When your patient’s blood pressure won’t come down

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Applied Evidence

When your patient’s blood pressure won’t come down

J Fam Pract. 2009 December;58(12):640-645

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References

1. Chobanian A, 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). Hypertension. 2003;42:1206-1252.

2. Fields L, Burt V, Cutler J, et al. The burden of adult hypertension in the United States 1999-2000: A rising tide. Hypertension. 2004;44:1-7.

3. Fang J, Alderman MH, Keenan NL, et al. Hypertension control at physicians’ offices in the United States. Am J Hypertens. 2008;21:136-142.

4. American Heart Association Statistics Committee and Stroke Statistics Subcommittee Heart disease and stroke statistics–2007 update. Circulation. 2007;115:e69-e171.

5. Sarafidis PA, Bakris GL. Resistant hypertension: an overview of evaluation and treatment. J Am Coll Cardiol. 2008;52:1749-1757.

6. Calhoun DA, Jones D, Textor S, 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.

7. Phillips LS, Branch WT, Book CB, et al. Clinical inertia. Ann Intern Med. 2001;135:825-834.

8. Van Wijk BL, Klungel OH, Heerdink ER, et al. Rate and determinants of 10-year persistence with antihypertensive drugs. J Hypertens. 2005;23:2101-2107.

9. Wexler R, Pleister A, Feldman D. Sociology meets genetics: sociogenetic implications for future management of hypertension and heart failure. Curr Treat Options Cardiovasc Med. 2009;11:305-315.

10. Ogedegbe G, Pickering TG, Clemow L, et al. The misdiagnosis of hypertension: the role of patient anxiety. Arch Intern Med. 2008;168:2459-2465.

11. Dawes MG, Bartlett G, Coats AJ, et al. Comparing the effects of white coat hypertension and sustained hypertension on mortality in a UK primary care setting. Ann Fam Med. 2008;6:390-396.

12. Pierdomenico SD, Lapenna D, Bucci A, et al. Cardiovascular outcome in treated hypertensive patients with responder, masked, false resistant, and true resistant hypertension. Am J Hypertens. 2005;18:1422-1428.

13. Verberk WJ, Kroon AA, Kessels AGH, et al. Home blood pressure monitoring: a systematic review. J Am Coll Cardiol. 2005;46:743-751.

14. Pickering TG, Miller NH, Ogedegbe G, et al. AHA/ASH/PCNA scientific statement. Call to action on use and reimbursement for home blood pressure monitoring. Hypertension. 2008;52:10-29.

15. O’Brien E. Ambulatory blood pressure measurement: the case for implementation in primary care. Hypertension. 2008;51:1435-1441.

16. O’Brien E, Asmar R, Beilin L, et al. On behalf of the European Society of Hypertension Working Group on Blood Pressure Monitoring. European Society of Hypertension recommendations for conventional ambulatory and home blood pressure measurements. J Hypertens. 2003;21:821-848.

17. Mourad A, Carney S, Gillies A, et al. Arm position and blood pressure: a risk factor for hypertension. J Hum Hypertens. 2003;17:389-395.

18. Myers MG. Automated blood pressure measurement in routine clinical practice. Blood Press Monit. 2006;11:59-62.

19. Myers MG, Valdivieso M, Kiss A. Use of automated office blood pressure measurement to reduce white coat hypertension. J Hypertens. 2009;27:280-286.

20. He J, Paul J, Whelton P, Appel L, et al. Long-term effects of weight loss and dietary sodium reduction on incidence of hypertension. Hypertension. 2000;35:544-549.

21. PREMIER Collaborative Research Writing Group. Effects of comprehensive lifestyle modification on blood pressure control. JAMA. 2003;289:2083-2093.

22. Cook NR, Cutler JA, Obarzanek E, et al. Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP). BMJ. 2007;334:885-888.

23. Dickinson BD, Havas S. Reducing the population burden of cardiovascular disease by reducing sodium intake. Arch Intern Med. 2007;167:1460-1468.

24. Li J, White J, Guo L, et al. Salt inactivates endothelial nitric oxide synthase in endothelial cells. J Nutr. 2009;139:1-5.

25. Beevers G, Lip G, O’Brien E. ABCs of hypertension: the pathophysiology of hypertension. BMJ. 2001;322:912-916.

26. Peppard PE, Young T, Palta M, et al. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med. 2000;342:1378-1384.

27. Sowers JR, Whaley-Connell A, Epstein M. Narrative review: the emerging clinical implications of the role of aldosterone in the metabolic syndrome and resistant hypertension. Ann Intern Med. 2009;150:776-783.

28. Young T, Peppard P, Palta M, et al. Population-based study of sleep-disordered breathing as a risk factor for hypertension. Arch Intern Med. 1997;157:1746-1752.

29. Haentjens P, Van Meerhaeghe A, Moscariello A. The impact of continuous positive airway pressure on blood pressure in patients with obstructive sleep apnea syndrome: evidence from a meta-analysis of placebo-controlled randomized trials. Arch Intern Med. 2007;167:757-764.

30. Kawashima A, Francis IR, Baumgarten DA, et al. For the Expert Panel on Urologic Imaging. Renovascular hypertension. Reston, Va: American College of Radiology; 2007. Available at: www.guideline.gov/summary/summary.aspx?ss=15&doc_id=11590&nbr=6003. Accessed April 4, 2009.

TABLE
Medications and other agents that may cause hypertension

• Alcohol	• Cyclosporine	• Nicotine
• Antidepressants	• Erythropoietin	• NSAIDs
• Buspirone (Buspar)	• Estrogen preparations	• St. John’s wort
• Cocaine	• Licorice	• Tyramine-containing foods
• Corticosteroids	• Metoclopramide (Reglan)
NSAIDs, nonsteroidal anti-infiammatory drugs.
Source: Chobanian A, et al. Hypertension. 2003.¹

Is it resistant hypertension? Look for clues

FAST TRACK

Only about 5% of cases of hypertension can be attributed to secondary causes.

You go over Ms. Stevens’ history carefully. Her hypertension medications should be adequate, and she is compliant with the prescribed regimen. Lifestyle factors are clearly not to blame: She’s not obese, she follows a low-sodium diet, doesn’t drink or smoke, and gets plenty of exercise. You ask her about other medications or over-the-counter supplements she takes, and nothing on her list raises a red flag. This doesn’t seem to be pseudo-resistance, and though you’re aware that only about 5% of cases of hypertension can be attributed to secondary causes, you think Ms. Stevens may be one of those patients.²⁵

Numerous causes of secondary hypertension exist, and evaluations for such causes should be considered in all patients with resistant hypertension. Renal artery stenosis and pheochromocytoma are the most well-known causes, but less well known but significant contributors are obstructive sleep apnea and hyperaldosteronism.^1,6,26,27

The relationship between obstructive sleep apnea and hypertension is not clear, and most of the studies linking the 2 conditions are population based.²⁸ Nevertheless, because studies show that continuous positive airway pressure (CPAP) does improve blood pressure control in patients with obstructive sleep apnea, it is appropriate to investigate patients with resistant hypertension for this condition.²⁹

Aldosterone’s role in resistant hypertension appears to be greatest in those with insulin resistance. The mechanism appears to be amplified sodium retention resulting in increased volume expansion, negative effects on oxidative stress, and elevated inflammation.²⁷ Many patients with hypertension also have insulin resistance, so testing for hyperaldosteronism should be part of your investigation.

Test, and as necessary, test some more

Taking into consideration that 2 of the more common causes of secondary hypertension are obstructive sleep apnea and renal artery stenosis, you schedule an overnight sleep study for Ms. Stevens and a magnetic resonance arteriogram of the kidneys.^26,30 (For more on the diagnostic tests and treatments for secondary causes of resistant hypertension, see the ALGORITHM.)

Reconsider medications. Ms. Stevens is already receiving the maximum dose of amlodipine, so you increase her metoprolol succinate to 200 mg daily and ask her to return in 1 month after the results of her tests come in.

Change medications and keep testing. At her next visit, Ms. Stevens’ blood pressure is 150/88 mm Hg, and her pulse rate is 64. Results of her overnight sleep study and magnetic resonance arteriogram are normal. At this juncture, with her work-up for common secondary causes of hypertension negative, you consider changes in her medication regimen. Because her pulse rate of 64 rules out any increase in the metoprolol, you decide to add lisinopril-HCTZ 10/12.5 mg to her regimen and discontinue her triamterene-HCTZ. Because her blood pressure is still elevated at this visit, you schedule additional testing to look for other secondary causes.

More tests, higher doses. One month later, Ms. Stevens returns with a blood pressure of 146/88 mm Hg. Appropriate testing for primary aldosteronism, pheochromocytoma, Cushing’s disease, and coarctation are all normal. Her lisinopril-HCTZ dose is increased to 20/12.5 mg, and when she returns 1 month later her blood pressure reading is 138/88 mm Hg.

You conclude that she is a patient with hard-to-control hypertension with no underlying cause who requires a significant amount of medication. That is not an uncommon situation. Although her blood pressure is now controlled to an appropriate level, you make a chart notation to consider referral to a hypertension specialist if her blood pressure become elevated again and treatment changes are not effective.⁶

ALGORITHM
Hard-to-control hypertension? This treatment algorithm can help

ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; CPAP, continuous positive airway pressure; CT, computed tomography; GFR, glomerular filtration rate; TSH, thyroid-stimulating hormone.
Adapted from: Calhoun DA, et al. Hypertension. 2008.⁶

Another consideration: Pseudohypertension

This uncommon condition sometimes occurs in elderly patients who suffer from a stiffened or thickened brachial artery.¹ Because the blood pressure cuff cannot compress the artery, blood pressure readings overestimate true arterial pressure. The condition should be considered in patients when increased doses of medication fail to achieve the desired response, particularly in patients who exhibit postural hypotension.¹

This was not a likely explanation for Ms. Stevens, however, given the clinical scenario and her young age.

CORRESPONDENCE Randy Wexler, MD, MPH, B0902B Cramblett Hall, 456 W 10th Avenue, Columbus, OH 43210; randy.wexler@osumc.edu