular calcification

Cited by 61 publications

References 94 publications

Cross-Sectional Relations of Arterial Stiffness, Pressure Pulsatility, Wave Reflection, and Arterial Calcification

Cross-Sectional Relations of Arterial Stiffness, Pressure Pulsatility, Wave Reflection, and Arterial Calcification

Effect of apelin on the cardiac hemodynamics in hypertensive rats with heart failure

Osteopontin regulates macrophage activation and osteoclast formation in hypertensive patients with vascular calcification

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