Hypertension

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Chapter 40

Hypertension

1. Define hypertension. What is the prevalence of hypertension in the United States, Mexico, and worldwide?

    The Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure, in its seventh report (JNC 7), defined hypertension as an average of two or more diastolic readings more than 90 mm Hg on at least two consecutive visits, or an average of multiple systolic readings more than 140 mm Hg. Isolated systolic hypertension is diagnosed if systolic blood pressure (SBP) is more than 140 mm Hg with a diastolic blood pressure less than 90 mm Hg. A new category called prehypertension is now defined as a blood pressure less than the arbitrary cutoff of 140/90 mm Hg for hypertension but greater than an optimal blood pressure of 120/80 mm Hg. Patients with prehypertension, unlike hypertensive patients, do not require antihypertensive drug therapy, but should be counseled to start health-promoting lifestyle modifications aimed at preventing the development of hypertension. Hypertension is classified into 2 stages: stage I: 140/90 to 159/99 mm Hg and stage II 160/100 or higher. In the latest National Health and Nutrition Examination Survey 2005-2008, about 33% of adults 20 years of age or older have hypertension (Table 40-1).

TABLE 40-1

JNC 7 CATEGORIES OF HYPERTENSION

Category Blood Pressure
Normal <120/80 mm Hg
Prehypertension 120-130/80-89 mm Hg
Hypertension: Stage 1 140-159/90-99 mm Hg
Hypertension: Stage 2 ≥160/100 mm Hg

Modified from Chobanian AV, Bakris GL, Black HR, et al: Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-7), Bethesda, Md., 2003, National Institutes of Health, pp 54-55.

    Prevalence of hypertension worldwide varies from as low as 3% of men in rural India to 72% of men in Poland. Hypertension prevalence is about the same in the United States and Mexico, at about 33% of the adult population.

2. What are the goals of hypertension treatment?

    Reducing elevated blood pressure levels is an important strategy to prevent various complications of systemic hypertension, such as stroke, myocardial infarction (MI), heart failure, and renal disease. The best predictor of the efficacy in preventing various cardiorenal complications is the degree of reduction of blood pressure. The risk of death from ischemic heart disease or stroke in cohort longitudinal studies is lowest at a blood pressure of approximately 115/75 mm Hg and doubles beginning at 115/75 mm Hg with each 20 mm Hg increment in SBP.

    Although blood pressure less than 120/80 mm Hg is associated in observational cohort studies with the lowest risk of death from ischemic heart disease and stroke, the goal of blood pressure treatment recommended by JNC 7 (2001) is a blood pressure less than 140/90 mm Hg in patients with uncomplicated hypertension, and less than 130/80 mm Hg in higher risk hypertensive patients with chronic kidney disease and/or diabetes mellitus.

    The American Heart Association (AHA) Task Force released a scientific statement in 2007 for the treatment of hypertension in the prevention of coronary artery disease (CAD). This AHA Task Force recommended more aggressive control of blood pressure among those at high risk for CAD: individuals with diabetes mellitus, chronic kidney disease (as recommended in JNC 7), but also in patients with cardiovascular disease, congestive heart failure, or a 10-year Framingham risk score of 10% or more. These individuals are advised to maintain a blood pressure less than 130/80 mm Hg. Moreover, the AHA Task Force recommended a goal blood pressure of less than 120/80 in patients with congestive heart failure.

    Targeting an SBP of less than 120 mm Hg, as compared with less than 140 mm Hg, in patients with type 2 diabetes mellitus did not reduce the rate of a composite outcome of fatal and nonfatal major cardiovascular events in the recently reported Action to Control Cardiovascular Risk in Diabetes (ACCORD) blood pressure trial. However, SBP less than 120 mm Hg did significantly reduce stroke risk, a secondary study endpoint. Thus, it is NOT recommended at this time to target SBP less than 120 mm Hg in type 2 diabetic patients.

3. Is systolic or diastolic blood pressure more powerful as a predictor of cardiovascular complications of hypertension?

    Systolic and diastolic blood pressure levels are independently predictive of the risk of cardiovascular complications in hypertensive patients. However, SBP is more powerful in predicting cardiovascular complications, particularly in patients over the age of 50 years. Pulse pressure—the difference between systolic and diastolic blood pressure—is also an independent predictor of cardiovascular complications. A wide pulse pressure is usually indicative of a noncompliant stiff aorta with a reduced ability to distend and recoil back. Thus, during systolic ejection of blood from the left ventricle into the aorta and systemic circulation, the aorta does not distend and the force of ejection is transmitted more forcefully into the peripheral vessels, thus causing an exaggerated SBP level recording. During diastole, the elastic recoil of the aorta is more limited, contributing to a lower diastolic blood pressure. Thus, a noncompliant aorta would increase SBP and reduce diastolic blood pressure, resulting in a widened pulse pressure.

4. You have diagnosed a new case of hypertension. What is your next step?

    Arterioles are the vessels that sustain the most damage from persistent elevation of blood pressure. Therefore, the first step is to do a damage assessment by evaluating the target organs of hypertension, keeping in mind that their involvement is an expression of arteriolar damage with subsequent ischemia and ischemia-induced changes.

image Kidney: Signs of involvement range from minimal proteinuria or slight increase of serum creatinine to end-stage renal disease. Kidney size is evaluated by a variety of imaging methods and has prognostic significance. Hypertension is the second leading cause of renal failure in the United States, particularly in African Americans.

image Brain: The eye fundus appearance is the mirror of the brain circulation. Findings range from minor atherosclerotic changes to papilledema and hemorrhages, which can be seen with severe hypertension and hypertensive crisis. A careful neurologic examination may reveal signs of previously undiagnosed strokes, and history may reveal previous transient ischemic attacks.

image Heart: The direct consequence is left ventricular hypertrophy (LVH) with increased left ventricular (LV) mass; this is easily documented by electrocardiogram (ECG), two-dimensional, and M-mode echocardiogram or cardiac magnetic resonance imaging (MRI). LVH is strongly associated with an increased risk of sudden death and MI, and constitutes the basis for decreased LV compliance and subsequent diastolic dysfunction. A thorough evaluation for the presence of CAD, guided by a skillful interview, is required. Holter monitoring may be necessary for evaluating LVH-associated arrhythmias. The last step in the natural history of the disease is LV dilation and pump failure, with the classical signs of congestive heart failure (CHF).

5. What is resistant hypertension and how prevalent is it?

    Resistant hypertension is defined as blood pressure that remains above goal in spite of the concurrent use of three antihypertensive agents of different classes. Ideally, one of the three agents should be a diuretic and all agents should be prescribed at optimal dose amounts. Resistant hypertension identifies patients who are at risk of having reversible causes of hypertension or patients who, by virtue of persistently elevated blood pressure levels, may benefit from special diagnostic and therapeutic considerations. In a recent analysis of the National Health and Nutrition Examination Survey (NHANES), only 53% of hypertensive patients were controlled to less than 140/90; the majority of the remaining 47% of these patients probably have resistant hypertension. While the exact prevalence of resistant hypertension is unknown, it is estimated from published hypertension clinical trials, including the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack (ALLHAT) trial, that about 20% to 30% of hypertensive patients have resistant hypertension.

    Factors recognized to be associated with resistant hypertension include older age, high baseline blood pressure, obesity, excessive dietary salt ingestion, chronic kidney disease, diabetes mellitus, LVH, African American race, female gender, and residence in southeastern U.S. regions (Box 40-1). Medications that interfere with blood pressure control (Box 40-2), such as nonsteroidal antiinflammatory drugs (NSAIDs), should be specifically inquired about in hypertensive poorly controlled patients.

Box 40-1   PATIENT CHARACTERISTICS ASSOCIATED WITH RESISTANT HYPERTENSION

From Calhoun D, Jones D, Textor D, et al: Resistant hypertension: diagnosis, evaluation, and treatment: a scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research. Hypertension 51:1403-1419, 2008.

Box 40-2   MEDICATIONS THAT CAN INTERFERE WITH BLOOD PRESSURE CONTROL

COX-2, cyclooxygenase-2.

From Calhoun D, Jones D, Textor D, et al: Resistant hypertension: diagnosis, evaluation, and treatment: a scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research. Hypertension 51:1403-1419, 2008.

6. What is secondary hypertension?

    Up to 5% of all hypertension cases are secondary, meaning that a specific cause can be identified. Most of these causes are treatable (e.g., surgery for an adrenal tumor, stenting of a renal artery stenosis, or correction of an aortic coarctation). Given the low prevalence of secondary hypertension, routine screening for secondary hypertension is not usually recommended. A targeted approach is much more cost-effective, and clinical and laboratory clues are critically important in evaluating patients for specific causes of secondary hypertension. Signs, symptoms, and findings suggestive of secondary hypertension are discussed later and in Table 40-2.

TABLE 40-2

CLINICAL SIGNS, SYMPTOMS, AND FINDINGS SUGGESTIVE OF SECONDARY CAUSES OF HYPERTENSION

Signs, Symptoms, and Findings Suggested Secondary Cause
Onset at young age (<35 years) in female patient Renal artery medial fibromuscular dysplasia
Onset at a late age (>55 years), especially in a patient with atherosclerosis
Exaggerated drop in blood pressure and/or kidney function with initiation of ACEI
Abdominal bruit		 Renal artery stenosis
Unexplained hypokalemia Primary hyperaldosteronism
Paroxysmal episodes of palpitations, sweating, and headaches Pheochromocytoma
Use of birth control pills, laxatives, or licorice Drug-induced due to mineralocorticoid effects
Renal calculi, elevated calcium level Hyperparathyroidism
Reduced femoral pulses with high blood pressure values only in the upper extremities Aortic coarctation
Abdominal striae, truncal obesity Cushing disease
Loud snoring, witnessed apnea Obstructive sleep apnea
Worsening renal function, polycystic kidneys or small kidneys on ultrasound Renal parenchymal disease

ACEI, Angiotensin-converting enzyme inhibitor.

7. When should one suspect secondary hypertension?

    The following scenarios should trigger a search for possible causes of secondary hypertension (see Table 40-2):

image Onset at a young age (younger than 35 years) in female patients raises the suspicion of renal artery medial fibromuscular dysplasia.

image Onset at a late age (older than 55 years) suggests atherosclerotic renal vascular disease (renal artery stenosis).

image Unexplained hypokalemia—sometimes manifested by generalized weakness—either in the absence of diuretic use or an exaggerated hypokalemia following low doses of diuretics suggests primary hyperaldosteronism.

image Paroxysmal episodes of palpitations, sweating, and headaches suggest a pheochromocytoma.

image Abdominal/lumbar trauma may result in a perirenal hematoma with subsequent small unilateral kidney.

image A transient episode of periorbital swelling and dark-colored urine that went untreated may point to a chronic glomerulonephritis.

image Multiple episodes of cystitis or urinary infection left untreated or with incomplete treatment will lead to and suggest chronic pyelonephritis.

image Use of birth control pills by young women and laxative use by elderly people or licorice use, which has a mineralocorticoid effect, suggest mineralocorticoid-induced hypertension.

image A history of chronic pain may be the clue for analgesic nephropathy.

image Renal calculi may be the sign of hyperparathyroidism or the cause of obstructive nephropathy.

image Reduced femoral pulses with high blood pressure values only in the upper extremities suggests aortic coarctation.

image Abdominal bruits suggest renal artery stenosis. The cause may be either atherosclerosis in an elderly patient or fibromuscular dysplasia in a young woman. Renal artery stenosis is also suggested by an exaggerated drop in blood pressure following initiation of treatment with angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers.

image Bilateral abdominal palpable masses commonly are due to polycystic kidney disease. Typically the history reveals the presence of hypertension with renal failure in other family members.

image Abdominal striae are the sign of Cushing disease, along with the typical truncal obesity.

image Resistance to a multiple drug regimen can point to a secondary cause of hypertension. In fact, in clinical practice, resistant hypertension with failure to control blood pressure to recommended goals despite at least three antihypertensive agents in optimal dosages is the most important clue that should lead to a thorough evaluation for secondary causes of hypertension.

8. What is the recommended initial diagnostic workup for a hypertensive patient?

    Any newly diagnosed patient with hypertension should have measurements of serum creatinine, sodium, potassium, calcium, and hematocrit, full fasting lipid profile, 12-lead ECG, and chest radiograph. Because essential hypertension accounts for the large majority—more than 95%—of all hypertension, a thorough and costly diagnostic workup for secondary causes of hypertension is not routinely recommended unless there are clinical or laboratory clues suggesting secondary hypertension.

9. What are the most common causes of secondary hypertension among patients with treatment-resistant or uncontrolled hypertension, when do you suspect them, and how do you confirm them?

    Secondary hypertension is common among patients with resistant hypertension. The most common causes of secondary hypertension among patients with resistant hypertension are obstructive sleep apnea, renal parenchymal and vascular disease, and, possibly, primary aldosteronism. Rare causes of secondary hypertension include pheochromocytoma, Cushing syndrome, hyperparathyroidism, aortic coarctation, and intracranial tumors. Following are important clinical or laboratory clues to these secondary hypertension causes:

image Obstructive sleep apnea: Untreated obstructive sleep apnea is an increasingly recognized cause of secondary hypertension. Clues include loud snoring, witnessed apnea, and excessive daytime somnolence. Diagnosis is confirmed with a sleep study.

image Renal artery stenosis: This is suspected in patients with atherosclerotic peripheral or coronary vascular disease, early age (younger than 35 years) or late age (older than 55 years) at onset of hypertension, abnormal renal function or worsening renal function with the use of an ACE inhibitor or in patients with a unilateral small kidney. Renal ultrasonography is not recommended and magnetic resistance angiography is the most specific and reliable noninvasive diagnostic imaging modality. Contrast angiography is also useful for the diagnosis and for possible renal angioplasty. It is important to recognize that the anatomic diagnosis of a renal artery stenosis, independent of its cause, does not imply that the stenosis is the cause of hypertension. Causation can be confirmed by documenting the functionality of the lesion by measuring renal vein renin activity and documenting a renin activity ratio greater than 1.5 between the two sides. Fibromuscular dysplasia is a type of renal artery stenosis that most commonly occurs in younger women

image Primary hyperaldosteronism: This is suspected in hypertensive patients with unexplained hypokalemia. Diagnosis is suspected by a suppressed renin activity and a high 24-hour urinary aldosterone excretion in the course of a high dietary sodium intake and is confirmed radiographically with a localizing imaging procedure such as computed tomography (CT) or MRI with a specific adrenal protocol.

image Renal parenchymal disease: This is suspected in patients with chronic kidney disease and impaired renal function, but causation of the hypertension is often difficult to confirm because longstanding untreated hypertension may also cause renal parenchymal disease. Imaging techniques that evaluate kidney size, presence of hydronephrosis and obstructive nephropathy, calculi, polycystic kidney disease, or congenital malformations are useful to detect specific causes of renal parenchymal disease.

image Pheochromocytoma: A rare secondary cause of hypertension that often presents with paroxysmal and postural hypotension, usually in a younger adult, with intermittent episodes of headache, palpitation, and sweating. The best screening test is plasma-free metanephrines (normetanephrine and metanephrine).

10. A 32-year-old man complains of intermittent episodes of headaches, palpitations, and profuse sweating. Over the last year, he has been treated three times in the emergency department for hypertensive crisis. He does not remember what his blood pressure was, but he felt lightheaded when trying to stand, even before reaching the emergency department (ED). In your office, he always has a blood pressure below 120/70 mm Hg. He has noticed low-grade fever at times and has lost a few pounds. After you examine him, he feels funny, so you measure his blood pressure again. This time it is 165/110 mm Hg, with a heart rate of 115 beats/min. Laboratory studies only show a slightly elevated serum glucose and white blood cell count (WBC) of 18,000/mL with a normal differential. What is your diagnosis?

    This is a typical presentation for a pheochromocytoma. The clues given by the patient’s history are invaluable for diagnosis: Many patients with pheochromocytoma have a normal baseline blood pressure, with high blood pressure values only on occasion. Postural hypotension is a classical feature. High serum catecholamine levels explain the sweating and palpitations and the low fever, elevation of serum glucose, and leukocytosis. Gentle palpation of the abdomen during physical examination may sometimes trigger a crisis. Because of the general and metabolic manifestations of the disease, it may mimic a large variety of conditions (e.g., vasculitis, diabetes), and a high level of suspicion is always necessary.

    Some patients present with a high blood pressure that is constant rather than paroxysmal. A rule of 10 may be applied: 10% of all cases are familial, 10% are bilateral, 10% are due to a malignant adrenal tumor, 10% recur, 10% are extra-adrenal, 10% occur in children, 10% are associated with a multiple endocrine neoplasia (MEN) syndrome, and 10% present with a stroke as the inaugural symptom.

    Diagnosis of a pheochromocytoma is rewarding because this very sick patient who is prone to life-threatening complications can be virtually cured. The current recommendation for biochemical diagnosis of pheochromocytoma is urine testing for metanephrines and fractionated catecholamines. These tests only certify the presence of a catecholamine-secreting tumor; therefore, the next step is to localize it (90% are in the adrenal medulla; the other 10% are scattered where chromaffin tissue is found). The preferred treatment is laparoscopic adrenalectomy.

11. How important are nonpharmacologic strategies in hypertension treatment?

    Hypertension treatment is a lifelong commitment regardless of the recommended treatment modality. Thus, compliance to treatment is critically important in achieving the expected clinical benefits of treatments. Hypertensive patients should be appropriately educated about the natural history and complications of hypertension and the critical importance of compliance with any treatment recommendation. Goal blood pressure attainment is much more likely achieved with earlier initiation of combination antihypertensive drug therapies—particularly in stage 2 hypertension, characterized by blood pressure levels greater than 160/100 mm Hg—and by frequent monitoring of blood pressure at home and in the doctor’s office and appropriate uptitration of antihypertensive medications to reach accepted goals of blood pressure treatments.

    Patients and some physicians tend to be skeptical about the importance of lifestyle changes. Often the skepticism of the physician may be communicated to the patient even without the physician’s conscious effort. It is critically important that patients and their physicians believe in the benefit of lifestyle changes. Current hypertension guidelines describe lifestyle changes as therapeutic to emphasize their proven benefit. Therapeutic lifestyle changes—weight loss; reduced intake of saturated fat and salt; reduced dietary calorie intake; regular exercise and moderation of alcohol intake; consumption of adequate amounts of calcium, potassium, magnesium, and fiber; and smoking cessation—are at the top of the JNC 7 treatment algorithm recommended for all patients. Therapeutic lifestyle changes have been proven to be effective in reducing blood pressure levels by 10 to 20 mm Hg, changes that are at times similar to the efficacy of one additional antihypertensive drug. In patients with prehypertension—with blood pressure levels between 120/80 and 140/90 mm Hg—therapeutic lifestyle changes, but not pharmacologic treatment, are generally recommended to prevent hypertension development, with the exception of diabetics and/or patients with chronic kidney disease. Pharmacologic treatment is generally recommended not solely, but in addition to and as an adjunct to, therapeutic lifestyle changes in hypertensive patients—that is, patients with blood pressure levels greater than 140/90 mm Hg. Antihypertensive drug therapy is recommended at lower levels of blood pressure (more than 130/80 mm Hg) in higher-risk patients with diabetes mellitus and chronic kidney disease, and the goal of blood pressure treatment is also lower, namely less than 130/80 mm Hg. In patients with uncomplicated hypertension, goal blood pressure levels are less than 140/90 mm Hg.

12. True or false: Beta-adrenergic blocking agents (β-blockers) are preferred initial antihypertensive agents in hypertensive patients with no known hypertensive complications.

    False. In large placebo-controlled prospective clinical trials, diuretics and β-blockers as a group have been shown to reduce cardiovascular complications of hypertension. However, the evidence of these cardioprotective effects of thiazide diuretics in hypertensive patients is more compelling, and in clinical trials comparing diuretic and β-blockers, such as the Medical Research Council (MRC) trial, diuretics were more effective than β-blockers. Thus, the JNC 7 report recommends thiazide diuretics, not β-blockers, as preferred initial treatments in patients with uncomplicated hypertension—that is, patients with no compelling comorbid conditions that may favor specific antihypertensive agents.

    Compelling indications in hypertensive patients for the use of a β-blocker as an antihypertensive agent include a history of MI, compensated heart failure, and CAD. Contraindications to β-blockers must be carefully weighed against their potential therapeutic benefits. For example, a β-blocker should be avoided in a patient admitted to the hospital with acutely decompensated heart failure, but may be started at lower doses then gradually uptitrated in patients with well-compensated and stable heart failure. Withdrawal of β-blockers, particularly in patients with CAD, should be performed gradually to avoid rebound increase in anginal symptoms upon their discontinuation.

13. Are alpha-adrenergic blocking agents (α-blockers) effective in preventing cardiovascular complications of hypertension, and when is it appropriate to use them in hypertensive patients?

    α-Blockers are effective antihypertensive agents but have not been shown in either placebo-controlled or active-controlled clinical prospective trials to be effective in preventing cardiovascular complications of hypertension. In the ALLHAT trial, the largest hypertensive clinical trial that randomized hypertensive patients to an ACE inhibitor, a calcium channel blocker, or an α-blocker versus a thiazide diuretic, the α-blocker arm of the trial was prematurely terminated because of an almost doubling of the risk of heart failure and a 25% excess cardiovascular death rate among patients treated with an α-blocker compared with a thiazide diuretic. Thus, α-blockers are not recommended as initial antihypertensive agents.

    However, α-blockers may be used as a second- or third-line antihypertensive agent to treat hypertension and may be used because of a compelling and specific reason for the use of an α-blocker to minimize obstructive urinary symptoms in older men with benign prostatic hyperplasia.

14. When are ACE inhibitors specifically recommended in hypertensive patients?

    The JNC 7 report recommends a thiazide as an initial antihypertensive agent in patients with uncomplicated hypertension. Compelling indications for the selection of an ACE inhibitor include heart failure, previous MI, diabetes mellitus, chronic kidney disease, high CAD risk, and for recurrent stroke prevention. These recommendations are based on several randomized, prospective, controlled clinical trials confirming the benefits of ACE inhibitors in preventing cardiovascular or renal complications in these patients. ACE inhibitors prevent myocardial remodeling, heart failure progression, progressive ventricular enlargement after a recent MI, MIs, and stroke in patients with cardiovascular disease, and have also been proven to prevent progression of renal disease among diabetics with established diabetic renal disease.

15. What are the goals for hypertension treatment in African Americans recommended by the International Society of Hypertension in Blacks (ISHIB)?

    African Americans have a significantly higher prevalence of hypertension than any other racial ethnic group in the United States and suffer a much higher risk of hypertensive complications. Unlike the JNC 7 report, the ISHIB Consensus report recommend lower blood pressure goals in African Americans, specifically:

ISHIB also recommended earlier initiation of a two-drug combination at a blood pressure 15/10 mm Hg above goal blood pressure, rather than 20/10 mm Hg above goal (as recommended by the JNC 7 report).

16. What is the prevalence of hypertension among African Americans and Hispanic Americans compared to non-Hispanic whites?

    Hypertension affects about 33% of all adults aged 20 years or older in the United States (according to the NHANES [2005-2008] and the AHA Statistical Update on Cardiovascular Disease and Stroke [2012]). African Americans have a significantly higher prevalence of hypertension, at approximately 44%. This percentage has been rising in the last 20 years, more so than in whites. Hispanics have a lower hypertension prevalence, at approximately 25%.

Bibliography, Suggested Readings, and Websites

1. ACCORD Study Group. Effects of Intensive Blood Pressure Control in Type 2 Diabetics. N Engl J Med. 2010;362:1575–1585.

2. Agency for Healthcare Research and Quality. 2009 National Healthcare Disparities Report, Table 2_1_3.2b. Available at http://www.ahrq.gov/qual/qrdr09/2_diabetes/T2_1_3-2b.htm. Accessed March 20, 2013

3. ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major cardiovascular events in hypertensive patients randomized to doxazosin vs. chlorthalidone: the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA 283. 2000:1967–1975.

4. ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA. 2002;288:2981–2997.

5. Calhoun, D., Jones, D., Textor, D., et al. Resistant hypertension: diagnosis, evaluation, and treatment: a scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research. Hypertension. 2008;51:1403–1419.

6. Chobanian, A.V., Bakris, G.L., Black, H.R., et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289:2560–2572. Erratum, JAMA 290:197, 2003

7. Chobanian, A.V., Bakris, G.L., Black, H.R., et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Available at http://www.nhlbi.nih.gov/guidelines/hypertension/express.pdf. (PDF file). Accessed March 19, 2013

8. Cusham, W.C., Ford, C.E., Cutler, J.A., et al. Success and predictors of blood pressure control in diverse North American settings: the antihypertensive and lipid-lowering treatment to prevent heart attack trial (ALLHAT). J Clin Hypertens (Greenwich). 2002;4:393–404.

9. Cutler, J.A., Davis, B.R. Thiazide-type diuretics and 2-adrenergic blockers as first-line drug treatments for hypertension. Circulation. 2008;117:2691–2705.

10. Flack, J.M., Sica, D.A., Bakris, G., et al. on behalf of the International Society on Hypertension in Blacks: ISHIB consensus statement. Management of high blood pressure in Blacks. An update of the International Society on Hypertension in Blacks Consensus Statement. Hypertension. 2010;56:780–800.

11. Hajjar, I., Kotchen, T.A. Trends in prevalence, awareness, treatment, and control of hypertension in the United States, 1998-2000. JAMA. 2003;290:199–206.

12. Heart Outcomes Prevention Evaluation Study Investigators. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. N Engl J Med. 2000;342:145–153.

13. Kearney, P.M., Whelton, M., Reynolds, K., et al. Worldwide prevalence of hypertension: a systematic review. J Hypertens. 2004;1:11–19.

14. Lloyd-Jones, D.M., Evans, J.C., Larson, M.G., et al. Differential control of systolic and diastolic blood pressure: factors associated with lack of blood pressure control in the community. Hypertension. 2000;36:594–599.

15. ONTARGET Investigators. Telmisartan, ramipril or both in patients at high risk for vascular events. N Engl J Med. 2008;358:1547–1559.

16. Roger, V.L., Go, A.S., Lloyd-Jones, D.M., et al. Heart disease and stroke statistics—2012 update. a report from the American Heart Association. Circulation. 2012;125:e2–e220.

17. Rosendorff, C., Black, H.R., Cannon, C.P., et al. Treatment of hypertension in the prevention and management of ischemic heart disease: a scientific statement from the American Heart Association Council for High Blood Pressure Research and the Councils on Clinical Cardiology and Epidemiology and Prevention. Circulation. 2007;115:2761–2788.

18. Sorlie, P.D., Backlund, E., Johnson, N.J., et al. Mortality by Hispanic status in the United States. JAMA. 1993;270:2464–2468.

19. TRANSCEND Investigators. Effects of the angiotensin-receptor blocker telmisartan on cardiovascular events in high-risk patients intolerant to angiotensin-converting enzyme inhibitors: a randomized controlled trial. Lancet. 2008;372:1174–1183.

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