Blood pressure variability acts as an independent predictor and active contributor to hypertensive target organ damage, necessitating its integration into comprehensive hypertension management.
Systematic Review
Does integrating blood pressure variability control into hypertension management prevent target organ damage compared to solely targeting mean blood pressure?
This review highlights blood pressure variability as an independent driver of hypertensive target organ damage, advocating for its inclusion as a therapeutic target alongside mean blood pressure control.
Hypertensive target organ damage (TOD) is a pivotal driver of cardiovascular events and mortality. Despite widespread control of traditional blood pressure (BP) averages, TOD progression persists in some patients, underscoring the independent and significant role of blood pressure variability (BPV). Accumulating evidence has established BPV not only as an independent predictor of TOD risk but also as an active contributor to its pathogenesis by propelling the vicious cycle of "hypertension-arteriosclerosis." This article systematically reviews the epidemiological evidence supporting BPV as an independent risk factor, elucidates its mediating pathways through mechanisms such as endothelial dysfunction, inflammatory activation, and arterial stiffness, and discusses recent advances and future directions in precision management strategies focused on attenuating BPV. This review aims to provide a novel theoretical basis and practical guidance for risk assessment and individualized treatment in hypertension. We advocate shifting the clinical paradigm from solely targeting mean BP to integrating BPV control into a comprehensive management strategy. This integrated approach is critical for disrupting the vicious cycle of TOD and achieving effective prevention of cardiovascular events.
Huang et al. (Sat,) conducted a systematic review in Hypertension and hypertensive target organ damage. Blood pressure variability was evaluated. Blood pressure variability acts as an independent predictor and active contributor to hypertensive target organ damage, necessitating its integration into comprehensive hypertension management.
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