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Arterial stiffness and hypertension

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dc.contributor.authorKim, Hack-Lyoung-
dc.date.accessioned2023-12-05T05:43:01Z-
dc.date.available2023-12-05T14:43:45Z-
dc.date.issued2023-12-01-
dc.identifier.citationClinical Hypertension,Vol.29(1):31ko_KR
dc.identifier.issn2056-5909-
dc.identifier.urihttps://hdl.handle.net/10371/197608-
dc.description.abstractArterial stiffness and hypertension are closely related in pathophysiology. Chronic high blood pressure (BP) can lead to arterial wall damage by mechanical stress, endothelial dysfunction, increased inflammation, oxidative stress, and renin–angiotensin–aldosterone system (RAAS) activation. Hypertension also increases collagen fiber production and accelerates elastin fiber degradation. Stiffened arteries struggle with BP changes, raising systolic BP and pulse pressure. The resulting increased systolic pressure further hardens arteries, creating a harmful cycle of inflammation and calcification. Arterial stiffness data can predict target organ damage and future cardiovascular events in hypertensive patients. Thus, early detection of arterial stiffness aids in initiating preventive measures and treatment plans to protect against progression of vascular damage. While various methods exist for measuring arterial stiffness, pulse wave velocity is a non-invasive, simple measurement method that maximizes effectiveness. Healthy lifestyle changes, RAAS blockers, and statins are known to reduce arterial stiffness. Further research is needed to ascertain if improving arterial stiffness will enhance prognosis in hypertensive patients.ko_KR
dc.language.isoenko_KR
dc.publisherBMCko_KR
dc.subjectArterial damage-
dc.subjectArterial stiffness-
dc.subjectCardiovascular risk-
dc.subjectHypertension-
dc.subjectTarget organ damage-
dc.titleArterial stiffness and hypertensionko_KR
dc.typeArticleko_KR
dc.identifier.doi10.1186/s40885-023-00258-1ko_KR
dc.citation.journaltitleClinical Hypertensionko_KR
dc.language.rfc3066en-
dc.rights.holderThe Author(s)-
dc.date.updated2023-12-03T04:09:58Z-
dc.citation.endpage9ko_KR
dc.citation.number1ko_KR
dc.citation.startpage1ko_KR
dc.citation.volume29ko_KR
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