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Hypertension (Case 7)

Published on 24/06/2015 by admin

Filed under Internal Medicine

Last modified 24/06/2015

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Elie R. Chemaly MD, MSc and Michael Kim MD

Case: A 59-year-old African-American woman is referred by her primary physician. She has had a history of severe hypertension for 38 years. She complains of dizziness, occipital headaches with blurred vision, and palpitations correlated with high BP sometimes reaching 200 mm Hg systolic and 120 mm Hg diastolic. She also has claudication of the legs and thighs upon walking four street blocks. She has a history of thyroid disease and is presently hypothyroid. Her medications on presentation were valsartan/hydrochlorothiazide 320 mg/25 mg (one tablet daily in the morning), clonidine 0.3 mg (one tablet daily in the evening), verapamil SR 240 mg (one tablet twice a day), and levothyroxine 0.1 mg (one tablet daily). Although she takes her medications each day as directed, she confides to you that she is concerned that they are becoming increasingly difficult for her to afford on a limited budget. She has an extensive family history of hypertension, and her father died at the age of 57 years in his sleep. On examination she weighs 68 kg, her pulse is 60 bpm, and her BP is 148/88 mm Hg. Her examination is remarkable for bilateral femoral bruits.

Differential Diagnosis

Speaking Intelligently

The first assessment when approaching the hypertensive patient is to classify the patient based on the following:

1. The arterial BP measurements

2. The acuteness of the problem

3. The status of the patient in terms of antihypertensive therapy

4. The cause of hypertension in the patient: essential vs. secondary. In acute settings, BP elevation may be an appropriate response to stress such as hypoxia, hypercapnia, hypoxemia, or even intracranial hypertension (the Cushing response of hypertension and bradycardia).

PATIENT CARE

Clinical thinking.

• The definition of hypertension is an operational definition, which means that a BP is considered to be in the hypertensive range when it requires treatment to lower it, not just when it is above the number considered to be normal, and such treatment is required when the benefit of therapy outweighs the risk of therapy. This explains the changes in the definition of hypertension over the course of the years, motivated by treatment availability and data on treatment benefit and treatment targets.

• The seventh report of the Joint National Committee (JNC 7), published in 2003, has issued those definitions. 1 Based upon the average of two or more BP readings at each of two or more visits after an initial screen, the following classification is used:

• Normal blood pressure: systolic less than 120 mm Hg and diastolic less than 80 mm Hg

• Prehypertension: systolic 120 to 139 mm Hg or diastolic 80 to 89 mm Hg

• Hypertension:

Stage 1: systolic 140 to 159 mm Hg or diastolic 90 to 99 mm Hg

Stage 2: systolic ≥160 mm Hg or diastolic ≥100 mm Hg

• It is not the same thing to have hypertension and to have a BP that is not normal. The normal BP definition comes from studies recognizing a continuous rise in the risk of hypertension complications starting at a BP over 110/75 mm Hg (mainly cardiovascular morbidity and mortality).

• These definitions apply to adults on no antihypertensive medications and who are not acutely ill. If there is a disparity in category between the systolic and diastolic pressures, the higher value determines the severity of the hypertension. The systolic pressure is the greater predictor of risk in patients over the age of 50 to 60 years. Also, systolic blood pressure (SBP) is measured more reliably than diastolic blood pressure (DBP) and classifies most patients. Isolated systolic hypertension is common in elderly patients; younger hypertensive patients tend to have elevations of both SBP and DBP. An isolated elevation of the DBP is much less common.

• I need to know if the patient, especially in the acute setting, is presenting with malignant hypertension, hypertensive emergency, or hypertensive urgency.

• If the patient is already receiving antihypertensive therapy, the diagnosis of hypertension is made. I need to assess the particular therapeutic goal for the BP of this patient, since BP treatment goals vary from patient to patient (see JNC 7 report 1 ) and the appropriateness of the treatment.

• The decision to search for a secondary cause of hypertension and/or poor BP control is made on a case-by-case basis.

The history should search for precipitating or aggravating factors as well as an identifiable cause (secondary hypertension), establish the course of the disease, assess the extent of target organ damage, and look for other risk factors for cardiovascular disease.

• Duration and course of the disease

• Prior treatment, response, tolerance, and compliance. Noncompliance with treatment is an important cause of poor BP control.

• Medications, diet, and social history: Drugs that may aggravate or cause hypertension include sympathomimetics, steroids, NSAIDs, and estrogens; psychiatric medications causing a serotonin syndrome; cocaine and alcohol abuse. Withdrawal syndromes and rebound effects also need to be considered: alcohol, benzodiazepines, β-blockers, and clonidine.

• Family history

• Comorbidities, especially diabetes; diseases that can be secondary causes of hypertension (e.g., kidney disease); other cardiovascular risk factors (e.g., tobacco).

• Symptoms of sleep apnea: early-morning headaches, daytime somnolence, snoring, erratic sleep.

• Symptoms of severe hypertension, end-organ damage, or volume overload: epistaxis, headache, visual disturbances, neurologic deficits, dyspnea, chest pain, syncope, claudication.

• Symptoms suggestive of a secondary cause: headaches, sweating, tremor, tachycardia/palpitations, muscle weakness, and skin symptoms.

Physical Examination

• Proper measurement of BP: Away from stressors, with an appropriate cuff size, use Korotkoff phase V for auscultatory DBP. Korotkoff phase V is when the sounds disappear; one can use phase IV when they muffle if they do not disappear until a BP of 0 mm Hg. SBP, measured by auscultation, can and should also be measured through the radial pulse: when the cuff is inflated above the SBP, the radial pulse disappears. This maneuver allows the assessment of auscultatory gap (a stiff artery that does not oscillate and leads to an auscultatory underestimation of SBP) and pseudo-hypertension (a stiff artery not compressed by the cuff; SBP is overestimated). In selected settings, BP should be measured in both arms (especially in the younger patient to assess for coarctation of the aorta). Measurements should be repeated at different visits, unless BP is markedly elevated, before treatment.

• Vital signs , in particular heart rate in relationship to BP and treatments already taken. It may be important, especially in the acute setting, to know if the patient is febrile or hypoxic. Mental status is an important vital sign in the acute setting (hypertensive emergencies and urgencies).

• General appearance: body fat, skin (cutaneous manifestations of endocrinopathies causing secondary hypertension).

• Funduscopic examination to evaluate retinal complications.

• Thyroid examination.

• Cardiac auscultation (for murmurs and abnormal sounds: An S 4 gallop may indicate the stiff left ventricle of hypertensive heart disease).

• Vascular auscultation (carotid bruits, renal bruits, pulses): to assess atherosclerotic status and the presence of renal artery stenosis; the relationship between carotid artery disease, its treatment, and hypertension is not well understood.

• Abdominal examination , especially of the aorta and the kidneys.

• Neurologic examination , if applicable.

Tests for Consideration

IMAGING CONSIDERATIONS

Article Contents

Clinical management and treatment decisions, hypertension in black americans, pharmacologic treatment of hypertension in black americans.

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Supplementary Data

Suzanne Oparil, Case study, American Journal of Hypertension , Volume 11, Issue S8, November 1998, Pages 192S–194S, https://doi.org/10.1016/S0895-7061(98)00195-2

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Ms. C is a 42-year-old black American woman with a 7-year history of hypertension first diagnosed during her last pregnancy. Her family history is positive for hypertension, with her mother dying at 56 years of age from hypertension-related cardiovascular disease (CVD). In addition, both her maternal and paternal grandparents had CVD.

At physician visit one, Ms. C presented with complaints of headache and general weakness. She reported that she has been taking many medications for her hypertension in the past, but stopped taking them because of the side effects. She could not recall the names of the medications. Currently she is taking 100 mg/day atenolol and 12.5 mg/day hydrochlorothiazide (HCTZ), which she admits to taking irregularly because “... they bother me, and I forget to renew my prescription.” Despite this antihypertensive regimen, her blood pressure remains elevated, ranging from 150 to 155/110 to 114 mm Hg. In addition, Ms. C admits that she has found it difficult to exercise, stop smoking, and change her eating habits. Findings from a complete history and physical assessment are unremarkable except for the presence of moderate obesity (5 ft 6 in., 150 lbs), minimal retinopathy, and a 25-year history of smoking approximately one pack of cigarettes per day. Initial laboratory data revealed serum sodium 138 mEq/L (135 to 147 mEq/L); potassium 3.4 mEq/L (3.5 to 5 mEq/L); blood urea nitrogen (BUN) 19 mg/dL (10 to 20 mg/dL); creatinine 0.9 mg/dL (0.35 to 0.93 mg/dL); calcium 9.8 mg/dL (8.8 to 10 mg/dL); total cholesterol 268 mg/dL (< 245 mg/dL); triglycerides 230 mg/dL (< 160 mg/dL); and fasting glucose 105 mg/dL (70 to 110 mg/dL). The patient refused a 24-h urine test.

Taking into account the past history of compliance irregularities and the need to take immediate action to lower this patient’s blood pressure, Ms. C’s pharmacologic regimen was changed to a trial of the angiotensin-converting enzyme (ACE) inhibitor enalapril, 5 mg/day; her HCTZ was discontinued. In addition, recommendations for smoking cessation, weight reduction, and diet modification were reviewed as recommended by the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI). 1

After a 3-month trial of this treatment plan with escalation of the enalapril dose to 20 mg/day, the patient’s blood pressure remained uncontrolled. The patient’s medical status was reviewed, without notation of significant changes, and her antihypertensive therapy was modified. The ACE inhibitor was discontinued, and the patient was started on the angiotensin-II receptor blocker (ARB) losartan, 50 mg/day.

After 2 months of therapy with the ARB the patient experienced a modest, yet encouraging, reduction in blood pressure (140/100 mm Hg). Serum electrolyte laboratory values were within normal limits, and the physical assessment remained unchanged. The treatment plan was to continue the ARB and reevaluate the patient in 1 month. At that time, if blood pressure control remained marginal, low-dose HCTZ (12.5 mg/day) was to be added to the regimen.

Hypertension remains a significant health problem in the United States (US) despite recent advances in antihypertensive therapy. The role of hypertension as a risk factor for cardiovascular morbidity and mortality is well established. 2–7 The age-adjusted prevalence of hypertension in non-Hispanic black Americans is approximately 40% higher than in non-Hispanic whites. 8 Black Americans have an earlier onset of hypertension and greater incidence of stage 3 hypertension than whites, thereby raising the risk for hypertension-related target organ damage. 1 , 8 For example, hypertensive black Americans have a 320% greater incidence of hypertension-related end-stage renal disease (ESRD), 80% higher stroke mortality rate, and 50% higher CVD mortality rate, compared with that of the general population. 1 , 9 In addition, aging is associated with increases in the prevalence and severity of hypertension. 8

Research findings suggest that risk factors for coronary heart disease (CHD) and stroke, particularly the role of blood pressure, may be different for black American and white individuals. 10–12 Some studies indicate that effective treatment of hypertension in black Americans results in a decrease in the incidence of CVD to a level that is similar to that of nonblack American hypertensives. 13 , 14

Data also reveal differences between black American and white individuals in responsiveness to antihypertensive therapy. For instance, studies have shown that diuretics 15 , 16 and the calcium channel blocker diltiazem 16 , 17 are effective in lowering blood pressure in black American patients, whereas β-adrenergic receptor blockers and ACE inhibitors appear less effective. 15 , 16 In addition, recent studies indicate that ARB may also be effective in this patient population.

Angiotensin-II receptor blockers are a relatively new class of agents that are approved for the treatment of hypertension. Currently, four ARB have been approved by the US Food and Drug Administration (FDA): eprosartan, irbesartan, losartan, and valsartan. Recently, a 528-patient, 26-week study compared the efficacy of eprosartan (200 to 300 mg/twice daily) versus enalapril (5 to 20 mg/daily) in patients with essential hypertension (baseline sitting diastolic blood pressure [DBP] 95 to 114 mm Hg). After 3 to 5 weeks of placebo, patients were randomized to receive either eprosartan or enalapril. After 12 weeks of therapy within the titration phase, patients were supplemented with HCTZ as needed. In a prospectively defined subset analysis, black American patients in the eprosartan group (n = 21) achieved comparable reductions in DBP (−13.3 mm Hg with eprosartan; −12.4 mm Hg with enalapril) and greater reductions in systolic blood pressure (SBP) (−23.1 with eprosartan; −13.2 with enalapril), compared with black American patients in the enalapril group (n = 19) ( Fig. 1 ). 18 Additional trials enrolling more patients are clearly necessary, but this early experience with an ARB in black American patients is encouraging.

Efficacy of the angiotensin II receptor blocker eprosartan in black American with mild to moderate hypertension (baseline sitting DBP 95 to 114 mm Hg) in a 26-week study. Eprosartan, 200 to 300 mg twice daily (n = 21, solid bar), enalapril 5 to 20 mg daily (n = 19, diagonal bar). †10 of 21 eprosartan patients and seven of 19 enalapril patients also received HCTZ. Adapted from data in Levine: Subgroup analysis of black hypertensive patients treated with eprosartan or enalapril: results of a 26-week study, in Programs and abstracts from the 1st International Symposium on Angiotensin-II Antagonism, September 28–October 1, 1997, London, UK.

Approximately 30% of all deaths in hypertensive black American men and 20% of all deaths in hypertensive black American women are attributable to high blood pressure. Black Americans develop high blood pressure at an earlier age, and hypertension is more severe in every decade of life, compared with whites. As a result, black Americans have a 1.3 times greater rate of nonfatal stroke, a 1.8 times greater rate of fatal stroke, a 1.5 times greater rate of heart disease deaths, and a 5 times greater rate of ESRD when compared with whites. 19 Therefore, there is a need for aggressive antihypertensive treatment in this group. Newer, better tolerated antihypertensive drugs, which have the advantages of fewer adverse effects combined with greater antihypertensive efficacy, may be of great benefit to this patient population.

1. Joint National Committee : The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure . Arch Intern Med 1997 ; 24 157 : 2413 – 2446 .

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3. Veterans Administration Cooperative Study Group on Antihypertensive Agents : Effects of treatment on morbidity in hypertension: II. Results in patients with diastolic blood pressures averaging 90 through 114 mm Hg . JAMA 1970 ; 213 : 1143 – 1152 .

4. Pooling Project Research Group : Relationship of blood pressure, serum cholesterol, smoking habit, relative weight and ECG abnormalities to the incidence of major coronary events: Final report of the pooling project . J Chronic Dis 1978 ; 31 : 201 – 306 .

5. Hypertension Detection and Follow-Up Program Cooperative Group : Five-year findings of the hypertension detection and follow-up program: I. Reduction in mortality of persons with high blood pressure, including mild hypertension . JAMA 1979 ; 242 : 2562 – 2577 .

6. Kannel WB , Dawber TR , McGee DL : Perspectives on systolic hypertension: The Framingham Study . Circulation 1980 ; 61 : 1179 – 1182 .

7. Hypertension Detection and Follow-Up Program Cooperative Group : The effect of treatment on mortality in “mild” hypertension: Results of the Hypertension Detection and Follow-Up Program . N Engl J Med 1982 ; 307 : 976 – 980 .

8. Burt VL , Whelton P , Roccella EJ et al. : Prevalence of hypertension in the US adult population: Results from the third National Health and Nutrition Examination Survey, 1988–1991 . Hypertension 1995 ; 25 : 305 – 313 .

9. Klag MJ , Whelton PK , Randall BL et al. : End-stage renal disease in African-American and white men: 16-year MRFIT findings . JAMA 1997 ; 277 : 1293 – 1298 .

10. Neaton JD , Kuller LH , Wentworth D et al. : Total and cardiovascular mortality in relation to cigarette smoking, serum cholesterol concentration, and diastolic blood pressure among black and white males followed up for five years . Am Heart J 1984 ; 3 : 759 – 769 .

11. Gillum RF , Grant CT : Coronary heart disease in black populations II: Risk factors . Heart J 1982 ; 104 : 852 – 864 .

12. M’Buyamba-Kabangu JR , Amery A , Lijnen P : Differences between black and white persons in blood pressure and related biological variables . J Hum Hypertens 1994 ; 8 : 163 – 170 .

13. Hypertension Detection and Follow-up Program Cooperative Group : Five-year findings of the Hypertension Detection and Follow-up Program: mortality by race-sex and blood pressure level: a further analysis . J Community Health 1984 ; 9 : 314 – 327 .

14. Ooi WL , Budner NS , Cohen H et al. : Impact of race on treatment response and cardiovascular disease among hypertensives . Hypertension 1989 ; 14 : 227 – 234 .

15. Weinberger MH : Racial differences in antihypertensive therapy: evidence and implications . Cardiovasc Drugs Ther 1990 ; 4 ( suppl 2 ): 379 – 392 .

16. Materson BJ , Reda DJ , Cushman WC et al. : Single-drug therapy for hypertension in men: A comparison of six antihypertensive agents with placebo . N Engl J Med 1993 ; 328 : 914 – 921 .

17. Materson BJ , Reda DJ , Cushman WC for the Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents : Department of Veterans Affairs single-drug therapy of hypertension study: Revised figures and new data . Am J Hypertens 1995 ; 8 : 189 – 192 .

18. Levine B : Subgroup analysis of black hypertensive patients treated with eprosartan or enalapril: results of a 26-week study , in Programs and abstracts from the first International Symposium on Angiotensin-II Antagonism , September 28 – October 1 , 1997 , London, UK .

19. American Heart Association: 1997 Heart and Stroke Statistical Update . American Heart Association , Dallas , 1997 .

hypertension
blood pressure
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