Carotid artery intima-media thickness and hypertensive heart disease: a short review

Magnussen, Costan G.

doi:10.1186/s40885-017-0063-3

Cited by 31 publications

(19 citation statements)

References 37 publications

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“…Baldassarre et al showed on sample of 4,482 patients that CIMT was associated with increased cardiovascular risk [22], which was also confirmed by Kokubo et al in a study on 4,724 patients [24]. Utility of CIMT can predict vascular incident in asymptomatic patients [25]. In PE, the placental helix arteries fail to lose their musculoelastic layers, leading exclusively to decreased placental perfusion [26].…”

Section: Discussionmentioning

confidence: 82%

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Increased of the carotid intima media thickness in preeclampsia

Neto

Ramos

Medjedović

et al. 2020

Journal of Perinatal Medicine

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ObjectivesThe aim of the study was to determine carotid intima-media thickness (CIMT) values in patients who developed and did not develop preeclampsia (PE), and to determine whether CIMT values could be predictors of PE development.MethodsThe study included pregnant women who were examined by regular ultrasound examination at the Materno-Infantil Presidente Vargas Hospital (HMIPV) in Porto Alegre, Brazil, from April 2016 to September 2017. The examinations were performed every three months. Patients were divided into two groups. The first group included patients diagnosed with PE (n=21) and second group included patients who did not have PE (n=199). A high frequency ultrasound device (12 MHz) with a semi-automatic method was used to estimate CIMT.ResultsCIMT was significantly higher in pregnant women with PE than in women without PE (55±0.11 vs. 0.44±0.06, respectively; p<0.001). Using a cut-off value of 0.51 mm, CIMT had a specificity of 77.9% and sensitivity of 81% in the diagnosis of PE. With CIMT ≥0.6 mm, the probability of a patient developing PE was 44.4%; with CIMT >0.42 mm, the probability was only 4.2%.ConclusionsAn increase in CIMT was associated with the onset of PE. CIMT values were significantly higher in patients who develop PE.

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Section: Discussionmentioning

confidence: 82%

“…Increased CIMT is an independent predictor of stroke and cardiovascular events [20][21][22][23][24][25]. Eikendal et al have concluded in 3,067 adult patients younger than 45 years of age without symptomatic cardiovascular disease that CIMT may be a marker for cardiovascular risk [20].…”

Section: Discussionmentioning

confidence: 99%

Increased of the carotid intima media thickness in preeclampsia

Neto

Ramos

Medjedović

et al. 2020

Journal of Perinatal Medicine

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“…34 The intima-media thickness is also increased in hypercholesterolaemic patients compared to controls, 35 and has become a convenient marker for atherosclerosis. 36 Oxidation of LDL cholesterol is key in the initiation of atherosclerosis 7 and may also trigger vascular remodelling by enhancing smooth muscle cell proliferation and collagen deposition, leading to increased intima-media thickness. Increased deposition of elastic and collagen fibres was observed in the present study, shown by VVG-stained sections of aortic arch and thoracic aorta, suggesting increased atherogenesis, as shown previously.…”

Section: Discussionmentioning

confidence: 99%

Natural cocoa inhibits maternal hypercholesterolaemiainduced atherogenesis in rabbit pups

Blay

Adjenti

Adutwum-Ofosu

et al. 2019

CVJA

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Atherosclerosis begins during foetal development and is enhanced by maternal hypercholesterolaemia during pregnancy. This study assessed the effect of natural cocoa on atherosclerosis in offspring conceived in maternal hypercholesterolaemia. Female rabbits were fed a cholesterol-enriched diet for two weeks and hypercholesterolaemia was confirmed, after which they were crossed with normocholesterolaemic males. One group of hypercholesterolaemic mothers (HCC) received natural cocoa powder (NCP) in their drinking water, whereas the other group (HC) received only water. Histological analysis of three segments of the aorta (arch, thoracic and abdominal) from offspring of both groups was compared with a control group (NC). Intima-media thickness of the aortic arch in offspring born to hypercholesterolaemic rabbits (HC: 146 µm) was higher compared to HCC (99 µm) and control rabbits (58.5 µm). All the sections from the aortic arch of the HC group had atherosclerotic lesions while none of the sections of the aortic arch from the NC and HCC groups had lesions present. Inferentially, regular and voluntary consumption of NCP during pregnancy may inhibit aortic atherogenesis in offspring of hypercholesterolaemic mothers.

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“…Vascular remodeling (VR) persists throughout the course of hypertension and is characterized by chronic, continuous, and complex changes in vascular structure and abnormalities in vascular functions (Hayashiet al , 2009;Lemarie et al , 2010;Zhang et al , 2019). VR, as an important indicator of the progression of hypertension, is closely related to the severity and prognosis of the disease (Mulvany, 2012;Magnussen, 2017;Brown et al , 2018). Angiotensin II (AngII)-induced dysfunction of vascular smooth muscle cells (VSMCs) plays a critical role in hypertensive VR (Das et al , 2018), but the potential molecular mechanisms remain poorly understood.…”

Section: Introductionmentioning

confidence: 99%

The antagonistic effects and mechanisms of microRNA-26a action in hypertensive vascular remodeling

Zhang

Wang

Xing

et al. 2020

Preprint

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Background and Purpose: Hypertensive vascular remodeling (VR) is responsible for end-organ damage and is the result of increased extracellular matrix accumulation and excessive vascular smooth muscle cell (VSMC) proliferation. MicroRNA-26a (miR-26a), a non-coding small RNA, is involved in multiple cardiovascular diseases. We aimed to validate the effect and mechanisms of miR-26a in hypertensive VR. Experimental Approach: Spontaneously hypertensive rats (SHRs) were injected intravenously with recombinant adeno-associated virus-miR-26a. In vitro experiments, angiotensin II (AngII)-induced VSMCs were transfected with miR-26a mimic or inhibitor. Key Results: We found miR-26a downregulated in the thoracic aorta and plasma of SHRs. Overexpression of miR-26a inhibited extracellular matrix deposition by targeting connective tissue growth factor (CTGF) and mitigated VSMC proliferation by regulating the enhancer of zeste homolog 2 (EZH2)/p21 pathway both in vitro and in vivo. AngII-mediated Smad3 activation suppressed miR-26a expression, which in turn promoted Smad3 activation via targeted regulation of Smad4, leading to further downregulation of miR-26a. Conclusion and Implications: Our study reveals that AngII stimulates a Smads/miR-26a positive feedback loop, which further reduces miR-26a expression, leading to collagen production and VSMC proliferation and consequently, VR. MiR-26a has an antagonistic effect on hypertensive VR and can be a strategy for treating hypertensive VR.

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Carotid artery intima-media thickness and hypertensive heart disease: a short review

Cited by 31 publications

References 37 publications

Increased of the carotid intima media thickness in preeclampsia

Increased of the carotid intima media thickness in preeclampsia

Natural cocoa inhibits maternal hypercholesterolaemiainduced atherogenesis in rabbit pups

The antagonistic effects and mechanisms of microRNA-26a action in hypertensive vascular remodeling

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