Hypertension: Practice Essentials, Background, Pathophysiology (original) (raw)

Practice Essentials

High blood pressure (BP), or hypertension, is defined by two levels by the 2017 American College of Cardiology/American Heart Association (ACC/AHA) guidelines [1, 2] : (1) elevated BP, with a systolic pressure (SBP) between 120 and 129 mm Hg and diastolic pressure (DBP) less than 80 mm Hg, and (2) stage 1 hypertension, with an SBP of 130 to 139 mm Hg or a DBP of 80 to 89 mm Hg.

Hypertension is the most common primary diagnosis in the United States. [3] It affects approximately 86 million adults (≥20 years) in the United States [4] and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease.

Signs and symptoms of hypertension

The 2017 ACC/AHA guidelines provide the following definitions and classifications of elevated BP and stages of hypertension [1, 2] :

Of note, the International Society of Hypertension (ISH) and the European Society of Cardiology (ESC) have a higher BP threshold, defining hypertension as an SBP of 140 mm Hg or greater and/or a DBP of 90 mm Hg or above. [5, 6]

Hypertension may be primary, which may develop as a result of a variety of environmental or genetic causes, or it may be secondary to renal, vascular, and endocrine causes. Primary or essential hypertension accounts for 90-95% of adult cases, and secondary hypertension accounts for 2-10% of adult cases.

See Presentation for more detail.

Diagnosis of hypertension

The evaluation of hypertension involves accurately measuring the patient’s BP, performing a focused medical history and physical examination, and obtaining results of routine laboratory studies. [7, 8] A 12-lead electrocardiogram should also be obtained. These steps can help determine the following [7, 8, 9] :

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 complete blood cell (CBC) count, basic metabolic panel; chest radiograph, transthoracic echocardiogram; and urine microalbumin. [7]

See Workup for more detail.

Management of hypertension

Many guidelines exist for the management of hypertension. Most groups, including the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood (JNC), the American Diabetes Associate (ADA), and the ACC/AHA recommend lifestyle modification as the first step in managing hypertension.

Lifestyle modifications

JNC 7 recommendations to lower BP and decrease cardiovascular disease risk include the following, with greater results achieved when two or more lifestyle modifications are combined [7] :

The ACC/AHA 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 cardiovascular events. Other recommendations include increasing physical activity (30 minutes or more of moderate intensity activity on a daily basis) and losing weight (persons with overweight and obesity). [1]

The 2018 ESC and the European Society of Hypertension (ESH) guidelines recommend a low-sodium diet (limited to 2 g per day) as well as reducing body-mass index (BMI) to 20-25 kg/m2 and waist circumference (to < 94 cm in men and < 80 cm in women). [11] The 2023 ESH guidelines for managing arterial hypertension indicates a linear reduction in BP with sodium intake limited to as low as 800 mg/day; when dietary sodium intake fell from about 3.6 g/day to around 2.7 g/day, there was an associated 18-26% fall in cardiovascular disease. [6]

Pharmacologic therapy

If lifestyle modifications are insufficient to achieve the goal BP, there are several drug options for treating and managing hypertension. Thiazide diuretics, an angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB), or calcium channel blocker (CCB) are the preferred first-line agents. [1] Often, patients require several antihypertensive agents to achieve adequate BP control.

Compelling indications for specific agents include comorbidities such as heart failure, ischemic heart disease, chronic kidney disease, and diabetes. Drug intolerability or contraindications may also be factors. [7]

The following are drug class recommendations for compelling indications based on various clinical trials [7] :

Although the 2017 ACC/AHA guidelines favor CCBs or thiazide diuretics in the absence of other indications as first-line medications in Black hypertensive populations, [1] reports in relatively recent years have raised questions on the benefits of race or ethnicity-based medication prescribing. [12, 13, 14, 15, 16, 17, 18, 19, 20]

See Treatment and Medication for more details.

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Background

Hypertension is the most common primary diagnosis in the United States, [3] and it is one of the most common worldwide diseases afflicting humans. It 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 (BP) 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, relatively 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 86 million adults (34%) in the United States are affected by hypertension, which is defined as a systolic BP (SBP) of 130 mm Hg or more or a diastolic BP (DBP) of 80 mm Hg or more, taking antihypertensive medication, or having been told by clinicians on at least two occasions as having hypertension. [1] Substantial efforts have been made to enhance awareness and treatment of hypertension. However, a National Health Examination Survey (NHANES) spanning 2011-2014 revealed that 34% of US adults aged 20 years and older are hypertensive and NHANES 2013-2014 data showed that 15.9% of these hypertensive adults are unaware they are hypertensive; these data have increased from NHANES 2005-2006 data that showed 29% of US adults aged 18 years and older were hypertensive and that 7% of these hypertensive adults had never been told that they had hypertension. [4]

Of those with elevated BP, 78% were aware they were hypertensive, 68% were being treated with antihypertensive agents, and only 64% of treated individuals had controlled hypertension. [4] In addition, previous data from NHANES estimated that 52.6% (NHANES 2009-2010) to 55.8% (NHANES 1999-2000) of adults aged 20 years and older have elevated BP or stage 1 hypertension, defined as an untreated SBP of 120-139 mm Hg or untreated DBP of 80-89 mm Hg. [4] (See Epidemiology.)

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, healthcare 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

The definition of abnormally high blood pressure (BP) has varied among guidelines. Nevertheless, 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 2017 ACC/AHA guidelines, the classification of BP (expressed in mm Hg) for adults aged 18 years or older is as follows [1, 2] :

The classification above is based on the average of two or more readings taken at each of two or more visits after the initial screening. [1] Normal BP with respect to cardiovascular risk is less than 120/80 mm Hg. However, unusually low readings should be evaluated for clinical significance.

From another perspective, hypertension may be categorized as either primary 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 about 5-10% of the cases. [21] However, secondary forms of hypertension, such as primary hyperaldosteronism, account for as much as 30% of resistant hypertension (hypertension in which BP is >140/90 mm Hg despite the use of medications from three or more drug classes, one 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 target organ dysfunction. [7]

Acute end-organ damage in the setting of a hypertensive emergency may include the following [22] :

With the advent of antihypertensives, the incidence of hypertensive emergencies has declined from 7% to approximately 1%. [23] 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. [24] (See Medication.)

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Pathophysiology

The pathogenesis of primary hypertension is multifactorial and complex. [25] Multiple factors modulate the blood pressure (BP) including humoral mediators, vascular reactivity, circulating blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation. The pathogenesis of primary hypertension involves multiple factors, including genetic predisposition, excess dietary salt intake, adrenergic tone, and renal sodium and water handling that interact to produce BP elevations. Although genetics contribute, with rare exceptions this condition is polygenic. Emerging evidence suggests a role for immune cell activation and the microbiome in the pathogenesis of hypertension. [26]

The natural history of primary hypertension evolves from occasional to established hypertension. After a long 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.

A general progression of primary hypertension is as follows:

  1. Prehypertension in persons aged 10-30 years (by increased cardiac output)
  2. Early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent)
  3. Established hypertension in persons aged 30-50 years
  4. Complicated hypertension in persons aged 40-60 years

As evident from the above, younger individuals may present with hypertension associated with an elevated cardiac output (high-output hypertension). High-output hypertension results from volume and sodium retention by the kidney, leading to increased stroke volume and, often, with cardiac stimulation by adrenergic hyperactivity. Systemic vascular resistance is generally not increased at such earlier stages of hypertension. As hypertension is sustained, however, vascular adaptations including remodeling, vasoconstriction, and vascular rarefaction occur, leading to increased systemic vascular resistance. In this situation, cardiac output is generally normal or slightly reduced, and circulating blood volume is normal.

Cortisol reactivity, an index of hypothalamic-pituitary-adrenal function, may be another mechanism by which psychosocial stress is associated with future hypertension. [27] In a prospective sub-study 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 group developed hypertension in response to laboratory-induced mental stressors, and there was an association between cortisol stress reactivity and incident hypertension. [27]

Investigations into the pathophysiology of hypertension, both in animals and humans, have revealed that hypertension may have an immunologic 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 human immunovirus [HIV] deficiency) results in reduced BP 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. [28, 29]

One hypothesis is that prehypertension results in oxidation of lipids such as arachidonic acid that leads to the formation of isoketals or isolevuglandins, which function as neoantigens, which are then presented to T cells, leading to T-cell activation and infiltration of critical organs (eg, kidney, vasculature). [30] 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. [31, 32, 33]

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Etiology

Hypertension can 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 adherence.

Environmental and genetic/epigenetic causes

Hypertension develops secondary to environmental factors, as well as multiple genes, whose inheritance appears to be complex. [24, 34] Furthermore, obesity, diabetes, and heart disease also have genetic components and contribute to hypertension. Epidemiologic studies using twin data and data from Framingham Heart Study families reveal that blood pressure (BP) has a substantial heritable component, ranging from 33% to 57%. [35, 36, 37]

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. [38] Further research into these novel genes, some of which are immune-related, will likely increase the understanding of the pathophysiology of hypertension, 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. [39]

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. [40]

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, syndrome of apparent mineralocorticoid excess, and pseudohypoaldosteronism type II. [7]

Causes of secondary hypertension

Renal causes (2.5-6%) of hypertension include the renal parenchymal diseases and renal vascular diseases, as follows:

Renovascular hypertension (RVHT) causes 0.2-4% of cases of hypertension. Since the 1934 seminal experiment by Goldblatt et al, [41] 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 secondary hypertension. More specific diagnoses are made retrospectively when hypertension is improved after intravascular intervention.

Vascular causes include the following:

Endocrine causes may account for the largest proportion of secondary hypertension (10-20%) and include exogenous or endogenous hormonal imbalances. Exogenous causes include administration of steroids. Primary hyperaldosteronism is the most common endogenous hormone abnormality causing hypertension. Approximately 20% of cases of confirmed resistant hypertension are due to primary hyperaldosteronism. Pheochromocytomas and paragangliomas are rare, chromaffin cell tumors, that produce catecholamines. The prevalence of these tumors is 0.01-0.2% in the hypertensive population, but up to 4% in the resistant hypertension population. Cushing syndrome is caused by excess glucocorticoids and can present in a variety of ways, including weight gain, menstrual irregularities, mood disorders, muscle weakness, abdominal striae, and enlargement of the pad fat on the dorsal neck. Small cohort studies suggest a high prevalence of hypertension in patients with Cushing syndrome; further studies are needed for accurate correlation. [42]

Another common endocrine cause of hypertension is oral contraceptive use, likely due to activation of the renin-angiotensin-aldosterone system (RAAS). This is caused by increased hepatic synthesis of angiotensinogen in response to 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 coexistent renal disease, familial history of primary hypertension, age older than 35 years, and obesity.

Exogenous administration of steroids used for therapeutic purposes also increases 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:

Neurogenic causes include the following:

Drugs and toxins that cause hypertension include the following:

Other causes include the following:

Obstructive sleep apnea (OSA) is a common but frequently undiagnosed sleep-related breathing disorder defined as an average of at least five apneic and hypopneic episodes per sleep hour, with associated symptoms, including excessive daytime sleepiness. [43] Multiple studies have shown OSA to be an independent risk factor for the development of primary hypertension, even after adjusting for age, sex, 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. Apneic episodes are associated with striking increases in sympathetic nerve activity and enormous elevations of BP. Individuals with sleep apnea have increased cardiovascular mortality, in part likely related to the high incidence of hypertension.

Although treatment of sleep apnea with continuous airway positive pressure (CPAP) would logically seem to improve cardiovascular outcomes and hypertension, studies evaluating this mode of therapy have been disappointing. A 2016 review of several studies indicated that CPAP either had no effect or a modest BP-lowering effect. [44] Findings from the SAVE (Sleep Apnea Cardiovascular Endpoints) study showed no effect of CPAP therapy on BP above usual care. [45] It is likely that patients with sleep apnea have other etiologies of hypertension, including obesity, hyperaldosteronism, increased sympathetic drive, and activation of the renin/angiotensin system that contribute to their hypertension. Although CPAP remains an effective therapy for other aspects of sleep apnea, it should not be expected to normalize BP in the majority of patients.

Causes of hypertensive emergencies

The most common hypertensive emergency is a rapid unexplained rise in BP in patients with chronic essential hypertension. Most patients who develop hypertensive emergencies have a history of inadequate hypertensive treatment or an abrupt discontinuation of their medications. [46, 47]

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:

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Epidemiology

Hypertension is a worldwide epidemic; accordingly, its epidemiology has been well studied. Data from the US National Health and Nutrition Examination Survey (NHANES) spanning 2011-2014 found that of those in the population aged 20 years or older, an estimated 86 million adults had hypertension, with a prevalence of 34%. [4]

More recently, 2020 data from the Centers for Disease Control and Prevention's (CDC) National Center for Health Statistics (NCHS) spanning 2017-2018 show a 45.4% prevalence of hypertension among those aged 18 and older (see the following image; prevalence by sex and age). [49] Of the US adult population diagnosed with hypertension, a higher prevalence exists in males (51%) relative to females (39.7%).

Hypertension. Prevalence of hypertension among adu

Hypertension. Prevalence of hypertension among adults aged 18 and older, by sex and age: United States, 2017-2018. Courtesy of the Centers for Disease Control and Prevention (CDC), National Center for Health Statistics (NCHS).

There has been an interesting trend in the prevalence of hypertension, which fell in the early 2000s but began trending upward in 2014 (see the image below, which shows the prevalence of hypertension by year and sex). [49] The prevalence of hypertension declined during the first decade of this century, but it has since increased, particularly in men.

Hypertension. Age-adjusted trends in hypertension

Hypertension. Age-adjusted trends in hypertension among adults aged 18 and older: United States, 1999–2018. Courtesy of the Centers for Disease Control and Prevention (CDC), National Center for Health Statistics (NCHS).

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. [50] The high prevalence of hypertension exacts a tremendous public health burden. For example, as a primary contributor to heart disease and stroke, the first and third leading causes of death worldwide, respectively, high BP was the top modifiable risk factor for disability adjusted life-years lost worldwide in 2013. [51, 52]

Hypertension and sex- and age-related statistics

Females have a lower prevalence of hypertension until the fifth decade of life. Afterward, the prevalence of hypertension is increased in females compared to males. [1]

Hypertension and race and ethnicity

Black adults have among the highest rates of hypertension, with an increasing prevalence, in the United States and globally. [17, 18, 19, 53] 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). [54]

Table 2, below, summarizes age-adjusted prevalence estimates from the National Health Interview Survey (NHIS) and the NCHS according to racial/ethnic groups and diagnosed conditions in individuals aged 18 years and older.

Table 2. NHIS/NCHS Age-Adjusted Prevalence Estimates in Individuals Aged 18 Years and Older in 2015. (Open Table in a new window)

Race/Ethnic Group Have Hypertension, % Have Heart Disease, % Have Coronary Heart Disease, % Have Had a Stroke, %
White only 23.8 11.3 5.6 2.4
Black/African American 34.4 9.5 5.4 3.7
Hispanic/Latino 23.0 8.2 5.1 2.4
Asian 20.6 7.1 3.7 1.4
American Indian/Alaska Native 28.4 13.7 9.3 2.2 (this number is considered unreliable)
Source: Summary health statistics: National Health Interview Survey, 2015. Available at: https://ftp.cdc.gov/pub/Health_Statistics/NCHS/NHIS/SHS/2015_SHS_Table_A-1.pdf. Accessed: November 14, 2016.NCHS = National Center for Health Statistics; NHIS = National Health Interview Survey.

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Prognosis

Most individuals diagnosed with hypertension will have increasing blood pressure (BP) as they age. Untreated hypertension is notorious for raising the mortality risk 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 of organ damage in 50% of persons within 8-10 years after onset. Patients with resistant hypertension are also at higher risk for poor outcomes, particularly those with certain comorbidities (eg, chronic kidney disease, ischemic heart disease). [55] Patients with resistant hypertension who have lower BP appear to have a reduced risk for some cardiovascular events (eg, incident stroke, coronary heart disease, or heart failure). [55]

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, mortality doubles for both ischemic heart disease and stroke. [7]

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. [56, 57] 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 BP (< 120/80 mm Hg). [58, 59] Patients in the high range of prehypertension (130-139/85-89 mm Hg) had a 95% increased risk of stroke, compared to a 44% increased risk for those in the low range of prehypertension (120-129/80-84 mm Hg). [58, 59]

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 adherence, the 10-year survival of patients with hypertensive crises approaches 70%. [60]

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. [61] Multiple Risk Factor Intervention Trial (MRFIT) data showed that the relative mortality risk for coronary artery disease was 2.3 to 6.9 times higher for persons with mild to severe hypertension than it was for persons with normal BP. [62] 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% to 40%. [62]

The Framingham Heart Study also 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. [63]

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 BP 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 National Health Examination Survey (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. [64]

Clinical trials have demonstrated the following benefits with antihypertensive therapy [7] :

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. [7] However, for the same lowering in systolic BP reduction, it is estimated that 1 death is prevented per 9 patients treated when cardiovascular disease or end-organ damage is present. [7]

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Patient Education

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 improves compliance with medical therapy but also reduces cardiovascular risk factors.

Various strategies to decrease cardiovascular disease risk include the following:

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Author

Mackenzie Samson, MD Resident Physician, Department of Internal Medicine, Vanderbilt University Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Matthew R Alexander, MD, PhD Assistant Professor of Medicine, Department of Medicine, Division of Clinical Pharmacology, Division of Cardiovascular Medicine, Vanderbilt University School of Medicine; Assistant Professor of Molecular Physiology and Biophysics, Vanderbilt University

Matthew R Alexander, MD, PhD is a member of the following medical societies: American Association of Immunologists, American Heart Association, American Physiological Society, Federation of Clinical Immunology Societies, Vanderbilt Institute for Infection, Immunology, and Inflammation

Disclosure: Nothing to disclose.

Meena S Madhur, MD, PhD, FACC, FAHA Associate Professor with Tenure, Division Chief of Clinical Pharmacology, Department of Medicine, Division of Clinical Pharmacology and Division of Cardiology, Adjunct Associate Professor of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine; Adjunct Associate Professor of Medicine, Vanderbilt University School of Medicine

Meena S Madhur, MD, PhD, FACC, FAHA is a member of the following medical societies: American College of Cardiology, American Heart Association, American Physiological Society, American Society for Clinical Investigation

Disclosure: Nothing to disclose.

David G Harrison, MD Betty and Jack Bailey Professor of Medicine and Pharmacology, Director of Clinical Pharmacology, Vanderbilt University School of Medicine

David G Harrison, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, American Physiological Society, American Society for Clinical Investigation, Association of American Physicians, Central Society for Clinical and Translational Research, American Federation for Clinical Research, Society for Vascular Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH Professor of Medicine, Director of CME Programs, Team Leader, Root Cause Analysis, Tulane University Heart and Vascular Institute; Director of In-Patient Cardiology, Tulane Service, University Hospital; Visiting Physician, Medical Center of Louisiana at New Orleans; Faculty, Pennington Biomedical Research Institute, Louisiana State University; Professor, Tulane University School of Medicine

Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH is a member of the following medical societies: Alpha Omega Alpha, American Chemical Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Society for Pharmacology and Experimental Therapeutics, American Society of Hypertension, American Thoracic Society, Heart Failure Society of America, National Lipid Association, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic ArizonA

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Additional Contributors

Kamran Riaz, MD Clinical Assistant Professor, Department of Internal Medicine, Section of Cardiology, Wright State University, Boonshoft School of Medicine

Kamran Riaz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Society of Echocardiography, Ohio State Medical Association, Royal College of Physicians

Disclosure: Nothing to disclose.

Albert W Dreisbach, MD Associate Professor of Medicine, Division of Nephrology, University of Mississippi Medical Center

Disclosure: Nothing to disclose.

Acknowledgements

George R Aronoff, MD Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine

George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation

Disclosure: Nothing to disclose.

Michael S Beeson, MD, MBA, FACEP Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine and Pharmacy; Attending Faculty, Akron General Medical Center

Michael S Beeson, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Pamela L Dyne, MD Professor of Clinical Medicine/Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center

Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Mert Erogul, MD Assistant Professor of Emergency Medicine, University Hospital of Brooklyn: Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Mert Erogul, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Allysia M Guy, MD Staff Physician, Department of Emergency Medicine, State University of New York Downstate Medical Center

Disclosure: Nothing to disclose.

Dawn C Jung, MD Staff Physician, Department of Emergency Medicine, Suny Downstate Medical Center, Kings County Hospital Center

Dawn C Jung, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Claude Kortas, MD, MEd, FRCP(C) Program Director, Associate Professor, Department of Medicine, University of Western Ontario, Canada

Claude Kortas, MD, Med, FRCP(C) is a member of the following medical societies: American Society of Nephrology, College of Physicians and Surgeons of Ontario, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Stephen C Morris, MD Resident, Section of Emergency Medicine, Department of Surgery, Yale New Haven Hospital

Stephen C Morris, MD is a member of the following medical societies: American College of Emergency Physicians and American Medical Association

Disclosure: Nothing to disclose.

L Michael Prisant, MD, FACC, FAHA Cardiologist, Emeritus Professor of Medicine, Medical College of Georgia

L Michael Prisant, MD, FACC, FAHA is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Clinical Pharmacology, American College of Forensic Examiners, American College of Physicians, American Heart Association, and American Medical Association

Disclosure: Boehringer-Ingelheim Honoraria Speaking and teaching

Assaad J Sayah, MD Chief, Department of Emergency Medicine, Cambridge Health Alliance

Assaad J Sayah, MD is a member of the following medical societies: National Association of EMS Physicians

Disclosure: Nothing to disclose.

Zina Semenovskaya, MD Resident Physician, Department of Emergency Medicine, Kings County Hospital, State University of New York Downstate Medical Center College of Medicine

Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

Mark A Silverberg, MD, MMB, FACEP Assistant Professor, Associate Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate Medical Center

Mark A Silverberg, MD, MMB, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mark Zwanger, MD, MBA Assistant Professor, Department of Emergency Medicine, Jefferson Medical College of Thomas Jefferson University

Mark Zwanger, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American Medical Association

Disclosure: Nothing to disclose.