Hypertension 

  • Author: Kamran Riaz, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Jan 27, 2012
 

Background

Hypertension is one of the most common worldwide diseases afflicting humans. Because of the associated morbidity and mortality and the cost to society, hypertension is an important public health challenge. Over the past several decades, extensive research, widespread patient education, and a concerted effort on the part of health care professionals have led to decreased mortality and morbidity rates from the multiple organ damage arising from years of untreated hypertension.

Approximately 50 million people in the United States are affected by hypertension.[1, 2] Substantial improvements have been made with regard to improving awareness and treatment of hypertension. However, approximately 30% of adults are still unaware of their hypertension; up to 40% of people with hypertension are not receiving treatment; and, of those treated, up to 67% do not have their blood pressure (BP) controlled to less than 140/90 mm Hg.[1] (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, 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 and Management.)

Definition and classification

Defining abnormally high blood pressure 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 Clinical Presentation.)

Based on recommendations of the Seventh Report of the Joint National Committee of Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII), the classification of BP (expressed in mm Hg) for adults aged 18 years or older is as follows[1] :

  • Normal - Systolic lower than 120, diastolic lower than 80
  • Prehypertension - Systolic 120-139, diastolic 80-90
  • Stage 1 - Systolic 140-159, diastolic 90-99
  • Stage 2 - Systolic equal to or more than 160, diastolic equal to or more than 100

The classification above is based on the average of 2 or more readings taken at each of 2 or more visits after initial screening. Normal BP with respect to cardiovascular risk is less than 120/80 mm Hg. However, unusually low readings should be evaluated for clinical significance.

Prehypertension, a new category designated in the JNC VII 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. Essential hypertension is diagnosed in the absence of an identifiable secondary cause. Approximately 95% of the 50 million American adults with hypertension have essential hypertension, while secondary hypertension accounts for fewer than 5% of the cases. However, secondary forms of hypertension, such as primary hyperaldosteronism, account for 20% of resistant hypertension (hypertension that requires 4 or more medications to control).

Especially severe cases of hypertension may be further categorized. Severe hypertension is defined by a blood pressure above 180/110 without symptoms. Hypertensive urgency is defined as a BP above 180/110 with mild end organ effects, such as headache and dyspnea. Hypertensive emergency is a BP of 220/140 or greater with life-threatening end-organ dysfunction.

Hypertensive emergencies encompass a spectrum of clinical presentations in which uncontrolled BPs lead to progressive or impending end-organ dysfunction; in these conditions, the BP should be lowered aggressively over minutes to hours. Acute end-organ damage in the setting of a hypertensive emergency may include the following[3] :

  • 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
  • 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%.[4] In addition, the 1-year survival rate associated with this condition has increased from only 20% (prior to 1950) to a survival rate of more than 90% with appropriate medical treatment.[5] (See Medication.)

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Pathophysiology

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.

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 target organ damage to the aorta and small arteries, heart, kidneys, retina, and central nervous system is evident. The progression begins with prehypertension in persons aged 10-30 years (by increased cardiac output) to early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent) to established hypertension in persons aged 30-50 years, and, finally, to 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.

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Etiology

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. Hypertensive emergencies are most often precipitated by inadequate medication or poor compliance.

Environmental and genetic causes

Hypertension develops secondary to environmental factors, as well as to multiple genes, whose inheritance appears to be complex.[6, 7] Very rare secondary causes are related to single genes and include Liddle syndrome, glucocorticoid-remediable hyperaldosteronism, 11 beta-hydroxylase and 17 alpha-hydroxylase deficiencies, the syndrome of apparent mineralocorticoid excess, and pseudohypoaldosteronism type II.

Primary or essential hypertension accounts for 90-95% of adult cases, and a small percentage of patients (2-10%) have a secondary cause.

Causes of secondary hypertension

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

  • Polycystic kidney disease
  • Chronic kidney disease
  • Urinary tract obstruction
  • Renin-producing tumor
  • Liddle syndrome

Renovascular hypertension (RVHT) causes 0.2-4% of cases. Since Goldblatt’s seminal experiment in 1934, 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
  • Vasculitis
  • 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 an endocrine cause: oral contraceptive use. Activation of the renin-angiotensin-aldosterone system is the likely mechanism because hepatic synthesis of angiotensinogen is induced by the estrogen component of oral contraceptives. Approximately 5% of women prescribed oral contraceptives may develop hypertension, which abates within 6 months of 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.

Exogenous administration of the other steroids used for therapeutic purposes also increases blood pressure, especially in susceptible individuals, mainly by volume expansion. Nonsteroidal anti-inflammatory drugs (NSAIDs) may also have adverse effects on blood pressure. 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 and/or controlled hypertensive patient

Endogenous hormonal causes include the following:

  • Primary hyperaldosteronism
  • Cushing syndrome
  • Pheochromocytoma
  • Congenital adrenal hyperplasia

Neurogenic causes include the following:

  • Brain tumor
  • Bulbar poliomyelitis
  • Intracranial hypertension

Drugs and toxins that cause hypertension include the following:

  • Alcohol
  • Cocaine
  • Cyclosporine, tacrolimus
  • NSAIDs
  • Erythropoietin
  • Adrenergic medications
  • Decongestants containing ephedrine
  • Herbal remedies containing licorice or ephedrine

Other causes include the following:

  • Hyperthyroidism and hypothyroidism
  • Hypercalcemia
  • Hyperparathyroidism
  • Acromegaly
  • Obstructive sleep apnea
  • Pregnancy-induced hypertension

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.

Other causes of hypertensive emergencies include the use of recreational drugs, abrupt clonidine withdrawal, post pheochromocytoma removal, and systemic sclerosis.

Other causes include 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 (CNS) factors - CNS trauma or spinal cord disorders, such as Guillain-Barré syndrome
  • Coarctation of the aorta
  • Preeclampsia/eclampsia
  • Postoperative hypertension
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Epidemiology

Hypertension is a worldwide epidemic; accordingly, its epidemiology has been well studied.

A 2005 survey 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 have prehypertension, 12.8 million men and 12.2 million women have stage 1 hypertension, and 4.1 million men and 6.9 million women have stage 2 hypertension.[8] In many countries, 50% of the population older than 60 years has hypertension. Overall, approximately 20% of the world’s adults are estimated to have hypertension. The 20% prevalence is for hypertension defined as BP in excess of 140/90 mm Hg. The prevalence dramatically increases in patients older than 60 years.

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Prognosis

Most individuals diagnosed with hypertension will have increasing 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, is associated with a risk of atherosclerotic disease in 30% of people and organ damage in 50% of people after only 8-10 years of onset.

Death from both ischemic heart disease and stroke increase 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.

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%.[9]

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 highest blood pressure was compared to the lowest.[10] Multiple Risk Factor Intervention Trial (MRFIT) data showed that the relative risk for coronary heart disease mortality varied from 2.3-6.9 times higher for persons with mild to severe hypertension compared to persons with normal BP.[11] The relative risk for stroke ranged from 3.6-19.2. The population-attributable risk percentage for coronary artery disease varied from 2.3-25.6%, 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.[12]

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 NHANES I and III showed a decrease in mortality over time among hypertensive adults, but the mortality gap between hypertensive and normotensive adults remains high.[13]

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Patient Education

Hypertension is a lifelong disorder. For optimal control, a long-term commitment to lifestyle modifications and pharmacological 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
  • Appropriate amounts of aerobic physical activity
  • Diets low in salt, total fat, and cholesterol
  • Adequate dietary intakes of potassium, calcium, and magnesium
  • Limited alcohol consumption
  • Avoidance of cigarette smoking
  • Avoidance of the use of illicit drugs, such as cocaine

For excellent patient education resources, visit eMedicine's Diabetes Center and Cholesterol Center. Also, see eMedicine's patient education articles High Blood Pressure, High Cholesterol, Chest Pain, Coronary Heart Disease, and Heart Attack.

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Contributor Information and Disclosures
Author

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, and Royal College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

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

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

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.

References

  1. 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. Dec 2003;42(6):1206-52. [Medline].

  2. Hajjar I, Kotchen TA. Trends in prevalence, awareness, treatment, and control of hypertension in the United States, 1988-2000. JAMA. Jul 9 2003;290(2):199-206. [Medline].

  3. Bianchi S, Bigazzi R, Campese VM. Microalbuminuria in essential hypertension: significance, pathophysiology, and therapeutic implications. Am J Kidney Dis. Dec 1999;34(6):973-95. [Medline].

  4. Shayne PH, Pitts SR. Severely increased blood pressure in the emergency department. Ann Emerg Med. Apr 2003;41(4):513-29. [Medline].

  5. Rhoades R, Planzer R. Human Physiology. 3rd. Fort Worth, TX: Saunders College Publishing; 1996.

  6. 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. Jul 2009;11(1):17-26. [Medline]. [Full Text].

  7. 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. Aug 2009;24(8):2414-20. [Medline]. [Full Text].

  8. 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. Sep 2005;11(9):CR403-9. [Medline].

  9. Webster J, Petrie JC, Jeffers TA, Lovell HG. Accelerated hypertension--patterns of mortality and clinical factors affecting outcome in treated patients. Q J Med. Aug 1993;86(8):485-93. [Medline].

  10. 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. Jul 6 1999;131(1):7-13. [Medline].

  11. Mortality after 10 1/2 years for hypertensive participants in the Multiple Risk Factor Intervention Trial. Circulation. Nov 1990;82(5):1616-28. [Medline].

  12. Chen G, McAlister FA, Walker RL, Hemmelgarn BR, Campbell NR. Cardiovascular outcomes in framingham participants with diabetes: the importance of blood pressure. Hypertension. May 2011;57(5):891-7. [Medline].

  13. Ford ES. Trends in mortality from all causes and cardiovascular disease among hypertensive and nonhypertensive adults in the United States. Circulation. Apr 26 2011;123(16):1737-44. [Medline].

  14. 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. Feb 1998;31(2):712-8. [Medline].

  15. Heilpern K. Pathophysiology of hypertension. Ann Emerg Med. Mar 2008;51(3 Suppl):S5-6. [Medline].

  16. Zampaglione B, Pascale C, Marchisio M, Cavallo-Perin P. Hypertensive urgencies and emergencies. Prevalence and clinical presentation. Hypertension. Jan 1996;27(1):144-7. [Medline].

  17. Tymchak W, Armstrong PW, Westerhout CM, et al. Mode of hospital presentation in patients with non-ST-elevation myocardial infarction: implications for strategic management. Am Heart J. Sep 2011;162(3):436-43. [Medline].

  18. 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. Jun 1999;17(6):817-24. [Medline].

  19. 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. Jun 2011;32(12):1509-18. [Medline].

  20. 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. Jun 1 1995;122(11):833-8. [Medline].

  21. Hermida RC, Ayala DE, Mojón A, Fernández JR. Decreasing sleep-time blood pressure determined by ambulatory monitoring reduces cardiovascular risk. J Am Coll Cardiol. Sep 6 2011;58(11):1165-73. [Medline].

  22. [Guideline] American Diabetes Association. Standards of medical care in diabetes--2011. Diabetes Care. Jan 2011;34 Suppl 1:S11-61. [Medline]. [Full Text].

  23. 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. Nov 2001;19(11):1949-56. [Medline].

  24. Your Guide to Lowering Your Blood Pressure With DASH. National Institutes of Health; April 2006. 64. [Full Text].

  25. [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. Dec 6 2010;[Medline].

  26. 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. Jul 26 2011;343:d4366. [Medline].

  27. [Best Evidence] 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. Jan 25 2010;170(2):126-35. [Medline].

  28. Leung AA, Wright A, Pazo V, Karson A, Bates DW. Risk of Thiazide-induced Hyponatremia in Patients with Hypertension. Am J Med. Nov 2011;124(11):1064-72. [Medline].

  29. 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. Jan 22 2011;377(9762):312-20. [Medline].

  30. Ruggenenti P, Lauria G, Iliev IP, et al, for the DEMAND Study Investigators. 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. Nov 2011;58(5):776-83. [Medline].

  31. Isom HC, DeMoss RD. Structural role of pyridoxal 5'-phosphate, pyridoxal 5'-phosphate analogs, and other agents in the association of subunits of Bacillus alvei apotryptophanase. Biochemistry. Sep 23 1975;14(19):4298-304. [Medline].

  32. Slovis CM, Reddi AS. Increased blood pressure without evidence of acute end organ damage. Ann Emerg Med. Mar 2008;51(3 Suppl):S7-9. [Medline].

  33. Abalos E, Duley L, Steyn DW, Henderson-Smart DJ. Antihypertensive drug therapy for mild to moderate hypertension during pregnancy. Cochrane Database Syst Rev. Jan 24 2007;CD002252. [Medline].

  34. 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. [Full Text].

  35. 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. Jul 29 2000;356(9227):359-65. [Medline].

  36. Aronow WS, Fleg JL, Pepine CJ, 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. May 17 2011;57(20):2037-114. [Medline]. [Full Text].

  37. Kostis JB, Cabrera J, Cheng JQ, et al. Association between chlorthalidone treatment of systolic hypertension and long-term survival. JAMA. Dec 21 2011;306(23):2588-93. [Medline].

  38. Lao D, Parasher PS, Cho KC, Yeghiazarians Y. Atherosclerotic renal artery stenosis--diagnosis and treatment. Mayo Clin Proc. Jul 2011;86(7):649-57. [Medline]. [Full Text].

  39. Rastan A, Krankenberg H, Müller-Hülsbeck S, Sixt S, Tübler T, Müller C, 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. Aug 2008;4(2):208-13. [Medline].

  40. Epstein M. Calcium antagonists and renal disease. Kidney Int. Nov 1998;54(5):1771-84.

  41. Yakovlevitch M, Black HR. Resistant hypertension in a tertiary care clinic. Arch Intern Med. Sep 1991;151(9):1786-92. [Medline].

  42. de la Sierra A, Segura J, Banegas JR, et al. Clinical features of 8295 patients with resistant hypertension classified on the basis of ambulatory blood pressure monitoring. Hypertension. May 2011;57(5):898-902. [Medline].

  43. Catheter-based renal sympathetic denervation for resistant hypertension: durability of blood pressure reduction out to 24 months. Hypertension. May 2011;57(5):911-7. [Medline].

  44. Bisognano JD, Bakris G, Nadim MK, 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. Aug 9 2011;58(7):765-73. [Medline].

  45. Kronish IM, Woodward M, Sergie Z, Ogedegbe G, Falzon L, Mann DM. Meta-analysis: impact of drug class on adherence to antihypertensives. Circulation. Apr 19 2011;123(15):1611-21. [Medline].

  46. Pimenta E, Calhoun DA, Oparil S. Sleep apnea, aldosterone, and resistant hypertension. Prog Cardiovasc Dis. Mar-Apr 2009;51(5):371-80. [Medline].

  47. Pedrosa RP, Drager LF, Gonzaga CC, et al. Obstructive sleep apnea: the most common secondary cause of hypertension associated with resistant hypertension. Hypertension. Nov 2011;58(5):811-7. [Medline].

  48. Pickering TG, James GD, Boddie C, Harshfield GA, Blank S, Laragh JH. How common is white coat hypertension?. JAMA. Jan 8 1988;259(2):225-8. [Medline].

  49. Fahey T, Schroeder K, Ebrahim S. Interventions used to improve control of blood pressure in patients with hypertension. Cochrane Database Syst Rev. Apr 19 2006;CD005182. [Medline].

  50. 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. Mar 2011;26(3):280-6. [Medline].

  51. Bosworth HB, Powers BJ, Olsen MK, et al. Home blood pressure management and improved blood pressure control: results from a randomized controlled trial. Arch Intern Med. Jul 11 2011;171(13):1173-80. [Medline].

  52. Narkiewicz K. Diagnosis and management of hypertension in obesity. Obes Rev. May 2006;7(2):155-62. [Medline].

  53. Cummings DM, Amadio P Jr, Nelson L, Fitzgerald JM. The role of calcium channel blockers in the treatment of essential hypertension. Arch Intern Med. Feb 1991;151(2):250-9. [Medline].

  54. 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. Mar 2011;57(3):413-20. [Medline].

  55. Harel Z, Gilbert C, Wald R, 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. Jan 9 2012;344:e42. [Medline]. [Full Text].

  56. 1999 World Health Organization-International Society of Hypertension Guidelines for the Management of Hypertension. Guidelines Subcommittee. J Hypertens. Feb 1999;17(2):151-83. [Medline].

  57. 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 &DocID=48. Accessed May 14, 2009.

  58. 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. Feb 2010;41(2):307-12. [Medline].

  59. 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. May 2008;7(5):391-9. [Medline].

  60. Ault MJ, Ellrodt AG. Pathophysiological events leading to the end-organ effects of acute hypertension. Am J Emerg Med. Dec 1985;3(6 Suppl):10-5. [Medline].

  61. Barton JR. Hypertension in pregnancy. Ann Emerg Med. Mar 2008;51(3 Suppl):S16-7. [Medline].

  62. Brown MJ. Hypertension and ethnic group. BMJ. Apr 8 2006;332(7545):833-6. [Medline]. [Full Text].

  63. Cheung AT, Hobson RW 2nd. Hypertension in vascular surgery: aortic dissection and carotid revascularization. Ann Emerg Med. Mar 2008;51(3 Suppl):S28-33. [Medline].

  64. 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. Jan 1996;5(1):17-24; discussion 25. [Medline].

  65. 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. Apr 1989;149(4):780-8. [Medline].

  66. Diercks DB, Ohman EM. Hypertension with acute coronary syndrome and heart failure. Ann Emerg Med. Mar 2008;51(3 Suppl):S34-6. [Medline].

  67. 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. Jan 4 2001;344(1):17-22. [Medline].

  68. Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation. Oct 25 2005;112(17):2735-52. [Medline].

  69. Hollander JE. Cocaine intoxication and hypertension. Ann Emerg Med. Mar 2008;51(3 Suppl):S18-20. [Medline].

  70. Kaplan NM. Calcium entry blockers in the treatment of hypertension. Current status and future prospects. JAMA. Aug 11 1989;262(6):817-23. [Medline].

  71. 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. Jun 2005;21(8):657-72. [Medline].

  72. Kitiyakara C, Guzman NJ. Malignant hypertension and hypertensive emergencies. J Am Soc Nephrol. Jan 1998;9(1):133-42. [Medline].

  73. 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. Apr 19 2000;283(15):1967-75. [Medline].

  74. Marik PE, Varon J. Hypertensive crises: challenges and management. Chest. Jun 2007;131(6):1949-62. [Medline].

  75. Pancioli AM. Hypertension management in neurologic emergencies. Ann Emerg Med. Mar 2008;51(3 Suppl):S24-7. [Medline].

  76. 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. Sep 28 1989;321(13):868-73. [Medline].

  77. Redon J, Cifkova R, Laurent S, Nilsson P, Narkiewicz K, Erdine S, et al. Mechanisms of hypertension in the cardiometabolic syndrome. J Hypertens. Mar 2009;27(3):441-51. [Medline].

  78. Rodriguez MA, Kumar SK, De Caro M. Hypertensive crisis. Cardiol Rev. Mar-Apr 2010;18(2):102-7. [Medline].

  79. Strong Heart Study Data Book: A Report to American Indian Communities. Bethesda, MD: National Heart, Lung, and Blood Institute, NIH; 2001.

  80. The World Health Report 2002-Reducing Risks, Promoting Healthy Life. Geneva, Switzerland: World Health Organization; 2002. [Full Text].

  81. 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. Oct 1980;46(4):559-65. [Medline].

  82. 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. Jan 2000;13(1 Pt 1):103-4. [Medline].

 
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Anteroposterior x-ray from a 28-year old woman who presented with congestive heart failure secondary to her chronic hypertension, or high blood pressure. The enlarged cardiac silhouette on this image is due to congestive heart failure due to the effects of chronic high blood pressure on the left ventricle. The heart then becomes enlarged, and fluid accumulates in the lungs, known as pulmonary congestion.
Electrocardiogram (ECG) from a 47-year-old man with a long-standing history of uncontrolled hypertension. This image shows left atrial enlargement and left ventricular hypertrophy.
Electrocardiogram (ECG) from a 46-year-old man with long-standing hypertension. This ECG shows left atrial abnormality and left ventricular hypertrophy with strain.
Histologic section of an autopsy myocardial specimen from a patient with long-standing hypertension and associated coronary artery disease. This slide shows myocardial hypertrophy, contraction bands (typical of left ventricular hypertrophy), and "box car" nuclei.
Hypertrophied cardiac myocytes with enlarged "box car" nuclei.
 
 
 
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