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Hypertension affects approximately 75 million adults in the United States and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease. See the image below.
Essential update: Study finds significant increase in US emergency room visits for hypertension
Between 2006 and 2011, there was a 25% increase in the number of people visiting US emergency rooms for essential hypertension, according to a new analysis of data from the Nationwide Emergency Department Sample. The reason for the increase, however, remained uncertain. The rate of emergency department visits also increased significantly, according to the study, rising from 190.1 visits per 100,000 population in 2006 to 238.5 visits per 100,000 population in 2011. Over the same period, however, admission rates decreased, from 10.47% in 2006 to 8.85% in 2011.
Emergency department visits for hypertension with complications and secondary hypertension also rose, from 71.2 per 100,000 population in 2006 to 84.7 per 100,000 population in 2011, while again, admission rates fell, dropping from 77.79% in 2006 to 68.75% in 2011. The in-hospital mortality rate for admitted patients dropped as well, from 1.95% in 2006 to 1.25% in 2011.
Signs and symptoms
Hypertension is defined as a systolic blood pressure (SBP) of 140 mm Hg or more, or a diastolic blood pressure (DBP) of 90 mm Hg or more, or taking antihypertensive medication.
Based on recommendations of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), the classification of BP for adults aged 18 years or older has been as follows :
Normal: Systolic lower than 120 mm Hg, diastolic lower than 80 mm Hg
Prehypertension: Systolic 120-139 mm Hg, diastolic 80-89 mm Hg
Stage 1: Systolic 140-159 mm Hg, diastolic 90-99 mm Hg
Stage 2: Systolic 160 mm Hg or greater, diastolic 100 mm Hg or greater
Hypertension may be primary, which may develop as a result of environmental or genetic causes, or secondary, which has multiple etiologies, including renal, vascular, and endocrine causes. Primary or essential hypertension accounts for 90-95% of adult cases, and secondary hypertension accounts for 2-10% of cases.
See Clinical Presentation for more detail.
The evaluation of hypertension involves accurately measuring the patient’s blood pressure, performing a focused medical history and physical examination, and obtaining results of routine laboratory studies.[3, 4] A 12-lead electrocardiogram should also be obtained. These steps can help determine the following[3, 4, 5] :
Presence of end-organ disease
Possible causes of hypertension
Cardiovascular risk factors
Baseline values for judging biochemical effects of therapy
Other studies may be obtained on the basis of clinical findings or in individuals with suspected secondary hypertension and/or evidence of target-organ disease, such as CBC, chest radiograph, uric acid, and urine microalbumin.
See Workup for more detail.
Many guidelines exist for the management of hypertension. Most groups, including the JNC, the American Diabetes Associate (ADA), and the American Heart Association/American Stroke Association (AHA/ASA) recommend lifestyle modification as the first step in managing hypertension.
JNC 7 recommendations to lower BP and decrease cardiovascular disease risk include the following, with greater results achieved when 2 or more lifestyle modifications are combined :
Weight loss (range of approximate systolic BP reduction [SBP], 5-20 mm Hg per 10 kg)
Limit alcohol intake to no more than 1 oz (30 mL) of ethanol per day for men or 0.5 oz (15 mL) of ethanol per day for women and people of lighter weight (range of approximate SBP reduction, 2-4 mm Hg)
Reduce sodium intake to no more than 100 mmol/day (2.4 g sodium or 6 g sodium chloride; range of approximate SBP reduction, 2-8 mm Hg) 
Maintain adequate intake of dietary potassium (approximately 90 mmol/day)
Maintain adequate intake of dietary calcium and magnesium for general health
Stop smoking and reduce intake of dietary saturated fat and cholesterol for overall cardiovascular health
Engage in aerobic exercise at least 30 minutes daily for most days (range of approximate SBP reduction, 4-9 mm Hg)
The AHA/ASA recommends a diet that is low in sodium, is high in potassium, and promotes the consumption of fruits, vegetables, and low-fat dairy products for reducing BP and lowering the risk of stroke. Other recommendations include increasing physical activity (30 minutes or more of moderate intensity activity on a daily basis) and losing weight (for overweight and obese persons).
The 2013 European Society of Hypertension (ESH) and the European Society of Cardiology (ESC) guidelines recommend a low-sodium diet (limited to 5 to 6 g per day) as well as reducing body-mass index (BMI) to 25 kg/m2 and waist circumference (to < 102 cm in men and < 88 cm in women).[7, 8]
If lifestyle modifications are insufficient to achieve the goal BP, there are several drug options for treating and managing hypertension. Thiazide diuretics are the preferred agents in the absence of compelling indications.
Compelling indications may include high-risk conditions such as heart failure, ischemic heart disease, chronic kidney disease, and recurrent stroke, or those conditions commonly associated with hypertension, including diabetes and high coronary disease risk. Drug intolerability or contraindications may also be factors. An angiotensin-converting enzyme (ACE) inhibitor, angiotensin receptor blocker (ARB), calcium channel blocker (CCB), and beta-blocker are all acceptable alternative agents in such compelling cases.
The following are drug class recommendations for compelling indications based on various clinical trials :
Heart failure: Diuretic, beta-blocker, ACE inhibitor, ARB, aldosterone antagonist
Postmyocardial infarction: Beta-blocker, ACE inhibitor, aldosterone antagonist
High coronary disease risk: Diuretic, beta-blocker, ACE inhibitor, CCB
Diabetes: Diuretic, beta-blocker, ACE inhibitor, ARB, CCB
Chronic kidney disease: ACE inhibitor, ARB
Recurrent stroke prevention: Diuretic, ACE inhibitor
Hypertension is one of the most common worldwide diseases afflicting humans and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease. Despite extensive research over the past several decades, the etiology of most cases of adult hypertension is still unknown, and control of blood pressure is suboptimal in the general population. Due to the associated morbidity and mortality and cost to society, preventing and treating hypertension is an important public health challenge. Fortunately, recent advances and trials in hypertension research are leading to an increased understanding of the pathophysiology of hypertension and the promise for novel pharmacologic and interventional treatments for this widespread disease.
According to the American Heart Association (AHA), approximately 75 million adults in the United States are affected by hypertension, which is defined as a systolic blood pressure (SBP) of 140 mm Hg or more or a diastolic blood pressure (DBP) of 90 mm Hg or more or taking antihypertensive medication. Substantial improvements have been made with regard to enhancing awareness and treatment of hypertension. However, a National Health Examination Survey (NHANES) spanning 2005-2006 showed that 29% of US adults 18 years of age and older were hypertensive; 7% of hypertensive adults had never been told that they had hypertension.
Furthermore, of those with high blood pressure (BP), 78% were aware they were hypertensive, 68% were being treated with antihypertensive agents, and only 64% of treated individuals had controlled hypertension. In addition, data from NHANES 1999-2006 estimated that 30% of adults 20 years of age and older have prehypertension, defined as an untreated SBP of 120-139 mm Hg or untreated DBP of 80-89 mmHg. (See Epidemiology.)
Data from the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), which was released in 2003, were relatively similar to the NHANES data. The JNC 7 noted that approximately 30% of adults were unaware of their hypertension; up to 40% of people with hypertension were not receiving treatment; and, of those treated, up to 67% did not have their BP controlled to less than 140/90 mm Hg.
Hypertension is the most important modifiable risk factor for coronary heart disease (the leading cause of death in North America), stroke (the third leading cause), congestive heart failure, end-stage renal disease, and peripheral vascular disease. Therefore, health care professionals must not only identify and treat patients with hypertension but also promote a healthy lifestyle and preventive strategies to decrease the prevalence of hypertension in the general population. (See Treatment.)
Definition and classification
Defining abnormally high blood pressure (BP) is extremely difficult and arbitrary. Furthermore, the relationship between systemic arterial pressure and morbidity appears to be quantitative rather than qualitative. A level for high BP must be agreed upon in clinical practice for screening patients with hypertension and for instituting diagnostic evaluation and initiating therapy. Because the risk to an individual patient may correlate with the severity of hypertension, a classification system is essential for making decisions about aggressiveness of treatment or therapeutic interventions. (See Presentation.)
Based on recommendations of the JNC 7, the classification of BP (expressed in mm Hg) for adults aged 18 years or older is as follows :
Normal: systolic lower than 120 mm Hg, diastolic lower than 80 mm Hg
Prehypertension: systolic 120-139 mm Hg, diastolic 80-89 mm Hg
Stage 1: systolic 140-159 mm Hg, diastolic 90-99 mm Hg
Stage 2: systolic 160 mm Hg or greater, diastolic 100 mm Hg or greater
The classification above is based on the average of 2 or more readings taken at each of 2 or more visits after initial screening.[3, 5] Normal BP with respect to cardiovascular risk is less than 120/80 mm Hg. However, unusually low readings should be evaluated for clinical significance.
The Eighth Report of the JNC (JNC 8), released in December 2013, recommends less aggressive target blood pressures and treatment-initiation thresholds than the JNC7 for elderly patients and in patients younger than 60 years with diabetes and kidney disease, and no longer recommends just thiazide-type diuretics as initial therapy in most patients.[9, 10] In essence, the JNC 8 recommends treating to 150/90 mm Hg in patients over age 60 years; for everybody else, the goal BP is 140/90.
Prehypertension, a new category designated in the JNC 7 report, emphasizes that patients with prehypertension are at risk for progression to hypertension and that lifestyle modifications are important preventive strategies.
From another perspective, hypertension may be categorized as either essential or secondary. Primary (essential) hypertension is diagnosed in the absence of an identifiable secondary cause. Approximately 90-95% of adults with hypertension have primary hypertension, whereas secondary hypertension accounts for around 5-10% of the cases. However, secondary forms of hypertension, such as primary hyperaldosteronism, account for 20% of resistant hypertension (hypertension in which BP is >140/90 mm Hg despite the use of medications from 3 or more drug classes, 1 of which is a thiazide diuretic).
Especially severe cases of hypertension, or hypertensive crises, are defined as a BP of more than 180/120 mm Hg and may be further categorized as hypertensive emergencies or urgencies. Hypertensive emergencies are characterized by evidence of impending or progressive target organ dysfunction, whereas hypertensive urgencies are those situations without progressive target organ dysfunction.
In hypertensive emergencies, the BP should be aggressively lowered within minutes to an hour by no more than 25%, and then lowered to 160/100-110 mm Hg within the next 2-6 hours. Acute end-organ damage in the setting of a hypertensive emergency may include the following :
Neurologic: hypertensive encephalopathy, cerebral vascular accident/cerebral infarction, subarachnoid hemorrhage, intracranial hemorrhage
Cardiovascular: myocardial ischemia/infarction, acute left ventricular dysfunction, acute pulmonary edema, aortic dissection, unstable angina pectoris
Other: acute renal failure/insufficiency, retinopathy, eclampsia, microangiopathic hemolytic anemia
With the advent of antihypertensives, the incidence of hypertensive emergencies has declined from 7% to approximately 1%. In addition, the 1-year survival rate associated with this condition has increased from only 20% (prior to 1950) to more than 90% with appropriate medical treatment. (See Medication.)
The pathogenesis of essential hypertension is multifactorial and highly complex. Multiple factors modulate the blood pressure (BP) for adequate tissue perfusion and include humoral mediators, vascular reactivity, circulating blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation. A possible pathogenesis of essential hypertension has been proposed in which multiple factors, including genetic predisposition, excess dietary salt intake, and adrenergic tone, may interact to produce hypertension. Although genetics appears to contribute to essential hypertension, the exact mechanism has not been established.
Due to investigations into the pathophysiology of hypertension, both in animals and humans, growing evidence suggests that hypertension may have an immunological basis. Studies have revealed that hypertension is associated with renal infiltration of immune cells and that pharmacologic immunosuppression (such as with the drug mycophenolate mofetil) or pathologic immunosuppression (such as occurs with HIV) results in reduced blood pressure in animals and humans. Evidence suggests that T lymphocytes and T-cell derived cytokines (eg, interleukin 17, tumor necrosis factor alpha) play an important role in hypertension.
One hypothesis is that prehypertension results in oxidation and altered mechanical forces that lead to the formation of neoantigens, which are then presented to T cells, leading to T-cell activation and infiltration of critical organs (eg, kidney, vasculature). This results in persistent or severe hypertension and end organ damage. Sympathetic nervous system activation and noradrenergic stimuli have also been shown to promote T-lymphocyte activation and infiltration and contribute to the pathophysiology of hypertension.[16, 17, 18]
The natural history of essential hypertension evolves from occasional to established hypertension. After a long invariable asymptomatic period, persistent hypertension develops into complicated hypertension, in which end-organ damage to the aorta and small arteries, heart, kidneys, retina, and central nervous system is evident.
The progression of essential hypertension is as follows:
- Prehypertension in persons aged 10-30 years (by increased cardiac output)
- Early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent)
- Established hypertension in persons aged 30-50 years
- Complicated hypertension in persons aged 40-60 years
One mechanism of hypertension has been described as high-output hypertension. High-output hypertension results from decreased peripheral vascular resistance and concomitant cardiac stimulation by adrenergic hyperactivity and altered calcium homeostasis. A second mechanism manifests with normal or reduced cardiac output and elevated systemic vascular resistance due to increased vasoreactivity. Another (and overlapping) mechanism is increased salt and water reabsorption (salt sensitivity) by the kidney, which increases circulating blood volume.
Cortisol reactivity, an index of hypothalamic-pituitary-adrenal function, may be another mechanism by which psychosocial stress is associated with future hypertension. In a prospective substudy of the Whitehall II cohort, with 3 years follow-up of an occupational cohort in previously healthy patients, investigators reported 15.9% of the patient sample developed hypertension in response to laboratory-induced mental stressors and found an association between cortisol stress reactivity and incident hypertension.
Hypertension may be primary, which may develop as a result of environmental or genetic causes, or secondary, which has multiple etiologies, including renal, vascular, and endocrine causes. Primary or essential hypertension accounts for 90-95% of adult cases, and a small percentage of patients (2-10%) have a secondary cause. Hypertensive emergencies are most often precipitated by inadequate medication or poor compliance.
Environmental and genetic/epigenetic causes
Hypertension develops secondary to environmental factors, as well as multiple genes, whose inheritance appears to be complex.[14, 20] Furthermore, obesity, diabetes, and heart disease also have genetic components and contribute to hypertension. Epidemiological studies using twin data and data from Framingham Heart Study families reveal that BP has a substantial heritable component, ranging from 33-57%.[21, 22, 23]
In an attempt to elucidate the genetic components of hypertension, multiple genome wide association studies (GWAS) have been conducted, revealing multiple gene loci in known pathways of hypertension as well as some novel genes with no known link to hypertension as of yet. Further research into these novel genes, some of which are immune-related, will likely increase the understanding of hypertension's pathophysiology, allowing for increased risk stratification and individualized treatment.
Epigenetic phenomena, such as DNA methylation and histone modification, have also been implicated in the pathogenesis of hypertension. For example, a high-salt diet appears to unmask nephron development caused by methylation. Maternal water deprivation and protein restriction during pregnancy increase renin-angiotensin expression in the fetus. Mental stress induces a DNA methylase, which enhances autonomic responsiveness. The pattern of serine protease inhibitor gene methylation predicts preeclampsia in pregnant women.
Despite these genetic findings, targeted genetic therapy seems to have little impact on hypertension. In the general population, not only does it appear that individual and joint genetic mutations have very small effects on BP levels, but it has not been shown that any of these genetic abnormalities are responsible for any applicable percentage of cases of hypertension in the general population.
Secondary causes of hypertension related to single genes are very rare. They include Liddle syndrome, glucocorticoid-remediable hyperaldosteronism, 11 beta-hydroxylase and 17 alpha-hydroxylase deficiencies, the syndrome of apparent mineralocorticoid excess, and pseudohypoaldosteronism type II.
Causes of secondary hypertension
Renal causes (2.5-6%) of hypertension include the renal parenchymal diseases and renal vascular diseases, as follows:
Polycystic kidney disease
Chronic kidney disease
Urinary tract obstruction
Renovascular hypertension (RVHT) causes 0.2-4% of cases. Since the seminal experiment in 1934 by Goldblatt et al, RVHT has become increasingly recognized as an important cause of clinically atypical hypertension and chronic kidney disease—the latter by virtue of renal ischemia. The coexistence of renal arterial vascular (ie, renovascular) disease and hypertension roughly defines this type of nonessential hypertension. More specific diagnoses are made retrospectively when hypertension is improved after intravascular intervention.
Vascular causes include the following:
Coarctation of aorta
Collagen vascular disease
Endocrine causes account for 1-2% and include exogenous or endogenous hormonal imbalances. Exogenous causes include administration of steroids. The most common form of secondary hypertension is a renal cause (although the true prevalence of hyperaldosteronism is not clear).
Another common cause is endocrine: oral contraceptive use. Activation of the renin-angiotensin-aldosterone system (RAAS) is the likely mechanism, because hepatic synthesis of angiotensinogen is induced by the estrogen component of oral contraceptives. Approximately 5% of women taking oral contraceptives may develop hypertension, which abates within 6 months after discontinuation. The risk factors for oral contraceptive–associated hypertension include mild renal disease, familial history of essential hypertension, age older than 35 years, and obesity. It would be better to group oral contraceptives and steroids with drug-induced hypertension (see Table 1, below).
Exogenous administration of the other steroids used for therapeutic purposes also increases blood pressure (BP), especially in susceptible individuals, mainly by volume expansion. Nonsteroidal anti-inflammatory drugs (NSAIDs) may also have adverse effects on BP. NSAIDs block both cyclooxygenase-1 (COX-1) and COX-2 enzymes. The inhibition of COX-2 can inhibit its natriuretic effect, which, in turn, increases sodium retention. NSAIDs also inhibit the vasodilating effects of prostaglandins and the production of vasoconstricting factors—namely, endothelin-1. These effects can contribute to the induction of hypertension in a normotensive or controlled hypertensive patient.
Endogenous hormonal causes include the following:
Congenital adrenal hyperplasia
Neurogenic causes include the following:
Drugs and toxins that cause hypertension include the following:
Decongestants containing ephedrine
Herbal remedies containing licorice (including licorice root) or ephedrine (and ephedra)
Other causes include the following:
Hyperthyroidism and hypothyroidism
Obstructive sleep apnea
Obstructive sleep apnea (OSA) is a common but frequently undiagnosed sleep-related breathing disorder defined as an average of at least 10 apneic and hypopenic episodes per sleep hour, which leads to excessive daytime sleepiness. Multiple studies have shown OSA to be an independent risk factor for the development of essential hypertension, even after adjusting for age, gender, and degree of obesity.
Approximately half of individuals with hypertension have OSA, and approximately half with OSA have hypertension. Ambulatory BP monitoring normally reveals a "dip" in BP of at least 10% during sleep. However, if a patient is a "nondipper," the chances that the patient has OSA is increased. Nondipping is thought to be caused by frequent apneic/hypopneic episodes that end with arousals associated with marked spikes in BP that last for several seconds.
Numerous studies have shown that treatment of OSA by continuous positive airway pressure (CPAP) or position therapy lowers the awake and 24-hour blood pressure levels. Unfortunately, most cases of OSA go undiagnosed. Improved physician awareness and screening for this reversible cause of hypertension is likely to lead to great improvements in quality of life and a reduced incidence of cardiovascular complications.
Causes of hypertensive emergencies
The most common hypertensive emergency is a rapid unexplained rise in BP in a patient with chronic essential hypertension. Most patients who develop hypertensive emergencies have a history of inadequate hypertensive treatment or an abrupt discontinuation of their medications.[29, 30]
Other causes of hypertensive emergencies include the use of recreational drugs, abrupt clonidine withdrawal, post pheochromocytoma removal, and systemic sclerosis, as well as the following:
Renal parenchymal disease: chronic pyelonephritis, primary glomerulonephritis, tubulointerstitial nephritis (accounts for 80% of all secondary causes)
Systemic disorders with renal involvement: systemic lupus erythematosus, systemic sclerosis, vasculitides
Renovascular disease: atherosclerotic disease, fibromuscular dysplasia, polyarteritis nodosa
Endocrine disease: pheochromocytoma, Cushing syndrome, primary hyperaldosteronism
Drugs: cocaine,  amphetamines, cyclosporine, clonidine (withdrawal), phencyclidine, diet pills, oral contraceptive pills
Drug interactions: monoamine oxidase inhibitors with tricyclic antidepressants, antihistamines, or tyramine-containing food
Central nervous system factors: CNS trauma or spinal cord disorders, such as Guillain-Barré syndrome
Coarctation of the aorta
Hypertension is a worldwide epidemic; accordingly, its epidemiology has been well studied. Data from National Health and Nutrition Examination Survey (NHANES) spanning 1999-2002 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, 12.8 million men and 12.2 million women had stage 1 hypertension, and 4.1 million men and 6.9 million women had stage 2 hypertension. Data from NHANES spanning 2003–2006 showed that 33.6% of US adults 20 years of age have hypertension, resulting in an estimated 74.5 million US adults with hypertension.
In many countries, 50% of the population older than 60 years have hypertension. Overall, approximately 20% of the world’s adults are estimated to have hypertension. The 20% prevalence is for hypertension defined as blood pressure (BP) in excess of 140/90 mm Hg. The prevalence dramatically increases in patients older than 60 years.
In a large Spanish epidemiologic study over a 10-year period, investigators found that despite an increase in the intensity of hypertensive therapy, the prevalence of uncontrolled hypertension (systolic BP [SBP] ≤140 mm Hg and/or diastolic BP [DBP] ≤90 mm Hg) did not change significantly over time. In addition, there appeared to be worse control in at-risk individuals (SBP ≤130 mm Hg and/or DBP ≤80-85 mm Hg) who had comorbidities.
Hypertension and sex- and age-related statistics
Until age 45 years, a higher percentage of men than women have hypertension; from age 45 years onward, the percentages are nearly equal between men and women. In women, those who use oral contraceptives, particularly obese and older women, have a 2- to 3-fold higher risk of hypertension than women not using these agents.
Hypertension in black adults
Globally, black adults have among the highest rates of hypertension, with an increasing prevalence. Although white adults also have an increasing incidence of high BP, they develop this condition later in life than black adults and have much lower average BPs. In fact, compared to hypertensive white persons, hypertensive black individuals have a 1.3-fold higher rate of nonfatal stroke, a 1.8-fold higher rate of fatal stroke, a 1.5-fold higher mortality rate due to heart disease, and a 4.2-fold higher rate of end-stage renal disease (ESRD).
Table 1, below, summarizes age-adjusted prevalence estimates from the National Health Interview Survey (NHIS) and the National Center for Health Statistics (NCHS) according to racial/ethnic groups and diagnosed conditions in individuals 18 years of age and older.[34, 35]
Table 1. NHIS/NCHS Age-Adjusted Prevalence Estimates in Individuals Aged 18 Years and Older in 2008. (Open Table in a new window)
|Race/Ethnic Group||Have Hypertension, %||Have Heart Disease, %||Have Coronary Heart Disease, %||Have Had a Stroke, %|
|American Indian/Alaska Native||25.3||12.1||6.6 (this number is considered unreliable)||3.9 (this number is considered unreliable)|
|Source: Pleis JR, Lucus JW, Ward BW. Summary health statistics for US adults: National Health Interview Survey, 2008. Vital Health Stat 10. No. 242; 2009. Available at: http://www.cdc.gov/nchs/data/series/sr_10/sr10_242.pdf. Accessed: February 21, 2012.
NCHS = National Center for Health Statistics; NHIS = National Health Interview Survey.
Most individuals diagnosed with hypertension will have increasing blood pressure (BP) as they age. Untreated hypertension is notorious for increasing the risk of mortality and is often described as a silent killer. Mild to moderate hypertension, if left untreated, may be associated with a risk of atherosclerotic disease in 30% of people and organ damage in 50% of people within 8-10 years after onset.
Death from ischemic heart disease or stroke increases progressively as BP increases. For every 20 mm Hg systolic or 10 mm Hg diastolic increase in BP above 115/75 mm Hg, the mortality rate for both ischemic heart disease and stroke doubles.
Hypertensive retinopathy was associated with an increased long-term risk of stroke, even in patients with well-controlled BP, in a report of 2907 adults with hypertension participating in the Atherosclerosis Risk in Communities (ARIC) study.[36, 37] Increasing severity of hypertensive retinopathy was associated with an increased risk of stroke; the stroke risk was 1.35 in the mild retinopathy group and 2.37 in the moderate/severe group.
In a meta-analysis of pooled data from 19 prospective cohort studies involving 762,393 patients, Huang et al reported that, after adjustment for multiple cardiovascular risk factors, prehypertension was associated with a 66% increased risk for stroke, compared with an optimal blood pressure (< 120/80 mm Hg).[38, 39] Patients in the high range of prehypertension (130-139/85-89 mm Hg) had a 95% increased risk of stroke, compared with a 44% increased risk for those in the low range of prehypertension (120-129/80-84 mm Hg).[38, 39]
The morbidity and mortality of hypertensive emergencies depend on the extent of end-organ dysfunction on presentation and the degree to which BP is controlled subsequently. With BP control and medication compliance, the 10-year survival rate of patients with hypertensive crises approaches 70%.
In the Framingham Heart Study, the age-adjusted risk of congestive heart failure was 2.3 times higher in men and 3 times higher in women when the highest BP was compared to the lowest BP. Multiple Risk Factor Intervention Trial (MRFIT) data showed that the relative risk for coronary artery disease mortality was 2.3 to 6.9 times higher for persons with mild to severe hypertension than it was for persons with normal BP. The relative risk for stroke ranged from 3.6 to 19.2. The population-attributable risk percentage for coronary artery disease varied from 2.3 to 25.6%, whereas the population-attributable risk for stroke ranged from 6.8-40%.
The Framingham Heart Study found a 72% increase in the risk of all-cause death and a 57% increase in the risk of any cardiovascular event in patients with hypertension who were also diagnosed with diabetes mellitus.
Nephrosclerosis is one of the possible complications of long-standing hypertension. The risk of hypertension-induced end-stage renal disease is higher in black patients, even when blood pressure is under good control. Furthermore, patients with diabetic nephropathy who are hypertensive are also at high risk for developing end-stage renal disease.
Comparative data from the NHANES I and III showed a decrease in mortality over time in hypertensive adults, but the mortality gap between hypertensive and normotensive adults remained high.
Clinical trials have demonstrated the following benefits with antihypertensive therapy :
Average 35-40% reduction in stroke incidence
Average 20-25% reduction in myocardial infarction
Average >50% reduction in heart failure
Moreover, it is estimated that 1 death is prevented per 11 patients treated for stage 1 hypertension and other cardiovascular risk factors when a sustained reduction of 12 mm Hg in systolic BP over 10 years is achieved. However, for the same reduction is systolic BP reduction, it is estimated that 1 death is prevented per 9 patients treated when cardiovascular disease or end-organ damage is present.
Hypertension is a lifelong disorder. For optimal control, a long-term commitment to lifestyle modifications and pharmacologic therapy is required. Therefore, repeated in-depth patient education and counseling not only improve compliance with medical therapy but also reduce cardiovascular risk factors.
Various strategies to decrease cardiovascular disease risk include the following:
Prevention and treatment of obesity: an increase in body mass index (BMI) and waist circumference is associated with an increased risk of developing conditions with high cardiovascular risk, such as hypertension, diabetes mellitus, impaired fasting glucose, and left ventricular hypertrophy [LVH] 
Appropriate amounts of aerobic physical activity
Diets low in salt, total fat, and cholesterol
Adequate dietary intake of potassium, calcium, and magnesium
Limited alcohol consumption
Avoidance of cigarette smoking
Avoidance of the use of illicit drugs, such as cocaine
Harrison L. Hypertension ER Visits Surge 25% in Five Years. Medscape. Sep 11 2014. [Full Text].
Roger VL, Go AS, Lloyd-Jones DM, et al. Heart disease and stroke statistics--2012 update: a report from the American Heart Association. Circulation. 2012 Jan 3. 125(1):e2-e220. [Medline].
Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003 Dec. 42(6):1206-52. [Medline].
Katakam R, Brukamp K, Townsend RR. What is the proper workup of a patient with hypertension?. Cleve Clin J Med. 2008 Sep. 75(9):663-72. [Medline].
Institute for Clinical Systems Improvement (ICSI). Hypertension diagnosis and treatment. Bloomington, Minn: Institute for Clinical Systems Improvement (ICSI); 2010.
Whelton PK, Appel LJ, Sacco RL, Anderson CA, Antman EM, Campbell N, et al. Sodium, Blood Pressure, and Cardiovascular Disease: Further Evidence Supporting the American Heart Association Sodium Reduction Recommendations. Circulation. 2012 Nov 2. [Medline].
O'Riordan M. New European Hypertension Guidelines Released: Goal Is Less Than 140 mm Hg for All. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/806367. Accessed: June 24, 2013.
[Guideline] Mancia G, Fagard R, Narkiewicz K, et al. 2013 ESH/ESC Guidelines for the management of arterial hypertension. 23rd European Meeting on Hypertension & Cardiovascular Protection. Available at http://www.esh2013.org/wordpress/wp-content/uploads/2013/06/ESC-ESH-Guidelines-2013.pdf. Accessed: June 24, 2013.
[Guideline] James PA, Oparil S, Carter BL, et al. 2014 Evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2013 Dec 18. [Medline]. [Full Text].
Wood S. JNC 8 at last! Guidelines ease up on BP thresholds, drug choices. Heartwire. December 18, 2013. [Full Text].
Hajjar I, Kotchen TA. Trends in prevalence, awareness, treatment, and control of hypertension in the United States, 1988-2000. JAMA. 2003 Jul 9. 290(2):199-206. [Medline].
Bianchi S, Bigazzi R, Campese VM. Microalbuminuria in essential hypertension: significance, pathophysiology, and therapeutic implications. Am J Kidney Dis. 1999 Dec. 34(6):973-95. [Medline].
Shayne PH, Pitts SR. Severely increased blood pressure in the emergency department. Ann Emerg Med. 2003 Apr. 41(4):513-29. [Medline].
Rhoades R, Planzer R. Human Physiology. 3rd. Fort Worth, TX: Saunders College Publishing; 1996.
Gandhi SK, Powers JC, Nomeir AM, Fowle K, Kitzman DW, Rankin KM, et al. The pathogenesis of acute pulmonary edema associated with hypertension. N Engl J Med. 2001 Jan 4. 344(1):17-22. [Medline].
Guzik TJ, Hoch NE, Brown KA, et al. Role of the T cell in the genesis of angiotensin II induced hypertension and vascular dysfunction. J Exp Med. 2007 Oct 1. 204(10):2449-60. [Medline].
Madhur MS, Lob HE, McCann LA, et al. Interleukin 17 promotes angiotensin II-induced hypertension and vascular dysfunction. Hypertension. 2010 Feb. 55(2):500-7. [Medline].
Hamer M, Steptoe A. Cortisol responses to mental stress and incident hypertension in healthy men and women. J Clin Endocrinol Metab. 2012 Jan. 97(1):E29-34. [Medline].
Rule AD, Fridley BL, Hunt SC, Asmann Y, Boerwinkle E, Pankow JS, et al. Genome-wide linkage analysis for uric acid in families enriched for hypertension. Nephrol Dial Transplant. 2009 Aug. 24(8):2414-20. [Medline]. [Full Text].
Mitchell GF, DeStefano AL, Larson MG, et al. Heritability and a genome-wide linkage scan for arterial stiffness, wave reflection, and mean arterial pressure: the Framingham Heart Study. Circulation. 2005 Jul 12. 112(2):194-9. [Medline].
Levy D, DeStefano AL, Larson MG, et al. Evidence for a gene influencing blood pressure on chromosome 17. Genome scan linkage results for longitudinal blood pressure phenotypes in subjects from the framingham heart study. Hypertension. 2000 Oct. 36(4):477-83. [Medline].
Coffman TM. Under pressure: the search for the essential mechanisms of hypertension. Nat Med. 2011 Nov 7. 17(11):1402-9. [Medline].
Millis RM. Epigenetics and hypertension. Curr Hypertens Rep. 2011 Feb. 13(1):21-8. [Medline].
Goldblatt H, Lynch J, Hanzal RF, Summerville WW. STUDIES ON EXPERIMENTAL HYPERTENSION : I. THE PRODUCTION OF PERSISTENT ELEVATION OF SYSTOLIC BLOOD PRESSURE BY MEANS OF RENAL ISCHEMIA. J Exp Med. 1934 Feb 28. 59(3):347-79. [Medline]. [Full Text].
Silverberg DS, Iaina A, Oksenberg A. Treating obstructive sleep apnea improves essential hypertension and quality of life. Am Fam Physician. 2002 Jan 15. 65(2):229-36. [Medline].
Marik PE, Varon J. Hypertensive crises: challenges and management. Chest. 2007 Jun. 131(6):1949-62. [Medline].
Rodriguez MA, Kumar SK, De Caro M. Hypertensive crisis. Cardiol Rev. 2010 Mar-Apr. 18(2):102-7. [Medline].
Hollander JE. Cocaine intoxication and hypertension. Ann Emerg Med. 2008 Mar. 51(3 Suppl):S18-20. [Medline].
Qureshi AI, Suri MF, Kirmani JF, Divani AA. Prevalence and trends of prehypertension and hypertension in United States: National Health and Nutrition Examination Surveys 1976 to 2000. Med Sci Monit. 2005 Sep. 11(9):CR403-9. [Medline].
Catalá-López F, Sanfélix-Gimeno G, García-Torres C, Ridao M, Peiró S. Control of arterial hypertension in Spain: a systematic review and meta-analysis of 76 epidemiological studies on 341?632 participants. J Hypertens. 2012 Jan. 30(1):168-76. [Medline].
Cornoni-Huntley J, LaCroix AZ, Havlik RJ. Race and sex differentials in the impact of hypertension in the United States. The National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study. Arch Intern Med. 1989 Apr. 149(4):780-8. [Medline].
Strong Heart Study Data Book: A Report to American Indian Communities. Bethesda, MD: National Heart, Lung, and Blood Institute, NIH; 2001.
Ong YT, Wong TY, Klein R, Klein BE, Mitchell P, Sharrett AR, et al. Hypertensive Retinopathy and Risk of Stroke. Hypertension. 2013 Aug 12. [Medline].
Brooks M. Hypertensive Retinopathy Linked to Increased Stroke Risk. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/809541. Accessed: August 20, 2013.
Huang Y, Cai X, Li Y, et al. Prehypertension and the risk of stroke: a meta-analysis. Neurology. 2014 Mar 12. [Medline].
Hughes S. Even prehypertension increases stroke risk: meta-analysis. Medscape Medical News. March 14, 2014. [Full Text].
Webster J, Petrie JC, Jeffers TA, Lovell HG. Accelerated hypertension--patterns of mortality and clinical factors affecting outcome in treated patients. Q J Med. 1993 Aug. 86(8):485-93. [Medline].
Culleton BF, Larson MG, Kannel WB, Levy D. Serum uric acid and risk for cardiovascular disease and death: the Framingham Heart Study. Ann Intern Med. 1999 Jul 6. 131(1):7-13. [Medline].
Mortality after 10 1/2 years for hypertensive participants in the Multiple Risk Factor Intervention Trial. Circulation. 1990 Nov. 82(5):1616-28. [Medline].
Chen G, McAlister FA, Walker RL, Hemmelgarn BR, Campbell NR. Cardiovascular outcomes in framingham participants with diabetes: the importance of blood pressure. Hypertension. 2011 May. 57(5):891-7. [Medline].
Ford ES. Trends in mortality from all causes and cardiovascular disease among hypertensive and nonhypertensive adults in the United States. Circulation. 2011 Apr 26. 123(16):1737-44. [Medline].
Bombelli M, Facchetti R, Sega R, Carugo S, Fodri D, Brambilla G, et al. Impact of body mass index and waist circumference on the long-term risk of diabetes mellitus, hypertension, and cardiac organ damage. Hypertension. 2011 Dec. 58(6):1029-35. [Medline].
Redon J, Campos C, Narciso ML, Rodicio JL, Pascual JM, Ruilope LM. Prognostic value of ambulatory blood pressure monitoring in refractory hypertension: a prospective study. Hypertension. 1998 Feb. 31(2):712-8. [Medline].
Wong TY, Mitchell P. Hypertensive retinopathy. N Engl J Med. 2004 Nov 25. 351(22):2310-7. [Medline].
Zampaglione B, Pascale C, Marchisio M, Cavallo-Perin P. Hypertensive urgencies and emergencies. Prevalence and clinical presentation. Hypertension. 1996 Jan. 27(1):144-7. [Medline].
Staykov D, Schwab S. Posterior reversible encephalopathy syndrome. J Intensive Care Med. 2012 Feb. 27(1):11-24. [Medline].
McCord J, Mundy BJ, Hudson MP, Maisel AS, Hollander JE, Abraham WT. Relationship between obesity and B-type natriuretic peptide levels. Arch Intern Med. 2004 Nov 8. 164(20):2247-52. [Medline].
Wang IK, Muo CH, Chang YC, Liang JC, Chang CT, Lin SY, et al. Association between hypertensive disorders during pregnancy and end-stage renal disease: a population-based study. CMAJ. 2013 Jan 21. [Medline].
Grundy SM, Cleeman JI, Daniels SR, et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation. 2005 Oct 25. 112(17):2735-52. [Medline].
Pickering TG, James GD, Boddie C, Harshfield GA, Blank S, Laragh JH. How common is white coat hypertension?. JAMA. 1988 Jan 8. 259(2):225-8. [Medline].
Stiles S. Framingham Criteria Predict New Hypertension Better Than Prehypertension in Young Adults. Medscape Medical News. Available at http://www.medscape.com/viewarticle/811416. Accessed: September 30, 2013.
Carson AP, Lewis CE, Jacobs DR Jr, Peralta CA, Steffen LM, Bower JK, et al. Evaluating the Framingham Hypertension Risk Prediction Model in Young Adults: The Coronary Artery Risk Development in Young Adults (CARDIA) Study. Hypertension. 2013 Sep 16. [Medline].
Olin JW, Piedmonte MR, Young JR, DeAnna S, Grubb M, Childs MB. The utility of duplex ultrasound scanning of the renal arteries for diagnosing significant renal artery stenosis. Ann Intern Med. 1995 Jun 1. 122(11):833-8. [Medline].
US Food and Drug Administration. Information on gadolinium-based contrast agents. Available at http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm142882.htm. Accessed: February 22, 2012.
Cortigiani L, Bigi R, Landi P, Bovenzi F, Picano E, Sicari R. Prognostic implication of stress echocardiography in 6214 hypertensive and 5328 normotensive patients. Eur Heart J. 2011 Jun. 32(12):1509-18. [Medline].
O'Riordan M. AHA/ACC/CDC Issue 'Science Advisory' on Treating BP. Medscape. Nov 15 2013. [Full Text].
[Guideline] Go AS, Bauman M, King SM, et al. An effective approach to high blood pressure control: a science advisory from the American Heart Association, the American College of Cardiology, and the Centers for Disease Control and Prevention. Hypertension. 2013 Nov 15. [Medline]. [Full Text].
Redon J, Cifkova R, Laurent S, Nilsson P, Narkiewicz K, Erdine S, et al. Mechanisms of hypertension in the cardiometabolic syndrome. J Hypertens. 2009 Mar. 27(3):441-51. [Medline].
Forman JP, Scheven L, de Jong PE, Bakker SJ, Curhan GC, Gansevoort RT. Association between sodium intake and change in uric acid, urine albumin excretion, and the risk of developing hypertension. Circulation. 2012 Jun 26. 125(25):3108-16. [Medline].
Aburto NJ, Hanson S, Gutierrez H, Hooper L, Elliott P, Cappuccio FP. Effect of increased potassium intake on cardiovascular risk factors and disease: systematic review and meta-analyses. BMJ. 2013 Apr 3. [Medline].
Egan BM, Laken MA, Donovan JL, Woolson RF. Does dark chocolate have a role in the prevention and management of hypertension?: commentary on the evidence. Hypertension. 2010 Jun. 55(6):1289-95. [Medline].
Fahey T, Schroeder K, Ebrahim S. Interventions used to improve control of blood pressure in patients with hypertension. Cochrane Database Syst Rev. 2006 Apr 19. CD005182. [Medline].
Blumenthal JA, Babyak MA, Hinderliter A, Watkins LL, Craighead L, Lin PH, et al. Effects of the DASH diet alone and in combination with exercise and weight loss on blood pressure and cardiovascular biomarkers in men and women with high blood pressure: the ENCORE study. Arch Intern Med. 2010 Jan 25. 170(2):126-35. [Medline].
Boggs W. Benazepril plus amlodipine effective for high-risk, stage 2 hypertension. Medscape Medical News. May 3, 2013. [Full Text].
Bakris G, Briasoulis A, Dahlof B, Jamerson K, Weber MA, Kelly RY, et al. Comparison of Benazepril Plus Amlodipine or Hydrochlorothiazide in High-Risk Patients With Hypertension and Coronary Artery Disease. Am J Cardiol. 2013 Apr 11. [Medline].
Jamerson K, Weber MA, Bakris GL, Dahlöf B, Pitt B, Shi V, et al. Benazepril plus amlodipine or hydrochlorothiazide for hypertension in high-risk patients. N Engl J Med. 2008 Dec 4. 359(23):2417-28. [Medline].
Ruggenenti P, Lauria G, Iliev IP, Fassi A, Ilieva AP, Rota S, et al. Effects of manidipine and delapril in hypertensive patients with type 2 diabetes mellitus: the delapril and manidipine for nephroprotection in diabetes (DEMAND) randomized clinical trial. Hypertension. 2011 Nov. 58(5):776-83. [Medline].
O'Riordan M. Spironolactone Provides Benefit in Resistant Hypertension, Small Study Shows. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/806388. Accessed: July 29, 2013.
Pancioli AM. Hypertension management in neurologic emergencies. Ann Emerg Med. 2008 Mar. 51(3 Suppl):S24-7. [Medline].
Slovis CM, Reddi AS. Increased blood pressure without evidence of acute end organ damage. Ann Emerg Med. 2008 Mar. 51(3 Suppl):S7-9. [Medline].
Blowey DL, Duda PJ, Stokes P, Hall M. Incidence and treatment of hypertension in the neonatal intensive care unit. J Am Soc Hypertens. 2011 Nov-Dec. 5(6):478-83. [Medline].
Kostis JB, Cabrera J, Cheng JQ, Cosgrove NM, Deng Y, Pressel SL, et al. Association between chlorthalidone treatment of systolic hypertension and long-term survival. JAMA. 2011 Dec 21. 306(23):2588-93. [Medline].
Staessen JA, Fagard R, Thijs L, Celis H, Arabidze GG, Birkenhäger WH, et al. Randomised double-blind comparison of placebo and active treatment for older patients with isolated systolic hypertension. The Systolic Hypertension in Europe (Syst-Eur) Trial Investigators. Lancet. 1997 Sep 13. 350(9080):757-64. [Medline].
Aronow WS, Fleg JL, Pepine CJ, Artinian NT, Bakris G, Brown AS, et al. ACCF/AHA 2011 expert consensus document on hypertension in the elderly: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus documents developed in collaboration with the American Academy of Neurology, American Geriatrics Society, American Society for Preventive Cardiology, American Society of Hypertension, American Society of Nephrology, Association of Black Cardiologists, and European Society of Hypertension. J Am Coll Cardiol. 2011 May 17. 57(20):2037-114. [Medline].
Weinberger MH, Izzo JL Jr, Purkayastha D, Weitzman R, Black HR. Comparative efficacy and safety of combination aliskiren/amlodipine and amlodipine monotherapy in African Americans with stage 2 hypertension and obesity or metabolic syndrome. J Am Soc Hypertens. 2011 Nov-Dec. 5(6):489-97. [Medline].
Nishizaka MK, Zaman MA, Calhoun DA. Efficacy of low-dose spironolactone in subjects with resistant hypertension. Am J Hypertens. 2003 Nov. 16(11 Pt 1):925-30. [Medline].
de la Sierra A, Segura J, Banegas JR, Gorostidi M, de la Cruz JJ, Armario P, et al. Clinical features of 8295 patients with resistant hypertension classified on the basis of ambulatory blood pressure monitoring. Hypertension. 2011 May. 57(5):898-902. [Medline].
Krum H, Schlaich M, Whitbourn R, et al. Catheter-based renal sympathetic denervation for resistant hypertension: a multicentre safety and proof-of-principle cohort study. Lancet. 2009 Apr 11. 373(9671):1275-81. [Medline].
Catheter-based renal sympathetic denervation for resistant hypertension: durability of blood pressure reduction out to 24 months. Hypertension. 2011 May. 57(5):911-7. [Medline].
Esler MD, Krum H, Sobotka PA, et al. Renal sympathetic denervation in patients with treatment-resistant hypertension (The Symplicity HTN-2 Trial): a randomised controlled trial. Lancet. 2010 Dec 4. 376(9756):1903-9. [Medline].
Bisognano JD, Bakris G, Nadim MK, Sanchez L, Kroon AA, Schafer J, et al. Baroreflex activation therapy lowers blood pressure in patients with resistant hypertension: results from the double-blind, randomized, placebo-controlled rheos pivotal trial. J Am Coll Cardiol. 2011 Aug 9. 58(7):765-73. [Medline].
de La Sierra A, Larrousse M, Oliveras A, Armario P, Hernández-Del Rey R, Poch E, et al. Abnormalities of vascular function in resistant hypertension. Blood Press. 2012 Apr. 21(2):104-9. [Medline].
Kronish IM, Woodward M, Sergie Z, Ogedegbe G, Falzon L, Mann DM. Meta-analysis: impact of drug class on adherence to antihypertensives. Circulation. 2011 Apr 19. 123(15):1611-21. [Medline]. [Full Text].
Pedrosa RP, Drager LF, Gonzaga CC, Sousa MG, de Paula LK, Amaro AC, et al. Obstructive sleep apnea: the most common secondary cause of hypertension associated with resistant hypertension. Hypertension. 2011 Nov. 58(5):811-7. [Medline].
Martínez-Garcia MA, Capote F, Campos-Rodriguez F, et al, for the Spanish Sleep Network. Effect of CPAP on blood pressure in patients with obstructive sleep apnea and resistant hypertension: the HIPARCO randomized clinical trial. JAMA. 2013 Dec 11. 310(22):2407-15. [Medline].
O'Riordan M. CPAP reduces blood pressure in resistant hypertension. Heartwire. December 10, 2013. [Full Text].
Pezzin LE, Feldman PH, Mongoven JM, McDonald MV, Gerber LM, Peng TR. Improving blood pressure control: results of home-based post-acute care interventions. J Gen Intern Med. 2011 Mar. 26(3):280-6. [Medline]. [Full Text].
Bosworth HB, Powers BJ, Olsen MK, McCant F, Grubber J, Smith V, et al. Home blood pressure management and improved blood pressure control: results from a randomized controlled trial. Arch Intern Med. 2011 Jul 11. 171(13):1173-80. [Medline].
Leung AA, Wright A, Pazo V, Karson A, Bates DW. Risk of thiazide-induced hyponatremia in patients with hypertension. Am J Med. 2011 Nov. 124(11):1064-72. [Medline].
Harel Z, Gilbert C, Wald R, Bell C, Perl J, Juurlink D, et al. The effect of combination treatment with aliskiren and blockers of the renin-angiotensin system on hyperkalaemia and acute kidney injury: systematic review and meta-analysis. BMJ. 2012 Jan 9. 344:e42. [Medline]. [Full Text].
Cummings DM, Amadio P Jr, Nelson L, Fitzgerald JM. The role of calcium channel blockers in the treatment of essential hypertension. Arch Intern Med. 1991 Feb. 151(2):250-9. [Medline].
1999 World Health Organization-International Society of Hypertension Guidelines for the Management of Hypertension. Guidelines Subcommittee. J Hypertens. 1999 Feb. 17(2):151-83. [Medline].
Abalos E, Duley L, Steyn DW, Henderson-Smart DJ. Antihypertensive drug therapy for mild to moderate hypertension during pregnancy. Cochrane Database Syst Rev. 2007 Jan 24. CD002252. [Medline].
Abergel E, Chatellier G, Battaglia C, Menard J. Can echocardiography identify mildly hypertensive patients at high risk, left untreated based on current guidelines?. J Hypertens. 1999 Jun. 17(6):817-24. [Medline].
AHRQ: Agency for Healthcare Research and Quality. Comparative Effectiveness of Angiotensin-Converting Enzyme Inhibitors (ACEIs) and Angiotensin II Receptor Antagonists (ARBs) for Treating Essential Hypertension. Agency for Healthcare Research and Quality. Available at http://effectivehealthcare.ahrq.gov/healthInfo.cfm?infotype=rr&ProcessID=12%20&DocID=48. Accessed: May 14, 2009.
American College of Radiology. Manual on Contrast Media. Vers. 7. Available at http://www.acr.org/SecondaryMainMenuCategories/quality_safety/contrast_manual.aspx. Accessed: February 22, 2012.
Anderson CS, Huang Y, Arima H, Heeley E, Skulina C, Parsons MW, et al. Effects of early intensive blood pressure-lowering treatment on the growth of hematoma and perihematomal edema in acute intracerebral hemorrhage: the Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial (INTERACT). Stroke. 2010 Feb. 41(2):307-12. [Medline].
Anderson CS, Huang Y, Wang JG, Arima H, Neal B, Peng B, et al. Intensive blood pressure reduction in acute cerebral haemorrhage trial (INTERACT): a randomised pilot trial. Lancet Neurol. 2008 May. 7(5):391-9. [Medline].
Ault MJ, Ellrodt AG. Pathophysiological events leading to the end-organ effects of acute hypertension. Am J Emerg Med. 1985 Dec. 3(6 Suppl):10-5. [Medline].
Barton JR. Hypertension in pregnancy. Ann Emerg Med. 2008 Mar. 51(3 Suppl):S16-7. [Medline].
Brown MJ, McInnes GT, Papst CC, Zhang J, MacDonald TM. Aliskiren and the calcium channel blocker amlodipine combination as an initial treatment strategy for hypertension control (ACCELERATE): a randomised, parallel-group trial. Lancet. 2011 Jan 22. 377(9762):312-20. [Medline].
Chapman N, Huxley R, Anderson C, Bousser MG, Chalmers J, Colman S, et al. Effects of a perindopril-based blood pressure-lowering regimen on the risk of recurrent stroke according to stroke subtype and medical history: the PROGRESS Trial. Stroke. 2004 Jan. 35(1):116-21. [Medline].
Cheung AT, Hobson RW 2nd. Hypertension in vascular surgery: aortic dissection and carotid revascularization. Ann Emerg Med. 2008 Mar. 51(3 Suppl):S28-33. [Medline].
Chrysant SG, Fagan T, Glazer R, Kriegman A. Effects of benazepril and hydrochlorothiazide, given alone and in low- and high-dose combinations, on blood pressure in patients with hypertension. Arch Fam Med. 1996 Jan. 5(1):17-24; discussion 25. [Medline].
Chrysant SG, Izzo JL Jr, Kereiakes DJ, Littlejohn T 3rd, Oparil S, Melino M, et al. Efficacy and safety of triple-combination therapy with olmesartan, amlodipine, and hydrochlorothiazide in study participants with hypertension and diabetes: a subpopulation analysis of the TRINITY study. J Am Soc Hypertens. 2012 Mar-Apr. 6(2):132-41. [Medline].
Cushman WC, Bakris GL, White WB, Weber MA, Sica D, Roberts A, et al. Azilsartan medoxomil plus chlorthalidone reduces blood pressure more effectively than olmesartan plus hydrochlorothiazide in stage 2 systolic hypertension. Hypertension. 2012 Aug. 60(2):310-8. [Medline].
Cushman WC, Evans GW, Byington RP, Goff DC Jr, Grimm RH Jr. Effects of intensive blood-pressure control in type 2 diabetes mellitus. N Engl J Med. 2010 Apr 29. 362(17):1575-85. [Medline].
Daien V, Duny Y, Ribstein J, du Cailar G, Mimran A, Villain M, et al. Treatment of hypertension with renin-angiotensin system inhibitors and renal dysfunction: a systematic review and meta-analysis. Am J Hypertens. 2012 Jan. 25(1):126-32. [Medline].
Diercks DB, Ohman EM. Hypertension with acute coronary syndrome and heart failure. Ann Emerg Med. 2008 Mar. 51(3 Suppl):S34-6. [Medline].
Dungan JR, Conley YP, Langaee TY, Johnson JA, Kneipp SM, Hess PJ, et al. Altered beta-2 adrenergic receptor gene expression in human clinical hypertension. Biol Res Nurs. 2009 Jul. 11(1):17-26. [Medline]. [Full Text].
Epstein M. Calcium antagonists and renal disease. Kidney Int. 1998 Nov. 54(5):1771-84. [Medline].
Faselis C, Doumas M, Kokkinos JP, Panagiotakos D, Kheirbek R, Sheriff HM, et al. Exercise capacity and progression from prehypertension to hypertension. Hypertension. 2012 Aug. 60(2):333-8. [Medline].
[Guideline] Goldstein LB, Bushnell CD, Adams RJ, Appel LJ, Braun LT, Chaturvedi S, et al. Guidelines for the primary prevention of stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011 Feb. 42(2):517-84. [Medline].
Ha V, Sievenpiper JL, de Souza RJ, Chiavaroli L, Wang DD, Cozma AI, et al. Effect of fructose on blood pressure: a systematic review and meta-analysis of controlled feeding trials. Hypertension. 2012 Apr. 59(4):787-95. [Medline].
Hansson L, Hedner T, Lund-Johansen P, Kjeldsen SE, Lindholm LH, Syvertsen JO, et al. Randomised trial of effects of calcium antagonists compared with diuretics and beta-blockers on cardiovascular morbidity and mortality in hypertension: the Nordic Diltiazem (NORDIL) study. Lancet. 2000 Jul 29. 356(9227):359-65. [Medline].
Heilpern K. Pathophysiology of hypertension. Ann Emerg Med. 2008 Mar. 51(3 Suppl):S5-6. [Medline].
Hermida RC, Ayala DE, Mojón A, Fernández JR. Decreasing sleep-time blood pressure determined by ambulatory monitoring reduces cardiovascular risk. J Am Coll Cardiol. 2011 Sep 6. 58(11):1165-73. [Medline].
Izzo JL Jr, Weintraub HS, Duprez DA, Purkayastha D, Zappe D, Samuel R, et al. Treating systolic hypertension in the very elderly with valsartan-hydrochlorothiazide vs. either monotherapy: ValVET primary results. J Clin Hypertens (Greenwich). 2011 Oct. 13(10):722-30. [Medline].
Kandzari DE, Bhatt DL, Sobotka PA, et al. Catheter-based renal denervation for resistant hypertension: rationale and design of the SYMPLICITY HTN-3 Trial. Clin Cardiol. 2012 Sep. 35(9):528-35. [Medline].
Kaplan NM. Calcium entry blockers in the treatment of hypertension. Current status and future prospects. JAMA. 1989 Aug 11. 262(6):817-23. [Medline].
Khan NA, McAlister FA, Lewanczuk RZ, Touyz RM, Padwal R, Rabkin SW, et al. The 2005 Canadian Hypertension Education Program recommendations for the management of hypertension: part II - therapy. Can J Cardiol. 2005 Jun. 21(8):657-72. [Medline].
Kitiyakara C, Guzman NJ. Malignant hypertension and hypertensive emergencies. J Am Soc Nephrol. 1998 Jan. 9(1):133-42. [Medline].
Lloyd-Jones D, Adams RJ, Brown TM, Carnethon M, Dai S, De Simone G, et al. Heart disease and stroke statistics--2010 update: a report from the American Heart Association. Circulation. 2010 Feb 23. 121(7):e46-e215. [Medline].
Magee LA, Helewa M, Moutquin J-M et al. Diagnosis, Evaluation, and Management of the Hypertensive Disorders of Pregnancy. Journal of Obstetrics and Gynaecology Canada. March 2008. 30:S1-S48.
Major cardiovascular events in hypertensive patients randomized to doxazosin vs chlorthalidone: the antihypertensive and lipid-lowering treatment to prevent heart attack trial (ALLHAT). ALLHAT Collaborative Research Group. JAMA. 2000 Apr 19. 283(15):1967-75. [Medline].
Narkiewicz K. Diagnosis and management of hypertension in obesity. Obes Rev. 2006 May. 7(2):155-62. [Medline].
National Institutes of Health. Your Guide to Lowering Your Blood Pressure With DASH. April 2006. 64. [Full Text].
Novartis. Novartis announces termination of ALTITUDE study with Rasilez/Tekturna in high-risk patients with diabetes and renal impairment [press release]. December 20, 2011. Available at http://www.novartis.com/newsroom/media-releases/en/2011/1572562.shtml. Accessed: February 22, 2012.
O'Connor PJ, Vazquez-Benitez G, Schmittdiel JA, Parker ED, Trower NK, Desai JR, et al. Benefits of Early Hypertension Control on Cardiovascular Outcomes in Patients With Diabetes. Diabetes Care. 2012 Sep 10. [Medline].
O'Riordan M. Olmesartan label to include intestinal problems, FDA says. Medscape Medical News. July 3, 2013. [Full Text].
Pimenta E, Calhoun DA, Oparil S. Sleep apnea, aldosterone, and resistant hypertension. Prog Cardiovasc Dis. 2009 Mar-Apr. 51(5):371-80. [Medline].
Pleis JR, Lucus JW, Ward BW. Summary health statistics for US adults: National Health Interview Survey, 2008. Vital Health Stat 10. 2009. No. 242:[Full Text].
Podymow T, August P. Antihypertensive drugs in pregnancy. Semin Nephrol. 2011 Jan. 31(1):70-85. [Medline].
Pollare T, Lithell H, Berne C. A comparison of the effects of hydrochlorothiazide and captopril on glucose and lipid metabolism in patients with hypertension. N Engl J Med. 1989 Sep 28. 321(13):868-73. [Medline].
Rastan A, Krankenberg H, Müller-Hülsbeck S, et al. Improved renal function and blood pressure control following renal artery angioplasty: the renal artery angioplasty in patients with renal insufficiency and hypertension using a dedicated renal stent device study (PRECISION). EuroIntervention. 2008 Aug. 4(2):208-13. [Medline].
Roberts CL, Ford JB, Algert CS, Antonsen S, Chalmers J, Cnattingius S, et al. Population-based trends in pregnancy hypertension and pre-eclampsia: an international comparative study. BMJ Open. 2011 May 24. 1(1):e000101. [Medline]. [Full Text].
Shook RP, Lee DC, Sui X, Prasad V, Hooker SP, Church TS, et al. Cardiorespiratory fitness reduces the risk of incident hypertension associated with a parental history of hypertension. Hypertension. 2012 Jun. 59(6):1220-4. [Medline].
Slagman MC, Waanders F, Hemmelder MH, Woittiez AJ, Janssen WM, Lambers Heerspink HJ, et al. Moderate dietary sodium restriction added to angiotensin converting enzyme inhibition compared with dual blockade in lowering proteinuria and blood pressure: randomised controlled trial. BMJ. 2011 Jul 26. 343:d4366. [Medline]. [Full Text].
Svetkey LP, Moore TJ, Simons-Morton DG, Appel LJ, Bray GA, Sacks FM, et al. Angiotensinogen genotype and blood pressure response in the Dietary Approaches to Stop Hypertension (DASH) study. J Hypertens. 2001 Nov. 19(11):1949-56. [Medline].
Taubert D, Roesen R, Lehmann C, Jung N, Schomig E. Effects of low habitual cocoa intake on blood pressure and bioactive nitric oxide: a randomized controlled trial. JAMA. 2007 Jul 4. 298(1):49-60. [Medline].
The World Health Report 2002-Reducing Risks, Promoting Healthy Life. Geneva, Switzerland: World Health Organization; 2002. [Full Text].
Tseng CD, Yen AM, Chiu SY, Chen LS, Chen HH, Chang SH. A predictive model for risk of prehypertension and hypertension and expected benefit after population-based life-style modification (KCIS No. 24). Am J Hypertens. 2012 Feb. 25(2):171-9. [Medline].
Tymchak W, Armstrong PW, Westerhout CM, Sookram S, Brass N, Fu Y, et al. Mode of hospital presentation in patients with non-ST-elevation myocardial infarction: implications for strategic management. Am Heart J. 2011 Sep. 162(3):436-43. [Medline].
US Food and Drug Administration. FDA Drug Safety Communication: FDA approves label changes to include intestinal problems (sprue-like enteropathy) linked to blood pressure medicine olmesartan medoxomil. July 3, 2013. [Full Text].
Wallach R, Karp RB, Reves JG, Oparil S, Smith LR, James TN. Pathogenesis of paroxysmal hypertension developing during and after coronary bypass surgery: a study of hemodynamic and humoral factors. Am J Cardiol. 1980 Oct. 46(4):559-65. [Medline].
White WB, Weber MA, Sica D, Bakris GL, Perez A, Cao C, et al. Effects of the angiotensin receptor blocker azilsartan medoxomil versus olmesartan and valsartan on ambulatory and clinic blood pressure in patients with stages 1 and 2 hypertension. Hypertension. 2011 Mar. 57(3):413-20. [Medline].
Wolz M, Cutler J, Roccella EJ, Rohde F, Thom T, Burt V. Statement from the National High Blood Pressure Education Program: prevalence of hypertension. Am J Hypertens. 2000 Jan. 13(1 Pt 1):103-4. [Medline].
Yakovlevitch M, Black HR. Resistant hypertension in a tertiary care clinic. Arch Intern Med. 1991 Sep. 151(9):1786-92. [Medline].
|Race/Ethnic Group||Have Hypertension, %||Have Heart Disease, %||Have Coronary Heart Disease, %||Have Had a Stroke, %|
|American Indian/Alaska Native||25.3||12.1||6.6 (this number is considered unreliable)||3.9 (this number is considered unreliable)|
|Source: Pleis JR, Lucus JW, Ward BW. Summary health statistics for US adults: National Health Interview Survey, 2008. Vital Health Stat 10. No. 242; 2009. Available at: http://www.cdc.gov/nchs/data/series/sr_10/sr10_242.pdf. Accessed: February 21, 2012.
NCHS = National Center for Health Statistics; NHIS = National Health Interview Survey.
|Chronic kidney disease||Estimated glomerular filtration rate|
|Coarctation of the aorta||Computed tomography angiography|
|Cushing syndrome; other states of glucocorticoid excess (eg, chronic steroid therapy||Dexamethasone suppression test|
|Drug-induced/drug-related hypertension*||Drug screening|
|Pheochromocytoma||24-hour urinary metanephrine and normetanephrine|
|Primary aldosteronism, other states of mineralocorticoid excess||24-hour urinary aldosterone level, specific mineralocorticoid tests|
|Renovascular hypertension||Doppler flow ultrasonography, magnetic resonance angiography, computed tomography angiography|
|Sleep apnea||Sleep study with oxygen saturation (screening would also include the Epworth Sleepiness Scale [ESS])|
|Thyroid/parathyroid disease||Thyroid stimulating hormone level, serum parathyroid hormone level|
|Adapted from: Chobanian AV, Bakris GL, Black HR, et al, and the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. Dec 2003;42(6):1206-52.
* Some examples of agents that induce hypertension include nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors; illicit drugs; sympathomimetic agents; oral contraceptive or adrenal steroid hormones; cyclosporine and tacrolimus; licorice; erythropoietin; and certain over-the-counter dietary supplements and medicines, such as ephedra, ma huang, and bitter orange. Drug-related causes of hypertension may be due to nonadherence, inadequate doses, and inappropriate combinations.
|Chronic hypertension||Prepregnancy or before 20 weeks’ gestation; SBP =140 mm Hg or DBP 90 mm Hg that persists >12 weeks postpartum|
|Preeclampsia||After 20 weeks’ gestation; SBP =140 mm Hg or DBP 90 mm Hg with proteinuria (>300 mg/24 h)
Can progress to eclampsia
More common in nulliparous women, multiple gestation, women with hypertension =4 years, family history of preeclampsia, previous hypertension in pregnancy, and renal disease
|Chronic hypertension with superimposed preeclampsia||New-onset proteinuria after 20 weeks in hypertensive woman
In a woman with hypertension and proteinuria before 20 weeks’ gestation
Sudden 2- to 3-fold increase in proteinuria
Sudden increase in BP
Elevated AST or ALT levels
|Gestational hypertension||Temporary diagnosis
Hypertension without proteinuria after 20 weeks’ gestation
May be a preproteinuric phase of preeclampsia or a recurrence of chronic hypertension that abated in mid-pregnancy
May lead to preeclampsia
Severe cases may cause higher rates of premature delivery and growth retardation relative to mild preeclampsia
|Transient hypertension||Diagnosis made retrospectively
BP returns to normal by 12 weeks’ postpartum
May recur in subsequent pregnancies
Predictive of future primary hypertension
|ALT = alanine aminotransferase; AST = aspartate aminotransferase; BP = blood pressure; DBP = diastolic BP; SBP = systolic BP.
Adapted from: Chobanian AV, Bakris GL, Black HR, et al, and the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. Dec 2003;42(6):1206-52.