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Hypertension and Correlation to Cerebrovascular Change: A Brief Overview
Published in Ayman El-Baz, Jasjit S. Suri, Cardiovascular Imaging and Image Analysis, 2018
Heba Kandil, Dawn Sosnin, Ali Mahmoud, Ahmed Shalaby, Ahmed Soliman, Adel Elmaghraby, Jasjit S. Suri, Guruprasad Giridharan, Ayman El-Baz
Hypertension can be classified as primary (or essential or idiopathic), secondary, accelerated, hypertension urgency, or as malignant hypertension. Essential hypertension develops over years, even decades, with no single identified lifestyle or genetic cause. Approximately 90–95% of patients diagnosed with hypertension are classified as primary hypertension [1]. Secondary hypertension is a secondary disease which can develop due to conditions including adrenal and thyroid problems, obstructive sleep apnea, drugs and medications, chronic alcohol abuse, etc. [2]. An example of secondary hypertension is renal (or renovascular) hypertension, where hormones released by the kidneys increase blood pressure throughout the systemic circulation in response to narrowing of the arteries that supply blood to the kidneys. Accelerated hypertension (recent significant increase) and malignant hypertension are hypertensive emergencies, defined as high blood pressure (typically ≥180/≥120) with acute impairment of one or more organ systems. Diagnosis of malignant hypertension requires the presence of papilledema, or in the absence of stage III or IV retinopathy, damage to a minimum of three target organs [3]. Hypertensive urgency is severely elevated blood pressure with no organ damage.
Influence of renal artery stenosis morphology on hemodynamics
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2021
Zhuxiang Xiong, Ding Yuan, Jiarong Wang, Tinghui Zheng, Yubo Fan
Unlike myocardial ischemia which generally occurs during the increased myocardial oxygen demand, renovascular hypertension and renal dysfunction occur due to chronically abnormal renal perfusion in the resting state (Prince et al. 2019). Accordingly, on one hand, FFR may be the gold standard for assessment of functional measurement of renal artery and helps clinical judgments regarding the severity of RAS (Guo et al. 2015; Klein et al. 2017; Liu et al. 2020). On the other hand, a smaller FFR than 0.8 which is widely used as the threshold value of coronary FFR may be suggested to be hemodynamic significant to assist and evaluate the intervention of the renal artery. In addition, an increase of R-PSV/A-PSV (greater than 3.5) is suggested to be a risk factor of hemodynamic severity of RAS. Moreover, low WSS and high OSI are suggested to play an important role in the development of atherosclerosis in artery (Moore and Ku 1994; Samady et al. 2011). Therefore, the intervention indication of RAS should not be based solely on the degree or area of stenosis, the hemodynamic information of a patient-specific RAS may be obtained by CFD and used for the evaluation and intervention of RAS to guide clinical diagnosis and treatment.