Hypertension ESC

Guideline 2018
3.4 Blood pressure relationship with risk
of cardiovascular and renal events

• SBP appears to be a better predictor of events than DBP after

the age of 50 yo
• High DBP is associated with increased CV risk and is more
commonly elevated in younger (<50 years) vs. older patients.
• DBP tends to decline from midlife as a consequence of arterial
stiffening
Hypertension and total cardiovascular risk
assessment by SCORE
3.6 Importance of hypertension-mediated organ damage in refining
cardiovascular risk assessment in hypertensive patients

• HMOD more accurately describes hypertension-induced structural

and/or functional changes in major organs (i.e. the heart, brain,
retina, kidney, and vasculature)

• the inclusion of HMOD assessment is important in patients with

hypertension and helps identify high-risk or very high-risk
hypertensive patients who may otherwise be misclassified as
having a lower level of risk by the SCORE system
BLOOD PRESSURE MEASUREMENT
4.3 Out-of-office blood pressure
measurement
4.7 White-coat hypertension and masked
hypertension
• White-coat hypertension  is elevated in the office, but is
normal when measured by ABPM HBPM, or both.
• masked hypertension’  elevated when measured by HBPM
or ABPM
• ‘true normotension’ is used when both office and out-of-office
BP measure-ments are normal, and ‘sustained hypertension’ is
used when both are abnorma
Clinical evaluation and assessment of hypertension- mediated organ damage in patients with hypertension
Physical
examination
and clinical
investigations
The main advantage
of detecting HMOD is
that it may reclassify
a patient’s SCORE
risk assessment from
low to moderate or
from moderate to
high risk
Characteristics of hypertension- mediated organ damage
1. The heart in hypertension  EKG +transthoracic echocardiography in hypertension
The blood vessels in hypertension

• 5.5.2.1 Carotid artery

• Carotid intima-media thickness (IMT) quantified by carotid ultra-

sound, and/or the presence of plaques, predicts CV risk.
• carotid IMT >0.9 mm is considered abnormal ; but the upper limit of normality varies with
age.
• The presence of a plaque can be identified by an IMT >_1.5 mm, or by a focal increase
in thickness of 0.5 mm or 50% of the surrounding carotid IMT value.
• Stenotic carotid plaques have a strong predictive value for both he presence of carotid
plaques will automatically reclassify patients from intermediate to high
risk;
• routine carotid imaging is not recommended unless clinically indicated (i.e. presence of
carotid bruit, previous TIA or cerebrovascular disease, or as part of the assessment of
patients with evidence of vascular disease
5.5.2.2 Pulse wave velocity A PWV >10 m/s is considered a con-
servative estimate of significant alterations of aortic function in
middle-aged hypertensive patients.

5.5.2.3 Ankle–brachial index  A low ABI (i.e. <0.9) indicates lower

extremity artery disease (LEAD), is usually indicative of advanced
atherosclerosis
Treatment of hypertension
Office vs.
home and
ambulatory
blood pressure
targets
Treatment of
hypertension
 Moderation of alcohol
consumption
Hypertensive men who drink
alcohol should be advised to
limit their consumption to 14
units per week and women to 8
units per week (1 unit is equal
to 125 mL of wine or 250 mL of
beer). Alcohol-free days during
the week and avoidance of
binge drinking are also advised.
Drug treatment strategy for hypertension
Resistent Hypertension
Secondary Hipertension
Hypertension
urgencies and
emergencies
White-coat hypertension and Masked
hypertension
MANAGEMENT
• Oral Contraceptive pills and hypertension
- Combined estrogen–progesterone oral contraceptive pills can be associated with a small but significant increase in BP and the
development of hypertension in about 5% of users.
- The rise in BP appears to be related to the oestrogen content and may be less likely with the progestogen-only oral contraceptive
pill

• Hormone- replacement therapy and hypertension

- Hormone-replacement therapy and selective oestrogen receptor modulators should not be used for primary or secondary
prevention of CVD. 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
Hypertension and COPD
• Patients with hypertension and COPD are at particularly high CV risk.
• Treatment of COPD with anticholinergic agents and long-acting beta-2 adrenoceptor agonists may adversely
affect the CV system (increase heart rate and BP).
• In conclusion, management of hypertensive patients with COPD should include lifestyle changes, among
which cessation of smoking is essential. CCBs, ARBs or ACEIs, or the CCB/RAS blocker combination are
recommended as the initial drugs of choice.
• If the BP response is poor, or depending on other comorbidities, thiazides or thiazide-like diuretics and beta1-
selective beta-blockers can be considered.
Hypertension and Vascular Disease
1. Carotid atherosclerosis
• Reducing BP regresses carotid IMT and may delay the intimal atherosclerotic process.
• There appear to be differential drug effects on IMT regression, with CCBs having greater efficacy than diuretics and
beta blockers, and ACE inhibitors more than diuretics.
• Patients with carotid plaques are at high risk of atheroembolic stroke and CV events, and BP
lowering should be complemented by lifestyle advice and treatment with statins and antiplatelet therapy

2. Arterioscclerosis and increased arterial stiffness

• Large artery stiffening is a major factor contributing to the rise in SBP and fall in DBP with ageing. Arterial stiffness
is usually measured in studies as PWV.
• Pharmacodynamic RCTs and meta-analyses suggest that ACE inhibitors and ARBs may reduce PWV beyond the
effect of BP lowering on a long-term basis. Whether RAS blockers are more effective than other antihypertensive
drugs in this regard has not been demonstrated.
Hypertension in valvular disease and aotopathy
Coarctation of the aorta
• Treatment of aortic coarctation is predominantly surgical and usually done in childhood.
• Even after surgical correction, these patients may develop systolic hypertension at a young age and require long-term follow-up.
• Few patients with aortic coarctation remain undetected until adult life, and by then often have severe hypertension, HMOD (especially
LVH and LV dysfunction), and an extensive collateral circulation below the coarctation.

Prevention of aortic dilation and dissection of high risk subjects

• All hypertensive patients with aortic dilatation, whether associated with Marfan syndrome, bicuspid aortic valve disease, or not, should
have their BP controlled <_ 130/80 mmHg.
• In patients with Marfan syndrome, prophylactic use of ACE inhibitors, ARBs, or beta-blockers seems to be able to reduce either the
progression of the aortic dilation or the occurrence of complications.
Hypertension bicuspid aortic valve related aortopathy
• Tricuspid aortic valve disease is associated with an aortopathy, and the risk of development of aortic dilation is higher in patients with
bicuspid aortic valve disease than in the normal population and is probably exacerbated by hypertension.
• BP should be tightly controlled in patients with bicuspid aortic valve disease and targeted 130/80 mmHg if tolerated.
Hypertension and sexual dysfunction
• Compared with the normotensive population, the prevalence of sexual dysfunction is greater in hypertensive
individuals, in whom it presents an important cause of low adherence to or discontinuation of antihypertensive
treatment.
• Sexual dysfunction may be triggered or aggravated by treatment with thiazide or thiazide-like diuretics,
conventional beta-blockers, or centrally acting agents (e.g. clonidine), while ACE inhibitors, ARBs, CCBs, or
vasodilating betablockers may have neutral or even beneficial effects.
• However, it seems prudent for unstable patients with high CV risk or severe uncontrolled hypertension to defer
sexual activity until their condition is stabilized and treatment for erectile dysfunction can be initiated.
• In men reporting sexual dysfunction, the antihypertensive agents more likely to be associated with this effect
(e.g. beta-blockers and thiazide diuretics) should be avoided or replaced, unless strictly necessary for the
patient’s clinical condition
Hypertension and cancer therapy
• The increase frequently occurs during the first months after starting the anticancer therapy, It follows that
office BP should be measured weekly during the initial part of the first cycle of therapy and at least every 2–3
weeks thereafter.
• After the first cycle is completed and BP values appear to be stable, BP can be measured at the time of the
routine clinical evaluations or assessed by HBPM.
• Patients developing hypertension (>_140/90 mmHg), or showing an increase in DBP >_20 mmHg compared
with pretreatment values, should initiate or optimize antihypertensive therapy, for which RAS blockers and
CCBs may be considered the preferred drugs, and a RAS blocker-CCB combination is a frequently needed
strategy.
• CCBs should only be of the dihydropiridine type, because diltiazem and verapamil block the CYP3A4
isoenzyme, which is involved in the metabolic pathway of sorafenib, increasing the drug’s levels and leading
to potential toxicity
Managing concomitant cardiovascular disease risk

• Statin and lipid lowering drugs

• Patients with hypertension, and more so those with type 2 diabetes or metabolic syndrome, often have atherogenic
dyslipidaemia characterized by elevated triglycerides and LDL cholesterol (LDL-C), and low HDL cholesterol (HDL-C).
• When overt CVD is present and the CV risk is very high, statins should be administered to achieve LDL-C levels of <1.8
mmol/L (70 mg/dL) or a reduction of >_50% if the baseline LDL-C is between 1.8 and 3.5 mmol/L (70 and 135 mg/dL).
• In patients at high CV risk, an LDL-C goal of <2.6 mmol/L (100 mg/dL) or a reduction of >_50% if the baseline LDL-C
is between 2.6 and 5.2 mmol/L (100 and 200 mg/dL) is recommended.
• Beneficial effects of statin therapy have also been shown in patients with a previous stroke with LDL-C targets <2.6
mmol/L
(100 mg/dL). Whether they also benefit from a target of <1.8 mmol/L (70 mg/dL) is open to future research.
• Evidence suggests that many patients with hypertension would benefit from statin therapy
• Antiplatelet therapy and anticoagulant therapy
• The most common complications of hypertension are related to thrombosis.
• Hypertension predisposes to a prothromboticstate, and also predisposes to LEAD, heart failure, or AF,
which are common conditions associated with thromboembolism, whether systemic or venous.
• Antiplatelet and anticoagulant therapy use in patients with hypertension.
• In summary, aspirin is not recommended for primary prevention in hypertensive patients without CVD.
For secondary prevention, the benefit of antiplatelet therapy in patients with hypertension may be
greater than the harm.
Glucose lowering drugs and blood pressure
 New generations of antidiabetes drugs, i.e. dipeptidyl peptidase 4 inhibitors and glucagon-like peptide 1
agonists, slightly reduce BP, and also body weight with glucagon-like peptide 1 agonists.
 Two glucagon-like peptide 1 agonists (liraglutide and semaglutide) reduced CV and total mortality, but not
heart failure, in patients with type 2 diabetes.
 Glucagon-like peptide 1 agonists and dipeptidyl peptidase 4 inhibitors to prevent heart failure.
 Inhibitors of sodium-glucose co-transporter-2 are the only glucose-lowering drug class to reduce BP beyond
the projected impact of weight reduction on BP.
 Empaglifozine and canagliflozin have demonstrated a reduction in heart failure and total and CV mortality,
and a protective effect on renal function.
Patient follow up
• Patient at least once within the first 2 months to evaluate the effects on BP and assess possible side effects
until BP is under control.
• The frequency of review will depend on the severity of hypertension, the urgency to achieve BP control, and
the patient’s comorbidities.
• Once the BP target is reached, a visit interval of a few months is reasonable and evidence has been obtained
that no difference exists in BP control between 3 and 6 month intervals