Cardiovascular

Hypertension

BY: PHYSICIANS COMMITTEE FOR RESPONSIBLE MEDICINE

Overview and Risk Factors

Hypertension is a major risk factor for cardiovascular disease, including coronary heart disease and stroke, as well as for end-stage renal disease and peripheral vascular disease. The World Health Organization has identified hypertension as the most important preventable cause of premature death in developed countries.1 Hypertension, obesity, insulin resistance, and lipid abnormalities (hypertriglyceridemia and low HDL-cholesterol levels) make up the metabolic syndrome, a particularly virulent risk profile for cardiovascular disease.

About 65 million people in the United States have hypertension. However, because it is typically asymptomatic, affected individuals often do not know they have the condition. In fact, one third of hypertensive persons are unaware of their disease, and only about half of those who are aware achieve adequate blood pressure control.2

The vast majority of cases are primary or "essential" (ie, the cause is unknown). Approximately 5% to 10% of cases are due to renal or endocrine disease (eg, renovascular disease, thyroid disease, chronic steroid therapy, Cushing's disease, or pheochromocytoma).

Signs and symptoms, when they do occur, include headache, confusion, vision changes, nausea, vomiting, and fatigue.

Risk Factors

African Americans have a higher prevalence of high blood pressure compared with blacks in Africa and with North American whites; the mechanisms for this increased risk are unknown. The following factors increase the likelihood of developing hypertension:

  • Age. About two thirds of Americans over age 65 have high blood pressure.
  • Family history. Having relatives with cardiovascular disease increases risk.
  • Obesity. The prevalence of hypertension in obese adults is double that of normal-weight individuals.
  • Lack of exercise.
  • Dietary factors (discussed in Nutritional Considerations).
  • Renovascular disease/chronic kidney disease.
  • Adrenal gland abnormalities.
  • Hyperthyroidism.
  • Oral contraceptive use.
  • Pheochromocytoma (rare).
  • Smoking.
  • Medications. For example, corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs), antihistamines, diet pills, and some antidepressants.

Diagnosis and Treatment

Diagnosis

Sustained and untreated high blood pressure may lead to end-organ damage, including left ventricular hypertrophy, congestive heart failure (of which hypertension is the leading cause in developed countries), stroke, retinopathy, and kidney disease. Therefore, it is important that hypertension be diagnosed and treated early.

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure2 defines normal blood pressure as less than 120/80 mm Hg. Prehypertension is defined as a blood pressure between 120/80 and 139/89 mm Hg. This range signals increased risk for progression to hypertension and requires regular monitoring. Further, blood pressure of at least 130/85 mm Hg is a component of the metabolic syndrome.3 Hypertension is defined as an average seated blood pressure measurement of 140/90 mm Hg or greater during 2 or more office visits. Stage 1 hypertension is defined as a systolic blood pressure measurement of 140 to 159 mm Hg and a diastolic measurement of 90 to 99 mm Hg. Stage 2 hypertension is defined as a systolic measurement greater than 160 mm Hg or a diastolic measurement greater than 100 mm Hg.

Hypertensive crisis involves a diastolic pressure greater than 120 to 130 mm Hg.

Hypertensive urgency involves elevated blood pressure without end-organ damage, and hypertensive emergency is characterized by end-organ damage.4

Treatment

Goal blood pressure is less than 140/90 mm Hg, or less than 130/80 mm Hg for patients with uncomplicated diabetes or chronic kidney disease. The target for complicated diabetes is less than 125/75 mm Hg.

Prehypertension usually does not require drug therapy unless the patient is at high risk for a cardiac event. High-risk patients include those with coronary heart disease, diabetes, heart failure, chronic kidney disease, or a history of stroke. Nonetheless, lifestyle interventions should be instituted and the patient should be encouraged to monitor blood pressure at regular intervals.

Lifestyle modifications are an integral initial step in the treatment of hypertension. These may include a low-sodium, low-fat, vegetarian diet, maintenance of appropriate body weight, smoking cessation, reduction in alcohol use, increased physical activity, and possibly stress reduction (eg, through meditation or yoga).

Pharmacologic therapy includes the following:

A thiazide-type diuretic is often prescribed as first-line pharmacotherapy.  Such drugs are relatively inexpensive. Potential adverse effects include hypokalemia and erectile dysfunction.

Other drug classes that can be used in mono- or combination-therapy include the following:

  • Beta-adrenergic receptor blockers serve as optimal treatment post-myocardial infarction. However, they should be avoided in patients with reactive airway disease or second- or third-degree heart block.
  • Calcium channel blockers protect against recurrent myocardial infarction and/or stroke. They may cause pedal edema and/or conduction abnormalities.
  • Angiotensin-converting enzyme (ACE) inhibitors are advantageous in patients with diabetes, diabetic nephropathy, post-myocardial infarction, and heart failure. Side effects include cough and angiodema. They are contraindicated in pregnant women.
  • Angiotensin receptor blockers (ARBs) have similar benefits to ACE inhibitors (patients who suffer side effects of ACE inhibitors, notably cough, are often switched to ARBs).  They are also beneficial for patients with early renal insufficiency.  
  • Alpha-adrenergic blockers are indicated in patients with concomitant benign prostatic hyperplasia, because of their vasodilatory action on both blood vessels and prostatic smooth muscle. This class of drug is associated with a risk of postural hypotension.
  • Arterial vasodilators include specific drugs that have noteworthy side effects: hydralazine may cause lupus syndrome, while minoxidil may cause sodium and water retention and hirsutism.
  • Potassium-sparing diuretics are optimal for patients at risk of hypokalemia. However, close monitoring of potassium levels is required.

Treatment of hypertensive urgencies often involves a combination of oral medications, whereas hypertensive emergencies require hospitalization and IV therapy.

Asymptomatic hypertension with ventricular dysfunction should be treated with ACE inhibitors, ARBs, and/or beta-blockers. Patients who are symptomatic or have end-stage heart disease should also be treated with digoxin, loop diuretics, and/or aldosterone blockers (eg, spironolactone).

Patients with chronic kidney disease also benefit from ACE inhibitors and ARBs, sometimes in combination.

Pregnant women should be given methyldopa, beta-blockers, or vasodilators such as hydralazine.

Individuals with inadequate responses to single-drug treatment will require combination therapy. Most patients require at least two drugs to achieve target blood pressure, and the use of three or more drugs is common.

It may also be noteworthy that people with hypertension have lower melatonin levels than those with normal blood pressure,5 and some fail to experience the normal nocturnal decrease in blood pressure.6 In limited studies, melatonin supplements (2.5 mg at bedtime) lowered nocturnal blood pressure significantly (6 mm Hg and 4 mm Hg for systolic and diastolic, respectively) in men with high blood pressure.7 An assessment of their clinical value awaits further studies.

Nutritional Considerations

Nutritional factors play a large role not only in reducing the risk that hypertension will occur, but also in managing the condition after it has been diagnosed. The Dietary Approaches to Stop Hypertension (DASH) study showed that diets rich in fruits and vegetables and reduced in saturated fat can lower both the risk for high blood pressure and assist with blood pressure control in hypertensive persons.8,9 The DASH study was predicated on the observation that vegetarian diets are associated with markedly reduced risk of hypertension.

Some investigators have carried these observations a step further. Vegetarian and vegan diets reduce blood pressure in both normotensive and hypertensive individuals, and have the potential to reduce or eliminate medication use in some patients.10 The benefits of a vegetarian diet are probably the combined result of several factors, in addition to lower body weight in vegetarians. These include lower saturated fat and cholesterol intakes; greater amounts of potassium, folate, vitamin C, and flavonoids; and, possibly, a greater presence of L-arginine, an amino acid involved in production of nitric oxide, an important vasodilator.

Possible mechanisms underlying these results may include a combination of the following:

Reducing or eliminating meat may influence blood viscosity. Numerous studies have linked beef, veal, lamb, poultry, and animal fat to high blood pressure.11-14 Saturated fat appears to influence blood viscosity.15 A higher proportional intake of fatty acids from polyunsaturated sources (linoleic acid and alpha-linolenic acids), compared with saturated fats, is associated with a lower risk for developing hypertension.16

Vegetables and fruits are rich in potassium, which influences blood pressure. Potassium, from either food or supplements, reduces blood pressure and stroke risk.17 Fruits and vegetables are rich potassium sources. Some evidence also suggests that fruits and vegetables may lower blood pressure by providing antioxidant flavonoids that up-regulate endothelial nitric oxide production,18,19 and suppressing enzymes involved in the generation of superoxide radicals20 that are known to reduce nitric oxide availability.

Sodium intake above physiologic need is related to the development of hypertension.21 Hypertension is rare in societies whose dietary sodium intake is very low.22 A study determined that 9% to 17% of the risk for hypertension in Western countries was attributable to dietary sodium alone.23 The principal sources of sodium are canned foods, snack foods, discretionary use of salt in food preparation or consumption, and dairy products. In their natural state, vegetables, fruits, grains, and legumes are very low in sodium

Additional considerations include:

  • Limiting alcohol. In excess of moderate consumption (1-2 drinks/day), alcohol intake raises the risk for developing hypertension.24 The relationship between moderate alcohol intake and hypertension is complicated, and studies have found a lower risk for hypertension-related mortality in moderate drinkers, even in those with hypertension, compared with persons who rarely or never drink alcohol.25,26
  • Folic acid. The Nurses' Health Study found that women consuming the highest amounts of folate from diet and supplements (> 1000 µg per day) had only one third the risk for developing hypertension than did women consuming less than 200 µg per day.27 One possible explanation is that folate is an important cofactor for nitric oxide synthase and subsequent nitric oxide generation.
  • Vitamin C. Dietary reference intakes (DRI) of vitamin C may not be adequate in persons at risk for hypertension. Studies show that blood pressure rises as vitamin C depletion occurs in humans,28 and higher vitamin C intakes are associated with lower blood pressure.29 However, there do not appear to be any additional blood pressure-lowering effects of vitamin C over an intake of 500 mg per day.30
  • Healthy body weight. The Nurses' Health Study and the Health Professionals Follow-Up Study found a dose-response relationship between weight and risk for hypertension, and this risk included persons in the upper range for "normal" body weight.31 The same diet changes used for blood pressure regulation--diets rich in vegetables and fruits and low in meat, particularly vegetarian diets--also help reduce body weight. See Obesity Chapter.
  • Regular physical activity. Researchers have estimated that physical inactivity contributes 5% to13% of the risk for hypertension.23 Energy expenditure in the form of vigorous activity,32 or even walking and leisure-time physical activity, lowers the risk for developing hypertension.33

Orders

Vegetarian diet, low fat. Foods rich in vitamin C and potassium should be encouraged.

Sodium less than 2 g daily.

See Basic Diet Orders.

Smoking cessation and alcohol restriction, if applicable.

Individualized exercise prescription to increase physical activity, as appropriate. Consultation with physical therapist or exercise physiologist as needed.

What to Tell the Family

Hypertension usually has no symptoms, but can be deadly. It is important for the patient and the family to have their blood pressure checked regularly and to adhere to the prescribed treatment plan. A good-quality home blood pressure monitor makes tracking and treating hypertension much easier.

Hypertension is not treated with medication alone. Dietary and lifestyle changes can help reduce blood pressure and decrease, sometimes even eliminate, the need for medication. The family can support and enhance the patient's adherence to the recommended diet. Because overweight and hypertension sometimes run in families, it is important for the entire family to shift to healthier eating and exercise patterns. Smoking cessation and alcohol restriction should be encouraged.

References

1. Ezzati M, Lopez AD, Rodgers A, Vander Hoorn S, Murray CJ. Selected major risk factors and global and regional burden of disease. Lancet. 2002;360:1347-1360.

2. Chobanian AV, Bakris GL, Black HR, et al.  The 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.

3. International Diabetes Federation. The IDF consensus worldwide definition of the metabolic syndrome. Available at: http://www.idf.org/webdata/docs/IDF_Metasyndrome_definition.pdf. Accessed May 30, 2005.

4. Bales A. Hypertensive crisis. How to tell if it's an emergency or urgency.
Postgrad Med. 1999;105:119-126, 130.

5. Sewerynek E. Melatonin and the cardiovascular system. Neuro Endocrinol Lett. 2002;23(suppl 1):79-83.

6. Jonas M, Garfinkel D, Zisapel N, Laudon M, Grossman E. Impaired nocturnal melatonin secretion in non-dipper hypertensive patients. Blood Press. 2003;12:19-24.

7. Scheer FA, Van Montfrans GA, van Someren EJ, Mairuhu G, Buijs RM. Daily nighttime melatonin reduces blood pressure in male patients with essential hypertension. Hypertension. 2004;43:192-197.

8. Appel LJ, Champagne CM, Harsha DW, Cooper LS, Obarzanek E, Elmer PJ. Effects of comprehensive lifestyle modification on blood pressure control: main results of the PREMIER clinical trial. JAMA. 2003;289:2083-2093.

9. Svetkey LP, Simons-Morton D, Vollmer WM, et al. Effects of dietary patterns on blood pressure: subgroup analysis of the Dietary Approaches to Stop Hypertension (DASH) randomized clinical trial. Arch Intern Med. 1999;159:285-293.

10. Berkow SE, Barnard ND. Blood pressure regulation and vegetarian diets. Nutr Rev.2005;63:1-8.

11. Bener A, Al-Suwaidi J, Al-Jaber K, Al-Marri S, Dagash MH, Elbagi IE. The prevalence of hypertension and its associated risk factors in a newly developed country. Saudi Med J. 2004;25:918-922.

12. Miura K, Greenland P, Stamler J, Liu K, Daviglus ML, Nakagawa H. Relation of vegetable, fruit, and meat intake to 7-year blood pressure change in middle-aged men: the Chicago Western Electric Study. Am J Epidemiol. 2004;159:572-580.

13. Beegom R, Singh RB. Association of higher saturated fat intake with higher risk of hypertension in an urban population of Trivandrum in south India.  Int J Cardiol. 1997;58:63-70.

14. Ascherio A, Hennekens C, Willett WC, et al. Prospective study of nutritional factors, blood pressure, and hypertension among U.S. women. Hypertension. 1996;27:1065-1072.

15. Ernst E, Pietsch L, Matrai A, Eisenberg J. Blood rheology in vegetarians. Br J Nutr. 1986;56:555-560.

16. Djousse L, Arnett DK, Pankow JS, Hopkins PN, Province MA, Ellison RC. Dietary linolenic acid is associated with a lower prevalence of hypertension in the NHLBI Family Heart Study. Hypertension. 2005;45:368-373.

17. Whelton PK, He J, Appel LJ, et al. Primary prevention of hypertension: clinical and public health advisory from the National High Blood Pressure Education Program. JAMA. 2002;288:1882-1888.

18. Xu JW, Ikeda K, Yamori Y. Upregulation of endothelial nitric oxide synthase by cyanidin-3-glucoside, a typical anthocyanin pigment. Hypertension. 2004;44:217-222.

19. Achike FI, Kwan CY. Nitric oxide, human diseases and the herbal products that affect the nitric oxide signaling pathway. Clin Exp Pharmacol Physiol. 2003;30:605-615.

20. Tauber AI, Fay JR, Marletta MA. Flavonoid inhibition of the human neutrophil NADPH-oxidase. Biochem Pharmacol. 1984;33:1367-1369.

21. He J, Whelton PK. What is the role of dietary sodium and potassium in hypertension and target organ injury? Am J Med Sci. 1999;317:152-159.

22. Adrogue HJ, Wesson DE. Role of dietary factors in the hypertension of African Americans. Semin Nephrol. 1996;16:94-101.

23. Geleijnse JM, Kok FJ, Grobbee DE. Impact of dietary and lifestyle factors on the prevalence of hypertension in Western populations. Eur J Public Health. 2004;14:235-239.

24. Witteman JC, Willett WC, Stampfer MJ, et al. Relation of moderate alcohol consumption and risk of systemic hypertension in women. Am J Cardiol. 1990;65:633-637.

25. Malinski MK, Sesso HD, Lopez-Jimenez F, Buring JE, Gaziano JM. Alcohol consumption and cardiovascular disease mortality in hypertensive men. Arch Intern Med. 2004;164:623-628.

26. Renaud SC, Gueguen R, Conard P, Lanzmann-Petithory D, Orgogozo JM, Henry O. Moderate wine drinkers have lower hypertension-related mortality: a prospective cohort study in French men. Am J Clin Nutr. 2004;80:621-625.

27. Forman JP, Rimm EB, Stampfer MJ, Curhan GC. Folate intake and the risk of incident hypertension among U.S. women. JAMA. 2005;293:320-329.

28. Block G. Ascorbic acid, blood pressure, and the American diet. Ann NY Acad Sci. 2002;959:180-187.

29. Chen J, He J, Hamm L, Batuman V, Whelton PK. Serum antioxidant vitamins and blood pressure in the United States population. Hypertension. 2002;40:810-816.

30. Hajjar IM, George V, Sasse EA, Kochar MS. A randomized, double-blind, controlled trial of vitamin C in the management of hypertension and lipids. Am J Ther. 2002;9:289-293.

31. Field AE, Coakley EH, Must A, et al. Impact of overweight on the risk of developing common chronic diseases during a 10-year period. Arch Intern Med. 2001;161:1581-1586.

32. Hernelahti M, Kujala U, Kaprio J. Stability and change of volume and intensity of physical activity as predictors of hypertension. Scand J Public Health. 2004;32:303-309.

33. Nakanishi N, Suzuki K. Daily life activity and the risk of developing hypertension in middle-aged Japanese men. Arch Intern Med. 2005;165:214-220.


Sometimes the most elegant solution is the most simple. Why plant-based nutrition? Why not? Why develop heart disease? Cancer? Diabetes? The epidemic of chronic, degenerative disease that is sweeping the western world can not only be stopped, it can be reversed. The power lies in the hands of the consumer, in the choices we make about what to put on our plates.