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TENTH EDITION Kaplan’s Clinical Hypertension Norman M Kaplan, MD Clinical Professor of Medicine Department of Internal Medicine University of Texas Southwestern Medical School Dallas, Texas Ronald G Victor, MD Associate Director, Clinical Research Director, Hypertension Center The Heart Institute Cedars-Sinai Medical Center Los Angeles, California With a Chapter by Joseph T Flynn, MD, MS Professor of Pediatrics Division of Nephrology Seattle Children’s Hospital Seattle, Washington FM.indd i 8/28/2009 1:23:33 PM Acquisitions Editor: Frances R DeStefano Product Manager: Leanne McMillan Production Manager: Alicia Jackson Senior Manufacturing Manager: Benjamin Rivera Marketing Manager: Kimberly Schonberger Design Coordinator: Holly Reid McLaughlin Production Service: SPi Technologies ©2010 by LIPPINCOTT WILLIAMS & WILKINS, a WOLTERS KLUWER business 530 Walnut Street Philadelphia, PA 19106 USA LWW.com 9th Edition, © 2006 Lippincott Williams & Wilkins 8th Edition, © 2000 Lippincott Williams & Wilkins 7th Edition, © 1998 Lippincott Williams & Wilkins 6th Edition, © 1994 Williams & Wilkins 5th Edition, © 1990 Williams & Wilkins 4th Edition, © 1986 Williams & Wilkins 3rd Edition, © 1982 Williams & Wilkins 2nd Edition, © 1978 Williams & Wilkins 1st Edition, © 1973 Williams & Wilkins All rights reserved This book is protected by copyright No part of this book may be reproduced in any form by any means, including photocopying, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews Materials appearing in this book prepared by individuals as part of their official duties as U.S government employees are not covered by the above-mentioned copyright Printed in China Library of Congress Cataloging-in-Publication Data Kaplan’s clinical hypertension / editors, Norman M Kaplan, Ronald G Victor; with a chapter by Joseph T Flynn —10th ed p ; cm Rev ed of: Kaplan’s clinical hypertension / Norman M Kaplan 9th ed c2006 Includes bibliographical references and index ISBN-13: 978-1-60547-503-5 ISBN-10: 1-60547-503-3 Hypertension I Kaplan, Norman M., 1931- II Victor, Ronald G III Kaplan, Norman M., 1931- Kaplan’s clinical hypertension IV Title: Clinical hypertension [DNLM: Hypertension WG 340 K171 2010] RC685.H8K35 2010 616.1′32—dc22 2009029663 Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices However, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication Application of the information in a particular situation remains the professional responsibility of the practitioner The authors, editors, and publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accordance with current recommendations and practice at the time of publication However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions This is particularly important when the recommended agent is a new or infrequently employed drug Some drugs and medical devices presented in the publication have Food and Drug Administration (FDA) clearance for limited use in restricted research settings It is the responsibility of the health care provider to ascertain the FDA status of each drug or device planned for use in their clinical practice To purchase additional copies of this book, call our customer service department at (800) 638–3030 or fax orders to (301) 223–2320 International customers should call (301) 223–2300 Visit Lippincott Williams & Wilkins on the Internet: at LWW.com Lippincott Williams & Wilkins customer service representatives are available from 8:30 am to pm, EST 10 FM.indd ii 8/28/2009 1:23:33 PM To those such as Goldblatt and Grollman, Braun-Menéndez and Page, Lever and Pickering, Mancia, Brenner, and Laragh, Julius, Hansson, and Freis, and the many others, whose work has made it possible for us to put together what we hope will be a useful book on clinical hypertension FM.indd iii 8/28/2009 1:23:33 PM PREFACE TO THE TENTH EDITION ypertension is increasingly being diagnosed worldwide, in developed and undeveloped societies, as populations become fatter and older The literature on hypertension keeps pace with the increased prevalence of the disease The ability required of a simple author to digest and organize this tremendous body of information into a relatively short book that is both current and inclusive has become almost impossible Fortunately, Dr Ronald Victor has been willing and able to join as a coauthor After 10 years of close contact at the University of Texas Southwestern Medical School, I know him to be a clearheaded and open-minded clinician, teacher, and researcher Despite his move to smoggy Los Angeles, he brings a fresh perspective that adds greatly to this book As noted in the previous edition, I am amazed at the tremendous amount of hypertension-related literature published over the past years A considerable amount of significant new information is included in this edition, presented in a manner that I hope enables the reader to grasp its significance and place it in perspective Almost every page has been revised, using the same goals: H • Give more attention to the common problems; primary hypertension takes up almost half • Cover every form of hypertension at least briefly, providing references for those seeking more information Additional coverage is provided on some topics that have recently assumed importance • Include the latest data, even if available only in abstract form • Provide enough pathophysiology to permit sound clinical judgment • Be objective and clearly identify biases, although my views may differ from those of others I have tried to give reasonable attention to those with whom I disagree Dr Joseph T Flynn, Professor of Pediatrics, Division of Nephrology, Seattle Children’s Hospital, Seattle, Washington has contributed a chapter on hypertension in children and adolescents I have been fortunate in being in an academic setting wherein such endeavors are nurtured and wish to thank all who have been responsible for establishing this environment and all of our colleagues who have helped us through the years Norman M Kaplan, MD Ronald G Victor, MD iv FM.indd iv 8/28/2009 1:23:33 PM C O N T E N T S Dedication iii Preface to the Tenth Edition 10 11 12 13 14 15 16 iv Hypertension in the Population at Large Measurement of Blood Pressure 20 Primary Hypertension: Pathogenesis 42 Primary Hypertension: Natural History and Evaluation 108 Treatment of Hypertension: Why, When, How Far 141 Treatment of Hypertension: Lifestyle Modifications 168 Treatment of Hypertension: Drug Therapy 192 Hypertensive Crises 274 Renal Parenchymal Hypertension 288 Renovascular Hypertension 319 Primary Aldosteronism 339 Pheochromocytoma (with a Preface about Incidental Adrenal Masses) 358 Hypertension Induced by Cortisol or Deoxycorticosterone 378 Other Forms of Identifiable Hypertension 392 Hypertension with Pregnancy and the Pill 410 Hypertension in Childhood and Adolescence 430 Appendix: Patient Information Index 457 455 v FM.indd v 8/28/2009 1:23:33 PM FM.indd vi 8/28/2009 1:23:33 PM CHAPTER Hypertension in the Population at Large ypertension provides both despair and hope: despair because it is quantitatively the largest risk factor for cardiovascular diseases (CVD), it is growing in prevalence, and it is poorly controlled virtually everywhere; and hope because prevention is possible (though rarely achieved) and treatment can effectively control almost all patients, resulting in marked reductions in stroke and heart attack Although most of this book addresses hypertension in the United States and other developed countries, it should be noted that CVDs are the leading cause of death worldwide, more so in the economically developed countries, but also in the developing world As Lawes et al (2008) note: “Overall about 80% of the attributable burden (of hypertension) occurs in lowincome and middle-income economies.” In turn, hypertension is, overall, the major contributor to the risks for CVDs When the total global impact of known risk factors on the overall burden of disease is calculated, 54% of stroke and 47% of ischemic heart disease (IHD) are attributable to hypertension (Lawes et al., 2008) Of all the potentially modifiable risk factors for myocardial infarction in 52 countries, hypertension is exceeded only by smoking (Danaei et al., 2009) The second contributor to our current despair is the growing prevalence of hypertension as seen in the ongoing survey of a representative sample of the U.S population (Cutler et al., 2008; Lloyd-Jones et al., 2009) According to their analysis, the prevalence of hypertension in the United States has increased from 24.4% in 1990 to 28.9% in 2004 This increased prevalence primarily is a consequence of the population becoming older and more obese The striking impact of aging was seen among participants in the Framingham Heart Study: Among H those who remained normotensive at either age 55 or 65 (providing two cohorts) over a 20-year follow-up, hypertension developed in almost 90% of those who were now aged 75 or 85 (Vasan et al., 2002) The impact of aging and the accompanying increased prevalence of hypertension on both stroke and IHD mortality has been clearly portrayed in a meta-analysis of data from almost one million adults in 61 prospective studies by the Prospective Studies Collaboration (Lewington et al., 2002) As seen in Figure 1-1, the absolute risk for IHD mortality was increased at least twofold at every higher decade of age, with similar lines of progression for both systolic and diastolic pressure in every decade At the same time as populations are growing older, obesity has become epidemic in the United States (Hedley et al., 2004) and is rapidly increasing wherever urbanization is occurring (Yusuf et al., 2001) With weight gain, blood pressure (BP) usually increases and the increased prevalence of overweight is likely responsible for the significant increase in the BP of children and adolescents in the United States over the past 12 years (Ostchega et al., 2009) The third contributor to our current despair is the inadequate control of hypertension virtually everywhere According to similar surveys performed in the 1990s, with control defined at the 140/90 mm Hg threshold, control has been achieved in 29% of hypertensives in the United States, 17% in Canada, but in fewer than 10% in five European countries (England, Germany, Italy, Spain, and Sweden) (WolfMaier et al., 2004) Some improvement in the U.S control rate has subsequently been found but the percentage has reached only 45% (Lloyd-Jones et al., 2009) (Table 1-1), whereas better control rates are reported from Canada (Mohan & Campbell, 2008), Cuba (Ordunez-Garcia et al., 2006), Denmark Chap01.indd 8/28/2009 12:47:49 PM Kaplan’s Clinical Hypertension FIGURE 1-1 Ischemic heart disease (IHD) mortality rate in each decade of age plotted for the usual systolic (left) and diastolic (right) BPs at the start of that decade Data from almost one million adults in 61 prospective studies (Modified from Lewington S, Clarke R, Qizilbash N, et al Age-specific relevance of usual blood pressure to vascular mortality: A metaanalysis of individual data for one million adults in 61 prospective studies Lancet 2002;360:1903–1913.) (Kronborg et al., 2009), and England (Falaschetti et al., 2009) As expected, even lower rates of control have been reported from less developed countries such as China (Dorjgochoo et al., 2009) Moreover, in the United States, control rates among the most commonly afflicted, the elderly, are significantly TABLE 1.1 lower: only 29% of women 70 to 79 years of age are controlled (Lloyd-Jones et al., 2009) Furthermore, the relatively lower control rates among Hispanics and African Americans compared to whites remain unchanged (McWilliams et al., 2009) And of even greater concern, even when hypertensives are treated Trends in Awareness, Treatment, and Control of High Blood Pressure in U.S Adults (Over Age 20) 1976–2004 National Health and Nutrition Examination Survey (%) Awareness Treatment Control 1976–1980 1988–1991 1991–1994 2000–2004 2005–2006 51 31 10 73 55 29 68 54 27 70 59 34 79 61 45 Percentage of adults aged 18 to 74 years with SBP of 140 mm Hg or greater, with DBP of 90 mm Hg or greater, or taking antihypertensive medication Adapted from Lloyd-Jones D, Adams R, Carnethon M, et al Heart disease and stroke statistics-2009 update: A report from the American Heart Association statistics committee and stroke statistics subcommittee Circulation 2009;119:e21–e181 Chap01.indd 8/28/2009 12:47:49 PM Chapter • Hypertension in the Population at Large down to an optimal level, below 120/80 mm Hg, they continue to suffer a greater risk of stroke than normotensives with similar optimal BP levels (Asayama et al., 2009) Despite all of these problems, there is hope, starting with impressive evidence of decreased mortality from CVDs, at least in the United States (Parikh et al., 2009) and England (Unal et al., 2004) However, as well as can be ascertained, control of hypertension has played only a relatively small role in the decreased mortality from coronary disease in the United States (Ford et al., 2007) Nonetheless, there is also hope relative to hypertension Primary prevention has been found to be possible (Whelton et al., 2002) but continues to be rarely achieved (Kotseva et al., 2009) Moreover, the rising number of the obese seriously questions the ability to implement the necessary lifestyle changes in today’s world of faster foods and slower physical activity Therefore, controlled trials of primary prevention of hypertension using antihypertensive drugs have begun (Julius et al., 2006) On the other hand, the ability to provide protection against stroke and heart attack by antihypertensive therapy in those who have hypertension has been overwhelmingly documented (Blood Pressure Trialists, 2008) There is no longer any argument as to the benefits of lowering BP, though uncertainty persists as to the most cost-effective way to achieve the lower BP Meanwhile, the unraveling of the human genome has given rise to the hope that gene manipulation or transfer can prevent hypertension As of now, that hope seems extremely unlikely beyond the very small number of patients with monogenetic defects that have been discovered All in all, hope about hypertension seems overshadowed by despair However, health care providers must, by nature, be optimistic, and there is an inherent value in considering the despairs about hypertension to be a challenge rather than an acceptance of defeat As portrayed by Nolte and McKee (2008), the most realistic way to measure the health of nations is to analyze the mortality that is amenable to health care By this criterion, the United States ranks 19th among the 19 developed countries analyzed This sobering fact can be looked upon as a failure of the vastly wasteful, disorganized U.S health care system We prefer to look upon this poor rating as a challenge: current health care is inadequate, including, obviously, the management of hypertension, but the potential to improve has never been greater (Shih et al., 2008) Chap01.indd 3 This book summarizes and analyses the works of thousands of clinicians and investigators worldwide who have advanced our knowledge about the mechanisms behind hypertension and who have provided increasingly effective therapies for its control Despite their continued efforts, however, hypertension will almost certainly not ever be conquered totally, because it is one of those diseases that, in the words of a Lancet editorialist (Anonymous, 1993): …afflict us from middle age onwards [that] might simply represent “unfavorable” genes that have accumulated to express themselves in the second half of our lives This could never be corrected by any evolutionary pressure, since such pressures act only on the first half of our lives: once we have reproduced, it does not greatly matter that we grow “sans teeth, sans eyes, sans taste, sans everything.” In this chapter, the overall problems of hypertension for the population at large are considered We define the disease, quantify its prevalence and consequences, classify its types, and describe the current status of detection and control In the remainder of the book, these generalities will be amplified into practical ways to evaluate and treat hypertension in its various presentations CONCEPTUAL DEFINITION OF HYPERTENSION Although it has been more than 100 years since Mahomed clearly differentiated hypertension from Bright’s renal disease, authorities still debate the level of BP that is considered abnormal (Task Force, 2007) Sir George Pickering challenged the wisdom of that debate and decried the search for an arbitrary dividing line between normal and high BP In 1972, he restated his argument: “There is no dividing line The relationship between arterial pressure and mortality is quantitative; the higher the pressure, the worse the prognosis.” He viewed arterial pressure “as a quantity and the consequence numerically related to the size of that quantity” (Pickering, 1972) However, as Pickering realized, physicians feel more secure when dealing with precise criteria, even if the criteria are basically arbitrary To consider a BP of 138/88 mm Hg as normal and one of 140/90 mm Hg as high is obviously arbitrary, but medical practice requires that some criteria be used to determine the need for workup and therapy The criteria should be established on some rational basis that includes the 8/28/2009 12:47:50 PM Kaplan’s Clinical Hypertension risks of disability and death associated with various levels of BP as well as the ability to reduce those risks by lowering the BP As stated by Rose (1980): “The operational definition of hypertension is the level at which the benefits… of action exceed those of inaction.” Even this definition should be broadened, because action (i.e., making the diagnosis of hypertension at any level of BP) involves risks and costs as well as benefits, and inaction may provide benefits These are summarized in Table 1-2 Therefore, the conceptual definition of hypertension should be that level of BP at which the benefits (minus the risks and costs) of action exceed the risks and costs (minus the benefits) of inaction Most elements of this conceptual definition are fairly obvious, although some, such as interference with lifestyle and risks from biochemical side effects of therapy, may not be Let us turn first to the major consequence of inaction, the increased incidence of premature CVD, because that is the prime, if not the sole, basis for determining the level of BP that is considered abnormal and is called hypertension Risks of Inaction: Increased Risk of CVD The risks of elevated BP have been determined from large-scale epidemiologic surveys The Prospective Studies Collaboration (Lewington et al., 2002) obtained data on each of 958,074 participants in 61 prospective observational studies of BP and mortality Over a mean time of 12 years, there were TABLE 1.2 11,960 deaths attributed to stroke, 32,283 attributed to IHD, 10,092 attributed to other vascular causes, and 60,797 attributed to nonvascular causes Mortality during each decade of age at death was related to the estimated usual BP at the start of that decade The relation between usual systolic and diastolic BP and the absolute risk for IHD mortality is shown in Figure 1-1 From ages 40 to 89, each increase of 20 mm Hg systolic BP or 10 mm Hg diastolic BP is associated with a twofold increase in mortality rates from IHD and more than a twofold increase in stroke mortality These proportional differences in vascular mortality are about half as great in the 80 to 89 decade as it is in the 40 to 49 decade, but the annual absolute increases in risk are considerably greater in the elderly As is evident from the straight lines in Figure 1-1, there is no evidence of a threshold wherein BP is not directly related to risk down to as low as 115/75 mm Hg As the authors conclude: “Not only the present analyses confirm that there is a continuous relationship with risk throughout the normal range of usual blood pressure, but they demonstrate that within this range the usual blood pressure is even more strongly related to vascular mortality than had previously been supposed.” They conclude that a 10 mm Hg higher than usual systolic BP or mm Hg higher than usual diastolic BP would, in the long term, be associated with about a 40% higher risk of death from stroke and about a 30% higher risk of death from IHD These data clearly incriminate levels of BP below the level usually considered as indicative of Factors Involved in the Conceptual Definition of Hypertension Action Benefits Risks and Costs Action Reduce risk of CVD, debility, and death Assume psychological burdens of “the hypertensive patient” Interfere with QOL Require changes in lifestyle Add risks and side effects from therapy Add monetary costs of health care Decrease monetary costs of catastrophic events Inaction Preserve “nonpatient” role Maintain current lifestyle and QOL Avoid risks and side effects of therapy Increase risk of CVD, debility, and death Increase monetary costs of catastrophic events Avoid monetary costs of health care Chap01.indd 8/28/2009 12:47:51 PM A P P E N D IX Patient Information WHAT IS HYPERTENSION? CAN HYPERTENSION BE CURED? For most people, a blood pressure above 140/90 is considered as hypertension The upper number, the systolic pressure, is the highest pressure in the arteries when the heart beats and fills the arteries The lower number, the diastolic pressure, is the lowest pressure in the arteries when the heart relaxes between beats As part of aging, blood vessels usually become stiff or rigid, so that they are less able to dilate when blood enters from the heart Therefore, the systolic pressure usually increases with age Not usually Some people who lose considerable excess weight, reduce a high intake of sodium (or alcohol), and relieve stress may have a return of elevated blood pressure to a normal level WHAT CAUSES HYPERTENSION? In most patients, no specific cause for hypertension can be found In about 10%, a specific cause can be found and often relieved by either medical or surgical treatment The term used for the usual type of hypertension has been “essential,” but “primary” is preferable These factors are involved: • Hereditary • Obesity • High sodium intake • Psychological stress In addition, a number of other factors sometimes play a role, including • Excessive alcohol drinking (more than two to three portions a day) • Smoking • Sleep apnea • Herbal remedies • Diet pills and other stimulants, such as ephedra • Physical inactivity WHAT ARE THE CONSEQUENCES OF HYPERTENSION? By placing a burden on the heart and blood vessels, hypertension in concert with other risk factors induces heart attacks, heart failure, strokes, and kidney damage The other important cardiovascular risk factors are • Smoking • Abnormal blood lipids (an elevated LDL cholesterol or a low HDL cholesterol) • Diabetes HOW IS HYPERTENSION TREATED? Treatment should always include an improvement in all the unhealthy lifestyle habits, including • Stopping smoking • Losing excess weight • Increasing physical activity • Reducing sodium intake (easiest accomplished by reading labels on processed foods and avoiding any with more than 300 mg of sodium per portion) • Drinking no more than a healthy quantity of alcohol • One drink per day for women, two for men (The portions are 12 oz of beer, oz of wine, and 1.5 oz of whiskey.) 455 Appendix.indd 455 8/28/2009 3:47:31 PM 456 Appendix: Patient Information Antihypertensive drugs are usually needed These include three major types: • Diuretics, which remove some of the excess sodium and fluid from the circulation • b-Blockers, which decrease the rate and strength of heart contraction • Vasodilators, which open blood vessels • This group includes angiotensin-converting enzyme inhibitors, angiotensin blockers, and calcium channel blockers All of these may cause side effects, and your physician should be contacted if you feel unwell after starting one or more drugs The action of most drugs can be reduced by weight gain, excessive sodium or alcohol, and certain drugs such as nonsteroid anti-inflammatories (ibuprofen, naprosyn, celebrex, etc.) Inform your physician about all over-the-counter or prescription drugs you take Take your pills every day at the same time, usually soon after awakening HOW TO ENSURE GOOD CONTROL OF HYPERTENSION In the past, only occasional readings in the physician’s office were used to determine the degree of hypertension Increasingly, home measurements with a battery-operated, semiautomatic device are being used to ensure adequate but not excessive treatment With such a device, costing $40 to $100, you can monitor your blood pressure, particularly when changes in the type or doses of medications are made GUIDELINES FOR HOME BLOOD PRESSURE MONITORING Equipment The device should be checked against the mercury manometer in the physician’s office to ensure its Appendix.indd 456 accuracy The cuff should be large enough to encircle the upper arm For most adults, a “large adult cuff ” should be used If the device comes with a smaller cuff, a larger one can be substituted Procedure Do not smoke or drink coffee for 30 minutes before taking the reading Sit with the back and arm supported, the arm at the level of the heart (middle of the chest) After to minutes of quiet sitting, take two readings, a minute apart If the two readings differ by more than 10 mm (points), take additional readings each minute until they are within 10 mm Hg Record the readings in this manner: Date Time First Second Reading Reading Circumstances May May May 7 a.m p.m a.m 150/95 135/85 110/70 145/90 130/80 105/60 Before breakfast After exercise Dizzy after standing If the readings are being taken to diagnose hypertension, as many as possible, four or five a day, should be taken for a few weeks If the readings are being taken to monitor treatment, two or three readings one day a week may be adequate Take a reading if you feel unwell, such as being dizzy or light-headed or having a bad headache You usually cannot tell when your pressure is rising, but the pressure can rise if you are anxious The readings may vary as much as 40 mm Hg from one time to another They rarely remain the same Take your diary with you on your next appointment More information can be obtained from the American Heart Association by phone, at (800) 2428721, or on the web at http://www.americanheart.org 8/28/2009 3:47:31 PM IN D E X Note: Page numbers followed by “f ” indicate figures; those followed by “t” indicate tables A AASK (African American Study of Kidney Disease and Hypertension) See African American Study of Kidney Disease and Hypertension (AASK) AAST (aspartate aminotransferase), 419 AB/CD algorithm, 235, 235f, 241 Abdominal aorta, 25 Abdominal aortic aneurysm, 118 Abdominal bruits, 442, 442t Abdominal obesity, 126, 158, 204, 251 evaluation of hypertensive patients, 128 metabolic syndrome, 86, 251 primary hypertension, 86 resistant hypertension, 247 weight reduction, 173, 299 Absolute benefit of lowering blood pressure, 152 Absolute risk cardiovascular, and elevated blood pressure, 8–9, 9f in clinical trials, estimations based on, 143–144, 144t Acarbose, 252, 304, 304t Accelerated glomerular obsolescence, 274 Accelerated-malignant hypertension clinical features funduscopic findings, 275–276, 276f symptoms and signs, 275, 275t evaluation identifiable causes, 277–278 laboratory findings, 277 patient’s status assessment, 276, 277t mechanisms humoral factors, 275 initiation and progression, 274, 276f structural changes, 274 prognosis, 278 ACE I/D polymorphism, DD variant of, 322 Acebutolol antihypertensive drugs available in the U.S., 197t, 239t β-adrenergic blocking agents antihypertensive efficacy, 214 intrinsic sympathomimetic activity, 212 pharmacologic properties, 213t hypertension and lactation, 424 Acetaminophen, 175, 369 Acetylcholine, 67, 70 Acromegaly, 351, 394 ACTH (adrenocorticotropic hormone) See Adrenocorticotropic hormone (ACTH) ACTH-dependent Cushing syndrome, 379, 383 ACTH-independent Cushing syndrome, 378, 379, 383 Action, mode of adrenergic-inhibiting agents α-adrenergic receptor blockers, 210–211, 210f β-adrenergic blocking agents, 212, 212f aldosterone blockers, 205–206 angiotensin II receptor blockers (ARBs), 229–231 angiotensin-converting enzyme inhibitors (ACEIs) combination therapy, 225 effects, 224–225 monotherapy, 225 morbidity and mortality reduction, 225 pharmacodynamics, 223–224, 224f pharmacokinetics, 223, 224f calcium channel blockers (CCBs), 218t dihydropyridines (DHPs), 218 duration, 218–219, 219t non dihydropyridine (non-DHP), 218 sympathetic activation, 218 diuretics, 198, 199f, 205–206 Acupuncture, 185 Acute kidney disease acute glomerulonephritis, 291–292 acute kidney injury (AKI) gadolinium and nephrogenic systemic fibrosis, 291 recognition, 291 causes, 292 renal donors, 292 urinary tract obstruction and reflux, 292 Acute kidney injury (AKI) gadolinium and nephrogenic systemic fibrosis, 291 recognition, 291 Adducin gene, 199 Adenomas adrenal gland adrenal scintiscans, 352 aldosterone-producing adenomas (APA), 346t, 350 hypokalemia, 342 Cushing syndrome, 378, 379 pheochromocytoma hyperfunction evaluation, 360 malignancy evaluation, 378 management, 361 Adenosine, 45 Adolescence See Childhood and adolescence Adrenal glands deoxycorticosterone, 387 pheochromocytoma, 375 unilateral hyperplasia, 351 Adrenal hyperplasia bilateral Cushing syndrome, 378, 384 incidental adrenal mass, 359 pheochromocytomas, 366, 373 primary aldosteronism, 339, 350–351 congenital adrenal hyperplasia (CAH), 387–389 saline suppression test, 347 Adrenal incidentaloma differential diagnosis, 358, 359t hyperfunction evaluation clinically silent pheochromocytoma, 360 laboratory evaluation, 359, 360t primary aldosteronism, 360 subclinical cushing syndrome, 360 malignancy evaluation imaging phenotype, 358–359, 359t metastases, 359 size, 358 management adrenalectomy, 361–362 algorithm, 361, 361f fine needle aspiration (FNA) biopsy, 362 prevalence, 358 Adrenal venous sampling (AVS), 352 primary aldosteronism, 339, 352 primary hypertension, 132 Adrenalectomy adrenal incidentaloma, 361, 362 Cushing syndrome, 378, 384 primary aldosteronism CT scans, 352 diagnosis, 347 glucocorticoid-remediable, 349 pregnancy, 350 surgical treatment, 353 Adrenergic agents and neonatal hypertension, 44t Adrenergic-inhibiting drugs α-adrenergic receptor blockers ALLHAT experience, 211 antihypertensive efficacy, 211 mode of action, 210–211, 210f side effects, 211 β-adrenergic blocking agents antihypertensive efficacy, 214 mode of action, 212, 212f pharmacologic differences, 212–214, 213f, 213t side effects, 214–215 central α-agonists antihypertensive efficacy, 207 guanabenz, 208 guanfacine, 208–209 imidazoline receptor agonists, 209 mechanism, 208f methyldopa, 207 side effects, 207–208 drug targets, 207f peripheral adrenergic inhibitors guanadrel sulfate, 210 guanethidine, 210 reserpine, 209–210 vasodilating β-blockers, 215 Adrenocorticotropic hormone (ACTH) Cushing syndrome corticotrophin-releasing hormone stimulation test, 383 corticotropin (ACTH) assay, 383 inferior petrosal sinuses (IPSS), 383–384 pathophysiology, 378, 379t pituitary MRI, 383 pseudo-Cushing syndrome, 381 treatment, 385 pheochromocytoma hyperfunction evaluation, 360 paroxysmal hypertension, 364 renovascular hypertension, 366 primary aldosteronism glucocorticoid remediable, 348 therapy, 353 Adventitial fibromuscular dysplasia, 323t, 325 Advertising and cost-effectiveness, hypertention treatment, 155 Aerobic exercise hypertension management, children and adolescents, 443 magnesium supplementation, 181 African American Study of Kidney Disease and Hypertension (AASK) chronic kidney disease (CKD), 121 calcium channel blockers, 303 management, 295 hypertensive nephrosclerosis, 160 African–Americans See Blacks 457 Index.indd 457 8/28/2009 6:13:53 PM 458 Index Age calcium channel blockers, 219 cardiovascular diseases (CVD), 6, 7f childhood and adolescence, 436t–437t hypertension treatment, 151– 151f, 151t white-coat hypertension, 26–29 Aging nocturia, 63 of population, and treatment of hypertension, postural hypotension, 122 Air pollution and primary hypertension, 97 Alanine aminotransferase (ALT), 419 Albuminuria AT1 receptor blockers, 231 diabetics, 253 direct renin inhibitors, 233 primary hypertension, 120 renal parenchymal hypertension, 290, 300, 301 Alcohol intake, 43f, 93f, 402 Alcohol moderation beneficial effects, 183 blood pressure effects, 182 recommendations, 183 Aldosterone blockers antihypertensive efficacy, 206 mode of action, 205–206 side effects, 206 Aldosterone receptor blockers, 386 Aldosterone to renin ratio (ARR) false-positive tests, 346–347 measurement, 345, 345t plasma renin concentration (PRC), 344 prevalence, 345, 346t Aldosteronism, primary See Primary aldosteronism (PA) Alerting reactions and blood pressure measurement, 34 Aliskerin See Direct renin inhibitors (DRI) Aliskiren, 76 Allopurinol, 68, 88, 89, 131, 203, 303t, 495 ALT (alanine aminotransferase), 417 Altitude and primary hypertension, 95 Alzheimer disease, 120, 396 Ambulatory BP monitoring (ABPM), 411f, 439 advantages, 36 BP variability, 21, 21f, 24 evalution scheme, 36, 36f vs HBPM, 34 recommended thresholds, 37t technical qualities, 35, 36t white-coat hypertension (WCH), 26–27 natural history, 28 prognosis, 27–28, 28f American College of Obstetrics and Gynecology (ACOG), 424 American Diabetes Association, 227, 297 American Heart Association blood pressure measurement in children and adolescents, 438 office measurement of blood pressure, 31, 34, 36f American Stroke Association, 280 Amiloride, 205 Aminoglutethimide, 384t Amiodarone, 304t Amlodipine cardiovascular profile, 219–220 coronary artery disease, 160 diabetes, 252 drug therapy treatment, 195 U.S oral antihypertensive drugs, 240–241 Amphetamines, 404, 451 Anabolic steroids, 401t Androgens hydroxylase deficiency, 387 Index.indd 458 pheochromocytoma, 360 primary hypertension, 90 Anemia and chronic renal disease, 400 Aneroid sphygmomanometers, 31 Anesthesia acute physical stress, 438 hypertension treament, 256 pheochromocytoma, 374 Aneurysms pathophysiology, 392 primary hypertension, 118 renovascular hypertension, 325 renovascular hypertension (RVHT), 325 Angina β-adrenergic receptor blockers, 214 calcium channel blockers, 217 coronary artery disease, 254 Angioedema, 228 Angioplasty, renovascular hypertension, 319, 318, 330, 333–334 Angiotensin II ACEIs, 222, 223 atherosclerosis, pathogenesis of, 114 cardiac, 232 cerebrovascular disease, 231–232 diabetic nephropathy, 318 erythrocytosis, 228 immunization, 233–234 peripheral resistance, 228f pressure-natriuresis, resetting of, 60f, 61-62, 321 receptor genes (-1332G/A) polymorphism of, 115 receptors and effects, 50, 74–76, 413 Angiotensin II receptor blockers (ARBs), 229f, 230t aldosterone blockers, 202, 206, 214, 302 angioedema, 230, 232 Angiotensin-converting enzyme, 229fAngiotensin-converting enzyme gene, DD genotype, 302 antihypertensive efficacy, 231 black patients, 223 calcium channel blockers, given with, 147 cardiac disease, 232 cerebrovascular disease, 231–232 congestive heart failure, 117–118, 118t 154 cost-effectiveness of treatment of hypertension, 155, 156, 244 diabetic nephropathy, 206, 233, 253, 300, 301, 309 dialysis patients, 305 elderly patients, 321 kidney transplantation, 312 left ventricular hypertrophy, 253, 313 mode of action, 229–231 nondiabetic chronic renal disease, 229, 300 oral antihypertensive drugs available the U.S., 239–240 parenteral, for hypertensive emergencies, 282 peripheral vascular disease, 255 placebo-controlled trials in stroke patients, 148, 149t, 150, 231 post myocardial infarction, 333 potassium supplements for diuretic induced hypokalemia, 202 pregnancy, 233, 243t pressure-natriuresis, resetting of, 60, 60f, 63 renal disease, 231 renography, discontinuation before, 331 renovascular hypertension, 197, 300 side effects, 232 stroke, prevention of, 152f, 231, 254, 255 trials after, 148, 149t Angiotensin-converting enzyme inhibitors (ACEIs), 229, 333 aldosterone blockers, 202, 206, 302 aldosteronism, primary, 197 angina, 154 arterial and venous dilation, 282 arteritis with renovascular hypertension, 275, 321, 326 benefits of treatment vs placebo, 141, 149t, 152f black patients, 223, 241 caicium channel blockers combined with, 109t, 147 cerebrovascular disease, 226 characteristics of, 224t children and adolescents, dosage for, 444, 445t combination therapy, 221, 225 diabetic patients, 152, 226, 233, 301 dialysis patients, 299 diuretics, 148, 154, 155, 200, 211, 219 drug therapy for hypertension, 10, 12, 17, 111, 158, 159 elderly patients, 235, 248, 321 general guidelines for drug choices, 234 glomerulonephritis, acute, 291–292 heart disease, 226 heart transplantation, 399, 403 hypertensive emergencies in children and adolescents, 449 J-curves and antihypertensive therapy, 162 left ventricular hypertrophy, 200, 212 left ventricular mass index, 156 metabolic syndrome and obesity, 81 mode of action combination therapy, 225 effects, 224–225 monotherapy, 225 morbidity and mortality reduction, 225 pharmacodynamics, 223–224, 224f pharmacokinetics, 223, 224f morbidity and mortality, 201, 225, 232, 241 myocardial infarction, following, 154 oral antihypertensive drugs available in the U.S., 239–240t parenteral l, for hypertensive emergencies, 234, 281t peripheral vascular disease, 255–256 placebo-controlled trials, 148, 149t, 231 pregnancy, 228 pressure-natriuresis, resetting of, 200 renal disease, 226–227 renal disease, acute, 292 renal disease, nondiabetic chronic, 308 renin-angiotensin system, 222f renography, discontinuation before, 331 renovascular hypertension, 197, 198, 300 renovascular hypertension with ischemic nephropathy, 293, 319, 321 side effects chemical structure, 228 nonspecific side effects, 228–229 pharmacologic actions, 227–229, 227t statins and, 154 trials after 1995, 148, 149t younger, white patients, 241 Angiotensinogen genes of, 235T allele of, 199 obesity with primary hypertension, 59f, 84,199, 224f sodium, sensitivity, 54, 58, 180 Anglo-Scandinavian cardiac outcomes trial (ASCOT), 206, 211, 244, 245 Antacids, 400, 401t Antibiotics, 304t Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), 152, 201, 203, 211 α-adrenergic receptor blockers, 210 8/28/2009 6:13:53 PM Index angiotensin-converting enzyme, 63, 161f, 196, 222–223 drugs under investigation, 233–234 recommendations for treatment, 162 thiazide diuretics and new-onset diabetes, 203, 252 Antihypertensive drug therapy, 197t adherence dosing time, 195–196 follow-up visits, 196 guidelines, 194, 195t patient involvement, 194 side effects, 196 Valsartan Antihypertensive Longterm Use Evaluation (VALUE) trial, 195 adrenergic-inhibiting agents α-adrenergic receptor blockers, 210–211 β-adrenergic blocking agents, 212–215 central α-agonists, 207–209 drug targets, 209 peripheral adrenergic inhibitors, 209–210 vasodilating β-blockers, 215 angiotensin II receptor blockers (ARBs), 229f, 230t antihypertensive efficacy, 231 cardiac disease, 232 cerebrovascular disease, 231–232 mode of action, 229–231 renal disease, 231 side effects, 232 angiotensin-converting enzyme inhibitors (ACEIs), 229 cerebrovascular disease, 226 heart disease, 226 mode of action, 223–225 renal disease, 226–227 renin-angiotensin system, 222f side effects, 227–229 calcium channel blockers (CCBs) antihypertensive efficacy, 219–220 mode of action, 218–219 side effects, 221–222, 221t childhood and adolescence classes, 446 indications, 444 pediatric labeling, 446, 444t recommended doses, 444, 445t stepped-care approach, 446, 446f direct renin inhibitors (DRI), 232–233 direct vasodilators, 216t hydralazine, 216–217, 216f minoxidil, 217 nitrates, 217 diuretics aldosterone blockers, 205 loop diuretics, 204–205 mode of action, 205–206 nephron, 197f potassium-sparing agents, 205 thiazide, 200–204 Antioxidants blood pressure, 70 nebivolol, 215 polyphenols, 94, 184 renovascular hypertension, 70 vascular changes, 184 Anxiety β-adrenergic receptor blockers, 399t functional somatic disorders and hypertension, 397-398 pheochromocytoma, conditions simulating, 364t, 365 variability of blood pressure, 12, 22t, 34 Aorta abdominal aneurysm, 118 abdominal rupture, 25 Index.indd 459 aortic wall thickness, 44 coarctation of, 15t, 45, 48, 442t, 447 lesions, 392 management, 393 pathophysiology, 392–393 recognition, 393 symptoms and signs, 392, 393t Aortic dissection labetolol, 215 natural history of hypertension, 119 renovascular hypertension, 325 Aortic stenosis, 118 Apparent mineralocorticoid excess (AME), 385–386 Aspartate aminotransferase (AST), 419 Atherosclerotic lesions genetic associations, 322 history, 322–323, 324f Atrial fibrillation, 118 Atrial natriuretic peptides (ANP), 92, 343, 413f Avapro, 230t B Bariatric surgery, 87, 88, 173 Baroreceptors aortic arch, 45 heart transplantation, 399 postural hypotension in elderly patients, 122 variability of blood pressure, 21 Bed rest, blood pressure, 185 Benazepril amlodipine, combined with, 240t angiotensin-converting enzyme inhibitors, 222 characteristics, 224t oral antihypertensive drugs available in the U.S., 239t Bendrofluazide and erectile dysfunction, 204 Benefits alcohol, light to moderate consumption, 402 control of hypertension, 6, 7f dietary sodium reduction, 175-179 Benicar, 230t Benidipine, 218 Benign prostatic hypertrophy a1-adrenergic receptor blockers, 210-211 nocturia, 128 Benzthiazide, 198t β-adrenergic receptor blockers adrenergic-inhibiting drugs, 197t, 206-210 aldosterone blockers, used with, 205 angina, 254 athletes, 256 Black patients, 241 cardiac symptoms, efficacy in reducing, 154 carotid endarterectomy, 399 catecholamine surges with central α-agonist discontinuation, 207 children and adolescents, dosages for, 444, 445t children and adolescents, emergencies in, 449 classification of, 213f congestive heart failure, 154, 212 cost-effectiveness, 155 diabetic nephropathy, slowing progression of, 308 dialysis patients, 310 diuretics, combined with, 243 general guidelines for drug choices, 234 head injuries, 397 hydralazine given with, 216 infant dosage, 448t isolated systolic hypertension, 151t kidney transplantation, hypertension following, 312 459 left ventricular hypertrophy, 253 left ventricular mass index, 221f metabolic syndrome, 81, 251 morbidity and mortality in general guidelines for drug choices, 234, 235f obesity, 251 oral antihypertensive drugs available in the U.S., 239-240t paradoxical response, 401t pharmacologic properties, 213t physical stress, acute, 398 postural hypotension, 249 pseudoephedrine, 403 side effects, biochemical, of hypertension therapy, 10, 11 smoking-induced rise in blood pressure, 173 starting therapy at lower levels for higher risk patients, 159 surgery, special considerations for, 256 thiazide diuretics, hypokalemia in, 202 trials before 1995, 147, 148 White, younger patients, 241 β1-receptor cardioselectivity, 212-214 Betaxolol β-adrenergic receptor blockers, 213f, 213t oral antihypertensive drugs available in the U.S., 239t Bilateral adrenal hyperplasia (idiopathic hyperaldosteronism), 350–351, 351t Bilateral medullary hyperplasia, 350 Biochemical diagnosis of pheochromocytoma, 367–371 Biofeedback and blood pressure, 184 Birthplace and complications of hypertension, 114, 115 Bisoprolol combination therapy with thiazide diuretics, 201 HCTZ, combined with, 445t oral antihypertensive drugs available in the U.S., 239t surgery, 256 Blacks antihypertensive therapy, benefit from, 152 β-adrenergic receptor blockers, 211–215 calcium channel blockers, efficacy of, 219 children, tracking blood pressure in, 431 coronary heart disease mortality, dietary sodium reduction, 175 direct vasodilators, 216–217 end-stage renal disease, 293 first choice of drugs for hypertension, 238 general guidelines for drug choices, 234 glucocorticoid-remediable aldosteronism, 348 goal of antihypertensive therapy, 162 hydralazine and nitrate for congestive heart failure, 154 left ventricular hypertrophy and hypertension, 116 natural history of hypertension, 108–110 potassium supplementation, 179 pressure-natriuresis in renal sodium retention, 58–59, 60f prevalence of hypertension in U.S population, 13 renal disease, 120, 292 renovascular hypertension, 322 special considerations in choice of therapy, 248 strokes, 212 thiazide diuretics, 200 Blood pressure (BP) ambulatory monitoring See Ambulatory BP monitoring (ABPM) central blood pressure, 37, 37f, 37t classification 8/28/2009 6:13:53 PM 460 Index Blood pressure (BP) (Continued) borderline, 13 in children, 13 labile, 13 prehypertension, 12–13, 12t systolic hypertension, 13 home measurements, 34, 35t masked hypertension, 29 measurement ambulatory monitoring, 35–37, 36f childhood, tracking during, 430–432 office measurement guidelines, 30t, 33 patient and arm position, 29–30, 31f significance, 33 sphygmomanometer, 30–32 technique, 32–33 sleep and awakening early morning surge, 25 excessive dipping, 25 nondipping, 25 normal pattern, 24 variation baroreflex sensitivity, 23 biologic variations, 22 BP level, 2523 measurement variation, 21–22, 22t types, 22–23, 24t white-coat effect environment, 25–26 measurer, 26, 26f white-coat hypertension (WCH) features, 27–28 natural history, 28 prognosis, 28–29, 28f systolic and daytime ambulatory BP readings, 26–27, 27f Blood Pressure Lowering Treatment Trialists’ Collaboration, 152 BMI (body mass index), 125f, 173 Bogalusa Heart Study, 89 Bothrops jararaca, 223 Brain tumors, 396 Brainstem, compression of, 50 Breast cancer, 425 Brevibloc, 281t British National Institute for Clinical Excellence (NICE), 288 Bromocriptine, 384t, 401t Bronchopulmonary dysplasia, 447, 448t Bronchospasm and ACEIs, 228 Bucindolol, 213t Bumetanide, 205 C Caffeine hypertension, 400 neonatal hypertension, causes of, 448t primary hypertension, 92 Calcium channel blockers (CCBs) antihypertensive efficacy, 220t determinants, 219-220 renal effects, 220 mode of action, 218t dihydropyridines (DHPs), 218 duration, 218-219, 220t non dihydropyridine (non-DHP), 218 sympathetic activation, 218 side effects, 221-222, 221t Calcium, dietary, 95, 181 Blacks and natural history of hypertension, 126 Calcium, excretion of β-adrenergic receptor blockers, 213 decreased, with dietary sodium reduction, 177t hypokalemia, 203 Index.indd 460 Calcium metabolism alterations, 203 Calcium, parenteral, 222 Calcium, supplementation of clinical data, 179–180 recommendations, 180 Canadian Hypertension Education Program, 241 Cancer renal cell, 236, 335, 365 stomach, 53, 177t Cardiovascular diseases (CVD) childhood and adolescence blood pressure, 432-433 blood pressure tracking, 430-432 cognitive function, 432 increased carotid intimα-media thickness (cIMT),432 left ventricular hypertrophy (LVH), 432 renal damage, 431 decreased risk of natural vs treatment-induced BP, prevention of, 10 rationale for, 9, 10t increased risk of age role, 6, 7f cardiovascular events incidence, 5, 5f gender, 5–6 HBP in, 6f, 7f isolated diastolic hypertension (IDH), 8, 8f isolated systolic hypertension (ISH), 6–8 pulse pressure, race and, 6, 6f relative vs absolute risk, 8–9, 9f Carotid artery disease, 120 Carotid endarterectomy, 399 Carotid intimα-media thickness (cIMT), 432 Carotid sinus baroreceptors, 46, 49 Carteolol, 197t, 213t Carvedilol, 215, 303 Cataracts, dietary sodium, 180t Catecholamine brain tumors, levels in, 396 central α-agonists, 207, 209 crisis, tyramine-induced, 283 pheochromocytoma, 367-370, 371f, 372t, 374 CDC Diabetes Cost-Effectiveness Group, 155 Celebrex, 403 Celecoxib, 403 Celiprolol, 213t Central α-agonists antihypertensive efficacy, 207 guanabenz, 208 guanfacine, 208-209 imidazoline receptor agonists, 209 mechanism, 208f methyldopa, 209 side effects, 209–210 Cerebral blood flow (CBF) hypertensive encephalopathy, 278–279, 275t preeclampsia, 419 Cerebrovascular disease, 119-120 angiotensin II receptor blockers (ARBs), 230-231 angiotensin-converting enzyme inhibitors (ACEIs),225 Charcot-Bouchard aneurysms, 231 Chemical agents and hypertension, 401t–402t alcohol, 402 caffeine, 400 nicotine and smoking, 401, 402 Chemodectoma, 379 Chemotherapy, identifiable hypertension, 403 Childhood and adolescence acute severe hypertension hypertensive emergencies, treatment, 448 oral antihypertensive agents, 447, 449t symptoms, 448 antihypertensive medications classes, 444 indications, 441 pediatric labeling, 441, 441t recommended doses, 447, 449t stepped-care approach, 446, 446f blood pressure levels, 434t boys, age and height percentile, 436–439t definitions, 435 environmental factors, 435 genetic factors, 434 girls, age and height percentile, 437t–438t management algorithm, 440, 440f measurement frequency and therapy recommendations, 439, 439t cardiovascular disease blood pressure, 431 blood pressure tracking, 430-432 cognitive function, 432 increased carotid intimα-media thickness (cIMT), 432 left ventricular hypertrophy (LVH),432 renal damage, 432 classification and diagnosis ambulatory BP monitoring (ABPM), 437 confirmation of BP elevation, 436–437 diagnostic evaluation, 441–444, 443t differential diagnosis, 441, 441t masked hypertension, 441 white-coat hypertension, 441 infancy causes, 447, 448t recommended doses, 447, 449t nonpharmacologic management, 443 obesity, 431 prevalence, 429, 430, 430t prevention,433 Children blood pressure (BP) classification, 13 paraganglioma and pheochromocytoma, 365 Chlamydia pneumonia, antibodies to, 322 Chloral hydrate, 304t Chloride cotransport, 198 Chloride reabsorption, 204, 348t Chlorothiazide, 198, 444t, 449t Chlorpropamide, 304t Chlorthalidone antihypertensive drugs available in the U.S, 197t new-onset diabetes, 203 thiazide-like diuretics, 199 Cholelithiasis, 366 Chromaffin cells and pheochromocytoma, 362, 368, 369 Chromogranin A levels,369 Chronic artery disease (CAD), 154, 162 Chronic dialysis hypertension role causes, 310t, 311 mechanisms, 310, 310t management, 311, 311f Chronic hypertension causes, 423–424 mother and fetus risks, 422 oral drugs, 423, 423t and pregnancy, 422–423 Chronic kidney disease (CKD), 120–122, 158 classification,290t elderly patients, 306, 306f future therapies, 306 hypertension role, 293 intensive therapy management hazards, 295–298, 297f proteinuria, 295, 296 8/28/2009 6:13:53 PM Index mechanisms glomerular filtration rate, 294–295 high blood pressure, 293, 294t proteinuria, 294, 296t structural injury, initiation and progression, 294, 296f prevention trials aldosterone blockers, 302 β-blockers, 303 α-blockers, 303 calcium channel blockers, 302–303 diuretics,302 minoxidil, 303–304 therapy mode ACEI and ARB combination, 298, 299 ACEI/ARB therapy, higher dose, 301 ACEIs, 298, 299, 298f algorithm, 296 anemia, RAS inhibitors,302 ARB and direct renin inhibitor, 301 ARBs, 299 combination, 299–300 lifestyle changes, 299 prolonged RAS inhibition, 300 renin-angiotensin system (RAS) inhibitors, 301 Chronic renal disease angiotensin-converting enzyme inhibitors (ACEIs), 222–223 antihypertensive treatment, 183, 299 renal parenchymal hypertension, 289f torsemide, 205 Chymase, 73 Circulatory changes with normal pregnancy, 412–413, 413f Cirrhosis with ascites, 78t Classification of blood pressure (BP) guidelines for, 10, 13, 15t hypertension in children and adolescents, 432, 441 hypertension, types of, during pregnancy, 408 Claudication, intermittent, 113f, 115 Clindamycin, 304t Clinical features accelerated-malignant hypertension, 273, 278, 278f congenital adrenal hyperplasia, 388 Cushing syndrome, 381t diabetic nephropathy, 305 eclampsia, 422 obstructive sleep apnea (OSA), 394, 395t paraganglioma and pheochromocytoma, 366–367 primary aldosteronism (PA), 340 Clinical practice, application of trial results, 139, 141, 143t, 144t Clinical prediction rule for revascularization, 329, 329t Clinical trials, problems with, 139, 143, 147t, 148f Computed tomography (CT), 332 Congenital adrenal hyperplasia (CAH) 11-hydroxylase deficiency, 387, 389 17-hydroxylase deficiency, 389 adrenal hyperplasia, 387, 389 adrenal steroid synthesis, 387f syndromes, 387, 388t Coronary heart disease (CHD), 118 Cortisol/deoxycorticosterone (DOC) congenital adrenal hyperplasia (CAH) 11-hydroxylase deficiency, 387, 389 17-hydroxylase deficiency, 389 adrenal steroid synthesis, 387f syndromes, 387, 389 cushing syndrome See Cushing syndrome Index.indd 461 mineralocorticoid receptors apparent mineralocorticoid excess (AME), 386 enzyme-mediated receptor protection, 386f glucocorticoid resistance,386 glycyrrhetinic acid,386 Cushing syndrome, 358 causes corticotrophin-releasing hormone stimulation test, 383 corticotropin (ACTH) assay, 383 high-dose dexamethasone suppression, 383 inferior petrosal sinuses (IPSS), 383–384 pituitary MRI, 383 clinical features, 381t glucocorticoid excess, 380–381 pathophysiology ACTH dependent/independent, 378–381t causes, 378–380t variants, 379–380 pseudo-cushing syndrome, 381 screening tests dexamethasone suppression test and combined DST-CRH, 383 diagnostic pathways, 382f late-night salivary cortisol, 382–383 overnight plasma suppression, 382 urinary free cortisol, 382 significance, 378 treatment, 384, 385, 384t Cyclosproine, 312 Cystatin C, 120 D Dacarbazine, 376 Darusentan, 234 Day time blood pressure, variability of, 21 Death arterial lesions, with natural history of hypertension, 115 pheochromocytomas, from, 367 sudden death cardiac arrest, upon awakening, 25 exercise, during, 181 obstructive sleep apnea, and hypertension, 394-395 pheochromocytoma with paroxysmal hypertension, 396 target organ involvement, 115–118 thiazide diuretics, hypokalemia in, 201–202 Decongestants, 442 Definitions hypertension, conceptual, 3–11 hypertension, operational, 11–17 hypertensive crises, 274 hypertensive emergencies, 274 hypertensive urgencies, 274 postural hypotension, 122 primary aldosteronism, 339 Degenerin/epithelial sodium channel proteins, 73 Delivery eclampsia, management of, 422 preeclampsia, management of, 419 Dementia alcohol, 402 calcium channel blockers, 217–222 elderly patients, special considerations for, 248 natural history of hypertension, 120 Deoxycorticosterone (DOC) See Cortisol/ deoxycorticosterone (DOC) Depression Cushing’s syndrome, 381 functional somatic disorders, 397 461 Dexamethasone 11β-HSD2 deficiency, 386 glucocorticoid-remediable aldosteronism, 348 neonatal hypertension, causes of, 448t Dexamethasone suppression test Cushing’s syndrome, 360 high dose, 364 incidental adrenal masses, 362 Diabetes Control and Complications Trial, 308 Diabetes mellitus ACEIs, 253 alcohol, 182 ARBs, 300 atherosclerotic lesions with renovascular hypertension, 322 β-adrenergic receptor blockers, 211–215 calcium channel blockers, 236 children and adolescents, indications for treatment, 444 complications of, 252f, 253 cost-effectiveness of treatment, 155–156 diabetic nephropathy, 305–308 goal of antihypertensive therapy, 162 home measurement of blood pressure, 34 hypertensive patients, 125 hypoglycemia with ACEIs, 228 hypokalemia, 202 low birth weight, and later development of, 63–65 metabolic syndrome and obesity, 251–252 new-onset, 203, 225, 251, 252 nitric oxide availability with aging, 66 pheochromocytoma with hypotension, 365 placebo-controlled trials, 148, 149t preeclampsia, 413 prevention of, 126 primary hypertension, 87 prorenin, 75–76 renal parenchymal hypertension, 305–309 sodium-lithium countertransport, 434t special considerations in choice of therapy, 248–251 thiazide diuretics, 198 Type 1, 76, 306 Type 2, 81–86 weight reduction and lifestyle modifications, 299 Diabetes Prevention Program, 252–253 Diabetic nephropathy course, 306, 307f drugs selection ACEIs, ARBs, and DRIs, 308–309 additional drugs, 309 therapies, 309 management antihypertensive therapy, 308, 309f glycemic control, 308 mechanisms angiotensin II, 308 factors, 306, 307f glomerular hypertension, 306, 308 hypertension, 308 renin-angiotensin, 308 pathology and clinical features, 305 risk factor management, 305, 306t Direct renin inhibitors (DRI), 232–233, 300 Direct vasodilators, 316t hydralazine, 216–217, 216f minoxidil, 217 nitrates, 217 Diuretics aldosterone blockers, 205 loop diuretics, 204–205 mode of action, 205–206 nephron, 197f potassium-sparing agents, 205 8/28/2009 6:13:53 PM 462 Index Diuretics (Continued) thiazide antihypertensive efficacy, 200, 200f cardiovascular morbidity, protection, 201 chlorthalidone, 199 dosage, 201 durations of action, 200–201 indapamide, 199–200 metolazone, 200 mode of action, 198, 199f resistance, 201 response determinants, 198–199 side effects, 201–204 sodium reabsorption, 197f Dyslipidemia, 129 E Early childhood growth and cardiovascular disease, 432, 433 Early hypertension, 111 Eating postural hypotension, 122, 249 variability of blood pressure, 21 Eccentric hypertrophy of left ventricle, 117 Echocardiograms, left ventricular hypertrophy, 116–117 Eclampsia clinical features, 422 definition, 422 hypertensive encephalopathy, 280 management, 422 Ecstasy (methylenedioxy methamphetamine), 401t Edecrin, 198t, 239 See also Ethacrynic acid Edema calcium channel blockers, dependent, 236 chronic, and resetting pressure-natriuresis, 60 eclampsia and preeclampsia, 422, 413–419 glomerulonephritis, acute, 291–292 Efficacy of antihypertensive medication ACEIs, 200 aldosterone blockers, 206 α1-adrenergic receptor blockers, 211 β-adrenergic receptor blockers, 211–215 calcium channel blockers, 220 carvedilol, 215 clonidine, 209 general guidelines for drug choices, 234–237 hydralazine, 216 labetalol, 215 methyldopa, 207 minoxidil, 217 reserpine, 209–210 thiazide diuretics, 200 Efonidipine, 218 Ehlers-Danlos syndrome, 119 Ejaculation, failure of, 215 Ejection fraction, 117 Elderly patients aldosterone blockers, 205–206 calcium channel blockers, 217–219 cardiovascular disease and blood pressure levels, 4, 5f first choice of drugs for hypertension, 240–245 general guidelines for drug choices, 234 hypertensive emergencies and gradual lowering of blood pressure, 280 hyponatremia, 203 isolated systolic hypertension, 43–44, 71, 114, 122, 152f natural history of hypertension, 2f, 109t, 117, 119 over age, 109, 152, 154 Index.indd 462 pseudohypertension, 32 pulse pressure, renovascular hypertension, 319–335 sodium, dietary, 175 special considerations in choice of therapy, 248–251 systolic hypertension, thiazide diuretics, 198–201 untreated, in trials of established hypertension, 108, 109f, 114 white-coat hypertension, 26–29 Electrocardiograms, accelerated-malignant hypertension, 274, 275t Electron beam computed tomography, 332 Electronic devices for blood pressure measurement, 35, 36t, 37t 11β-hydroxylase (CYP11Bl), 387 11β-Hydroxysteroid dehydrogenase type isoform (11β-HSD2), 199, 385, 386 11β-hydroxysteroid dehydrogenase-1, 79 11-hydroxylase deficiency, 387, 388t, 389 Emboli fibromuscular dysplasia, 323, 324t renovascular hypertension, arteriography for, 319–335 Enalapril ACEIs, 224t angina, 254 benefits of ACEI treatment vs placebo, 149t characteristics, 224t coronary artery disease, 254 diabetic nephropathy, 226, 305 dose-response relationships, 237, 238f general guidelines for drug choices, 234 infant dosage, 248t obstructive sleep apnea, 395 oral antihypertensive drugs available in the U.S., 240t pediatric dosage, 444t starting therapy at lower levels for higher risk patients, 161 surgery, special considerations for, 256 timing of dosing, 195–196 Enalaprilat children and adolescents, emergencies, 450t parenteral, for hypertensive emergencies, 281t, 282 Encephalopathy differential diagnosis, 280, 280f eclampsia, 422 pathophysiology breakthrough vasodilation, 278, 279, 278f, 279f central nervous system changes, 279 preeclampsia, 418–419 End points of therapy See Goals of therapy Endarterectomy, 399 Endothelial dysfunction accelerated-malignant hypertension, 275 ACEIs, 225 acromegaly, 394 atherosclerosis, pathogenesis of, 114 inflammation, 83 lipid-lowering drugs and antihypertensive effects, 184 low birth weight, and later development of, 64 peripheral vascular disease, 255 preeclampsia, 413, 414f, 417 smoking attenuating relaxation, 94 weight reduction reversing, 173 Endothelial function diabetes with primary hypertension, 73 primary hypertension, 67 statins and ACEIs, 253 vasoactive substances, 68 Endothelial progenitor cells, 225 Endothelin calcium and cell membrane alterations in hypertension, 66 endothelial function, effect on, 61f, 62 Endothelin-1, 58t Endothelin antagonists, 234 drugs under investigation, 233–234 heart failure, 82 Erectile dysfunction, 204 Established hypertension clinical trials, 112–114 uncontrolled long-term observations, 111–112 Estimated glomerular filtration rate (eGFR), 120 Estrogen replacement therapy (ERT), 425–426 Ethacrynic acid, 205 Ethnic groups atheroscleroticstiffness, 115 natural history of hypertension, 124–125 special considerations in choice of therapy, 248 F False positive results in laboratory test, 130 Familial hyperaldosteronism, type I See Glucocorticoid-remediable aldosteronism (familial hyperaldosteronism, type I) Familial syndromes See Genetic factors; specific syndromes Family histories aldosteronism, 353 evaluation of hypertensive patients, 91 genetics, role of, 91 hypertension in children and adolescents, 441 Fat, dietary children and adolescents, 435 DASH diet, 183 Fatal familial insomnia, 397 Fatigue β-adrenergic receptor bldckers, 214 primary aldosteronism, hypokalemia in, 376 Fatty acid metabolites, 83 Felodipine calcium channel blockers, 220t, 236–237 enalapril, combined with, 224t grapefruit juice, interaction with, 247 hypertensive urgencies, 283–284 nondiabetic chronic renal disease, 299 oral antihypertensive drugs available in the U.S., 240t pediatric dosage, 250t timing of dosing for control of hypertension, 195 Females antihypertensive therapy, benefit from, 168 children and adolescents, blood pressure levels in, 426t medial fibromuscular dysplasia, 323 natural history of hypertension, 114 renovascular hypertension with ischemic nephropathy, 335 special considerations for, 248 Femoral pulses, 442 Fenofibrate, 304t Fenoldopam parenteral, for hypertensive emergencies, 281t, 282, 283 pediatric hypertensive emergencies, 444t, 446 Fentanyl hydromorphone, 305t Fetal development, 65, 94 Fever, high, and pheochromocytoma, 375 Fiber, dietary, 183 Fibrinoid necrosis, 275 8/28/2009 6:13:53 PM Index Fibromuscular dysplasia, 323–325, 324t Filters used with renal angioplasty, 312 Finger devices for measurement of blood pressure, 32 First choice of drugs for hypertension, 244, 250–251 Fish-oil supplements (omegα-3 fatty acids), 184 Florinef, 347 Fluid intake, limited eclampsia, management of, 283 glomerulonephritis, acute, 291–292 Fluid retention guanethidine, 210 thiazide diuretics, 206 Fluid volume chronic dialysis, 309 pheochromocytoma, 358 Food and Drug Modernization Act (FDAMA), 444, 444t Framingham Heart Study, 14f aging, impact of, and accompanying hypertension, cardiovascular disease and blood pressure levels, Furosemide, 204–205 G GABA agonists, 384t Gabapentin, 304t Garlic, 185 Gastric bypass surgery, 173 Gastrointestinal symptoms, acceleratedmalignant hypertension, 275t Gastroplasty, 173 Gender differences atherosclerotic stiffness, 115 incidence of hypertension, 14, 14f left ventricular hypertrophy, 116 prevalence of hypertension in U.S population, 13 risk of IHD mortality and blood pressure levels, tracking blood pressure in children, 430 white-coat hypertension, 27 Gene therapy for primary hypertension, 42 Genetic factors aldosterone-producing adenomas, 350 associations with, in primary hypertension, 42–43 atherosclerotic lesions with renovascular hypertension, 320 β-adrenergic receptor blockers, 211 Blacks and natural history of hypertension, 123, 124t blood pressure in children, 435, 436t 11β-HSD2 deficiency, 385, 386 glucocorticoid-remediable aldosteronism, 343, 347–349 inherited defects in renal sodium excretion, 63 inherited renal tubular disorders, 348 left ventricular hypertrophy and hypertension, 116 natural history of hypertension, 108 preeclampsia, 386 primary aldosteronism, 352 primary hypertension, role in, 42, 43, 46 sodium, sensitivity to, 53 thiazide diuretics, 198 Genetic testing, 372 Genitourinary system, 211 Gestational hypertension (GH), 410 Gingival hyperplasia, 221 Gitelman’s syndrome, 93f Glaucoma, 25 Gliclazide, 304t Index.indd 463 Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries-I Trial, 118 Glomerular filtration rate (GFR), 294 ACEIs, 299 calculation of, 294 CCBs, 302 diabetic nephropathy, 305, 306, 307f, 308 evaluation of hypertensive patients, 117, 118 nondiabetic chronic renal disease, 308, 309 pressure-natriuresis, resetting of, 60 renal disease, 120–121 Glomerular hypertension, diabetic nephropathy, 305–306 Glomerulonephritis, acute hypertensive encephalopathy, 278 renal disease, acute, 292 Glomerulopathy, and renal sodium retention, 54–55 Glomerulosclerosis contralateral kidney, with renal stenosis, 326 diabetic nephropathy, 293 Glucagon-stimulation test, 371 Glucocorticoid receptor resistance, 386 Glucocorticoid-remediable aldosteronism (familial hyperaldosteronism, Type I) clinical and laboratory features, 348–349 diagnosis, 349 genetic confirmation, 348, 349f Gordon syndrome, 350 Liddle syndrome, 349 mineralocorticoid receptor activation, 349 nonglucocorticoid-remediable aldosteronism, 349 Glucocorticoids Cushing’s syndrome, 379 Takayasu’s arteritis, 119 Glucose intolerance Cushing’s syndrome, 379 thiazide diuretics, 203 Glucose, serum acute physical stress and hypertension, 398 benign pheochromocytoma, postoperative care, 375 control of, and diabetic nephropathy, 308 diabetes with primary hypertension, 81 metabolism of, and dietary magnesium, 181 myocardial infarction and β-blockers, 154 prehypertension, 109 side effects, biochemical, of hypertension therapy, 10 Glyburide, 304t Glycyrrhizin acid, 386 Goals of therapy elderly patients, 248–249 end points of therapy, determining, 143 lack of consistent recommendations, 162 medication for pediatric hypertension, 449 pediatric hypertensive emergencies, 308 Gordon’s syndrome, 348t, 350 Gout alcohol, 402 thiazide diuretics, hyperuricemia in, 198 Gradual lowering of blood pressure dose-response relationships, 237 elderly patients, 249 hypertensive emergencies, 280 hypertensive encephalopathy, 278, 279 hypertensive urgencies, oral medication for, 284, 285 stroke, acute ischemic, 285 Grapefruit juice calcium channel blockers, drug interactions with, 236 resistant hypertension, 247 Growth factors, vascular, 124 463 Guanabenz central α-agonists, 207–208, 239t oral antihypertensive drugs available in the U.S., 240t pilots, special considerations for therapy for, 248 Guanadrel oral antihypertensive drugs available in the U.S., 240t peripheral adrenergic inhibitors, 215, 239t pilots, special considerations for therapy for, 248 Guanethidine oral antihypertensive drugs available in the U.S., 240t peripheral adrenergic inhibitors, 215, 239t pilots, special considerations for therapy for, 248 Guanfacine central α-agonists, 207–208, 239t oral antihypertensive drugs available in the U.S., 240t Guidelines for therapy blood pressure levels in children and adolescents, 435–439 drugs, choosing, 234–240 elderly patients, 249t lack of consistent recommendations, 162 oral contraceptives, with hypertension, 425 problems with, 146 Guillain-Barre syndrome, 397 H Hair, 217 Hazard difference in clinical trials, 144 HCTZ (hydrochlorothiazide) See Hydrochlorothiazide (HCTZ) Head injuries, 280t, 397 Headache, 127–128 patient histories, 127t Hearing loss, 205 Heart outcomes prevention evaluation (HOPE), 149t, 196, 226 Heart rate, cardiac output, 47, 48, 225 Heart transplantation, 399, 403 HELLP syndrome and preeclampsia, 419, 420, 420t Hematocrit, primary hypertension, 129 Hemodynamics characteristics of antihypertensive drugs, 299 preeclampsia, 413 primary aldosteronism, hypertension, 341f renovascular hypertension, 321f, 414f Hemolysis accelerated-malignant hypertension, 277 HELLP syndrome with preeclampsia, 419 Hepatic metabolism, β-adrenergic receptor biockers, 212 Home BP monitoring (HBPM), 20, 34, 35t Hydrochlorothiazide (HCTZ), 199, 241, 445t Hyperkalemia, 227–228, 227t Hypertension drug comparisons adverse effects, 236–237 efficacy, 234–235, 235f morbidity and mortality reductions, 235–236 poor control patients, 193–194 physicians, 193 therapy, 194 prevention, 257 resistant hypertention associated conditions, 247 diagnosis and management, 246, 247f 8/28/2009 6:13:53 PM 464 Index Hypertension (Continued) identifiable causes, 247 inadequate response, 246 nonadherence, 246–247 treatment, 247–248 therapy choice considerations, 248–257 discontinuation, 245–246 dose-response relationships, 237–238, 237f–238f first drug, 240–245 oral antihypertensive drugs, 239t–240t second drug, 245, 245f third and fourth drug, 245 treatment antihypertensive drug See Antihypertensive drug therapy lifestyle modifications See Lifestyle modifications Hypertension Detection and Follow-up Program (HDFP), 12f, 147t, 148, 148f Hypertension treatment benefits animal experiments, 142 antihypertensive therapy, clinical trails, 142 cost-effectiveness, 155–156 epidemiologic evidence, 141 natural experiments, 141–142 progression, 141 goals adequate therapy, 163 J-curve, 161–162 population strategies, 163 recommendations, 162 guidelines absolute cardiovascular risk, 156–157, 157f Institution of Drug Therapy, thresholds, 158t irrationalities and inconsistencies, 156 level of BP, 156 prognosis factors, 159t recommendations, 159 risk assessment, 157–158 risk stratification, 160t overall management, 160–161, 157f randomized clinical trial (RCT) problems antihypertensive treatment, 142 guidelines, 146 meta-analyses and systematic reviews, 146 overestimations, 143–144, 144t, 145f solutions, 144–145 trial data validity, 144–145 underestimations, 143 thresholds, high risk patients CAD, 160, 160f CKD, 159–160, 161f trial results blacks, 152 brain disease, 154 cardiac patients, 154 diabetic patients, 152–154, 153t elderly patients with ISH, 150, 150f, 151 less severe hypertension, 146–147 malignant hypertension, 146 over age, 79, 152, 151f, 151t placebo-controlled trials after 1995, 148, 149f, 149t, 150 trials before 1995, 147–148, 147t women, 152 TROPHY trial, 158 Hypertensive crises accelerated-malignant hypertension See Accelerated-malignant hypertension definitions accelerated-malignant hypertension, 274 Index.indd 464 hypertensive emergency, 274, 275t hypertensive encephalopathy, 274 hypertensive urgency, 274 hypertensive encephalopathy See Encephalopathy uncontrolled severe hypertension, 284 Hypertensive emergencies definitions, 274, 275t drug selection criteria, 283 initiating therapy, 280 monitoring therapy, 280–281 parenteral drugs, 281t clevidipine, 282 diuretic, 283 esmolol, 283 fenoldopam, 282 hydralazine, 283 labetalol, 283 nicardipine, 282 nitroglycerin, 282 nitroprusside, 282 phentolamine, 283 Hypertensive urgencies, 283 definitions, 274 management, 285 oral agents selection, 284t captopril, 284 clonidine, 284 diuretics, 285 labetalol, 285 nifedipine, 284 Hyperthyroidism, 393 Hyperuricemia, 203 Hypoglycemia, 228 Hypokalemia, 342 diuretic-induced hypokalemia prevention, 202 repletion, 202–203 sudden death, 202 urinary K+ loss, 201–202 ventricular arrhythmias, 202 Hypomagnesemia, 203 Hyponatremia, 203 Hypothyroidism, 393 I Identifiable hypertension acute physical stresses cardiovascular surgery, 399, 399t perioperative hypertension, 398–399 aorta coarctation lesions, 392 management, 393 pathophysiology, 392–393 recognition, 393 symptoms and signs, 392, 393t chemical agents, 401t–402t alcohol, 402 caffeine, 400 nicotine and smoking, 400, 402 chemotherapy, 403 functional somatic disorders, 397t anxiety-induced hyperventilation, 398, 398f white-coat hypertension, 397 hormonal disturbances acromegaly, 394 hyperparathyroidism, 393–394 hyperthyroidism, 393 hypothyroidism, 393 vitamin D deficiency, 394 immunosuppressive agents, 403 intravascular volume, increased erythropoietin therapy, 400 polycythemia and hyperviscosity, 400 neurologic disorders, 397 Alzheimer disease, 396 brain tumors, 396 head injury, 397 quadriplegia, 397 nonsteroidal anti-infl ammatory drugs (NSAIDs), 403 obstructive sleep apnea (OSA) clinical features and diagnosis, 394, 395t incidence, 394–395, 396f mechanisms, 395 treatment, 395 street drugs, 404 sympathomimetic agents, 403 Isolated diastolic hypertension (IDH), 8, 8f Idiopathic hyperaldosteronism See Bilateral adrenal hyperplasia (idiopathic hyperaldosteronism) Imidazoline receptor agonists, 208f, 209 Immunosuppressive agents See Cyclosproine; Tacrolimus Incidentalomas ACTH-independent Cushing’s syndrome, 383 incidental adrenal masses, 360 primary aldosteronism, screening for, 344 Indapamide benefits of ACEI treatment vs placebo, 149t, 152 oral antihypertensive drugs available in the U.S., 239t–240t potassium loss decreased with dietary sodium reduction, 178 special considerations for prevention of stroke, 231 thiazide-like diureties, 199–200 Indigo carmine, 401t Indinavir, 4002t Industrialized societies excess sodium intake in primary hypertension, 51 natural history of hypertension, 108 physical activity, lack of, 168 Infancy, hypertension causes, 447, 448t recommended doses, 447, 449t Infants and neonates hypertension, 421, 423 left ventricular hypertrophy, 116–117 low birth weight, and later cardiovascular disease, 64, 65, 433 office measurement of blood pressure, 29–33 Infection and renovascular hypertension, 322 Inferior petrosal sinus sampling, 382f, 383 Inflammatory markers aldosterone and primary hypertension, 132 cytokines, reduced, with weight reduction, 86 estrogen replacement therapy and hypertension, 425 evaluation of hypertensive patients, 131 metabolic syndrome and primary hypertension, 94 primary hypertension, 131 Ischemic heart disease (IHD), 1, 2f, Ischemic nephropathy bilateral renovascular disease, 326–327 definition, 326 therapies, 326 Isolated diastolic hypertension (IDH), 8, 8f Isolated systolic hypertension (ISH), 6–8 vs combined systolic and diastolic hypertension, 108, 109t elderly patients, 150, 150f 8/28/2009 6:13:53 PM Index J J-curve of blood pressure, 162, , 251 John Henryism, 124 Joint National Committee (JNC-7), blood pressure classification, 11–12 K Keith–Wagener retinopathy, 274 Keloids and hypertension, 124 Ketamine, 374 Ketoconazole, 384t Ketorolac, 304t Kidney transplantation immunosuppression, 312 management, 312–313 native kidney hypertension, 312 posttransplantation hypertension causes, 312t posttransplantation renal artery stenosis, 312 Korotkoff sounds amplification of, 33 children and adolescents, 440 office measurement of blood pressure, 30t L Large-vessel disease, 118–119 Left ventricular hypertrophy (LVH), 432 associations, 116–117 consequences, 117 patterns, 117 prevalence, 116 regression, 117 Lifestyle modifications acupuncture, 185 alcohol moderation beneficial effects, 183 blood pressure effects, 182 recommendations, 183 antioxidants, 184 caffeine, 184 calcium supplementation clinical data, 181–182 recommendations, 182 cardiovascular disease, protection, 172 dietary fat, 183–184 dietary nitrate, 183 dietary sodium reduction antihypertensive effect, 175–178 background, 175 benefits, 178 data outcome, safety, 179 harmful perturbations, 178 mortality, 178 myocardial infarction, 178 fiber, 183 folate, 185 garlic and herbal remedies, 185 increased physical activity clinical data, 181–182 recommendations, 182 individual therapy, problems, 172 lipid-lowering diet and drugs, 184 magnesium supplementation, 181 melatonin, 185 potassium supplementation clinical data, 179–180, 180–181 recommendations, 180 preventive potential benefits, 168, 169t diabetes, 168 Dietary Approaches to Stop Hypertension (DASH), 169t, 170–172, 171f hypertension, incidence, 170, 171t Index.indd 465 JNC-7 report, 168–169 trial of nonpharmacologic interventions in the elderly (TONE), 170, 170f protein intake, 184 relaxation, 184–185 surgical sympathectomy, 185 tobacco avoidance, 172–173 weight reduction clinical data, 173–174, 173t, 174f recommendations, 174–175 M Magnetic resonance imaging (MRI), 332 Metolazone, 200 Microalbuminuria, 120, 306 Mineralocorticoid receptors apparent mineralocorticoid excess (AME), 385–386 enzyme-mediated receptor protection, 385f glucocorticoid resistance, 386 glycyrrhetinic acid, 386 Minoxidil, CKD anemia, 303 dietary protein restriction, 303 dose modification, 304, 304t lipid-lowering agents, 303–304 timing of, 303 Multiple Risk Factor Intervention Trial population risk from hypertension, 16, 16f race, coronary heart disease mortality, and blood pressure levels, N Nadolol β-adrenergic receptor blockers, 197t, 212, 213t, 239t nondiabetic chronic renal disease, 309f oral antihypertensive drugs available in the U.S., 239t National Health and Nutrition Examination Surveys (NHANES), 13 current state of control of hypertension, 192 dietary protein and blood pressure, 184 elderly hypertensive patients, 121 isolated systolic hypertension and cardiovascular risk, lead and primary hypertension, 97 mortality rate, and improved control of hypertension, 16 obesity, 125–126 prevalence of hypertension in U.S population, 13 pulse pressure, widening of, National Health Epidemiologic Follow-up Study, 14 National Heart, Lung, and Blood Institute, 147t National High Blood Pressure Education Program hypertension, types of, during pregnancy, 350 population risk from hypertension, 16 preeelampsia, 413–414 preeelampsia, management of, 418 recommendations for treatment, 193 National Institute for Clinical Excellence (NICE), 193 Natriuresis accelerated-malignant hypertension, 274 renal sodium retention, 54–55, 55f 20-HETE, 58t Nebivolol, 213t, 215 Nefazodone, 304t Nephrectomy renovascular hypertension, 320 renovascular hypertension with hypoplastic kidney, 327 465 Nephrons ischemia of, and primary hypertension, 62 reduced number, and hypertension, 63–64, 433 Nephropathy ACEIs, 220, 226 contrast media, 332 diabetes, 86–87 renovascular hypertension, 326–327 Nephrotic syndrome, 326, 344t Neurologic status accelerated-malignant hypertension, 275t hypertensive emergencies and gradual lowering of blood pressure, 280 hypertensive encephalopathy, 280 Neuropathy, autonomic, 309 Neurovascular decompression, 50 New Zealand guidelines for starting antihypertensive therapy, 196, 197t Nicardipine, hypertensive emergencies, 282 Nicotine and smoking, 400, 402 Nocturia, 128 Nonsteroidal antiinflammatory drugs (NSAIDs), 403 O Obesity, 433 aerobic exercise, 181 Black patients, 162 children, 430–433 Cushing’s syndrome, 360 diabetes with primary hypertension, 86–87 hypertensive patients, 128–129 metabolic syndrome, 86 obstructive sleep apnea, 394–395 population risk from hypertension, 16–17 prehypertension, 109–110 prevention of hypertension in U.S population, 17 primary hypertension, 81–86 resistant hypertension, 247 special considerations in choice of therapy, 251–252 Obesity-related hypertension adipocytokine interaction, 83, 83f epidemics, 81–82, 82f neural mechanisms liver fat accumulation, 85 neurogenic hypertension variant, 85 obstructive sleep apnea, 84–85, 84f RAAS overactivity, 86 T cell activation, 86 prevention, 88–89, 89t Obstructive sleep apnea (OSA) clinical features and diagnosis, 394, 395t and hypertension incidence, 394–395, 396f mechanisms, 395 treatment, 395 Octreotide, 384t Office measurement of blood pressure, 29–33, 30t Oliguria, 291 Olmesartan, 240t Omapatrilat, 234 Omega-3 fatty acids (fish oil supplements), 184 Once-daily therapy, 240t, 241 Opiates, 209, 364 Oral contraceptives (OC), pregnancy clinical course, 424 guidelines, 425, 426t incidence, 424 mechanism, 424 predisposing factors, 424 risks, 424–425, 425t Orlistat, 175 Oslo Trial, 112t, 147t 8/28/2009 6:13:53 PM 466 Index Osteopenia, 381t Osteoporosis alcohol consumption, moderate, 183 calcium supplementation, 180–181 sodium intake, 177t, 178 thiazide diuretics, 202 Ouabain, 56 Overdoses calcium channel blockers, 222 dose-response relationships, 237–238 Oxidative stress peripheral resistance, 57, 58t preeclampsia, 417 P Paraganglioma and pheochromocytoma acute hypertensive crises, 374 biochemical diagnosis dopamine-secreting paraganglioma, 371 end-stage renal disease, 369-370 pharmacological testing, 371 plasma/urine metanephrines, 368-369 scientific rationale, 367-368, 368f technique, 369, 370f, 370t children, 375 clinical features catecholamine-secreting tumors, 366–367 deaths, 371 disease-causing genes, 369 familial paraganglioma, 366 hypotension, 365 less-common presentations, 369 MEN2 differing phenotypes and VHL syndrome, 365–366 neurofibromatosis, 366 paroxysmal hypertension, 364-365 pheo mimics, 367 pheo-like spells, differential diagnosis, 363-364, 364t pseudopheochromocytoma, 367 revised rule of 10 s, 365 signs and symptoms, 363-364, 364t location, 362t malignant pheochromocytoma, 375–376 postoperative follow-up, 375 pregnancy, 375 preoperative management β-blocker, 373 α-blocker, 373 calcium channel blockade, 374 catecholamine-synthesis inhibition, 374 prevalence, 363, 363f screening indications, 367, 367t surgery and anesthesia, 374–375 tumor localization abdominal CT and MRI, 371–372, 372f genetic testing, 372-373 imaging studies, 372 Patient’s hypertension information causes, 455 consequences, 455 control, 456 definition, 455 home blood pressure monitoring guidelines equipment, 456 procedure, 456 treatment antihypertensive drugs, 456 lifestyle habits, 455 Peripheral vascular disease (PVD), 119 Pheochromocytoma adrenal hypertension, 362 incidental adrenal mass adrenal incidentaloma, 358 differential diagnosis, 358, 369t Index.indd 466 hyperfunction evaluation, 359–360, 360t malignancy evaluation, 358–359, 359t management, 361–362, 361f prevalence, 358 paraganglioma See Paraganglioma and pheochromocytoma Plasma renin activity (PRA), 344–347 Polypill, 11 Population groups, hypertension conceptual definition, 3–11, 5f–9f, 10t factors, 4t patient role and quality of life (QOL) worsening, 10 polypill, 11 therapy, biochemical side effects, 10–11 control rates, 1, 2t incidence, 14 ischemic heart disease (IHD) mortality rate, 1, 2f operational definitions, 11–13, 12f, 12t prevalence, 14 U.S adult population, 13–14 prevention, 17 risk SBP, percentage distribution, 16, 16f strategy for, 16–17 types and causes, 14–15, 15t Potassium supplementation clinical data, 179-180, 180f recommendations, 180 Potassium-sparing agents, 205 Preeclampsia (PE) cerebral blood flow, 419 definition, 410 diagnosis consequences, 418 differential diagnosis, 419 early detection, 418 hyperuricemia, 419 overdiagnosis, 418 proteinuria, 418 early and late onset genesis, 416, 417f epidemiology causes, 414 risk factors, 414, 415t HELLP syndrome, 419 intravascular coagulation, 419, 420f long-term consequences, 421 management nonpharmacologic management, 420 pharmacologic therapy, 421, 421t severe PE, 420, 420t maternal syndrome, 417–418 pathophysiology deficient trophoblastic migration, 415, 416f placental stimulus, 415–416 uteroplacental hypoperfusion, 415 prevention, 421–422 uteroplacental and maternal hemodynamics, 414, 414f Pregnancy and pill blood pressure monitoring ambulatory monitoring, 411–412, 412f home readings, 411 office readings, 411 pulse wave analysis, 412 chronic hypertension causes, 423–424 mother and fetus risks, 422-423 oral drugs, 423, 423t circulatory changes, 412–413, 413f eclampsia clinical features, 422 definition, 422 management, 422 estrogen replacement therapy (ERT), 425–426 oral contraceptives (OC) clinical course, 424 guidelines, 425, 426t incidence, 424 mechanism, 424 predisposing factors, 424 risks, 424–425, 425t postpartum syndromes and lactation, 424 peripartum cardiomyopathy, 424 preeclampsia (PE) See Preeclampsia (PE) types classification, 410 preeclampsia diagnostic issues, 410–411 Prehypertension, 109–110, 109f–110f Primary aldosteronism (PA) adrenal pathology types adrenal computed tomography, 352 adrenal scintigraphy, 352 adrenal venous sampling, 352 aldosterone-producing adenomas, 350, 350f associated conditions, 351 bilateral adrenal hyperplasia, 350–351, 351t carcinoma, 351 diagnosis flow chart, 352, 353f extrα-adrenal tumors, 351 unilateral hyperplasia, 351 aldosterone to renin ratio (ARR) screening, 339 clinical features blood pressure (BP), 340–341 complications, 341 hemodynamics, 341, 341f pathophysiology, 340, 340f sodium retention mechanism, 342 definitions, 340 diagnosis confirmatory tests, 347 guidelines, 344 monogenic forms, 348, 348t plasma aldosterone:renin ratio, 344–347 pregnancy, 350 urine potassium, 344, 344t effects, 343 familial hyperaldosteronism type II, 343 glucocorticoid-remediable aldosteronism clinical and laboratory features, 348–349 diagnosis, 349 genetic confirmation, 348, 349f Gordon syndrome, 350 Liddle syndrome, 349 mineralocorticoid receptor activation, 349 nonglucocorticoid-remediable aldosteronism, 349 hypokalemia incidence, 342 incidence, 340 medical treatment, 353–354 mineralocorticoid excess syndromes, 339, 340t renin release suppression, 342 resistant hypertension, 343 surgical treatment postoperative complications, 353 postoperative course, 353 preoperative management, 353 surgical technique, 353 Primary hyperparathyroidism (PHPT), 393–394 Primary hypertension complications arterial lesions, 114–115 cerebrovascular disease, 119–120 8/28/2009 6:13:53 PM Index death causes, 115 heart disease, 115–118 large-vessel disease, 118–119 renal disease, 120–121 diabetes, 86-87 early hypertension, 111 environmental determinants alcohol, 94-95, 95f caffeine, 94 nutrients, 96–97 temperature and altitude, 95 tobacco, 94 toxic exposures, 97 vitamin D, 95-96 established hypertension clinical trials, 112–114 uncontrolled long-term observations, 111–112 gender differences, 90 androgens, 90 estrogen, 90 hemorheological factors, 90 general considerations, 42–43, 43f genes and environment family history, 91 genetic determinants, 91–92 racial and ethnic aspects, 92–94 hemodynamic subtypes diastolic hypertension, 44 isolated systolic hypertension, 44 systolic hypertension, 43–44 metabolic syndrome diagnostic criteria, 86, 86t pathogenesis, 87, 87f natural history, 108, 109f Americans, 125 blacks, 123–124, 124t diabetes, 125 elderly, 121–123 obesity, 125–126, 125f prevention, 126 women, 123 obesity See also Obesity-related hypertension epidemics, 82, 82f prevention, 88, 89t patient evaluation history, 126–128, 127t identifiable causes, 131–132, 131t–132t laboratory tests, 129–131, 130f overall cardiovascular risk status, 132–134, 133t–134t physical examination, 128–129, 128t, 129f prehypertension, 109–110, 109f–110f renal mechanisms See also Renal mechanisms congenital oligonephropathy, 64–65 excess sodium, 51–53 high-salt diet, 53 inherited renal defects, sodium excretion, 63 limitations, 65 postnatal weight gain, 65 pressure-natriuresis, 58–63 reduced nephron number, 63, 64f salt sensitivity and resistance, 57–58 renin-angiotensin-aldosterone system, 73, 74f aldosterone and sodium channel regulation, 73–75 plasma renin activity (PRA), 76–79 receptor-mediated actions, 75–76 T cells and Ang II–induced hypertension, 80–81 sympathetic nervous system adrenergic receptors, 46–47, 47f angiotensin II, central effects, 50 baroreceptors, 45, 50 brainstem compression, 50 Index.indd 467 central sympathetic outflow, 46 cortical influences, 47 emotional and physical stress, 49–50 excitatory reflexes, 45 long-term sympathetic regulation, 47–48 mechanism, 46f sympathetic overactivity, 48, 49f uric acid, 89–90 vascular mechanisms endothelial dysfunction and nitric oxide (NO), 66–70 microvascular rarefaction, 73 vascular remodeling, 70-73 vasoconstriction, 66, 66f Prospective Studies Collaboration, aging, impact of, and accompanying hypertension, gender, risk of IHD mortality and blood pressure levels, mortality and risk of inaction, Q Quadriplegia, 397 Quality of life adverse effects in drugs, 236 anxiety-related symptoms, 126 labeling as hypertensive, 10 Quality-adjusted life-years laboratory tests for evaluation of hypertensive patients, 129–131 treatment of hypertension, 155–156 Quinapril ACEIs, 197t benefits of treatment vs placebo, 149t characteristics, 224t oral antihypertensive drugs available in the U.S., 240t R Race See also Ethnic groups calcium channel blockers, efficacy of, 237 coronary heart disease mortality and blood pressure levels, incidence of hypertension, 14, 14f prevalence of hypertension in U.S population, 13 Radiofrequency ablation of pheochromocytomas, 374 Ramipril ACEIs, 216t, 241 aortic stenosis, 225 benefits of treatment vs.placebo, 153t characteristics, 224t diabetic patients, 133t nondiabetic chronic renal disease, 308 Oral antihypertensive drugs available in the U.S., 240t placebo-controlled trials for cardiac symptoms, 150 timing of dosing, 195–196 Ramipril Efficacy in Nephropathy (REIN) trial, 303 Randomized, controlled trials, 147–150, 147t, 149t Randomized Evaluation Study (RALES), 205 Randomized placebo-controlled trials after 1995, 148–150 Randomized placebo-controlled trials before 1995, 147–148 Rauwolfia, 185, 209 Raynaud’s phenomenon, 220 Rebound of blood pressure central α-agonists, 207 clonidine, 209, 284 467 Relative risk, cardiovascular, 161f Relaxation therapy, 184 Remodeling of vascular system complications of hypertension, natural history of, 124 hypertension, in, 75, 75f Remodeling, prevention of angiotensin-converting enzyme inhibitors, 222 left ventricular hypertrophy, after Ml, 116–117 Renal artery occlusion, 298 Renal artery stenosis accelerated-malignant hypertension, 280 ACEIs, 251 kidney transplantation, 312 nodular glomerulosclerosis, 306 prevalence of, 320t primary aldosteronism, 362 renovascular hypertension, 319–320 vascular damage and level of blood pressure, 141 Renal blood flow asymmetry of, 330 central α-agonists, 207 fenoldopam, 282 ischemia, 323 pregnancy, 349, 350 prostaglandins, 62 Renal mechanisms adult salt-dependent hypertension, 63, 64f congenital oligonephropathy, 64–65 excess sodium animal studies, 53, 54f epidemiological studies, 51–52, 52f–53f feeding trials, 53 human genetic studies, 53 migration studies, 52 population-level dietary interventions, 52–53 high-salt diet sodium retention, 54, 54t volume-dependent mechanisms, 54–56, 55f, 56f volume-independent mechanisms, 56–57 limitations, 65 postnatal weight gain, 65 pressure-natriuresis experimental support, 59, 60f extrarenal mechanism, 62–63 intrarenal mechanisms, 61 intrarenal RAAS, 61–62, 61f nocturia, 63 pressure-sodium excretion curve, 60, 60f renal dopaminergic system, 62 renal inflammation, 63 renal medullary endothelin system, 62 salt sensitivity and resistance clinical research methodology, 57–58 monogenic human hypertension and hypotension, 57, 59f pathophysiological mechanisms, 58t sodium excretion, 63 Renal parenchymal hypertension acute kidney disease See Acute kidney disease chronic dialysis hypertension role, 310, 310t management, 310–312 chronic kidney disease (CKD) See Chronic kidney disease (CKD) diabetic nephropathy See Diabetic nephropathy end-stage renal disease (ESRD) issues data, 288–290 hypertension role, 290 practical solutions, 290–291, 290t risk factors prevalence, 288, 289f 8/28/2009 6:13:54 PM 468 Index Renal parenchymal hypertension (Continued) kidney transplantation immunosuppression, 312 management, 312–313 native kidney hypertension, 312 posttransplantation hypertension causes, 312t posttransplantation renal artery stenosis, 312 renal replacement therapy (RRT), 288–289 Renin-angiotensin-aldosterone system, 73, 74f aldosterone, sodium channel regulation, 73–75 Ang II, receptor-mediated actions, 75, 75f plasma renin activity (PRA) clinical assays, 76–77, 77f factors affecting, 77, 78t primary hypertension, 77–79 schematic representation, 77, 78f prorenin and renin, 75–76 T cell induced hypertension adaptive immunity, 80, 80f experimental evidence, 81 translational evidence, 81 Renin-secreting tumors, 335 Renovascular hypertension (RVHT) classification and course aneurysms, 325 aortic dissection, 325 arteritis, 325 atherosclerotic lesions, 322–323 emboli, 325 fibromuscular dysplasia, 323–325, 324f renal artery stenosis types, 322, 324t types, 323t clinical features clinical clues, 325t cortical atrophy, 326 dyslipidemia, 326 hyperaldosteronism, 326 hypoplastic kidney, 327 ischemic nephropathy, 326–327 nephrotic syndrome, 326 polycythemia, 326 renal transplantation, 327 diagnostic tests catheter-directed arteriography, 331–332 clinical prediction rule, 328, 328t duplex ultrasonography, resistive index, 330 evaluation and therapy algorithm, 328, 329f peripheral blood, 329 renal scans, 330–331, 331f renal vein renins comparison, 329–330 renin measurements, 328 revascularization response factors, 327t spiral computed tomography and magnetic resonance angiography, 332, 332f factors, 319 mechanisms animal models, 320–321, 321f, 322t humans studies, 321 prevalence, 320 renin-secreting tumors, 335 vs renovascular disease, 319–320, 320t therapy angioplasty, 333–334, 334t medical therapy, 333 selection, 334–335 surgery, 334 Resistant hypertension associated conditions, 247 diagnosis and management, 246, 247f Index.indd 468 identifiable causes, 247 inadequate response, 246 nonadherence, 246 treatment, 247–248 S Sphygmomanometer automated oscillometric devices, 32 bladder size, 31 cuff position, 31 manometer, 31–32 wrist and finger devices, 32 Stroke See Cerebrovascular disease Sympathetic nervous system adrenergic receptors, 46–47, 47f baroreceptors, 45 central sympathetic outflow, 46 cortical influences, 47 excitatory reflexes, 45 increased MSNA, 50 long-term sympathetic regulation, 47–48 mechanism angiotensin II, central effects, 50 baroreceptor resetting, 50 brainstem compression, 50 central and reflex mechanisms, 46f emotional and physical stress, 49–50 refractory hypertension, 51 sympathetic overactivity, 48, 49f T Tacrolimus, 312 Takayasu’s arteritis natural history of hypertension, 119 recognition of coarctation, 393 renovascular hypertension, 323t, 325 Tamsulosin, 211 Target organ damage, 53–57 Tobacco avoidance, 172–173 Torsemide, 205 Trial of preventing hypertension (TROPHY), 158 Triamterene, 205 U U.K Prospective Diabetes Study, 159–160 Ultrasonography childhood and adolescence, 447 renovascular hypertension, 330 Umbilical artery catheterization, 447 Uncontrolled hypertension, 285 Unilateral adrenal hyperplasia, 340t Universal (national) healthcare coverage, 193 Untreated patients in clinical trials, 112–114 Uric acid, serum, 131 Urinary tract, 292 Urine analysis, 129, 277 U.S Nurses Study, 424 U.S Public Health Service Cooperative Study, 185 Uterine vasculature, and preeciampsia, 415 V Valsartan control of hypertension, 195 HCTZ, combined with, 241 oral antihypertensive drugs available in the U.S., 239t–240t Valsartan Antihypertensive Long-term Use Evaluation (VALUE) trial, 195, 252f Valsartan Heart Failure Trial, 206 Vaniilylmandelic acid (VAM), 368f, 369 Vanlev, 234 Variability of blood pressure, 22–24 Vascular mechanisms endothelial cell dysfunction, NO antioxidant vitamins, 70 measurement, 69 NOS inhibition, 68–69 redox-dependent signaling pathways, 69f superoxide, 67, 68f, 70 vascular tone regulation, 67f microvascular rarefaction, 73 vascular remodeling assessment, 71–73, 72f mechanisms, 70, 71f vasoconstriction, 66, 66f Vascular resistance baroreceptor resetting, 50 cellular mechanisms, 66 diastolic hypertension, 44 hypertrophic remodeling, 71 peripheral adrenergic inhibitors, 209–210 primary hypertension, 57 Vascular system, 10t Vasculitis, large-artery, 324–325 Vasoactive agents, 68f Vasoconstriction, 66 Vasodilation β-adrenergic receptor blockers, 211–215 children and adolescents, 431t direct, oral antihypertensive drugs available in the U.S., 239t–240t Vasopeptidase inhibitors, 234 Vasopressin, 61, 62, 379, 383, 399 Vegetarian diets, 183 Venous pooling, 122 Vesicoureteric reflux, 292 Veterans Administration Cooperative Study Group on Antihypertensive Agents, 112t, 146–147 Vigabatrin, 304t Vincristine, 376 Vioxx, 403 Virilization, 387, 388t, 389 Vitamin C, 422 Vitamin D, 95, 203, 305, 394, 448 Vitamin E, 70, 422 von Hippel-Lindau syndrome, 365, 366 W Waist circumference, 174, 433 Wegener's granulomatosis, 325 Weight gain β-adrenergic receptor blockers, 213 postnatal, accelerated, 65, 433 smoking cessation, 172 Weight loss children and adolescents, 443 diabetics, 252 discontinuation of therapy following, 245–246 lifestyle modifications, 168–172 obstructive sleep apnea, 395 Weight reduction clinical data, 173–174, 173t, 174f recommendations, 174–175 Weight Watchers program, 174 White-coat hypertension (WCH) blood pressure measurement in children and adolescents, 440–441 blood pressure variability, 26–29 elderly hypertensive patients, 27 features, 27–28 history and prognosis of, 28–29 home measurement of blood pressure, 34 natural history, 28 8/28/2009 6:13:54 PM 469 Index prognosis, 28–29, 28f systolic and daytime ambulatory BP readings, 26–27, 27f Whites angiotensin-converting enzyme inhibitors, 226 β-adrenergic receptor blockers, 213 first choice of drugs for hypertension, 240 general guidelines for drug choices, 235–238 renovascular hypertension, 320 tracking blood pressure in children, 430–432 Wilms tumors, 335 Index.indd 469 Women See Females World Health Organization-International Society of Hypertension (WHO/ISH), 12 Wrist devices for measurement of blood pressure, 32 primary hypertension, 43 renovascular hypertension with ischemic nephropathy, 326–327 Z Zaroxolyn,198t See also Metolazone Y Yoga, 184 Young adults blood pressure tracking, 430–432 medial fibromuscular dysplasia, 323–325 8/28/2009 6:13:54 PM ... 20 Primary Hypertension: Pathogenesis 42 Primary Hypertension: Natural History and Evaluation 108 Treatment of Hypertension: Why, When, How Far 141 Treatment of Hypertension: Lifestyle Modifications... retention: Liddle syndrome, Gordon syndrome Endocrine Acromegaly Hypothyroidism Hyperthyroidism Hypercalcemia (hyperparathyroidism) Adrenal disorders Cortical disorders Cushing syndrome Primary aldosteronism... Adrenal Masses) 358 Hypertension Induced by Cortisol or Deoxycorticosterone 378 Other Forms of Identifiable Hypertension 392 Hypertension with Pregnancy and the Pill 410 Hypertension in Childhood
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