• Race

   

  Blacks have a higher prevalence and incidence of hypertension than whites.  The prevalence of hypertension was increased by 50% in African Americans. In  Mexican Americans, the prevalence and incidence of hypertension is similar to or  lower than in whites. The National Health and Nutrition Examination Survey  (NHANES) III reported an age-adjusted prevalence of hypertension at 20.6% in  Mexican Americans and 23.3% in non-Hispanic whites.

   

   

   
  • Are there ethnic differences in the pathogenesis of hypertension, and do  these differences influence the choice of treatment? To understand ethnic  influence, an understanding of the renin angiotensin system is essential. Renin  secretion is suppressed when the kidney detects that the amount of sodium  excretion is increased; thus, a clue to the excess sodium in the circulation.  Black people tend to develop hypertension at an earlier age and have lower  rennin activity; target organ damage also differs in black people from that in  white people. 
  • Most studies in the United Kingdom and the United States report a higher  prevalence and lower awareness of hypertension in black people than in white  people. Mortality from hypertension in African-Caribbean–born people is 3.5  times the national rate; similar data have been published for African American  citizens. Strokes are more common in black people, but coronary heart disease is  more common in Asians. Both groups have a higher incidence of chronic renal  failure than white people, but this is more due to hypertension in black people  and diabetes in Asians. 
  • Black people have a poorer response to treatment with ACE inhibitors  compared to white people; the evidence for beta-blockers being less effective in  black people is also clear. However, diuretics are more effective at a young age  in black people.
   
   

  Sex

   

  The age-adjusted prevalence of hypertension was 34%, 25.4%, and 23.2% for men  and 31%, 21%, and 21.6% for women among African Americans, whites, and Mexican  Americans, respectively. In the NHANES III study, the prevalence of hypertension  was 12% for white men and 5% for white women aged 18-49 years. However, the  age-related blood pressure rise for women exceeds that of men. The prevalence of  hypertension was reported at 50% for white men and 55% for white women aged 70  years or older.

   

  Age

   

  A progressive rise in blood pressure with increasing age is observed. The  third NHANES survey reported that the prevalence of hypertension grows  significantly with increasing age in all sex and race groups. The age-specific  prevalence was 3.3% in white men (aged 18-29 y); this increased to 13.2% in the  group aged 30-39 years. The prevalence further increased to 22% in the group  aged 40-49 years, to 37.5% in the group aged 50-59 years, and to 51% in the  group aged 60-74 years. In another study, the incidence of hypertension appeared  to increase approximately 5% for each 10-year interval of age. Age-related  hypertension appears to be predominantly systolic rather than diastolic. The  systolic blood pressure rises into the eighth or ninth decade, while the  diastolic blood pressure remains constant or declines after age 40  years.¹

  
  

• Hypertension is one of the most common worldwide diseases afflicting humans.  Because of the associated morbidity and mortality and the cost to society,  hypertension is an important public health challenge. Over the past several  decades, extensive research, widespread patient education, and a concerted  effort on the part of health care professionals have led to decreased mortality  and morbidity rates from the multiple organ damage arising from years of  untreated hypertension. Hypertension is the most important modifiable risk  factor for coronary heart disease (the leading cause of death in North America),  stroke (the third leading cause), congestive heart failure, end-stage renal  disease, and peripheral vascular disease. Therefore, health care professionals  must not only identify and treat patients with hypertension but also promote a  healthy lifestyle and preventive strategies to decrease the prevalence of  hypertension in the general population.

• Regulation of blood pressure

   

  Regulation of normal blood pressure is a complex process. Although a function  of cardiac output and peripheral vascular resistance, both of these variables  are influenced by multiple factors.

   

  The factors affecting cardiac output include sodium intake, renal function,  and mineralocorticoids; the inotropic effects occur via extracellular fluid  volume augmentation and an increase in heart rate and contractility. Peripheral  vascular resistance is dependent upon the sympathetic nervous system, humoral  factors, and local autoregulation. The sympathetic nervous system produces its  effects via the vasoconstrictor alpha effect or the vasodilator beta effect. The  humoral actions on peripheral resistance are also mediated by other mediators  such as vasoconstrictors (angiotensin and catecholamines) or vasodilators  (prostaglandins and kinins). For additional resource, please visit Angiotensin II Receptor  Blockade.

   

  Autoregulation of blood pressure occurs by way of intravascular volume  contraction and expansion, as well as by transfer of transcapillary fluid.  Interactions between cardiac output and peripheral resistance are autoregulated  to maintain a set blood pressure in an individual. For example, constriction of  the arterioles elevates arterial pressure by increasing total peripheral  resistance, whereas venular constriction leads to redistribution of the  peripheral intravascular volume to the central circulation, thereby increasing  preload and cardiac output.
  

• Causes

   

   

   
  • Primary or essential hypertension (90-95%) 
  • Secondary hypertension: A small percentage of patients (2-10%) have a  secondary cause. The following is a list of secondary causes of hypertension: 
  •  
     
    • Renal (2.5-6%)  
       
      • Renal parenchymal disease  
      • Polycystic kidney disease  
      • Urinary tract obstruction  
      • Renin-producing tumor  
      • Liddle syndrome
       
    • Renovascular hypertension (0.2-4%) 
    • Vascular  
       
      • Coarctation of aorta  
      • Vasculitis  
      • Collagen vascular disease
       
    • Endocrine (1-2%) - Oral contraceptives 
    • Adrenal  
       
      • Primary aldosteronism  
      • Cushing syndrome  
      • Pheochromocytoma  
      • Congenital adrenal hyperplasia
       
    • Hyperthyroidism and hypothyroidism 
    • Hypercalcemia 
    • Hyperparathyroidism 
    • Acromegaly 
    • Neurogenic  
       
      • Brain tumor  
      • Bulbar poliomyelitis  
      • Intracranial hypertension
       
    • Pregnancy-induced hypertension 
    • Drugs and toxins  
       
      • Alcohol  
      • Cocaine  
      • Cyclosporin  
      • Erythropoietin  
      • Adrenergic medications

• Arterial blood pressure is a product of cardiac output and systemic vascular  resistance. Therefore, determinants of blood pressure include factors that  affect both cardiac output and arteriolar vascular physiology. There is  potential relevance of blood viscosity, vascular wall sheer conditions (rate and  stress), and blood flow velocity (mean and pulsatile components) on vascular and  endothelial function regulating blood pressure in humans. Furthermore, changes  in vascular wall thickness affect the amplification of peripheral vascular  resistance in hypertensive patients and result in reflection of waves back to  the aorta, increasing systolic blood pressure.
  
  

• Pathogenesis of hypertension

   

  The pathogenesis of essential hypertension is multifactorial and highly  complex. Multiple factors modulate the blood pressure for adequate tissue  perfusion and include humoral mediators, vascular reactivity, circulating blood  volume, vascular caliber, blood viscosity, cardiac output, blood vessel  elasticity, and neural stimulation. A possible pathogenesis of essential  hypertension has been proposed in which multiple factors, including genetic  predisposition, excess dietary salt intake, and adrenergic tone, may interact to  produce hypertension. Although genetics appears to contribute to essential  hypertension, the exact mechanism has not been established.

   

  The natural history of essential hypertension evolves from occasional to  established hypotension. After a long invariable asymptomatic period, persistent  hypertension develops into complicated hypertension, in which target organ  damage to the aorta and small arteries, heart, kidneys, retina, and central  nervous system is evident. The progression begins with prehypertension in  persons aged 10-30 years (by increased cardiac output) to early hypertension in  persons aged 20-40 years (in which increased peripheral resistance is prominent)  to established hypertension in persons aged 30-50 years, and, finally, to  complicated hypertension in persons aged 40-60 years.

   

  The early stage of hypertension has been described as high-output  hypertension. High-output hypertension results from decreased peripheral  vascular resistance and concomitant cardiac stimulation by adrenergic  hyperactivity and altered calcium homeostasis. In contrast, the chronic phase of  essential hypertension characteristically has normal or reduced cardiac output  and elevated systemic vascular resistance.

   

  The vasoreactivity of the vascular bed, an important phenomenon mediating  changes of hypertension, is influenced by the activity of vasoactive factors,  reactivity of the smooth muscle cells, and structural changes in the vessel wall  and vessel caliber, expressed by a lumen-to-wall ratio. Patients who develop  hypertension are known to develop a systemic hypertensive response secondary to  vasoconstrictive stimuli. Alterations in structural and physical properties of  resistance arteries, as well as changes in endothelial function, are probably  responsible for this abnormal behavior of vasculature. Furthermore, vascular  remodeling occurs over the years as hypertension evolves, thereby maintaining  increased vascular resistance irrespective of the initial hemodynamic  pattern.

   

  Genetic factors

   

  Hypertension is likely to be related to multiple genes. Hypertension develops  secondary to multiple environmental factors, as well as to several genes, whose  inheritance appears to be complex. Very rare secondary causes are related to  single genes.

   

  Role of the vascular endothelium

   

  The vascular endothelium is presently considered a vital organ, where  synthesis of various vasodilating and constricting mediators occurs. The  interaction of autocrine and paracrine factors takes place in the vascular  endothelium, leading to growth and remodeling of the vessel wall and to the  hemodynamic regulation of blood pressure.

   

  Numerous hormonal, humeral vasoactive, and growth and regulating peptides are  produced in the vascular endothelium. These mediators include angiotensin II,  bradykinin, endothelin, nitric oxide, and several other growth factors.  Endothelin is a potent vasoconstrictor and growth factor that likely plays a  major role in the pathogenesis of hypertension. Angiotensin II is a potent  vasoconstrictor synthesized from angiotensin I with the help of an  angiotensin-converting enzyme (ACE). Another vasoactive substance manufactured  in the endothelium is nitric oxide. Nitric oxide is an extremely potent  vasodilator that influences local autoregulation and other vital organ  functions. Additionally, several growth factors are manufactured in the vascular  endothelium; each of these plays an important role in atherogenesis and target  organ damage. These factors include platelet-derived growth factor, fibroblast  growth factor, insulin growth factor, and many others.
  

• Diet

   

  A number of studies have documented an association between sodium chloride  intake and blood pressure. The effect of sodium chloride is particularly  important in individuals who are middle-aged to elderly with a family history of  hypertension. A moderate reduction in sodium chloride intake can lead to a small  reduction in blood pressure. The American Heart Association recommends that the  average daily consumption of sodium chloride not exceed 6 g, this may lower  blood pressure by 2-8 mm Hg.
  
   

   
  • The Dietary Approaches to Stop Hypertension (DASH) eating plan encompasses a  diet rich in fruits, vegetables, and low-fat dairy products and may lower blood  pressure by 8-14 mm Hg.² 
  • Dietary potassium, calcium, and magnesium consumption have an inverse  association with blood pressures. Lower intake of these elements potentiates the  affect of sodium on blood pressure. Oral potassium supplementation may lower  both systolic and diastolic pressure. Calcium and magnesium supplementation have  elicited small reductions in blood pressures. 
  • In population studies, low levels of alcohol consumption have shown a  favorable effect on blood pressure, with reductions of 2-4 mm Hg. However, the  consumption of 3 or more drinks per day is associated with elevation of blood  pressure. Alcohol intake should be restricted to less than 1 oz of ethanol in  men and 0.5 oz in women. 
  • Weight reduction may lower blood pressure by 5-20 mm Hg per 10 kg of weight  loss in a patient who weighs more than 10% of ideal body weight.

• The central nervous system

   

  Long-standing hypertension may manifest as hemorrhagic and atheroembolic  stroke or encephalopathy. Both the high systolic and diastolic pressures are  harmful; a diastolic pressure of more than 100 mm Hg and a systolic pressure of  more than 160 mm Hg have led to a significant incidence of strokes. Other  cerebrovascular manifestations of complicated hypertension include hypertensive  hemorrhage, hypertensive encephalopathy, lacunar-type infarctions, and  dementia.

• Complications

   

   

   
  • Central nervous system - Intracerebral hemorrhage, lacunar infarcts,  encephalopathy, thrombotic stroke, transient ischemic attack 
  • Ophthalmologic - Fundal hemorrhages, exudates, papilledema 
  • Cardiac - LVH, congestive heart failure, angina pectoris, myocardial  infarction 
  • Vascular - Aortic dissection, diffuse arthrosclerosis 
  • Renal - Nephrosclerosis, renal artery stenosis
   
   

  Prognosis

   

   

   
  • Most individuals diagnosed with hypertension will have increasing blood  pressure as they age. 
  • Untreated hypertension is notorious for increasing the risk of mortality and  is often described as a silent killer. 
  • Mild-to-moderate hypertension, if left untreated, is associated with a risk  of atherosclerotic disease in 30% of people and organ damage in 50% of people  after only 8-10 years of onset.
   
   

  Patient Education

   

   

   
  • Hypertension is a lifelong disorder. For optimal control, a long-term  commitment to lifestyle modifications and pharmacological therapy is required.  Therefore, repeated in-depth patient education and counseling not only improve  compliance with medical therapy but also reduce cardiovascular risk factors. 
  • Various strategies to decrease cardiovascular disease risk include the  following: 
  •  
     
    • Prevention and treatment of obesity 
    • Appropriate amounts of aerobic physical activity 
    • Diets low in salt, total fat, and cholesterol 
    • Adequate dietary intakes of potassium, calcium, and magnesium 
    • Limited alcohol consumption 
    • Avoidance of cigarette smoking
     
  • For excellent patient education resources, visit eMedicine's Diabetes Center and Cholesterol Center. Also, see eMedicine's patient education  articles High Blood Pressure, High  Cholesterol, Chest Pain, Coronary  Heart Disease, and Heart  Attack.

• Metabolic syndrome

   

  The metabolic syndrome is an assemblage of metabolic risk factors that  directly promote the development of atherosclerotic cardiovascular disease.  Dyslipidemia, hypertension, and hyperglycemia are the most widely recognized  metabolic risk factors. The combination of these risk factors leads to a  prothrombotic, proinflammatory state in humans and identifies individuals who  are at elevated risk for atherosclerotic cardiovascular disease.

   

  The predominant underlying risk factors for the metabolic syndrome appear to  be abdominal obesity and insulin resistance. Other associated conditions are  physical inactivity, aging, hormonal imbalance, and atherogenic diet. Insulin  resistance, an essential cause of the metabolic syndrome, predisposes to  hyperglycemia and type 2 diabetes mellitus. Individuals who insulin resistant  may not be clinically obese, but they commonly have an abnormal fat distribution  that is characterized by predominant upper body fat. Upper body obesity can  occur either intraperitoneally (visceral fat) or subcutaneously, both of which  correlate strongly with insulin resistance and the metabolic syndrome.

   

  The rising prevalence of the metabolic syndrome is secondary to the  increasing burden of obesity in our society. The adipose tissue in people who  are obese is insulin resistant, raises nonesterified fatty acid levels, alters  hepatic metabolism, and produces several adipokines. These include increased  production of inflammatory cytokines, plasminogen activator inhibitor-1, and  other bioactive products, while the synthesis of potentially protective  adipokine, adiponectin, is reduced. Recently, this syndrome has been noted to be  associated with a state of chronic, low-grade inflammation. Although the  metabolic syndrome unequivocally predisposes to type 2 diabetes mellitus, this  syndrome is multidimensional risk factor for atherosclerotic cardiovascular  disease.

• Mortality/Morbidity

   

   

   
  • In the Framingham Heart Study, the age-adjusted risk of congestive heart  failure was 2.3 times higher in men and 3 times higher in women when highest  blood pressure was compared to the lowest. Multiple Risk Factor Intervention  Trial (MRFIT) data showed that the relative risk for coronary heart disease  mortality varied from 2.3-6.9 times higher for persons with mild-to-severe  hypertension compared to persons with normal blood pressure. 
  • The relative risk for stroke ranged from 3.6-19.2. The  population-attributable risk percentage for coronary artery disease varied from  2.3-25.6%, whereas the population-attributable risk for stroke ranged from  6.8-40%.

• Renal disease

   

  Despite widespread treatment of hypertension in the United States, the  incidence of end-stage renal disease continues to rise. The explanation for this  rise may be concomitant diabetes mellitus, the progressive nature of  hypertensive renal disease despite therapy, or a failure to reduce blood  pressure to a protective level. A reduction in renal blood flow in conjunction  with elevated afferent glomerular arteriolar resistance increases glomerular  hydrostatic pressure secondary to efferent glomerular arteriolar constriction.  The result is glomerular hyperfiltration, followed by development of  glomerulosclerosis and further impairment of renal function.

   

  Two studies have demonstrated that a reduction in blood pressure may result  in improved renal function. Therefore, earlier detection of hypertensive  nephrosclerosis using means to detect microalbuminuria and aggressive  therapeutic interventions, particularly with ACE inhibitor drugs, may prevent  progression to end-stage renal disease.

   

  Nephrosclerosis is one of the possible complications of long-standing  hypertension. The risk of hypertension-induced end-stage renal disease is higher  in black patients, even when the blood pressure is under good control.  Furthermore, patients with diabetic nephropathy who are hypertensive are also at  high risk for developing end-stage renal disease. The renin-angiotensin system  activity influences the progression of renal disease. Angiotensin II acts at  both the afferent and the efferent arterioles, but more so on the efferent  arteriole, which leads to an increase of the intraglomerular pressure. The  excess glomerular pressure leads to microalbuminuria. Reducing intraglomerular  pressure using an ACE inhibitor has been shown to be beneficial in patients with  diabetic nephropathy, even in those who are not hypertensive. The beneficial  effect of ACE inhibitors on the progression of renal insufficiency in patients  who are nondiabetic is less clear.

   

  Hypertension in renal disease

   

  Hypertension is commonly observed in patients with kidney disease. Volume  expansion is the main cause of hypertension in patients with glomerular disease  (nephrotic and nephritic syndrome). Hypertension in patients with vascular  disease is the result of the activation of the renin-angiotensin system, which  is often secondary to ischemia. Most patients with chronic renal failure are  hypertensive (80-90%). The combination of volume expansion and the activation of  the renin-angiotensin system is believed to be the main factor behind  hypertension in patients with chronic renal failure.

• Clinical trials

   

  Multiple clinical trials suggest that most antihypertensive drugs provide the  same degree of cardiovascular protection for the same level of blood pressure  control. Well-designed prospective randomized trials, such as the Swedish Trial  in Old Patients with Hypertension (STOP-2), the Nordic Diltiazem (NORDIL) trial,  and the Intervention as a Goal in Hypertension Treatment (INSIGHT) trial, have  shown a similar outcome with older drugs (eg, diuretics, beta-blockers) compared  to the newer antihypertensive agents (eg, ACE inhibitors, calcium channel  blockers).

   

  No consensus exists regarding optimal drug therapy for treatment of  hypertension; most clinicians recommend initiating therapy with a single agent  and advancing to the low-dose combination therapy. Any of the first-line  medications decrease blood pressure in 40-60% of patients with mild-to-moderate  hypertension. In unresponsive patients, switching to a second drug (rather than  combining it with the first drug) or switching to a third drug if the second  drug is not effective may allow a 70-80% response rate to monotherapy.  Therefore, attempt to identify a particular class of drug to which the patient  responds rather than adding multiple drugs (as in combination therapy).

   

  The JNC VII report recommends either a thiazide diuretic or a beta-blocker as  the initial therapy of uncomplicated hypertension. A low dose of thiazide  diuretic (12.5-25 mg hydrochlorothiazide) is a low-cost therapy with fewer  complications, and it provides equivalent cardiovascular protection. Patients  unresponsive to low-dose thiazide therapy should try an ACE inhibitor,  beta-blocker, or calcium channel blocker, sequentially. Patients unresponsive to  a diuretic may not respond to a calcium channel blocker, and an ACE inhibitor or  a beta-blocker should be tried as a second-line agent in these patients. Calcium  channel blocking agents and diuretics may be more effective in hypertensive  black patients.

   

  Initial therapy based on the JNC VII report recommendations is as  follows:
  

   
   
  • Prehypertension (systolic 120-139, diastolic 80-89): No antihypertensive  drug is indicated. 
  • Stage 1 hypertension (systolic 140-159, diastolic 90-99): Thiazide-type  diuretics are recommended for most. ACE inhibitor, angiotensin II receptor  blocker (ARB), beta-blocker, calcium channel blocker, or combination may be  considered. 
  • Stage 2 hypertension (systolic more than 160, diastolic more than 100):  Two-drug combination (usually thiazide-type diuretic and ACE inhibitor or ARB or  beta-blocker or calcium channel blocker) is recommended for most. 
  • For the compelling indications, other antihypertensive drugs (eg, diuretics,  ACE inhibitor, ARB, beta-blocker, calcium channel blocker) may be considered as  needed.
   

  Randomized trials

   

  Two randomized controlled trials, the Hypertension Detection and Follow-up  Program (HDFP) and the Medical Research Council (MRC) trials, randomized  patients with elevated levels of diastolic blood pressure to either  diuretic-based stepped-care treatment or usual care. The usual care group  received some form of therapy from their own physicians, whereas the  stepped-care group received systematic care. In both studies, stepped-care  treatment reduced diastolic blood pressure by 5 mm more than that reduced in the  control group. Both trials showed a benefit from stepped-care therapy compared  to the control group. In the HDFP trial, stepped-care led to relative risk  reduction of 17% for total mortality; 76 hypertensive patients needed to be  treated with stepped-care therapy for 5 years to prevent one death.

   

  A meta-analysis published in the Journal of the American Medical  Association (JAMA) in 1997 included several randomized controlled  clinical trials. The total number of participants randomized to active therapy  was 24,294, and the number for the control therapy was 23,926. Active treatment  reduced diastolic blood pressure by at least 5 mm Hg. The meta-analysis showed a  risk reduction of coronary heart disease of 8-14% and the reduction in stroke  incidence of 35-40%. Subsequent meta-analysis reported that benefits of active  treatment are similar in men and women.
• • Key messages of the Seventh Report of the Joint National Committee on  Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC  VII) are as follows: 
  •  
     
    • In those older than 50 years, systolic blood pressure (BP) of greater than  140 mm Hg is a more important cardiovascular disease risk factor than diastolic  BP. 
    • Beginning at 115/75 mm Hg, the cardiovascular disease risk doubles for each  increment of 20/10 mm Hg. 
    • Individuals who are normotensive at 55 years will have a 90% lifetime risk  of developing hypertension. 
    • Prehypertension (systolic 120-139, diastolic 80-89) requires  health-promoting lifestyle modifications to prevent the progressive rise in  blood pressure and cardiovascular disease. 
    • In uncomplicated hypertension, a thiazide diuretic, either alone or combined  with drugs from other classes, should be used for the drug treatment of most. 
    • In specific high-risk conditions, there are compelling indications for the  use of other antihypertensive drug classes (eg, ACE inhibitors,  angiotensin-receptor blockers, beta-blockers, calcium channel blockers). 
    • Two or more antihypertensive medications will be required to achieve goal BP  (<140/90 mm Hg or <130/80 mm Hg) for patients with diabetes and chronic  kidney disease. 
    • For patients whose BP is more than 20 mm Hg above the systolic BP goal or  more than 10 mm Hg above the diastolic BP goal, initiation of therapy using 2  agents, one of which usually will be a thiazide diuretic, should be considered. 
    • Regardless of therapy or care, hypertension will be controlled only if  patients are motivated to stay on their treatment plan.
• • Resistant hypertension: Some patients may have persistent diastolic blood  pressures above 100 mm Hg despite the use of 3 or more antihypertensive  medications. These patients may be experiencing of the following factors as the  cause of resistant hypertension: 
  •  
     
    • Inadequate treatment was described as the most common cause of resistant  hypertension in several published series. Patients may not be on an effective  drug, or concomitant volume expansion may occur as a side effect of the drug. 
    • Extracellular volume expansion: Volume expansion may contribute to the  inability to lower systemic blood pressure. The volume expansion may occur  because of renal insufficiency, sodium retention due to treatment with  vasodilators, high-salt diet, or insufficient dosing of diuretic. This situation  can be treated with more aggressive diuretic therapy until clinical signs of  extracellular volume depletion (eg, orthostatic hypotension) develop. 
    • Poor compliance: Noncompliance with medical therapy or dietary modifications  (eg, salt restriction) may play a role in causing resistant hypertension.  Address noncompliance with extensive patient education, simplification of the  drug regimen, and use of drugs with the fewest adverse effects. 
    • Secondary hypertension: Whenever confronted with resistant hypertension, try  to exclude any secondary causes of hypertension. A reevaluation of the patient's  history, physical examination, and laboratory results may provide clues to  secondary hypertension (eg, renal artery stenosis, primary hyperaldosteronism). 
    • White coat hypertension: Blood pressure rise secondary to anxiety may be  observed in 20-30% of patients. This may be avoided by having patients rest  prior to measurement, having a nurse check the blood pressure, or arranging to  have the blood pressure monitored at home. Development of hypotensive symptoms  on medications is an indication of white coat hypertension. White coat  hypertension can also be evaluated by the use of a 24-hour ambulatory  monitor.
     
  • Pseudohypertension may be observed in elderly individuals who have  thickened, calcified arteries. Much higher cuff pressure may be required to  occlude a thickened brachial artery, and diastolic pressure may also be  overestimated. Consider pseudohypertension in situations in which no organ  damage occurs despite marked hypertension, when patients develop hypotensive  systems on medications, and when calcification of the brachial artery is  observed on radiologic examination. Direct measurement of intra-arterial  pressure may be required in this setting. 
  • Vasoactive substances: Resistant hypertension may be encountered in patients  who are ingesting vasoactive substances despite taking antihypertensive drugs  regularly. Use of salt and alcohol are the common examples; others include use  of cocaine, amphetamines, anabolic steroids, oral contraceptives, cyclosporine,  antidepressants, and nonsteroidal anti-inflammatory drugs.
• • Hypertension in special populations 
  •  
     
    • Age 
    •  
       
      • The systolic pressure continues to progressively rise throughout life,  reaching the highest levels in later stages of life. Isolated systolic  hypertension may be present in 10% of the population aged 70 years and in 24% of  those aged 80 years. Furthermore, severe arteriosclerosis may lead to  pseudohypertension. Isolated hypertension results in low cardiac output because  of the decreased stroke volume and high peripheral resistance. This may reduce  glomerular filtration further, which is why low activity of renal angiotensin  aldosterone cascade is encountered in elderly individuals who are hypertensive. 
      • Despite low PRA, blood pressure responds well to ACE inhibitor and  angiotensin receptor inhibitor therapy. Low doses of diuretics may also be  effective. Calcium antagonists are quite useful because of their strong  antihypertensive effects. Often, combining 2 drugs at a lower dose may be  preferable to using a single drug at a high dose that has the potential for  adverse effects.
       
    • Sex: The prevalence of hypertension is similar between men and women, but  women are protected from coronary heart disease prior to menopause.  Premenopausal women have a higher resting heart rate, a higher cardiac index,  and a lower peripheral resistance than men. These changes are not encountered in  postmenopausal females. Therefore, in premenopausal situations, a medication  such as beta-blocker may be effective. However, postmenopausal hypertension is  treated similarly to that in men. 
    • Race 
    •  
       
      • Blacks have a higher prevalence of hypertension and a much higher frequency  of end organ damage, such as occurs in end-stage renal disease, strokes, and  heart failure. Black patients also develop more severe LVH than white patients.  Renal function in hypertensive black patients continues to deteriorate over time  despite aggressive management of the blood pressures. 
      • Black patients respond less well to beta-blockers, ACE inhibitors, and  angiotensin receptor blockers than white patients. At times, this relative lack  of efficacy may be overcome by increasing the dosage of the medications. Blacks  may respond well to treatment with calcium antagonists, diuretics, and  postsynaptic alpha-blockers.
       
    • Obesity 
    •  
       
      • Hypertensive patients who are obese have a higher cardiac output and a lower  peripheral vascular resistance than hypertensive patients who are not obese. The  increase in cardiac output manifests secondary to increased preload. The  end-diastolic volume and pressure are elevated, leading to left ventricular  dilatation. Left ventricular wall thickening also occurs secondary to increased  afterload, which increases the risk of congestive heart failure. The concomitant  diabetes often present in patients who are obese produces a devastating effect  on kidneys and leads to a much higher incidence of renal failure. 
      • No class of drugs seems to be of particular advantage in hypertensive  patients who are obese, but thiazide diuretics may be helpful, unless the  patient also has coexisting diabetes. In patients who are diabetic and who may  have microalbuminuria, ACE inhibitors or calcium antagonists are recommended  because they may slow declining renal function. Because of the high preload and  afterload, drugs that have negative inotropic effects, such as beta-blockers,  should be avoided.

• Surgical Care

   

  Aortorenal bypass using saphenus vein graft or hypogastric artery is a common  revascularization technique for renovascular hypertension. Surgical resection is  the treatment of choice for pheochromocytoma because hypertension is cured by  tumor resection. In patients with fibromuscular renal disease, angioplasty has a  60-80% success rate for cure or improvement of hypertension. Surgical correction  of renal artery stenosis has resulted in cure of hypertension in approximately  61% of patients and amelioration in 27% of patients with fibromuscular lesions.  With respect to renal artery stenosis secondary to atherosclerotic lesions,  surgical correction has resulted in cure of hypertension in 38% of patients and  amelioration in about 41% of patients. See Medical Care for more details.

   

  Consultations

   

  Consultations with a nutritionist and exercise specialist are often helpful  in changing lifestyle and initiating weight loss. Consultations with an  appropriate consultant are indicated for management of secondary hypertension  attributable to a specific cause.

• Activity

   

  Up to 60% of all individuals with hypertension are more than 20% overweight.  The centripetal fat distribution is associated with insulin resistance and  hypertension. Even modest weight loss (5%) can lead to reduction in blood  pressure and improved insulin sensitivity. Regular aerobic physical activity can  facilitate weight loss, decrease blood pressure, and reduce the overall risk of  cardiovascular disease. Blood pressure may be lowered by 4-9 mm Hg with  moderately intense physical activity. These activities include brisk walking for  30 minutes a day, 5 days per week. More intense workouts for 20-30 minutes, 3-4  times a week may also lower blood pressure and have additional health  benefits.

• Deterrence/Prevention

   

   

   
  • A comprehensive strategy for reduction in mortality and morbidity from  hypertension must include prevention strategies, earlier detection, and adequate  treatment. Ideally, a population strategy should be used in order to lower blood  pressure in the community. More intensive efforts are required to lower blood  pressure in high-risk population groups, which include individuals with a family  history of hypertension, black ancestry, obesity, excessive sodium consumption,  physical inactivity, and/or alcohol consumption. Even a small reduction in blood  pressure confers significant health benefits. A 2-mm Hg reduction in diastolic  pressure is estimated to decrease the risk of stroke by 15% and the risk of  coronary heart disease by 6%. 
  • Prevention of hypertension may be achieved by the following interventions: 
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    • Weight control 
    • Increased physical activity 
    • Moderated sodium and alcohol intake 
    • Increased potassium intake 
    • A dietary pattern rich in fruits and vegetables and low-fat meat, fish, and  dairy products

• Medical/Legal Pitfalls

   

   

   
  • Hypertension is one of the most common modifiable risk factors for  atherosclerotic disease. 
  • According to the JNC VI enrollment report, only 53% of patients with  hypertension are being treated in the United States. Of these, only 27% have  adequately controlled blood pressure, and only 45% of treated patients have a  blood pressure less than 140/90 mm Hg. 
  • Despite an array of pharmaceutical agents to treat hypertension, JNC VI  recommends diuretics and beta-blockers as the preferred initial agents because  of proven efficacy and lower cost. 
  • Patients with hypertension should be identified and staged based on blood  pressure determinations and cardiovascular risk and the presence or absence of  target organ damage. 
  • JNC VI recommends lower target blood pressure goals in 2 select populations:  (1) patients with diabetes mellitus (blood pressure <130/85 mm Hg) and (2)  patients with renal disease (blood pressure <130/85 mm Hg; if urinary protein  is >1 g/d, a blood pressure <125/75 mm Hg). 
  • Malignant hypertension is a medical emergency and requires hospitalization  and urgent therapy. The blood pressure should be reduced rapidly, but diastolic  blood pressure should be maintained at approximately 95 mm Hg.

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• In the next 10 years, 20.7 million people will die of cardiovascular disease in  the Americas if the level of intervention stays the same. Yet at least 80% of  all heart disease is preventable.

• Although many cardiovascular diseases (CVDs) can be treated or prevented, an  estimated 17 million people die of CVDs each year. A substantial number of these  deaths can be attributed to tobacco smoking, which increases the risk of dying  from coronary heart disease and cerebrovascular disease 2–3 fold. The risk  increases with age and is greater for women than for men. In contrast, cardiac  events fall 50% in people who stop smoking and the risk of CVDs, including acute  myocardial infarction, stroke and peripheral vascular disease, also decreases  significantly over the first two years after stopping smoking.

   

  Continuing to smoke after myocardial infarction or coronary revascularization  can have serious clinical consequences. Even eight years after myocardial  infarction, the mortality of post-myocardial infarction patients who continue to  smoke is double that of quitters. Further, those who do not stop smoking after  coronary revascularization also have a two-fold higher risk of re-infarction and  death.

   

  Studies indicate that although doctors are knowledgeable about the risks of  CVDs associated with tobacco smoking, they are not sufficiently prepared to help  their patients stop smoking. Even though physicians identify a substantial  number of smokers during consultations, for example, many patients do not  receive counseling to help them quit. Smoking cessation is the most  cost-effective intervention for patients with documented CVDs, and efficacious  programmes have been developed. The challenge is to get these programmes more  widely used, and doctors and nurses should seize every opportunity to encourage  patients to stop smoking.

• Hypertension is already a highly prevalent cardiovascular risk factor  worldwide because of increasing longevity and prevalence of contributing factors  such as obesity. Whereas the treatment of hypertension has been shown to prevent  cardiovascular diseases and to extend and enhance life, hypertension remains  inadequately managed everywhere.

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  	Cardiovascular disease

       

  	WHO > Programmes  and projects

   

   

  Main content

      

  Cardiovascular diseases          Cardiovascular disease is caused by disorders of the heart and blood vessels,  and include coronary heart disease (heart attacks), cerebrovascular disease  (cerebrovascular disease), raised blood pressure (hypertension), peripheral  artery disease, rheumatic heart disease, congenital heart disease and heart  failure. The major causes of cardiovascular disease are tobacco use, physical  inactivity, and an unhealthy diet.   Cardiovascular disease is the number one cause of death globally and is  projected to remain the leading cause of death. An estimated 17.5 million people  died from cardiovascular disease in 2005, representing 30 % of all global  deaths. Of these deaths, 7.6 million were due to heart attacks and 5.7 million  were due to stroke. Around 80% of these deaths occurred in low and middle income  countries (LMIC). If appropriate action is not taken, by 2015, an estimated 20  million people will die from cardiovascular disease every year, mainly from  heart attacks and strokes.

• What causes heart attacks and strokes?

   

  Heart attacks and strokes are mainly caused by a blockage tat prevents blood  from flowing to the heart or the brain. the most common reason for this is  build-up of fatty deposits on the inner walls of the blood vessels that supply  the heart or the brain. This makes the blood vessels narrower and less flexible.  It is sometimes called hardening of the arteries or atherosclerosis. The blood  vessels are then more likely to get blocked by blood clots. When that happens,  the blood vessels cannot supply blood to the heart and brain, which become  damaged.

• Why does fat build up in blood vessels?

   

  There are three main reasons for fatty build-up, and you can control them  all:

   
   
  • Smoking and other tobacco use  
  • unhealthy diet  
  • not staying active.
   

  An early form of fatty deposits, known as ''fatty streaks'', can even be  found in some children younger than 10 years. These deposits get slowly worse as  the person gets older. To find out more about how you can prevent this from  happening to you and your family, read WHO publication ''Avoiding heart attacks  and strokes''.

• Key massages to protect heart health:

   
   
  • Heart attacks and strokes are major killers in all parts of the world. Butt  they can often be prevented.  
  • You can protect yourself from heart attacks and strokes by investing a  little time and effort.  
  • Tobacco use, an unhealthy die, and physical inactivity increase the risk of  heart attacks and strokes.  
  • Stopping tobacco use reduces the chance of a heart attack or stroke from the  moment you stop.  
  • Engaging in physical activity for at least 30 minutes on most days of the  week will help to keep away heart attacks and strokes.  
  • Eating at least five servings of fruit and vegetables a day, and limiting  your salt intake to less than one teaspoon a day, can help to prevent heart  attacks and strokes.  
  • High blood pressure has no symptoms, but can cause a sudden stroke or heart  attack. Have your blood pressure checked regularly.  
  • Diabetes increases the risk of heart attacks and stroke. If you have  diabetes control your blood pressure and blood sugar to minimize your risk.  
  • Being overweight increases the risk of heart attacks and strokes. To  maintain an ideal body weight, take regular physical activity and eat a healthy  diet.  
  • heart attacks and strokes can strike suddenly and can be fatal if assistance  is not sought immediatly.

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• Cardiovascular disease is caused by disorders of the heart and blood vessels,  and includes coronary heart disease (heart attacks), cerebrovascular disease  (stroke), raised blood pressure (hypertension), peripheral artery disease,  rheumatic heart disease, congenital heart disease and heart failure. The major  causes of cardiovascular disease are tobacco use, physical inactivity, and an  unhealthy diet.

   

  Cardiovascular disease is the number one cause of death globally and is  projected to remain the leading cause of death. An estimated 17.5 million people  died from cardiovascular disease in 2005, representing 30 % of all global  deaths. Of these deaths, 7.6 million were due to heart attacks and 5.7 million  were due to stroke. Around 80% of these deaths occurred in low- and  middle-income countries (LMIC). If appropriate action is not taken, by 2015, an  estimated 20 million people will die from cardiovascular disease every year,  mainly from heart attacks and strokes.