HYPERTENSION

Hypertension can be defined as a condition in which blood pressure (BP) is

elevated to a level likely to lead to adverse consequences. There is no clear-cut
blood pressure threshold separating normal blood pressure from high blood
pressure, with hypertension arbitrarily defined as a systolic blood pressure equal
to or greater than 140 mmHg and/or diastolic blood pressure equal to or greater
than 90 mmHg. The risk of complications is related to the degree to which blood
pressure is elevated

. • The World Health Organization has identified hypertension as the leading risk
factor for death worldwide. The complications of hypertension include stroke,
myocardial infarction, heart failure, renal failure and dissecting aortic aneurysm.
Modest reductions in blood pressure result in substantial reductions in the
relative risks of these complications.

• Hypertension should not be seen as a risk factor in isolation, and decisions on

management should not focus on blood pressure alone but on the total
cardiovascular risk present for an individual, which, in the absence of established
cardiovascular (CV) disease, should be calculated using a validated CV risk
calculator such as QRisk2.

• The diagnosis of hypertension should be based on the results of ambulatory

blood pressure monitoring or home blood pressure monitoring, not on clinic
blood pressure readings

. • Non-pharmacological interventions are important and include weight

reduction, avoidance of excessive salt and alcohol, increased intake of fruit and
vegetables and regular physical activity. Other cardiovascular risk factors, such as
smoking, dyslipidaemia and diabetes, should be addressed.

• Different antihypertensive drugs are available. Drug choice should aim to

maximise blood-pressure-lowering effectiveness and minimise patient side effects
. • The most appropriate choice of initial drug therapy depends on the age and
racial origin of the patient, as well as the presence of other medical conditions.
For patients younger than 55 years, an angiotensin-converting enzyme (ACE)
inhibitor is recommended as first-line treatment. For older patients and people of
black African or Caribbean origin of any age, a calcium channel blocker is an
appropriate initial choice. Most people need a combination of drugs to achieve
adequate blood pressure control.

HEART FAILURE
• Heart failure is a common condition that affects the quality of life, causing
fatigue, breathlessness and oedema. It often has a poor prognosis.

• Heart failure is a maladaptive condition with haemodynamic and

neurohormonal disturbances. Increased understanding of its pathophysiology and
the strength of the evidence base allow a rational approach to therapeutic
management.

• The aims of drug treatment are to control symptoms and improve survival. By
slowing disease progression, the aim is to maintain quality of life.

• Angiotensin-converting enzyme (ACE) inhibitors, β-blockers and

mineralocorticoid receptor antagonists are first-line options in treating patients
with systolic dysfunction.

• Angiotensin II receptor blockers (ARBs) are an alternative choice in patients

intolerant of or resistant to ACE inhibitors or mineralocorticoid receptor
antagonist therapy.

• Diuretics are used for symptomatic management of heart failure and are
combined with other agents in the treatment of systolic dysfunction.

• The use of sacubitril/valsartan should be considered under specialist advice in

patients with systolic dysfunction who have ongoing symptoms of heart failure
despite optimal therapy
. • Ivabradine should be considered under specialist advice in patients with
systolic dysfunction who have had a hospital admission for heart failure in the
preceding 12 months but have stabilised on standard therapy for at least 4 weeks.

• Digoxin may still have a role in improving symptoms and reducing the rate of
hospitalisation for patients with heart failure in sinus rhythm, but it has not been
demonstrated to affect mortality. The combination of hydralazine and nitrate may
still have a place for specific patients on the advice of a specialist.

• Heart failure is a condition in which integration of pharmaceutical care within

multidisciplinary models of patient care can improve clinical outcomes for
patients and contribute to the continuity of care

CHD
• Coronary heart disease (CHD) is common, often fatal and frequently
preventable.

• High dietary fat, smoking and sedentary lifestyle are risk factors for CHD and
require modification if present.

• Hypertension, hypercholesterolaemia, diabetes mellitus, obesity and personal

stress are also risk factors and require optimal management

. • Stable angina should be managed with nitrates for pain relief and β-blockers,
unless contraindicated, for long-term prophylaxis. Where β-blockers are
inappropriate, the use of calcium channel blockers and/or nitrates may be
considered

. • Acute coronary syndromes arise from unstable atheromatous plaques and

may be classified as to whether there is ST-elevation myocardial infarction
(STEMI) or non-ST-elevation myocardial infarction (NSTEMI).

• ST elevation on the electrocardiogram (ECG) indicates an occluded coronary

artery and is used to determine treatment with fibrinolysis or primary
angioplasty.
 • P atients with NSTEMI may have experienced myocardial damage, are at
increased risk of death and may benefit from a glycoprotein IIb/IIIa inhibitor

VENOUS THROMBOEMBOLISM
• Venous thromboembolism (VTE) is the development of a ‘thrombus’, principally
containing fibrin and red blood cells, in the venous circulation. This most often
occurs as a deep vein thrombosis (DVT) in the deep, as distinct from the
superficial, veins of the legs.

• If part of a thrombus in the venous circulation breaks off and enters the right
heart, it may become lodged in the pulmonary arterial circulation, causing
pulmonary embolism (PE).

• Combinations of sluggish blood flow and hypercoagulability are the most

common causes of VTE. Vascular injury is also a recognised causative factor.

• Treatment of VTE involves the use of anticoagulants and, in severe cases,

thrombolytic drugs

. • Anticoagulant therapy often involves an immediate-acting agent, such as

heparin, followed by maintenance treatment with an oral anticoagulant, such as
warfarin.

• Another option is the use of a direct oral anticoagulant (DOAC), also

sometimes known as a non–vitamin K antagonist oral anticoagulant/novel oral
anticoagulant (NOAC), with a marketing authorisation for such use. The use of
heparin in the early stages is not necessary with all of the DOACs, but
requirements change, and thus product literature should be consulted.

• Unfractionated heparins increase the rate of interaction of thrombin with

antithrombin III 1000-fold and prevent the production of fibrin from fibrinogen.

• Low-molecular-weight heparins inactivate factor Xa, have a longer half-life and

produce a more predictable response than unfractionated heparins
. • Warfarin is the most widely used coumarin because of potency, reliable
bioavailability and an intermediate half-life of elimination (36 hours).

• Warfarin consists of an equal mixture of two enantiomers, (R)- and (S)-

warfarins, that have different anticoagulant potencies and routes of metabolism.
The latter enantiomer is a much more potent anticoagulant.

• DOACs currently available include dabigatran etexilate, a direct thrombin

(factor IIa) inhibitor, and apixaban, e doxaban and rivaroxaban, which are direct
inhibitors of activated factor Xa.

Arterial thromboembolism
• Arterial thromboembolism is normally associated with vascular injury and
hypercoagulability

 ACUTE MI IS THE COMON CAUSE OF arterial throbosis

• Arterial thromboembolism affecting the cerebral circulation results in either

transient ischaemic attacks (TIAs) or, in more severe cases, cerebral infarction
(stroke).

• Arterial thrombosis is the development of a ‘thrombus’ consisting of platelets,

fibrin, red blood cells and white blood cells in the systemic circulation.

• An embolus may result in peripheral arterial occlusion, either in the lower

limbs or in the cerebral circulation (where it may cause thromboembolic stroke).