Epidemiology of Hypertension 

Updated: Dec 30, 2020
Author: Albert W Dreisbach, MD; Chief Editor: Vecihi Batuman, MD, FASN 

National Estimates of Hypertension

Hypertension is a worldwide epidemic; accordingly, its epidemiology has been well studied in the United States and internationally.

National High Blood Pressure Education Program

In 1991, the National High Blood Pressure Education Program (NHBPEP) estimated 43.3 million adults had hypertension in United States.[1] Hypertension was defined as systolic blood pressure (SBP) equal to or greater than 140 mm Hg and diastolic BP (DBP) as equal or more than 90 mm Hg or defined as those taking medication for hypertension. The prevalence according to age group, sex, and race is shown in Table 1, below.

Table 1. Prevalence (%) of Hypertension in the United States, 1989-1994* [1] (Open Table in a new window)

Age Groups (y)

 

All Races

White

Black

 

Men (%)

Women (%)

Total (%)

Men (%)

Women (%)

Total (%)

Men (%)

Women (%)

Total (%)

18-24

 

2.6

4.6

0.7

2.5

4.6

0.5

2.6

4.1

1.4

25-34

 

5.4

8.4

2.4

4.9

8.1

1.6

8.2

10.6

6.2

35-44

 

13.0

16.0

10.2

11.3

14.3

8.5

25.9

29.5

22.9

45-54

 

27.6

30.0

25.2

25.8

29.1

22.6

46.9

44.3

48.8

55-64

 

43.7

44.2

43.2

42.1

43.0

41.4

60.0

58.0

63.0

65-74

 

59.6

55.8

62.7

58.6

54.9

61.7

71.0

65.2

75.6

75+

 

70.3

60.5

76.2

69.7

59.0

76.1

75.5

71.3

77.9

Total

 

23.4

23.5

23.3

23.2

23.4

23.1

28.1

27.9

28.2

* Includes racial/ethnic groups not shown separately because of small sample sizes.

NHANES and NCHS

According to data from the National Health Examination Surveys (NHANES), the age-adjusted prevalence of hypertension varies from 18% to 32%. The National Center for Health Statistic Surveys (NCHS) reported the awareness for hypertension increased from 53% over 1960-1962 to 89% over 1988-1991.[2] The percentage of patients engaged in hypertension treatment increased from 35% to 79% during this period.[2]

In a separate report, age- and sex-adjusted rates of prehypertension and stage I hypertension increased among non-Hispanic white, black, and Hispanic persons between 1988-1992 and 1999-2000; however, the age- and sex-adjusted rates of stage 2 hypertension decreased among non-Hispanic whites between 1988-1992 and 1999-2000, whereas they were unchanged for black and Hispanic persons.[3]

A 2005 NHANES report in the United States found that in the population aged 20 years or older, an estimated 41.9 million men and 27.8 million women had prehypertension (SBP, 120-139 mm Hg; DBP, 80-99 mm Hg), 12.8 million men and 12.2 million women had stage 1 hypertension (SBP, 140-159 mm Hg; DBP, 90-99 mm Hg), and 4.1 million men and 6.9 million women had stage 2 hypertension (SBP ≥160 mm Hg; DBP ≥100 mm Hg).[2]

Hypertension is a common and manageable chronic condition. Based on 2011-2012 national data, treatment of hypertension exceeded the Healthy People 2020 target goal of 69.5%.[4] However, the control of hypertension neither met the goal of the Healthy People 2020 (61.2% by 2020) nor the Million Hearts Initiative (65% by 2017). These results provide evidence for continued efforts to improve the management of hypertension in order to attain these goals.

2011-2012 NHANES data showed an increase in prevalence in hypertension in all age groups from 23.4% to 29.1% compared to 1991.[4] The prevalence in non-Hispanic Black persons rose from 28.2% to 42% during the same period. Among adults with hypertension in 2011-2012, 82.8% were aware of their hypertension, 75.7% were currently taking medication to lower their BP, and 51.9% had their BP controlled to less than 140/90 mm Hg. However, awareness, treatment, and control of hypertension were similar among non-Hispanic Black, non-Hispanic White, and Hispanic adults.[4] A multinational study in high-, middle-, and low-income countries showed that 46.5% of participants with hypertension were aware of their diagnosis, with BP control in only 32.5% of those being treated.[5] The percentage BP control was greater in high-income countries than in low-income countries (46.7% vs 31.7%) and was associated with lower rates of awareness, treatment, and control in low-income countries but not in other countries.[5]

Data from NHANES spanning 2011-2014 in the United States found that in the population aged 20 years or older, an estimated 86 million adults had hypertension, with a prevalence of 34%.[6]  2017 Data from the NCHS spanning 2015-2016 show a hypertension prevalence of 29.0% among those aged 18 and older.[7]  There was also an increasing trend of hypertension in adults between 1999-2000 and 2009-2010, and 2013-2014, with mild declines in 2011-2012 and 2015-2016.[7]

Multi-Ethnic Study of Atherosclerosis

The Multi-Ethnic Study of Atherosclerosis is a US-based study that examined the associations of left ventricular (LV) mass and geometry with hypertension incidence in 2,567 normotensive participants. The study found that higher LV mass was associated with incident hypertension. Over 4.8 years, 745 participants developed hypertension.[8]

 

Worldwide Estimates of Hypertension

Globally, an estimated 26% of the world’s population (972 million people) has hypertension, and the prevalence is expected to increase to 29% by 2025, driven largely by increases in economically developing nations.[9] The high prevalence of hypertension exacts a tremendous public health burden. As a primary contributor to heart disease and stroke, the first and third leading causes of death worldwide, respectively, high blood pressure was the top modifiable risk factor for disability adjusted life-years lost worldwide in 2013.[10, 11]

The prevalence of hypertension dramatically increases in patients older than 60 years: In many countries, 50% of individuals in this age group have hypertension. Worldwide, hypertension contributes to more than 7.1 million deaths per year.[12]

National health surveys in various countries have shown a high prevalence of poor control of hypertension.[13] These studies have reported that prevalence of hypertension is 22% in Canada, of which 16% is controlled; it is 26.3% in Egypt, of which 8% is controlled; and it is 13.6% in China, of which 3% is controlled.

 

Age Distribution for Hypertension

The ACCORD study was equally powered it may demonstrated benefit of the intensive control group as well.[14, 15]

A progressive rise in BP with increasing age is observed. Age-related hypertension appears to be predominantly systolic rather than diastolic. The SBP rises into the eighth or ninth decade, whereas the DBP remains constant or declines after age 40 years.[3]  Until age 45 years, a higher percentage of men than women have hypertension; from age 45 to 64 years, the percentages are nearly equal between men and women. Beyond age 64 years, a higher percentage of women have hypertension than men.[16]

The third NHANES survey reported that the prevalence of hypertension grows significantly with increasing age in all sex and race groups.[17] The age-specific prevalence was 3.3% in white men (aged 18-29 y); this rate increased to 13.2% in the group aged 30-39 years. The prevalence further increased to 22% in the group aged 40-49 years, to 37.5% in the group aged 50-59 years, and to 51% in the group aged 60-74 years.[17] In another study, the incidence of hypertension appeared to increase approximately 5% for each 10-year interval of age.

Cardiovascular disease risk

According to the 2003 Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), in individuals older than 50 years, SBP of greater than 140 mm Hg is a more important cardiovascular disease risk factor than DBP.[18] It recommended targets of 130 mm Hg in diabetics or patients with chronic kidney disease. Beginning at a BP of 115/75 mm Hg, the cardiovascular disease risk doubles for each increment of 20/10 mm Hg. Individuals who are normotensive (SBP < 120 mm Hg; DBP < 80 mm Hg) at 55 years will have a 90% lifetime risk of developing hypertension.

Trials

The question of appropriate targets for SBP was addressed in three studies since JNC 7 was released.

  • In 2010, the results of the Action to Control Cardiovascular Risk in Diabetes (ACCORD BP) study were reported.[15] In this study, 4733 type II diabetic patients (34% had cardiovascular disease, all had normal renal function, and 24% were Black) were randomized to an SBP of 130-140 mm Hg or below 120 mm Hg. Mean follow-up was 4.7 years. Although the hazard ratio (HR) was 0.88 for the primary cardiovascular endpoint (composite of nonfatal myocardial infarction [MI], nonfatal stroke, or death from cardiovascular causes) for the intensive control group and it trended toward greater benefit of tight control, this did not reach statistical significance. However, the rate of total stroke was reduced by 40%, the frequency of macro-albuminuria at the final visit was lower in the intensive treatment group, and there was no difference in the frequency of end-stage renal disease (ESRD) or the need for dialysis.[15] Quality of life (QOL) and frequency of orthostatic hypotension was similar in both groups. Adverse reactions in the intensive treatment group included hypotension and increased frequency of an estimated glomerular filtration rate (eGFR) below 30 mL/min/1.73 m2.

  • In 2013, the results of the Secondary Prevention of Small Subcortical Strokes (SPS3) were released.[19] This open-label randomized trial included 3020 patients from North America, Latin America, and Spain who had recent magnetic resonance image (MRI)-defined symptomatic lacunar infarctions and randomized them to an SBP of 130-139 mm Hg or below 130 mm Hg. The population was 36% diabetic and 17% of African ethnic origin. Nonsignificant reductions were seen in the all stroke (HR 0.81, P < 0.08), disabling or fatal stroke (HR 0.81, P< 0.32), and composite outcome of MI or vascular death (HR 0.84. P< 0.32), but there was a significant 63% reduction in the rate of intracerebral hemorrhage (HR 0.37, P< 0.03).

  • In 2014, the JNC 8 panel did not reach consensus; therefore, a group of panel members independently published evidence-based recommendations for a SBP to target of less than 150/90 mm Hg in patients older than 60 years and below 140/90 mm Hg in younger patients, even for those with diabetes and underling chronic kidney disease.[20] Thus, the target of 130/80 mm Hg for chronic kidney disease and diabetes from JNC 7 was no longer recommended  although there was a suggestion that tighter control may be warranted in the setting of proteinuria. These recommendations were based partly on data from the ACCORD trial showing there was no statistical benefit of intensive control on cardiovascular mortality in diabetics. A great deal of controversy surrounded these new recommendations, especially as they would impact older women and Black individuals.[21]

The Systolic Blood Pressure Intervention Trial (SPRINT) results released in 2015 brought the JNC 8 recommendations into question.[22] SPRINT was a controlled trial in 9361 nondiabetic hypertensive patients with a high risk for cardiovascular disease who were over age 50 years and randomized to a target SBP of 130-40 mm Hg or less than 120 mm Hg (same as in the ACCORD trial). Exclusion criteria were a history of prior cerebrovascular accident and diabetes. Participans were 28% with chronic kidney disease (mean eGFR: 47.3 mL/min/1.73 m2) and 31% Black. The data safety monitoring board ended the study early at 3.6 years (before the maximum 6-year follow-up) because of a clear benefit in the intensive therapy group: The lower SBP target of 120 mm Hg was associated with a 24% reduction of the primary composite endpoint (MI, non-MI acute coronary syndrome, acute decompensated heart failure, or death from cardiovascular disease).

Both the ACCORD and SPRINT trials demonstrated that the SBP target of 120 mm Hg was feasible and sustainable. However, SPRINT found an increased risk of acute kidney injury in those with an initial normal baseline renal function, syncope, and emergency department visits for hypotension in the intensively treated group.[22] SPRINT had twice the population and thus had more power to detect a treatment benefit when compared to ACCORD or SPS-3.[23, 24, 25] ACCORD and SPRINT also showed an adverse effect of intensive treatment on eGFR in participants with an initial normal renal function. There was no significant change in renal function with intensive treatments in patients with chronic kidney disease at baseline in SPRINT, and there was no increase in the incidence of ESRD in either study in the intensive treatment groups.

A 2016 observational database review of 187,106 type 2 diabetics in the Swedish national diabetes registry demonstrated improved cardiovascular outcomes including non-fatal acute MI (HR 0.76, P  = 0.003), total acute MI (HR 0.85, P = 0.04), total cardiovascular disease (HR 0.82, P = 0.002), and non-fatal coronary heart disease (HR 0.88, P = 0.03) in the group with an SBP of 110-119 mmg Hg compared to the reference group SBP of 130-139 mm Hg.[26] There was no indication of a J point-shaped relationship between SBP and the cardiovascular endpoint, with the exception of increased heart failure and total mortality.

 

Prevalence of Hypertension by Sex

The third report of teh National Health Examination Surveys (NHANES III) revealed an age-adjusted hypertension prevalence of 34%, 25.4%, and 23.2% for men and 31%, 21%, and 21.6% for women among Blacks, Whites, and Mexican Americans, respectively.[3] The prevalence of hypertension was 12% for White men and 5% for White women aged 18-49 years; however, the age-related BP rise for women exceeded that of men. The prevalence of hypertension was reported at 50% for White men and 55% for White women aged 70 years or older.[3]

 

Prevalence of Hypertension by Race or Ethnicity

Black individuals have a higher prevalence and incidence of hypertension than white persons.[27] The prevalence of hypertension has been reported to be increased by 50% in blacks. Most studies in the United Kingdom and the United States report not only a higher prevalence but also a lower awareness of hypertension in black people than in white people. Mortality from hypertension in African-Caribbean–born people is 3.5 times the national rate; similar data have been published for African American citizens.

The prevalence and incidence of hypertension in Mexican Americans are similar to or lower than those in non-Hispanic whites.[28] NHANES III reported an age-adjusted prevalence of hypertension at 20.6% in Mexican Americans and 23.3% in non-Hispanic whites.[3, 17] In general, Mexican Americans and Native Americans have lower BP control rates than non-Hispanic white persons and black individuals.[29]

To understand ethnic influence, an understanding of the renin-angiotensin system (RAS) is essential. Renin secretion is suppressed when the kidney detects that the amount of sodium excretion is increased; thus, this is a clue to the excess sodium in the circulation. Black people tend to develop hypertension at an earlier age and have lower renin activity; target organ damage also differs in black people from that in white people.

In addition, black people have a poorer response to treatment with angiotensin converting enzyme (ACE) inhibitors compared with white people; the evidence for beta-blockers being less effective in black people is also clear. However, diuretics are more effective at a young age in black people.

In comparative assessments of black people and Asians, strokes are more common in black people, but coronary heart disease is more common in Asians. Both groups have a higher incidence of chronic renal failure than white people, but this is more due to hypertension in black people and diabetes in Asians.

 

Genetics of Hypertension

There are rare forms of hypertension due to single genetic mutations, so called Mendelian forms. These involve mutations in the epithelial sodium channel (ENaC) in the distal renal tubule (Liddle syndrome), mineralocorticoid receptor, chimeric CYP11B2 (familial hyperaldosteronism type I), and others. The inheritance of the mutation almost always results in the development of hypertension.[30]  (See the Medscape Drugs and Diseases topic Pathophysiology of Hypertension.)

However, hypertension is a broad phenotype, which results from perturbations of many mechanistic pathways and usually requires multiple hits to manifest. Large genetic epidemiologic studies known as genome-wide association studies (GWAS) with over 100,000 subjects have identified 30 or more variants with a relatively modest contribution of the risk of hypertension, such as in the adrenergic receptor (ADRB1) and angiotensinogen genes.[31]

Polymorphisms in the gene KCNK3, which reduce the expression of the TASK-1 potassium channels, were associated with increased plasma aldosterone and mean arterial pressure across all ethnic groups in genetic consortia in 7840 individuals in the Multi-Ethnic Study of Atherosclerosis Study (MESA).[32] The angiotensin II AT1 receptor polymorphism at position 1166 has been associated with severe hypertension.[33] Studies have found polymorphisms in the alpha-2 and beta-2 adrenergic receptors were significantly associated with blood pressure variation.[33, 34]

Alpha adducin gene ADD1 codes for a cytoskeletal protein involved in salt transport in rats models and may play a role in salt-sensitive hypertension.[33, 34] A Chinese case control study of 170 patients with essential hypertension and 154 normotensive subjects showed an association of G614T polymorphisms of ADD1 and essential hypertension.[35]

GNB (G protein beta-2 subunit) 825T allele had a strong association with hypertension in the 35 populations in the International Sodium Potassium and Blood Pressure (INTERSALT) study.[34, 36]  Rare exome sequence variants of CLCN6 chloride channel in 9950 European Americans and 4547 Blacks has been associated with lower systolic and diastolic pressures and a reduced hypertensive risk.[37] Despite their small impact on risk, these genes and pathways may serve to identify targets for novel drugs.