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Hypertension Clinical Presentation

  • Author: Meena S Madhur, MD, PhD; Chief Editor: David J Maron, MD, FACC, FAHA  more...
 
Updated: Sep 30, 2014
 

History

The 2013 joint European Society of Hypertension (ESH) and the European Society of Cardiology (ESC) guidelines recommend that ambulatory blood-pressure monitoring (ABPM) be incorporated into the assessment of cardiovascular risk factors and hypertension.[7, 8]

Following the documentation of hypertension, which is confirmed after an elevated blood pressure (BP) on at least 3 separate occasions (based on the average of 2 or more readings taken at each of ≥2 follow-up visits after initial screening), a detailed history should extract the following information:

  • Extent of end-organ damage (eg, heart, brain, kidneys, eyes)
  • Assessment of patients’ cardiovascular risk status
  • Exclusion of secondary causes of hypertension

Patients may have undiagnosed hypertension for years without having had their BP checked. Therefore, a careful history of end-organ damage should be obtained. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) identifies the following as targets of end-organ damage[3] :

  • Heart: left ventricular hypertrophy, angina/previous myocardial infarction, previous coronary revascularization, and heart failure
  • Brain: stroke or transient ischemic attack, dementia
  • Chronic kidney disease
  • Peripheral arterial disease
  • Retinopathy

The JNC 7 identifies the following as major cardiovascular risk factors[3] :

  • Hypertension: component of metabolic syndrome
  • Tobacco use, particularly cigarettes, including chewing tobacco
  • Elevated LDL cholesterol (or total cholesterol ≥240 mg/dL) or low HDL cholesterol: component of metabolic syndrome
  • Diabetes mellitus: component of metabolic syndrome
  • Obesity (BMI ≥30 kg/m 2): component of metabolic syndrome
  • Age greater than 55 years for men or greater than 65 years for women: increased risk begins at the respective ages; the Adult Treatment Panel III used earlier age cut points to suggest the need for earlier action
  • Estimated glomerular filtration rate less than 60 mL/min
  • Microalbuminuria
  • Family history of premature cardiovascular disease (men < 55 years; women < 65 years)
  • Lack of exercise

Obtain a history of the patient’s use of over-the-counter medications; herbal medicines such as herbal tea containing licorice (the issue is products containing licorice root; large amount of licorice in the US is licorice candy, but black licorice and over-the-counter licorice root supplements are increasingly available); ephedrine/ephedra; current and previous unsuccessful antihypertensive medication trials; oral contraceptives; ethanol; and illicit drugs such as cocaine. The patient’s lifestyle factors should also be included, such as changes in weight, dietary intake of sodium and cholesterol, exercise level, and psychosocial stressors.[5]

The historical and physical findings that suggest the possibility of secondary hypertension are a history of known renal disease, abdominal masses, anemia, and urochrome pigmentation. A history of sweating, labile hypertension, and palpitations suggests the diagnosis of pheochromocytoma. A history of cold or heat tolerance, sweating, lack of energy, and bradycardia or tachycardia may indicate hypothyroidism or hyperthyroidism. A history of obstructive sleep apnea may be noted. A history of weakness suggests hyperaldosteronism. Kidney stones raise the possibility of hyperparathyroidism.

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Physical Examination

An accurate measurement of blood pressure is the key to diagnosis. Several determinations should be made over a period of several weeks. At any given visit, an average of 3 blood pressure readings taken 2 minutes apart using a mercury manometer is preferable.[3, 5] On the first visit, blood pressure should be checked in both arms and in one leg to avoid missing the diagnosis of coarctation of aorta or subclavian artery stenosis.

The patient should rest quietly for at least 5 minutes before the measurement. Blood pressure should be measured in both the supine and sitting positions, auscultating with the bell of the stethoscope. As the improper cuff size may influence blood pressure measurement, a wider cuff is preferable, particularly if the patient’s arm circumference exceeds 30 cm. Although somewhat controversial, the common practice is to document phase V (a disappearance of all sounds) of Korotkoff sounds as the diastolic pressure.

Ambulatory or home blood pressure monitoring provides a more accurate prediction of cardiovascular risk than do office blood pressure readings.[46] "Non-dipping" is the loss of the usual physiologic nocturnal drop in blood pressure and is associated with an increased cardiovascular risk.

A study by Wong and Mitchell indicated that independent of other risk factors, there is a link between the presence of certain signs of hypertensive retinopathy (eg, retinal hemorrhages, microaneurysms, cotton-wool spots) and an increased cardiovascular risk (eg, stroke, stroke mortality).[47] Therefore, a funduscopic evaluation of the eyes should be performed to detect any evidence of early or late, chronic or acute hypertensive retinopathy, including arteriovenous nicking or changes in the vessel wall (eg, copper wiring, silver wiring, SOT , hard exudates, flame-shaped hemorrhages, papilledema). Indeed, ocular changes can be the initial finding in an asymptomatic patient necessitating a primary care referral; acute and chronic changes may manifest in the eyes. Alternatively, a symptomatic patient may be referred to the ophthalmologist for visual changes due to hypertensive changes.

Palpation of all peripheral pulses should be performed. Absent, weak, or delayed femoral pulses suggests coarctation of the aorta or severe peripheral vascular disease. In addition, examine the neck for carotid bruits, distended veins, or enlarged thyroid gland.[3, 5] Listen for renal artery bruit over the upper abdomen; the presence of a bruit with both a systolic and diastolic component suggests renal artery stenosis.

A careful cardiac examination is performed to evaluate signs of LVH. These include displacement of apex, a sustained and enlarged apical impulse, and the presence of an S4. Occasionally, a tambour S2 is heard with aortic root dilatation.

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Hypertension and Cerebrovascular Disease

Blood pressure is a powerful determinant of risk for ischemic stroke and intracranial hemorrhage; in fact, long-standing hypertension may manifest as hemorrhagic and atheroembolic stroke or encephalopathy. Both the high systolic and diastolic pressures are harmful; a diastolic pressure of more than 100 mm Hg and a systolic pressure of more than 160 mm Hg are associated with a significant incidence of strokes. The American Heart Association notes that individuals whose blood pressure level is lower than 120/80 mm Hg have about 50% the lifetime stroke risk of that of hypertensive individuals.

The main pathologic findings are in the heart, which shows an increase in mass caused principally by left ventricular hypertrophy. Histologically, the individual myocytes are enlarged and show nucleomegaly (“box car” nuclei) (see the image below). Hearts that are enlarged secondary to hypertension have an increased incidence of arrhythmia and death. Other cerebrovascular manifestations of complicated hypertension include hypertensive hemorrhage, hypertensive encephalopathy, lacunar-type infarctions, and dementia.

Hypertrophied cardiac myocytes with enlarged "box Hypertrophied cardiac myocytes with enlarged "box car" nuclei.

Hypertensive encephalopathy is one of the clinical manifestations of cerebral edema and microhemorrhages seen with dysfunction of cerebral autoregulation and is characterized by hypertension, altered mentation, and papilledema.

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Hypertensive Emergencies

The history and physical examination determine the nature, severity, and management of the hypertensive event. The history should focus on the presence of end-organ dysfunction, the circumstances surrounding the hypertension, and any identifiable etiology. The physical examination should assess whether end-organ dysfunction is present (eg, neurologic, cardiovascular). BP should be measured in both the supine position and the standing position (assess volume depletion). BP should also be measured in both arms (a significant difference may suggest aortic dissection).

The most common clinical presentations of hypertensive emergencies are cerebral infarction (24.5%), pulmonary edema (22.5%), hypertensive encephalopathy (16.3%), and congestive heart failure (12%). Other clinical presentations associated with hypertensive emergencies include intracranial hemorrhage, aortic dissection, and eclampsia,[48] as well as acute myocardial infarction. Hypertension is also one of several conditions that have been increasingly recognized as having an association with posterior reversible encephalopathy syndrome (PRES), a condition characterized by headache, altered mental status, visual disturbances, and seizures.[49]

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Hypertensive Heart Disease

Uncontrolled and prolonged BP elevation can lead to a variety of changes in the myocardial structure, coronary vasculature, and conduction system of the heart. These changes in turn can lead to the development of left ventricular hypertrophy (LVH), coronary artery disease, various conduction system diseases, and systolic and diastolic dysfunction of the myocardium, which manifest clinically as angina or myocardial infarction, cardiac arrhythmias (especially atrial fibrillation), and congestive heart failure (CHF). Thus, hypertensive heart disease is a term applied generally to heart diseases—such as LVH, coronary artery disease, cardiac arrhythmias, and CHF—that are causedbydirectorindirecteffects of elevated BP.

Although these diseases generally develop in response to chronically elevated BP, marked and acute elevation of BP can also lead to accentuation of an underlying predisposition to any of the symptoms traditionally associated with chronic hypertension.

In a study by Tymchak et al, patients presenting with acute heart failure as a manifestation of hypertensive emergency were more likely to be black and have a history of heart failure; they were also more likely to have higher B-type natriuretic peptide (BNP) and creatinine levels and lower left ventricular ejection fraction. Note that BNP is inversely proportional to the degree of a patient’s obesity.[50]

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Hypertension in Pediatric Patients

Advances in the ability to identify, evaluate, and care for infants with hypertension, coupled with advances in the practice of neonatology in general, have led to an increased awareness of hypertension in modern neonatal ICUs (NICUs) since its first description in the 1970s.

The true incidence of hypertension in the pediatric population is not known, although various health data showed a decreasing trend between 1963 and 1988, followed by an upward trend. Hypertension is now commonly discovered in children, and the long-term health risks to these children may be substantial.

Systemic hypertension is less common in children than in adults, but the incidence of hypertension in children is approximately 1-5%. The presence of hypertension in younger children is usually indicative of an underlying disease process (secondary hypertension). In children, approximately 5-25% of cases of secondary hypertension are attributed to renovascular disease.

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Hypertension in Pregnancy

Hypertension is the most common medical problem encountered during pregnancy, complicating 2-3% of pregnancies. Hypertensive disorders during pregnancy are classified into the 4 following categories, as recommended by the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy:

  • Chronic hypertension
  • Preeclampsia-eclampsia
  • Preeclampsia superimposed on chronic hypertension
  • Gestational hypertension (transient hypertension of pregnancy or chronic hypertension identified in the latter half of pregnancy); this terminology is preferred over the older but widely used term pregnancy-induced hypertension (PIH) because it is more precise.

A large, population-based study compared 26,651 pregnant women with hypertensive disorders to 213,397 pregnant women without hypertensive disorders to determine risk of end-stage renal disease. Results showed that the incidence of chronic kidney disease was almost 11-fold higher in the hypertensive group. This group also exhibited a 14-fold increased risk for end-stage renal disease. The risk was much greater for women with preeclampsia or eclampsia. This study highlights the importance of adequate follow-up of BP after pregnancy.[51]

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Primary Aldosteronism

Mineralocorticoid excess secondary to primary hyperaldosteronism is infrequently observed and is characterized by excessive production of aldosterone. Renal sodium retention, kaliuresis, hypokalemia, and hypochloremic metabolic alkalosis are the common manifestations. It should be considered in patients who have an exaggerated hypokalemic response to a thiazide diuretic or who have hypokalemia unprovoked by a diuretic. These patients develop increased intravascular volume, resulting in hypertension. The BP increase may vary from mild hypertension to marked elevation in primary hyperaldosteronism. Patients may have underlying adenoma or hyperplasia of the adrenal gland and rarely have an extra-adrenal source for aldosterone.

The incidence of primary hyperaldosteronism was 1.5% in one study.[11] However, the true incidence of primary aldosteronism is still not clear, largely because of the lack of criterion-standard testing. In contrast, inappropriately high output of aldosterone for a given salt state of a patient (ie, not meeting criteria for a diagnosis of primary aldosteronism) is much more common, especially in patients with metabolic syndrome.[52]

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Contributor Information and Disclosures
Author

Meena S Madhur, MD, PhD Assistant Professor, Department of Medicine, Divisions of Clinical Pharmacology and Cardiology, Vanderbilt University School of Medicine

Meena S Madhur, MD, PhD is a member of the following medical societies: American College of Cardiology, American Heart Association

Disclosure: Nothing to disclose.

Coauthor(s)

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.

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.

Chief Editor

David J Maron, MD, FACC, FAHA Clinical Professor of Medicine (Cardiovascular), Director, Preventive Cardiology, ISCHEMIA Trial Co-Chair/PI, Stanford University School of Medicine

David J Maron, MD, FACC, FAHA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association

Disclosure: Received ownership interest from Cardiovascular Care Group for other.

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.

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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.
Hypertrophied cardiac myocytes with enlarged "box car" nuclei.
Table 1. NHIS/NCHS Age-Adjusted Prevalence Estimates in Individuals Aged 18 Years and Older in 2008.
Race/Ethnic Group Have Hypertension, % Have Heart Disease, % Have Coronary Heart Disease, % Have Had a Stroke, %
White only 23.3 12.1 6.5 2.7
Black/African American 31.8 10.2 5.6 3.6
Hispanic/Latino 21.0 8.1 5.7 2.6
Asian 21.0 5.2 2.9 1.8
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.



Table 2. Identifiable Hypertension and Screening Tests
Condition Screening Test
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.[3]



* 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.



Table 3. Hypertensive Disorders in Pregnancy
Classification Characteristics
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



Thrombocytopenia



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.[3]



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