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Essential hypertension—definition, epidemiology, and pathophysiology 

Essential hypertension—definition, epidemiology, and pathophysiology

Chapter:
Essential hypertension—definition, epidemiology, and pathophysiology
Author(s):

Bryan Williams

DOI:
10.1093/med/9780199204854.003.161701_update_001

Update:

Definitions – increasing use of automated home BP readings and ambulatory BP measurements to diagnose hypertension. Epidemiology – recognition that automated home BP and ambulatory BP measurements predict cardiovascular events better than does office BP monitoring.

Updated on 29 Oct 2015. The previous version of this content can be found here.
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date: 24 April 2017

‘Essential hypertension’ is high blood pressure for which there is no clearly defined aetiology. From a practical perspective, it is best defined as that level of blood pressure at which treatment to lower blood pressure results in significant clinical benefit—a level which will vary from patient to patient depending on their absolute cardiovascular risk.

Historically, most guidelines define ‘hypertension’ as an office blood pressure greater than or equal to 140/90 mmHg, but some recent recommendations prefer home or ambulatory blood pressure (blood pressure) averages. When using 24 h ambulatory blood pressure or home blood pressure averages to define hypertension, the diagnostic thresholds are lower than those used with office measurement, with a value of 135/85 mmHg typically used for both daytime ambulatory blood pressure and home measurements.

Isolated diastolic hypertension (systolic blood pressure (SBP) <140 mmHg, diastolic blood pressure (DBP) >90 mmHg) is more common in younger people, and isolated systolic hypertension (SBP >140 mmHg, DBP <90 mmHg) is the most common form of hypertension in older people.

American guidelines include a category of ‘prehypertension’ (SBP 120–139 mmHg and/or, DBP 80–89 mmHg), the reason for this being that blood pressure in this range is associated with both adverse cardiovascular outcome and a high rate of progression to hypertension.

Epidemiology

In 2000, it was estimated 25% of the world’s adult population were hypertensive, and predicted that this would rise to 29% by 2025. By the age of 60, more than one-half of adults in most regions of the world will be hypertensive.

There is a continuous relationship between blood pressure and cardiovascular risk from blood pressure values as low as 115/75 mmHg. The relationship is steeper for stroke than it is for coronary heart disease, and is magnified by age. There is a doubling in risk of stroke and ischaemic heart disease mortality for every 20/10 mmHg increase in blood pressure.

Most people with hypertension are over the age of 50 years, and in these SBP is by far the most important contributor to the burden of cardiovascular disease attributable to hypertension.

Pathogenesis and pathophysiology

The pathogenesis of essential hypertension is a complex interplay between (1) genetic predisposition, (2) lifestyle and environmental influences, and (3) disturbances in vascular structure and neurohumoral control mechanisms.

Genetic predisposition—blood pressure runs in families, with a remarkably consistent level of correlation of around 0.2 between first-degree relatives found in many studies. This means that if the blood pressure of one member of the family deviates from the norm by +10 mmHg, the first-degree relative will deviate by +2 mmHg on average. Variants in a large number of genes, involving virtually all of the main physiological systems affecting blood pressure, have shown association with blood pressure in one or more studies, but the effect of any individual variant is likely to be modest.

Lifestyle and environmental influences—the exploding prevalence of hypertension in economically developing regions reflects lifestyle changes, so-called ‘Westernization’, more than anything else, with the most important influences on blood pressure being sodium intake, obesity, and alcohol intake.

Pathophysiology—a characteristic finding in essential hypertension is an inappropriate increase in peripheral vascular resistance relative to the cardiac output. This is due to remodelling of small arteries (arterioles), which is characterized by an increase in their media/lumen ratio, but it is not clear whether these changes are a consequence or a cause of raised blood pressure. The functional integrity of large conduit arteries, i.e. the aorta, which becomes stiffer, also influences the development of hypertension—especially systolic hypertension. Endothelial dysfunction and decreased nitric oxide production are found in hypertension, but are more likely a consequence than a cause of elevated blood pressure. The specific role of the renin–angiotensin–aldosterone system in the development of essential hypertension remains unclear, but therapeutic agents that inhibit this system have proved to be very effective treatments. The sympathetic nervous system is involved in the acute and chronic regulation of blood pressure, but whether disturbances in it play a major role in the initiation and maintenance of chronic essential hypertension remains unknown.

The hypertensive phenotype and target-organ damage

Although blood pressure measurement is used to define hypertension, hypertension is more than just blood pressure. Essential hypertension is commonly associated with metabolic disturbances (the ‘insulin resistance phenotype’) and multisystem structural damage that conspire to enhance cardiovascular risk beyond that which can be attributed to blood pressure alone.

Left ventricular hypertrophy is a classic feature of untreated or inadequately treated long-standing hypertension, and is a very potent predictor of premature cardiovascular disease and death. Inhibition of the renin–angiotensin–aldosterone system is particularly effective at regressing left ventricular hypertrophy, which is associated with dramatically improved prognosis for people with hypertension.

Hypertension is the single most important risk factor for stroke, and is increasingly recognized as a major factor contributing to the rate of cognitive decline in later life. Patients with renal disease often have hypertension, people with hypertension can develop renal disease, and the age-related decline in GFR is more rapid in people with essential hypertension, but renal function is usually well preserved throughout life in patients with mild to moderate essential hypertension. Retinal changes caused by hypertension are discussed in Chapter 16.17.2.

Implications of the evolution of hypertensive injury

The process of hypertensive injury to target organs evolves silently over many years. Current treatment guidelines have been developed from an evidence base relating to changes in hard clinical endpoints derived from studies in very elderly patients at the end of the hypertensive disease process. Future treatment strategies must surely focus on preventing the evolution of the silent disease process, rather than simply battling with its consequences.

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