Abstract

It is estimated that approximately 1 billion individuals worldwide have hypertension, and more than 7 million deaths per year may be attributable to hypertension-induced complications and organ damage (1). The mechanisms underlying hypertension are complex and incompletely understood. To better control hypertension-induced end-organ damage, it is important to investigate new and effective targets for therapeutic intervention. Besides blood pressure level itself, recent studies have demonstrated that the spontaneous variation in blood pressure, called blood pressure variability (BPV), is another key determinant of hypertensive end-organ damage. Clinical trials have demonstrated that, for nearly any level of 24-h mean arterial blood pressure, hypertensive subjects with low 24-h BPV had a significantly lower prevalence and severity of organ damage than those with high BPV (2). Furthermore, the cardiovascular complications of hypertension may in fact depend on the degree of 24-h BPV (3). Tatasciore et al. showed that awake systolic BPV, via non-invasive ambulatory blood pressure monitoring, correlates with subclinical target-organ damage that is independent of mean blood pressure level in hypertensive subjects (4). In contrast, ambulatory blood pressure levels and BPV are closely associated with carotid artery alteration, as found in the Ohasama study, suggesting that these parameters are independent risk

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