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It is time to contend with the endothelial consequences of prehypertension

Journal of Human Hypertension volume 29, pages 457–458 (2015)Cite this article

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Worldwide, >1 billion people over the age of 25 years suffer from high blood pressure, defined as systolic pressure ⩾140 mm Hg and/or diastolic ⩾90 mm Hg, making hypertension the single most important cause of early mortality.1 Hypertension claims more lives annually than obesity, prediabetes and high cholesterol combined and was responsible for ~9.4 million deaths (13% of total global mortality) in 2010.2 Although trends in awareness, treatment and control of hypertension have significantly improved, particularly in the United States and Western Europe, reducing its population prevalence continues to be a major global health crisis. From 2001 to 2009, the number of Americans with hypertension actually increased, with current estimates indicating ~78 million people are affected,3 accounting for 1000 deaths each day.4 Yet, in low- and middle-income countries, hypertension has emerged as an even more serious public health problem. Indeed, although the number of people with hypertension is highest in these regions compared with high-income countries,1 many more people are undiagnosed and poorly treated, accelerating their burden of atherothrombotic disease.5 Future projections are discouraging. Analysis from the World Economic Forum and the Harvard School of Public Health in collaboration with the World Health Organization indicates that low- and middle-income countries will suffer an economic loss of nearly $4 trillion in the next decade solely attributed to cardiovascular diseases (CVD), most from the widespread clinical consequences of raised blood pressure.6 In the US alone, the prevalence of hypertension is expected to increase by 27 million people in the next 15 years, placing an inconceivable annual financial toll of $400 billion in hypertension-related medical costs.7

What is more concerning is that we have come to realize that the adverse vascular impacts of elevated blood pressure commence and progress well before someone becomes hypertensive (<140/90 mm Hg). This notion was first put forth by Robinson and Brucer in late 1930s following a series of studies showing a progressive rise of early death from CVD in persons with blood pressure between 120 and 140 mm Hg.8 As a result of these important findings, Robinson and Brucer introduced the term ‘prehypertension’ to indicate an increased mortality risk zone of raised blood pressure. Seventy-five years later, we have amassed a large body of impressive data from many epidemiological and prospective cohort studies that clearly show a considerable vascular risk in the prehypertensive blood pressure range,9 now defined as untreated systolic pressure 120–139 mm Hg and/or diastolic pressure 80–89 mm Hg.10 Chronic elevations in blood pressure in the prehypertensive range are atherogenic, contributing to widespread vascular and structural damage to all organs and tissues, particularly the heart, brain and kidneys. Increased carotid intima-media thickness, coronary artery calcification, abnormal left ventricular morphology and diastolic dysfunction, reduced large-artery elasticity, aortic stiffening and vascular endothelial dysfunction are some of the major abnormalities that commence and progress in the prehypertensive state. The population burden of disease attributable to prehypertension, which affects ~80 million Americans, is responsible for half of all deaths from ischemic heart disease and stroke worldwide.5 Most of the mortality risk occurs in those with systolic pressure <140 mm Hg. Moreover, each 20/10 mm Hg increase in pressure above 115/75 mm Hg doubles the risk of death from atherothrombotic vascular disease, even before the onset of overt hypertension.11 The cardiovascular health consequences of prehypertension afflict men, women and children of all ethnicities who are independent of traditional risk factors, and invariably affect people across all socioeconomic and education levels.9 Despite this breadth of evidence, the precise mechanisms underlying the considerable CVD risks associated with prehypertension elude us. Recently, however, new scientific findings provide important evidence showing that prehypertension diminishes the inherent properties of the vascular endothelium to protect against thrombotic clots.

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  1. Department of Health and Nutritional Sciences, South Dakota State University, Brookings, SD, USA

    G P Van Guilder

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Van Guilder, G. It is time to contend with the endothelial consequences of prehypertension. J Hum Hypertens 29, 457–458 (2015). https://doi.org/10.1038/jhh.2014.122

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