Hypertension is a multisystem disease whose hallmark is the elevation of blood pressure. Primary hypertension has no apparent cause, constitutes the majority of cases, and is treated with measures to reduce blood pressure. Secondary hypertension does have an abnormality that is causing the elevation in blood pressure, such as a tumor that secretes hormones that raise blood pressure; removing the cause may be curative. Primary hypertension is generally not curable and needs to be managed as a chronic disease.
"Evaluate or refer to source of care within 1 month. For those with higher pressures (e.g., >180/110 mmHg), evaluate and treat immediately or within 1 week depending on clinical situation and complications... 2 drug combination for most."
If the diastolic pressure is below 110 mm Hg, it should be confirmed on two addition visits as some patients will have a lower blood pressure on repeat measurements.[9] A larger cuff should be used for obese patients.[10]
White coat hypertension is a temporary increase in the blood pressure caused by being examined by a medical professional in a clinical environment. If the only measurements being taken are in medical offices, white coat hypertension may cause the appearance of sustained hypertension.[11]
White coast hypertension may not be as important to treat.[12]
Elderly patients may have pseudohypertension due to inability of the blood pressure cuff to compress stiff arteries.[13] Pseudohypertension may be detected by Osler's maneuver.[13]
Since secondary hypertension may be curable, ruling it out is essential. A starting point is listening for an abdominal bruit, especially if it is both systolic and diastolic, may help detect underlying renal artery stenosis.[16]
Among patients with resistant hypertension (blood pressure >140/90 mm Hg despite a three drug regimen, 20% of patients had serum aldosterone and plasma renin activity ratio of more than 65:16 with a aldosterone concentration above 416 pmol/L. However, only 10% of all patients had primary aldosteronism. Half of these patients have a normal serum potassium.[17]
The European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC) 2007 guidelines add to diabetes and chronic kidney disease that tight control (<130/80 mmHg) is needed for patients with:[18]
An industry-sponsored, unblinded randomized controlled trial suggests benefit from treating any patient with a cardiac risk to a goal systolic pressure of 130 mm Hg.[30] The HOPE trial reported similar results.[31] Although 39% of HOPE patients had diabetes, the benefit occurred in patients with and without diabetes.
Overly aggressive treatment of hypertension may be harmful due to the "j-curve" effect.[32][33] It is not clear if this is due to excessive reduction in systolic pressure[34] or low diastolic pressure after treatment[33] or due to general bad health rather than treatment[35].
"Thiazide-type diuretics for most" patients are recommended by the JNC7 clinical practice guidelines.[1]Chlorthalidone may be the best choice based on the Multiple Risk Factor Intervention Trial[37] and other studies.[38][39][40] In the MRFIT trial, the clinics that predominantly used chlorthalidone reported lower mortality than the clinics using hydrochlorothiazide (5% versus 7%).
"First-line low-dose thiazides reduce all morbidity and mortality outcomes. First-line ACE inhibitors and calcium channel blockers may be similarly effective but the evidence is less robust. First-line high-dose thiazides and first-line beta-blockers are inferior to first-line low-dose thiazides" according to the Cochrane Collaboration.[41]
ß-blockers are the preferred initial medication for patients with coronary heart disease according to a systematic review.[42]
"ß-blockers, especially in combination with a thiazide diuretic, should not be used in patients with the metabolic syndrome or at high risk of incident diabetes" is noted by the European ESH/ESC clinical practice guidelines.[18] The ESH/ESC guidelines cite the LIFE[27] and ASCOT[43] trials. Unlike the ALLHAT study[44], both of these trials were in largely anglo populations, supported by industry, and at the same institution. All patients in the LIFE trial had left ventricular hypertrophy (LVH). Based on these two trials, a meta-analysis has concluded that beta blockers should not be the first choice treatment.[45]
For Stage 2 Hypertension (SBP ≥ 160 or DBP≥100) consider starting two medications for more effect.[46][1]
Several randomized controlled trials have compared initial medications for hypertension. As summarized in the table, the disparate results may be due to racial and gender differences in responses to medications.[24][47][49][25][48]
* Obesity and female[50] are also associated with low renin.
Some authors have proposed that either the renin level or the renin level indexed to urinary sodium excretion in 24 hours.[51][52]
Efficacy of different drugs. From Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents.[25]
However, the Veterans Affairs Cooperative trial suggests the initial drug may be better selected based on the patient's age, race, and gender.[25][26] The patient's demographic roughly corresponds with their renin profile, but is more predictive than the renin profile.[26] The molecular basis is being determined.[53] In the Veterans Affairs Cooperative, among the high renin demographic (young whites), diuretics had similar efficacy to placebo; whereas in the low renin demographic (older blacks), the ace-inhibitors had similar efficacy to placebo in the Veterans Affairs Cooperative Study Group on Antihypertensive Agents (see figure).[25] Similarly, a meta-analysis has concluded that beta-blockers are a good first choice for younger patients, but not for older patients.[54]
More recently, plasma renin activity was found to predict response to adrenergic beta-antagonists versus diuretics better than using demographic predictors.[55]
Race, gender, and age demographic may partly predict frequency of drug toxicity to different anti-hypertensive medications.[56]
There are contraindications to each of the four major classes, even when other indicators suggest a particular class might be best for the hypertensive patients:
While labile hypertension may be due to a pheochromocytoma, it may be due to baroreflex failure. This can be treated with clonidine 0.3 to 2.4 mg orally total per day.[57]
The AHA defines resistant hypertension as "blood pressure that remains above goal in spite of the concurrent use of 3 antihypertensive agents of different classes."
First, 'pseudoresistance' should be considered:[61]
A low sodium (50 mmol or 1150 mg of sodium) diet may help.[71]
The AHA recommends that one of the three medicines use for hypertension should be a diuretic.[61]
"Three drugs at half standard dose in combination" may be better than one drug at standard dose according to a systematic review.[42]
In an unblinded, uncontrolled extension of the ASCOT randomized controlled trial, spironolactone 25-50 mg per day as a fourth medication reduced the blood pressure by 21.9/9.5. This result was not affected by whether one of the first three medications included a diuretic.[72] A second study study, also uncontrolled, corroborated the role of spironolactone.[73] In this study, 54% of patients were African-American, 45% had primary hyperaldosteronism.
Treatment must be from a critical care perspective. While the blood pressure must be lowered quickly to avoid end-stage organ failure or crises such as cerebral hemorrhage, lowering it too quickly may create a different end-stage organ failure through decreased perfusion. "Treat the patient, not the number".
Treatment of hypertension in the geriatrics is effective.[20]
However, treatment of patients over age 80 is not clear.[20][34] A randomized controlled trial included in this meta-analysis found that treating patients aged 80 years or older for two years who have a systolic pressure over 160 mm hg (the average entry pressure was 173/91 mm Hg) and treating to 150/80 mm Hg reduced morbidity.[77] In this trial, the average seated blood pressure at the end of the study in the treatment group was 143/78.
The Cochrane Collaboration has also performed a meta-analysis of this topic and concluded "treating healthy persons (60 years or older) with moderate to severe systolic and/or diastolic hypertension reduces all cause mortality and cardiovascular morbidity and mortality. The decrease in all cause mortality was limited to persons 60 to 80 years of age."[20]
↑Reeves RA (1995). "The rational clinical examination. Does this patient have hypertension? How to measure blood pressure". JAMA273 (15): 1211–8. PMID 7707630. [e]
↑ (July 1985) "MRC trial of treatment of mild hypertension: principal results. Medical Research Council Working Party". British medical journal (Clinical research ed.)291 (6488): 97–104. PMID 2861880. PMC 1416260. [e]
↑ (January 1997) "Five-year findings of the hypertension detection and follow-up program. I. Reduction in mortality of persons with high blood pressure, including mild hypertension. Hypertension Detection and Follow-up Program Cooperative Group. 1979". JAMA : the journal of the American Medical Association277 (2): 157–66. PMID 8990344. [e]
↑Neaton JD, Grimm RH, Prineas RJ, et al (August 1993). "Treatment of Mild Hypertension Study. Final results. Treatment of Mild Hypertension Study Research Group". JAMA : the journal of the American Medical Association270 (6): 713–24. PMID 8336373. [e]
↑ 25.025.125.225.325.4Materson BJ, Reda DJ (1994). "Correction: single-drug therapy for hypertension in men". N. Engl. J. Med.330 (23): 1689. PMID 8177286. [e]
↑ 26.026.126.2Preston RA, Materson BJ, Reda DJ, et al (1998). "Age-race subgroup compared with renin profile as predictors of blood pressure response to antihypertensive therapy. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents". JAMA280 (13): 1168–72. PMID 9777817. [e]
↑ (November 1990) "Mortality after 10 1/2 years for hypertensive participants in the Multiple Risk Factor Intervention Trial". Circulation82 (5): 1616–28. PMID 2225366. [e]
↑ 47.047.1Wing LM, Reid CM, Ryan P, et al (2003). "A comparison of outcomes with angiotensin-converting--enzyme inhibitors and diuretics for hypertension in the elderly". N. Engl. J. Med.348 (7): 583-92. DOI:10.1056/NEJMoa021716. PMID 12584366. Research Blogging.
↑Laragh JH, Baer L, Brunner HR, Buhler FR, Sealey JE, Vaughan ED (1972). "Renin, angiotensin and aldosterone system in pathogenesis and management of hypertensive vascular disease.". Am J Med52 (5): 633-52. PMID 4337477. [e]
↑McDowell SE, Coleman JJ, Ferner RE (2006). "Systematic review and meta-analysis of ethnic differences in risks of adverse reactions to drugs used in cardiovascular medicine". BMJ332 (7551): 1177–81. DOI:10.1136/bmj.38803.528113.55. PMID 16679330. Research Blogging.
↑ 61.061.161.261.3Calhoun, D. A., Jones, D., Textor, S., Goff, D. C., Murphy, T. P., Toto, R. D., et al. (2008). 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, HYPERTENSIONAHA.108.189141. DOI:10.1161/HYPERTENSIONAHA.108.189141.
↑Ferrannini E, Buzzigoli G, Bonadonna R, et al (August 1987). "Insulin resistance in essential hypertension". N. Engl. J. Med.317 (6): 350–7. PMID 3299096. [e]
↑Mejia AD, Egan BM, Schork NJ, Zweifler AJ (February 1990). "Artefacts in measurement of blood pressure and lack of target organ involvement in the assessment of patients with treatment-resistant hypertension". Ann. Intern. Med.112 (4): 270–7. PMID 2297205. [e]
↑Isaksson H, Danielsson M, Rosenhamer G, Konarski-Svensson JC, Ostergren J (May 1991). "Characteristics of patients resistant to antihypertensive drug therapy". J. Intern. Med.229 (5): 421–6. PMID 2040868. [e]
↑ Beckett, N. S., Peters, R., Fletcher, A. E., Staessen, J. A., Liu, L., Dumitrascu, D., et al. (2008). Treatment of Hypertension in Patients 80 Years of Age or Older. N Engl J Med, NEJMoa0801369. DOI:10.1056/NEJMoa0801369