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High blood pressure: the silent killer

High blood pressure: the silent killer

Key learning points:

– High blood pressure or hypertension is diagnosed when it is persistently at 140/90mm Hg or above

– High blood pressure does not usually cause any symptoms and is only diagnosed when carefully measured

– Adequate control of high blood pressure significantly prevents strokes, heart attacks, heart failure, kidney failure, atrial fibrillation and aortic disease

High blood pressure (BP) or hypertension is one of the major modifiable risk factors for cardiovascular morbidity and mortality. Treatment of hypertension not only reduces the incidence of death and morbidity from strokes and heart attacks but also prevents heart failure, renal failure, aortic disease, peripheral vascular disease and dementia.

 There is accumulating evidence from large outcome studies that support a move towards lower BP treatment targets in patients with hypertension, particularly for those with concomitant risk factors or evidence of established target organ damage. At present, the achieved rates for BP control in the UK are very poor. One of the many possible reasons is the under-utilisation of effective drug combinations.

How does high BP affect people?

Normal BP is usually about 120/80 mm Hg. Both high and very low BP can cause health problems. Low BP (hypotension) is where BP in the arteries is abnormally low to restrict the amount of blood flowing to the brain and other vital organs, causing symptoms such as unsteadiness, dizziness, light-headedness or even fainting. High BP or hypertension is when BP is equal to or above 140/90mm Hg, according to current guidelines.

Importance of diagnosing high BP

Hypertension is the most important risk factor for cardiovascular disease (CVD), which is the leading cause of death in both men and women – in both the developed and the developing world.1 The prevalence of hypertension increases with age across all race and sex groups. Women have lower systolic BP levels than men during early adulthood, while the opposite is true after the sixth decade of life. Diastolic BP tends to be marginally lower in women than men, regardless of age. Similarly, in early adulthood hypertension is less common among women than men. However, after the fifth decade of life, the incidence of hypertension increases more rapidly in women; thus, women older than 60 years have higher rates of hypertension compared with men.

The highest prevalence rates of hypertension are observed in elderly black women, with hypertension occurring in more than 75% of black women older than 75 years.2 Hypertension is also the most common chronic medical condition affecting one-in-three individuals in the UK.

Hypertension increases the risk of strokes, heart attacks, heart failure, renal failure, aortic disease, peripheral vascular disease, dementia, diabetes, atrial fibrillation and sudden death.3 However the disease does not usually cause any symptoms or signs and that is why it is termed the ‘silent killer’. Therefore the only way to diagnose hypertension is to measure BP. Hypertension is diagnosed if BP is persistently 140/90mm Hg or above for two to four weeks. Ambulatory BP monitoring or home BP monitoring are offered to rule out white-coat hypertension. The results of many trials of antihypertensive drug treatment indicate that the reduction of BP in hypertensive individuals reduces their risk of cardiovascular events by about 16% for coronary heart disease and by 36% for stroke.4 With successive outcome trials in hypertension and CVD it is clear that the more the BP is lowered with treatment, the greater the cardiovascular protection afforded.5

Causes of hypertension

In the majority of individuals no cause is found for the high BP and therefore hypertension is termed primary or essential. Possible causes could be obesity, lack of exercise, a high intake of alcohol or an unhealthy diet with high salt content or low consumption of vegetables and fruit.

In 20-30% of patients a secondary cause of high BP can be found with appropriate investigations and the hypertension is potentially curable. These causes include overactive adrenal glands (high aldosterone, high epinephrine/norepinephrine, or high cortisol), kidney diseases (narrowing of the kidney arteries), drugs (pain killers, liquorice, steroids) and obstructive sleep apnoea.

How can hypertension go unnoticed?

As mentioned above, the only way to diagnose hypertension is by measuring BP either in the clinic, at home or by 24-hour ambulatory monitoring. Hypertension does not usually cause any symptoms. In rare cases it can cause headaches if BP is very high. For many patients the first sign of hypertension is target organ damage or a complication such as a stroke or a heart attack.

Investigations for hypertension

Investigations for hypertension can be subdivided into the following:6

            – Routine investigations.

            – Assess target organ damage and cardiovascular risk.

            – Investigations to diagnose secondary hypertension.

Routine investigations should include urine dipstick testing for blood and protein, full blood count, urea and electrolytes, total and LDL-cholesterol and triglycerides, blood glucose level, HbA1c, thyroid function tests and liver function tests.

Investigations to assess for target organ damage include electrocardiogram, echocardiogram, renal ultrasound and fundoscopy. All these investigations are ideally done in primary care. Investigations to diagnose secondary hypertension are best done in secondary or tertiary care and may include plasma renin activity and plasma aldosterone level (to rule out hyperaldosteronism), 24-hour urinary sodium excretion (to assess salt intake), 24-hour urinary metanephrines excretion or plasma free metanephrines (to rule out pheochromocytoma), CT renal angiography or magnetic resonance angiography (to rule out renal artery stenosis), and plasma or urinary cortisol level (to rule out Cushing’s syndrome).

Treatment of hypertension

Lifestyle and dietary interventions

All patients with high BP should be offered advice about reducing their salt and alcohol consumption, and increasing their intake of vegetables and fruit.

Patients should also be advised to stop smoking, increase exercise and maintain an ideal body weight.

Antihypertensive drug treatment

The current NICE guidelines, Hypertension: clinical management of primary hypertension in adults,6 suggest offering antihypertensive drug treatment based on the stage of hypertension.

            – Individuals with stage 3 severe hypertension (clinic BP of 180/110mm Hg or higher) should be started on antihypertensive drug treatment immediately.

            – Individuals of any age with stage 2 moderate hypertension (ambulatory/home BP of 150/95mm Hg or higher; clinic BP of 160/100mm Hg or higher) should be offered antihypertensive drug treatment irrespective of the target organ damage.

            ­– Individuals younger than 80 years with stage 1 mild hypertension (ambulatory or home BP of 135/85 to 150/95mm Hg; clinic BP of 140/90 to 160/100mm Hg) and with target organ damage, CVD, renal disease,
diabetes or a 10-year cardiovascular risk of 20% or higher should be offered antihypertensive drug treatment.

            – Individuals younger than 40 with stage 1 mild hypertension and no evidence of target organ damage, CVD, renal disease or diabetes, should be referred for specialist evaluation.

Initiating and stepping up of antihypertensive drug treatment

Step 1 treatment

1. Individuals younger than 55 years should be offered an angiotensin converting enzyme inhibitor (ACEi) or an angiotensin II receptor blocker (ARB). 

2. Individuals older than 55 years and people of African or Caribbean origin (of any age) should be offered a calcium channel blocker (CCB) or a thiazide-like diuretic 
(for instance, chlorthalidone or indapamide).

Step 2 treatment

BP control on monotherapy is rarely achieved, except in patients with mild high BP. Therefore if BP is not well controlled with an ACEi or an ARB, a CCB is added. If a CCB is not tolerated, a thiazide-like diuretic should be offered. For black African or Caribbean origin patients on a CCB, an ARB (rather than an ACEi) should be added.6 If BP is still not well controlled on the two-drug combination, optimising the doses should be considered before moving to step 3 treatment.

Step 3 treatment

For most patients with hypertension, treatment with three antihypertensive drugs will be needed – an ACEi (or ARB) combined with a CCB and a thiazide-like diuretic.7,8

Step 4 treatment (resistant hypertension)

Hypertension is classed as resistant when the BP remains above the target of less than 140/90mm Hg, despite treatment with a combination of three or more antihypertensive medications, including a diuretic, at maximal tolerated doses. A referral to a specialist hypertension unit is warranted for exclusion of secondary causes. An important common cause of apparently resistant hypertension is non-adherence to drug treatment.9 This should be explored fully before escalating drug treatment. Adding a low-dose spironolactone or a higher dose of thiazide-like diuretic should be considered. If BP remains uncontrolled with four drugs, a referral to a specialist hypertension unit should be considered.

High BP treatment targets

For patients below 80 years of age, target clinic BP should be less than140/90mm Hg. For patients aged 80 years and over with treated hypertension, target clinic BP should be less than 150/90mm Hg. However healthcare professionals involved in the management of patients with hypertension know from observational studies that there is a progressive increase in CVD risk with BP above 115/75mm Hg.10 However, there was limited data from randomised controlled trials guiding the lowering of BP beyond 140/90mm Hg. The recent publication of the Systolic Blood Pressure Intervention Trial (SPRINT)11 has provided the much-awaited evidence needed to revise BP targets to help improve cardiovascular outcomes.

The SPRINT trial

The SPRINT researchers randomly assigned 9,361 individuals with a systolic BP of 130mm Hg or higher with an increased cardiovascular risk to a target of 120mm Hg or lower (intensive treatment) or a target of 140mm Hg or lower (standard treatment).

The study was stopped early after a median follow-up of just over three years as individuals in the intensive treatment group had a 25% lower relative risk of major cardiovascular events, compared with those assigned to the standard-treatment group. Furthermore, individuals in the intensive-treatment group had a 27% lower relative risk of all-cause mortality. The SPRINT trial will undoubtedly change practice and guidelines.


High BP is a major risk factor for strokes, heart attacks, heart failure, kidney failure and cardiovascular morbidity and mortality. Treatment not only reduces the incidence of strokes and coronary events but also prevents left ventricular hypertrophy, heart failure, renal failure and dementia.12 Appropriate management of individuals with high BP should include correction of other cardiovascular risk factors. The fact remains that many individuals in the UK with high BP are inadequately controlled. Finally, it is imperative for healthcare professionals to assess treatment non-adherence by toxicological urine testing to prevent wrong measures being taken.


1.         Ezzati M, Lopez AD, Rodgers A, Vander Hoorn S, Murray CJ. Selected major risk factors and global and regional burden of disease. The Lancet 2002;360:1347-60.

2.         Roger VL, Go AS, Lloyd-Jones DM, Adams RJ, Berry JD, Brown TM, et al. Heart disease and stroke statistics –2011 update: a report from the American Heart Association. Circulation 2011;123:e18-e209.

3.         Stamler J, Neaton JD, Wentworth DN. Blood pressure (systolic and diastolic) and risk of fatal coronary heart disease. Hypertension 1989;13:I2-12.

4.         Thomopoulos C, Parati G, Zanchetti A. Effects of BP lowering on outcome incidence in hypertension. 1. Overview, meta-analyses, and meta-regression analyses of randomized trials. Journal of Hypertension 2014;32:2285-95.

5.         Staessen JA, Wang JG, Thijs L. Cardiovascular protection and BP reduction: a meta-analysis. The Lancet 2001;358:1305-15.

6.         NICE. CG127 Hypertension: clinical management of primary hypertension in adults, 2011. (accessed 19 April 2016).

7.         Antonios TF, Cappuccio FP, Markandu ND, Sagnella GA, MacGregor GA. A diuretic is more effective than a beta-blocker in hypertensive patients not controlled on amlodipine and lisinopril. Hypertension 1996;27:1325-8.

8.         MacGregor GA, Viskoper JR, Antonios TF, He FJ. Efficacy of candesartan cilexetil alone or in combination with amlodipine and hydrochlorothiazide in moderate-to-severe hypertension. Hypertension 2000;36:454-60.

9.         Jung O, Gechter JL, Wunder C, Paulke A, Bartel C, Geiger H, et al. Resistant hypertension? Assessment of adherence by toxicological urine analysis. Journal of Hypertension 2013;31:766-74.

10.       Lewington S, Clarke R, Qizilbash N, Peto R, Collins R. Age-specific relevance of usual BP to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. The Lancet 2002;360:1903-13.

11.       Group SR, Wright JT, Williamson JD, Whelton PK, Snyder JK, Sink KM, et al. A Randomized Trial of Intensive versus Standard Blood-Pressure Control. The New England Journal of Medicine 2015;373:2103-16.

12.       Thomopoulos C, Parati G, Zanchetti A. Effects of BP-lowering treatment. 6. Prevention of heart failure and new-onset heart failure - meta-analyses of randomized trials. Journal of Hypertension 2016;34:373-84.

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