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Effective treatment combines lifestyle changes especially the reduction of sodium intake , discontinuation of interfering substances, and the sequential addition of antihypertensive drugs to the initial triple therapy. Ultimately, replacing all current drugs by a simpler treatment regimen using SPC treatment is recommended to reduce pill burden and improve adherence to treatment. The optimal drug treatment of resistant hypertension has been poorly studied.
The most effective strategy seems to be additional diuretic treatment to decrease volume overload, together with the restriction of salt intake, particularly in patients with CKD. BP control may be improved by increasing the dose of the existing diuretic or by switching to a more potent thiazide-like diuretic chlorthalidone or indapamide.
Although resistant hypertension may show a BP reduction if the existing diuretic dose is further increased, most patients require the administration of additional drugs. Moreover, the efficacy and safety of spironolactone for the treatment of resistant hypertension has not yet been established in patients with significant renal impairment. Moreover, electrolytes and eGFR should be monitored soon after initiation and at least annually thereafter. Neither was as effective as spironolactone, but they did reduce BP significantly vs.
Direct vasodilators, such as hydralazine or minoxidil, are infrequently used because they may cause severe fluid retention and tachycardia. New BP-lowering drugs nitric oxide donors, vasopressin antagonists, aldosterone synthase inhibitors, neutral endopeptidase inhibitors, and endothelin antagonists are all under investigation. When spironolactone is not tolerated, replace with amiloride or eplerenone. Secondary hypertension is hypertension due to an identifiable cause, which may be treatable with an intervention specific to the cause.
A high index of suspicion and early detection of secondary causes of hypertension are important because interventions may be curative, especially in younger patients [e.
Interventions that treat the cause of secondary hypertension later in life are less likely to be curative i. Screening all hypertensive patients for secondary hypertension is not feasible or cost-effective; however, there are some general patient characteristics that suggest those more likely to have secondary hypertension and in whom screening should be considered after confirming that BP is elevated with ABPM Table It is beyond the scope of these Guidelines to describe the detailed clinical management of specific causes of secondary hypertension.
However, the commoner causes of secondary hypertension, clinical history, and screening tests are described in Table 26 , and the typical age distribution of these causes of secondary hypertension is shown in Table Review of these tables demonstrates that most screening can be undertaken with blood and urine tests, abdominal ultrasound, and echocardiography.
Referral to a specialist centre is recommended for additional investigations to confirm a suspected diagnosis of secondary hypertension and for clinical management. Other causes of secondary hypertension due to drugs and substances, and rarer monogenic causes, are described below and are summarized in Tables 28 and Medications and other substances that may increase blood presssure Medications and other substances may cause a sufficient increase in BP to raise the suspicion of secondary hypertension Table Consequently, a careful drug history is important when considering a diagnosis of secondary hypertension.
Moreover, other commonly used drugs such as non-steroidal anti-inflammatory drugs or glucocorticoids can antagonize the BP-lowering effect of antihypertensive medications in patients treated for hypertension, and may contribute to a loss of BP control. Genetic causes of secondary hypertension are usually due to single-gene disorders see section 6. Thus, they are usually associated with a suppressed plasma renin concentration PRC or plasma renin activity PRA , which is unusual in younger patients and especially those treated with antihypertensive medications e.
Thus, the finding of a suppressed PRC or PRA, especially whilst taking these drugs, should raise the suspicion of secondary hypertension due a salt-retaining state. Importantly, beta-blockers in particular, but also non-steroidal anti-inflammatory drugs, alpha-methyl dopa, or clonidine, suppress PRC and PRA. Hypertension emergencies are situations in which severe hypertension grade 3 is associated with acute HMOD, which is often life-threatening and requires immediate but careful intervention to lower BP, usually with intravenous i.
The hallmark of this condition is small artery fibrinoid necrosis in the kidney, retina, and brain. Patients with severe hypertension associated with other clinical conditions who are likely to require an urgent reduction of BP, e. Patients with sudden severe hypertension due to phaeochromocytoma , associated with organ damage. The most common emergency symptoms will depend of the organs affected but may include headache, visual disturbances, chest pain, dyspnoea, dizziness, and other neurological deficits.
In patients with hypertensive encephalopathy, the presence of somnolence, lethargy, tonic clonic seizures, and cortical blindness may precede a loss of consciousness; however, focal neurological lesions are rare and should raise the suspicion of stroke. Acute stroke , especially intracerebral haemorrhage, when associated with severe hypertension has often been termed a hypertension emergency, but a more cautious approach is now recommended for acute BP lowering in the emergency setting of acute stroke see section 8.
However, these patients will require urgent outpatient review to ensure that their BP is coming under control. Acute and severe increases in BP can sometimes be precipitated by ingestion of sympathomimetics such as meta-amphetamine or cocaine.
This can result in a hypertension emergency when there is evidence of acute HMOD. It is emphasized that many patients in an emergency department with acute pain or distress may experience an acute elevation in BP that will be restored to normal when the pain and distress are relieved, rather than requiring any specific intervention to lower BP.
For patients with a suspected hypertension emergency, a diagnostic workup is shown in Table Apart from acute BP lowering in stroke, there are no RCTs evaluating different treatment strategies for hypertensive emergencies. The key considerations in defining the treatment strategy are: Establishing the target organs that are affected, whether they require any specific interventions other than BP lowering, and whether there is a precipitating cause for the acute rise in BP that might affect the treatment plan e.
The type of BP-lowering treatment required. With regard to drug treatment, in a hypertension emergency, i. Recommended drug treatments for specific hypertension emergencies , are shown in Table 31 and an expanded range of possible drug choices is shown in Table Rapid uncontrolled BP lowering is not recommended as this can lead to complications. Hypertensive emergencies requiring immediate blood pressure lowering with intravenous drug therapy. Although i. However, low initial doses should be used because these patients can be very sensitive to these agents and treatment should take place in hospital.
Further comprehensive details on the clinical management of hypertension emergencies are available. The survival of patients with hypertension emergencies has improved dramatically over past decades, but these patients remain at high risk , and should be screened for secondary hypertension see section 8. After discharge from hospital, when BP has reached a safe and stable level on oral therapy, we recommend frequent, at least monthly, visits in a specialized setting until the optimal target BP is achieved and long-term specialist follow-up thereafter.
As discussed in section 4, white-coat hypertension is defined as an elevated office BP despite a normal out-of-office BP. Compared with normotensive people, white-coat hypertension is associated with an increased prevalence of dysmetabolic risk factors and asymptomatic organ damage. It is also associated with a greater risk of developing type 2 diabetes and sustained hypertension, as well as an overall increased risk of CV events. Office and out-of-office BP both home and ambulatory BP should be measured frequently, e. Treatment should consider lifestyle changes to reduce the elevated CV risk.
Whether or not patients with white-coat hypertension should receive antihypertensive drugs is unresolved. In white-coat hypertension, antihypertensive drugs have been shown to effectively and persistently lower office BP, with no concomitant reduction indeed, even a small increase of ambulatory BP values. However, it should be considered that people with white-coat hypertension have inevitably been well represented in trials documenting the protective effect of antihypertensive drugs, particularly those addressing conditions in which white-coat hypertension is more common, such as grade 1 hypertension or hypertension in older patients.
As reported in section 4. Such people usually have dysmetabolic risk factors and asymptomatic organ damage, which are substantially more frequent than in people who are truly normotensive. Masked hypertension is commoner in younger rather than older individuals, and in those with an office BP in the borderline hypertension range i.
Masked hypertension is associated with progression to sustained office hypertension, increased frequency of developing type 2 diabetes, and the presence of HMOD. The long-term risk of fatal and non-fatal CV events approaches that of patients with sustained hypertension. CV risk factors including organ damage and ideally both home and ambulatory BP should then be periodically monitored. Factors contributing to the out-of-office BP elevation e. The impact of antihypertensive drug treatment on CV outcomes in people with masked hypertension has never been studied.
Nevertheless, treatment with BP-lowering medication should be considered because these patients are at high CV risk, often have HMOD, and the adverse prognostic importance of out-of-office BP elevations has been well documented. Presently, no data are available from outcome trials for patients with MUCH; however, mindful of their high CV risk, treatment uptitration should be considered to ensure that that both office and out-of-office BP are controlled. The prevalence of hypertension increases with age.
Most hypertension across the age span is due to systolic hypertension; however, elevations of DBP and isolated diastolic hypertension, when they occur, are more common in younger rather than older patients. All younger adults with grade 2 or more severe hypertension should be offered lifestyle advice and drug treatment, as well as high-risk younger adults with grade 1 hypertension i. There is controversy about whether younger adults with uncomplicated grade 1 hypertension should be treated because of the obvious difficulty in conducting conventional clinical outcome trials in younger adults in whom the outcomes only occur after many years.
Thus, despite the absence of RCT evidence demonstrating the benefits of antihypertensive treatment in younger adults with uncomplicated grade 1 hypertension, treatment with BP-lowering drugs may be considered prudent.
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If a decision is taken not to offer treatment or treatment is declined, lifestyle advice should be prescribed, and longer-term follow-up is essential as BP will invariably rise. Other interventions, e. Some young, healthy people, and men in particular, may present with isolated grade 1 systolic hypertension i.
A recent examination of prospective data from the Chicago Heart Association Detection Project found that young men with isolated systolic hypertension had a CV risk similar to that of individuals with high—normal BP and that isolated systolic hypertension in the young was closely associated with smoking. For many years, advanced age has been a barrier to the treatment of hypertension because of concerns about potential poor tolerability, and even harmful effects of BP-lowering interventions in people in whom mechanisms preserving BP homeostasis and vital organ perfusion may be more frequently impaired.
This approach is not appropriate, because evidence from RCTs has shown that in old and very old patients, antihypertensive treatment substantially reduces CV morbidity and CV and all-cause mortality , see section 7. Moreover, treatment has been found to be generally well tolerated.
However, older patients are more likely to have comorbidities such as renal impairment, atherosclerotic vascular disease, and postural hypotension, which may be worsened by BP-lowering drugs. Older patients also frequently take other medications, which may negatively interact with those used to achieve BP control. A further important caveat is that RCTs have not included very frail patients, dependent patients, and patients with postural hypotension. It is thus uncertain whether, and to what extent, such patients would benefit from BP-lowering treatment in the context of their comorbidities and reduced life expectancy.
That said, age alone must never be a barrier to treatment because high BP is an important risk factor even at the most advanced ages. It is recommended that older patients are treated according to the treatment algorithm outlined in section 7. In very old patients, it may be appropriate to initiate treatment with monotherapy. In all older patients, when combination therapy is used, it is recommended that this is initiated at the lowest available doses.
In all older patients, and especially very old or frail patients, the possible occurrence of postural BP should be closely monitored and symptoms of possible hypotensive episodes checked by ABPM. Unless required for concomitant diseases, loop diuretics and alpha-blockers should be avoided because of their association with injurious falls. A key emphasis in treating older patients, and especially the very old, is to carefully monitor for any adverse effects or tolerability problems associated with BP-lowering treatment, keeping in mind that adverse effects can be more frequent than reported in RCTs, in which specific medical expertise and close patient supervision may minimize adverse effects and tolerability problems.
An important consideration is frail, dependent older patients, including those with orthostatic hypotension. These have been excluded from RCTs. The SPRINT trial showed the benefits of BP-lowering treatment being extended to recruited patients who were at the frailer end of the spectrum, including those with reduced gait speed.
In some patients, the best achievable BP may be higher than the recommended target, but it should be recognised that any amount of BP lowering is likely to be worthwhile and associated with a reduced risk of major CV events especially stroke and heart failure and mortality. Maternal risks include placental abruption, stroke, multiple organ failure, and disseminated intravascular coagulation.
Hypertension in pregnancy is not a single entity but comprises: Pre-existing hypertension: precedes pregnancy or develops before 20 weeks of gestation, and usually persists for more than 6 weeks post-partum and may be associated with proteinuria. Gestational hypertension: develops after 20 weeks of gestation and usually resolves within 6 weeks post-partum. Pre-existing hypertension plus superimposed gestational hypertension with proteinuria.
It occurs more frequently during the first pregnancy, in multiple pregnancy, in hydatidiform mole, in antiphospholipid syndrome, or with pre-existing hypertension, renal disease, or diabetes. It is often associated with foetal growth restriction due to placental insufficiency and is a common cause of prematurity. Antenatally unclassifiable hypertension: this term is used when BP is first recorded after 20 weeks of gestation and it is unclear if hypertension was pre-existing.
Reassessment 6 weeks post-partum will help distinguish pre-existing from gestational hypertension. BP in pregnancy should be measured in the sitting position or the left lateral recumbent during labour with an appropriately sized arm cuff at heart level and using Korotkoff V for DBP.
Manual auscultation remains the gold standard for BP measurement in pregnancy, because automated devices tend to under-record the BP and are unreliable in severe pre-eclampsia. Only validated devices should be used in pregnancy. ABPM helps avoid unnecessary treatment of white-coat hypertension, and is useful in the management of high-risk pregnant women with hypertension and those with diabetic or hypertensive nephropathy.
Basic laboratory investigations recommended for monitoring pregnant hypertensive women include urine analysis, blood count, haematocrit, liver enzymes, serum creatinine, and serum uric acid increased in clinically evident pre-eclampsia. Hyperuricaemia in hypertensive pregnancies identifies women at increased risk of adverse maternal and foetal outcomes. All pregnant women should be assessed for proteinuria in early pregnancy to detect pre-existing renal disease and, in the second half of pregnancy, to screen for pre-eclampsia.
In addition to basic laboratory tests, the following investigations may be considered: Ultrasound investigation of the kidneys and adrenals, and plasma or urinary fractionated metanephrine assays in pregnant women with a history suggestive of phaeochromocytoma. Doppler ultrasound of uterine arteries performed after 20 weeks of gestation to detect those at higher risk of gestational hypertension, pre-eclampsia, and intrauterine growth retardation.
Women at high or moderate-risk of pre-eclampsia should be advised to take — mg of aspirin daily from weeks 12— Moderate-risk of pre-eclampsia includes one or more of the following risk factors: First pregnancy. The goal of drug treatment of hypertension in pregnancy is to reduce maternal risk; however, the agents selected must be safe for the foetus. The benefits of drug treatment for mother and foetus in hypertension in pregnancy have not been extensively studied, with the best data from a single trial using alpha-methyldopa, performed 40 years ago.
However, secondary analysis suggested that tighter control of BP may reduce the risk of developing more severe hypertension and pre-eclampsia.
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Most women with pre-existing hypertension and normal renal function will not have severe hypertension and are a low risk for developing complications during pregnancy. Indeed, some of these women may be able to withdraw their medication in the first half of pregnancy because of the physiological fall in BP. Women with pre-existing hypertension may continue their current antihypertensive medication, but ACE inhibitors, ARBs, and direct renin inhibitors are contraindicated due to adverse foetal and neonatal outcomes.
Methyldopa, labetalol, and CCBs are the drugs of choice. Beta-blockers may induce foetal bradycardia; consequently, if used, their type and dose should be carefully selected, with atenolol best avoided. Diuretic therapy is generally avoided because plasma volume is reduced in women who develop pre-eclampsia.
There are no data to define the optimal BP treatment target in pregnant women. Nevertheless, for pragmatic reasons, if treatment is initiated it is important to suggest a treatment target to calibrate how much treatment to give. The selection of the antihypertensive drug and its route of administration depends on the expected time of delivery. Pharmacological treatment with i. Intravenous hydralazine is no longer the drug of choice as it is associated with more perinatal adverse effects than other drugs.
Intravenous urapidil can also be considered. In hypertensive crises, i. Both labetalol and nicardipine have shown to be safe and effective for the treatment of severe pre-eclampsia if i. BP-lowering therapy is necessary. Intravenous sodium nitroprusside is contraindicated in pregnancy because of an increased risk of foetal cyanide poisoning. The drug of choice when pre-eclampsia is associated with pulmonary oedema is nitroglycerin glyceryl trinitrate , given as an i. Delivery is indicated i urgently in pre-eclampsia with visual disturbances or haemostatic disorders, and ii at 37 weeks in asymptomatic women.
Post-partum hypertension is common in the first week. Any drug recommended can be used according to the hypertension treatment algorithm shown in Figure 4 , with the caveats: i methyldopa should be avoided because of the risk of post-partum depression and ii consideration should be given to drug choice in breastfeeding women. All antihypertensive drugs taken by the nursing mother are excreted into breast milk. Most are present at very low concentrations except for propranolol and nifedipine, with breast milk concentrations similar to those in maternal plasma.
Reference to prescribing information in breastfeeding women is important. Women experiencing hypertension in their first pregnancy are at increased risk in a subsequent pregnancy. The earlier the onset of hypertension in the first pregnancy, the higher the risk of recurrence in a subsequent pregnancy. Women who develop gestational hypertension or pre-eclampsia are at increased risk of hypertension, stroke, and ischaemic heart disease in later adult life. Therefore, annual visits to a primary care physician to check BP and metabolic factors are recommended for these patients. Further detail on the management of hypertension and other CV disorders in pregnancy is available.
The rise in BP appears to be related to the oestrogen content and may be less likely with the progestogen-only oral contraceptive pill. Older studies have demonstrated a relationship between the oral contraceptive pill and venous thrombosis and venous thromboembolism, and, to a lesser extent, myocardial infarction especially with concomitant smoking history and stroke. Thus, the use of oral contraceptives should consider the risks and benefits for the individual patient. Changes in BP should be carefully evaluated with follow-up readings.
In such patients, alternative forms of contraception should be offered. Discontinuation of combined oestrogen—progestin oral contraceptives in women with hypertension may improve their BP control. Cross-sectional studies have long established that menopause doubles the risk of developing hypertension, even after adjusting for factors such as age and BMI.
In summary, current evidence suggests that the use of hormone-replacement therapy is not associated with an increase in BP. Moreover, it is not contraindicated in women with hypertension, and women with hypertension may be prescribed hormone-replacement therapy as long as BP levels can be controlled by antihypertensive medication. In comparison with the non-black population, hypertension is more prevalent in the black population living in Europe, similarly to that reported for the USA. Afro-American US patients, in contrast to the much scarcer database available for European black people, and thus we extrapolate from US data.
However, this extrapolation requires some caution as differences between the North American and the European black population exist, especially with regard to socioeconomic status, CV risk, , and the response to antihypertensive drug treatment. However, to achieve an effective BP reduction and BP control, salt restriction is particularly important in black patients, in whom it may lead to greater BP falls and more favourably impact on the effectiveness of BP-lowering drug treatment. Angioedema appears more common with ACE inhibitors in black patients, which may favour the preferred use of ARBs in this population.
Despite some progress in recent years, data on hypertension prevalence, management, and control in European black patients and in other immigrant populations such as European individuals from South Asia are still scarce, , which makes this field an important area for future research. There is no evidence that the BP response to treatment in other ethnic groups differs from that reported in the general population in Europe. Except in patients with low grade 1 hypertension or frail older patients, in whom initial treatment with a single drug may be more appropriate.
High BP is a common feature of type 1 and, particularly, type 2 diabetes. Moreover, masked hypertension and a blunted nocturnal fall in BP are not infrequent in people with diabetes. Substantial evidence supports the benefits of BP reduction in people with diabetes to reduce major macrovascular and microvascular complications of diabetes, as well as reducing mortality.
Proven benefits of BP-lowering treatment in diabetes also include a significant reduction in the rate of end-stage renal disease, , retinopathy, 1 and albuminuria. When considering treatment for hypertension, it is important to exclude significant postural hypotension, which can be marked in people with diabetes due to autonomic neuropathy. This approach ensures that the treatment strategy includes an ACE inhibitor or ARB, which has been shown to reduce albuminuria and the appearance or progression of diabetic nephropathy more effectively than other drug classes.
Recent RCTs have shown that some antidiabetes agents the selective inhibitors of sodium glucose cotransporter 2 in the kidney can reduce office and ambulatory BP by several mmHg, , and that this occurs even when people are treated with antihypertensive drugs. This may help improve BP control see below , which is especially difficult in diabetes, and may reduce the progression of CKD — see also section 8.
There has been considerable debate about the target BP that should be achieved in people with diabetes see section 7. BP targets for renoprotection for patients with diabetic kidney disease are discussed in section 8. A recent meta-analysis has shown that BP lowering significantly reduced end-stage renal disease in patients with CKD, but only in those with albuminuria and without any beneficial effect on CV events.
Reduction of albuminuria has also been considered as a therapeutic target. Analyses of data from RCTs have reported that changes in urinary albumin excretion are predictors of renal and CV events.
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The combination of two RAS blockers is not recommended. Lifestyle advice, especially sodium restriction, may be especially effective at aiding BP lowering in patients with CKD. Thus, careful monitoring of blood electrolytes and eGFR is essential, but clinicians should not be alarmed by the anticipated decline in GFR when treatment is initiated. This decline usually occurs within the first few weeks of treatment and stabilizes thereafter.
If the decline in GFR continues or is more severe, the treatment should be stopped, and the patient investigated to determine the presence of renovascular disease. Hypertension is the most frequent comorbidity in patients with COPD, and coincidence of the two diseases may affect 2. The presence of COPD also has an impact on the selection of antihypertensive drugs, which should consider their effects on pulmonary function. Concern has been predominantly directed to the use of beta-blockers, although there is evidence that in COPD these drugs maintain their CV-protective effects.
That said, when tolerated, the use of cardiac beta1-selective beta-blockers in patients with COPD has proven to be safe in different settings, including hypertension. Therefore, in general, diuretics are not recommended for widespread use in hypertensive patients with COPD. In conclusion, management of hypertensive patients with COPD should include lifestyle changes, among which cessation of smoking is essential. If the BP response is poor, or depending on other comorbidities, thiazides or thiazide-like diuretics and beta1-selective beta-blockers can be considered.
There are strong epidemiological relationships between CAD and hypertension. More compelling is the beneficial effect of BP treatment on reducing the risk of myocardial infarction. Similar findings were also reported from another analysis of RCT data evaluating the relationships between achieved BP and risks of CV outcomes. Other analyses do not support the existence of a J-curve, even in hypertensive patients at increased CV risk.
Hypertension is the leading risk factor for the development of heart failure, 7 and most patients with heart failure will have an antecedent history of hypertension. Hypertension also causes LVH, which impairs LV relaxation so-called diastolic dysfunction and is a potent predictor of heart failure, even when LV systolic function is normal and there is no preceding myocardial infarction HFpEF. Hypertension-dependent fibrosis and structural alteration of large and small arteries microvascular disease also contribute.
Treating hypertension has a major impact on reducing the risk of incident heart failure and heart failure hospitalization, especially in old and very old patients. It is unclear how low BP should be lowered in patients with heart failure. However, some patients may achieve even lower BP levels than this because of the desirability to remain on treatment with guideline-directed heart failure medications, which, if tolerated, should be continued because of their protective effect.
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Heart failure guideline-directed medications are recommended for the treatment of hypertension in patients with HFrEF. HFpEF patients commonly have multiple comorbidities that may adversely affect outcomes and complicate management.
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A lowest safety BP value is not given as many patients receiving intensive treatment for heart failure may achieve much lower BP levels than recommended BP targets. Hypertension is a major risk factor for haemorrhagic and ischaemic stroke, and a risk factor for recurrent stroke.
BP management during the acute phase of haemorrhagic and ischaemic stroke remains an area of uncertainty. BP is often elevated at presentation with acute stroke, but often declines without intervention. In acute intracerebral haemorrhage, an increased BP is common and is associated with a greater risk of haematoma expansion, increased risk of death, and a worse prognosis for neurological recovery. Thus, careful lowering of BP via i.
The beneficial effects of BP reduction are even less clear in acute ischaemic stroke. A key consideration is whether the patient will receive thrombolysis, because observational studies have reported an increased risk of intracerebral haemorrhage in patients with a markedly elevated BP who received thrombolysis. The benefit of acute BP lowering in patients with acute ischaemic stroke who do not receive thrombolysis is uncertain.
A meta-analysis suggested that BP lowering early after acute ischaemic stroke had a neutral effect on the prevention of death or dependency. We recommend resumption of BP-lowering therapy several days after stroke, or immediately after TIA, for previously treated or untreated patients with hypertension, for prevention of both recurrent stroke and other CV events. The appropriate BP targets to prevent recurrent stroke are uncertain, but should be considered in the context of a consistent finding in many meta-analyses that stroke is the one major CV event that is reduced at lower achieved BP levels.
Prevention of stroke is a consistent benefit of antihypertensive therapy and has been observed in all large RCTs using different drug regimens. However, individual RCTs comparing modern treatment regimens , and meta-analyses suggest that beta-blockers are less effective at stroke prevention than other classes of antihypertensive agents.
Thus, optimal antihypertensive treatment for stroke prevention should not include beta-blockers unless there is a compelling indication for their use, mindful of the fact that the most common recurrent event after stroke is a further stroke rather than myocardial infarction. One study showed that achieving better BP control over 4 years reduced the progression of cerebral white matter lesions and the decrease in global cognitive performance.
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