CVS e-book Flashcards

1
Q

What is cardiovascular disease?

A

Cardiovascular disease can be described as a disease of the heart and circulation, and includes ischaemic heart disease, acute coronary syndrome/s, myocardial infarction, stroke and congenital heart disease. Cardiovascular disease results principally from atherosclerosis of the arteries in which fatty plaques (atheroma) build up in various arteries of the circulation. The build-up of atheroma can result in formation of local thrombosis (blood clot) which ultimately blocks the flow of blood. Cardiovascular disease becomes increasingly common with age particularly in those aged > 60 years.

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2
Q

What are the risk factors associated with cardiovascular disease?

A
 Smoking/tobacco use 
 High cholesterol
 Hypertension 
 Obesity
 Lack of physical exercise 
 Diabetes
 Excessive alcohol use 
 Poor diet
 Psychosocial stress
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3
Q

What is meant by primary prevention of cardiovascular disease?

A

From a public health perspective the aims of primary prevention are to prevent the development of cardiovascular disease at both the individual and the population level. For this reason identifying and assessing at-risk individuals is important in order that lifestyle changes and lipid modification are offered.

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4
Q

What is meant by secondary prevention of cardiovascular disease?

A

Secondary prevention is concerned with prevention of further cardiovascular events occurring in an individual who is already known to have cardiovascular disease and who has experienced a cardiovascular event, for example, myocardial infarction. Secondary prevention includes lifestyle changes, drug treatments and rehabilitation appropriate to the cardiovascular event experienced. An example is secondary prevention after myocardial infarction where lifestyle modification, drug treatment, such as the quartet of ACE inhibitors, beta blockers, antiplatelets and statins, are used together with a programme of cardiac rehabilitation.

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5
Q

Normal blood pressure readings

A

Normal systolic blood pressure readings are considered to be below 120mmHg (and above 90mmHg). Normal diastolic blood pressure readings are considered to be below 80mmHg (and above 60mmHg).

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6
Q

Classification - Hypertension

A

Hypertension can be classified as either primary (or essential) where there is no known identified cause or secondary where the underlying cause is known.
Essential hypertension has been associated with factors such as stress response, race, age, heredity, and socioeconomic background.
Primary hypertension accounts for approximately 95% of cases.
Secondary hypertension can be caused by renal disease, endocrine disease (e.g. diabetes), vascular disease, pregnancy, drugs (e.g. steroids, alcohol, oral contraceptives, ciclosporin).
Other related factors include obesity, inactivity, smoking, alcohol intake, dietary salt intake.

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7
Q

Pathophysiology - hypertension

A

Arterial blood pressure is a combination of both cardiac output and systemic vascular resistance (also known as total peripheral resistance).
If either of these factors is increased then arterial blood pressure also increases. An increase in either the stroke volume or heart rate correspondingly increases cardiac output.
Systemic vascular resistance is increased by mechanisms which cause vasoconstriction such as arteriosclerosis, atherosclerosis, and increased blood viscosity.
The regulation of blood pressure involves a balance between the sympathetic (increases cardiac output) and parasympathetic (decreases vascular resistance) nervous systems along with hormonal, humoral and growth factors produced by the vascular endothelium.

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8
Q

Stage 1 hypertension

A

Clinic blood pressure is 140/90mmHg or higher and subsequent ambulatory blood pressure monitoring (ABPM) daytime average or home blood pressure monitoring (HBPM) average blood pressure is 135/85mmHg.

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9
Q

Stage 2 hypertension

A

Clinic blood pressure is 160/100mmHg or higher and subsequent ambulatory blood pressure monitoring (ABPM) daytime average or home blood pressure monitoring (HBPM) average blood pressure is 150/95mmHg.

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10
Q

Severe hypertension

A

Clinic systolic blood pressure is 180mmHg or higher or clinic diastolic blood pressure is 110mmHg or higher

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11
Q

Clinical features - Hypertension

A

Hypertension, once diagnosed, is a chronic life-long condition where treatment is aimed at controlling the condition to prevent serious pathological consequences.
It is usually asymptomatic which may cause problems with adherence to medication regimens. Patients may stop taking medication due to the side effects. Patients may think that their BP is fine since they feel no ill effects when they stop taking the medication.
However, long term pathological consequences of uncontrolled hypertension are extremely serious. These include end-stage renal disease, cardiovascular disease, arteriosclerosis, retinopathy and stroke. The presence of other factors such as smoking, excessive alcohol intake, excessive dietary salt and co-morbidities such as diabetes increase these risks even further

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12
Q

Diagnosis hypertension

A

Diagnosis should not be based upon one isolated BP reading. If a high BP measurement is obtained, the measurement should be repeated using both arms initially. BP readings may differ in the right and left arms due to the nature of the vasculature being measured. If the difference between the right and left arms is greater than 20mmHg on two readings then the arm with the higher reading should be used routinely for measurements.

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13
Q

The following tests and investigations should be offered before commencing any
antihypertensive therapies:

A

 Urea and electrolytes, including serum creatinine (U&Es)
 Estimated glomerular filtration rate (eGFR)
 Plasma glucose
 Lipid profile including serum total cholesterol and HDL cholesterol
 Urinalysis for proteinurea and estimation of the albumin:creatinine ratio.
 Urinalysis for haematuria
 Examination of the fundi of the eye for the presence of hypertension-related retinopathy
 Electrocardiogram (ECG)

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14
Q

When to treat hypertension

A

Lifestyle interventions should be first line in any patient over the age of 40 years with stage 1 hypertension and no other risk factors. Patients under the age of 40 years with stage 1 hypertension should be considered for specialist referral.

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15
Q

The following groups of patients should be offered antihypertensive therapy first line:

A

 Any patient under the age of 80 years with stage 1 hypertension with one or more of the following risk factors:
o Target organ damage (e.g. left ventricular hypertrophy)
o Established cardiovascular disease
o Renal disease
o Diabetes
o A 10 year cardiovascular disease risk of > 20% (calculated using the QRISK tool)
o Any patient of any age with stage 2 hypertension (BP > 160/100mmHg) or greater

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16
Q

QRISK 2 risk assessment tool

A

used to assess cardiovascular disease risk for primary prevention in people up to and including 84 years of age.

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17
Q

Lifestyle modifications in hypertension

A

 Weight loss including eating a healthy diet (DASH diet)
 Increasing physical activity / taking regular exercise
 Reducing salt in the diet
 Stopping smoking
 Decreasing alcohol intake
 Decreasing coffee and caffeine intake

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18
Q

Several classes of medicines are used to manage hypertension and this will depend on the patient’s age and ethnicity. Below is a list of drug classes which are prescribed in the management of hypertension:

A
 ACE inhibitors
 Beta blockers
 Calcium channel blockers
 Diuretics
o Thiazides
o Loop diuretics
o Aldosterone antagonists
 Nitrates
 Direct acting vasodilators
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19
Q

Treatment targets - hypertension

A

NICE recommends that patients aged under 80 years of age who have treated hypertension have a ‘clinic’ blood pressure target set to below 140/90mmHg. Those patients aged 80 years and over with treated hypertension should have a ‘clinic’ blood pressure target set to below 150/90mmHg.

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20
Q

Hypertension in pregnancy

A

Hypertension in pregnancy can occur as chronic hypertension which is already present before 20 weeks gestational age. Gestational hypertension is new hypertension occurring after 20 weeks gestational age without significant proteinurea (protein in the urine).
Further complications from hypertension during pregnancy can arise such as pre-eclampsia.
Pre-eclampsia occurs when significant protein is found in the urine. Symptoms associated with the condition include severe headaches, visual disturbances, new epigastric pain which is persistent, nausea and vomiting and sudden swelling of the face and extremities.
Eclampsia is defined as the occurrence of one or more seizures in a patient with preeclampsia.
There is increased risk of complications to both the mother and foetus from hypertension during pregnancy.
Hypertension in pregnancy is defined by NICE as: ‘a single diastolic blood pressure reading of 90mmHg or greater on two occasions more than 4 hours apart AND/OR a single diastolic blood pressure reading of more than 110mmHg’

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21
Q

which drugs are associated with an increased risk of congenital malformations when taken during pregnancy.

A

ACE inhibitors, ARBs and chlorothiazide have all been associated with an increased risk of congenital malformations when taken during pregnancy.

22
Q

Hypertension and type 1 diabetes

A

Management of hypertension in Type 1 diabetes is usually undertaken in consultation with specialists in secondary care.
Antihypertensive drug therapy is started at a threshold of a blood pressure > 135/85mmHg provided there is no evidence of albuminuria or metabolic syndrome.
Antihypertensive treatment is started at a threshold blood pressure of > 130/80mmHg when there is present:
 Albuminuria, and
 Two or more features of metabolic syndrome

23
Q

Hypertension and type 2 diabetes

A

Management of diabetes in type 2 diabetes depends on whether the hypertension is previously diagnosed and treated, and whether nephropathy is present.
For patients without previously diagnosed hypertension and nephropathy and a confirmation of BP consistently above 140/80mmHg then lifestyle advice (diet and exercise) should be provided. Lifestyle advice is also provided when the BP is consistently above 130/80mmHg in the presence of nephropathy, retinopathy or cerebrovascular damage.
If lifestyle advice does not reduce blood pressure below the targets given above then offer the patient antihypertensive medication. First line drug therapy is an ACE inhibitor unless the patients are of African or Caribbean origin or are women who may become pregnant.

24
Q

Postural hypotension

A

Postural hypotension (low BP) occurs in a number of individuals and is characterised by symptoms of dizziness and falls. In order to diagnose postural hypotension a blood pressure (BP) measurement is first taken while the patient is sitting or lying down (supine). Then a second BP reading is taken while the patient is standing and has been standing for at least one minute prior to taking the reading.
A diagnosis of postural hypotension is made when the difference between the lying and the standing systolic BP measurement is > 20mmHg.
An example is:
Lying or sitting BP = 120/76mmHg and standing BP = 97/60mmHg. The difference in systolic BP measurements is 23mmHg.

25
Q

In order to address postural hypotension the following should be undertaken:

A

 Review all medication
 Take subsequent BP measurements with the patient standing
 If symptoms persist refer the patient for Specialist review
 Drugs used to manage postural hypotension include fludrocortisone and midodrine

26
Q

Definition of heart failure

A

Heart failure is generally defined by a failure to meet normal perfusion demands of the body or a condition in which perfusion needs can only be met with an elevated filling pressure.
The signs and symptoms of heart failure include breathlessness, fluid retention and fatigue, and are suggestive of impaired cardiac output, volume overload or a combination of both.

27
Q

Aetiology of heart failure

A
Heart failure (HF) is not a single disease state but a complex clinical syndrome made up of a constellation of signs and symptoms with many possible underlying causes. Heart failure is caused by structural or functional abnormalities of the heart. It is usually a progressive condition (chronic) occurring over a number of years, however acute heart failure can occur either as an initial diagnosis or as a sudden worsening of chronic heart failure.
An underlying aetiology and diagnosis should always be sought as these directly influence the treatment of heart failure.
In failure the heart is unable to pump blood sufficiently quickly around the body to meet the body’s demands. When the heart fails as a pump, compensatory mechanisms kick in. The results of compensatory mechanisms include fluid retention via the kidneys and vasoconstriction of blood vessels. Two neurohumoral systems (compensatory mechanisms) are stimulated; the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system.
Activation of the RAAS causes sodium and water retention and vasoconstriction, thus increasing peripheral resistance.
Stimulation of the sympathetic nervous system increases myocardial contractility, tachycardia and vasoconstriction. As a result of these two systems the heart beats faster,
the heart muscle stretches (to hold more blood) and becomes thinner. This structural damage is called remodelling
28
Q

Natriuretic peptides

A

Natriuretic peptides are hormones released by the blood stream in response to the body’s increased ventricular wall stress, myocardial damage and volume overload. Natriuretic peptides are released by the cardiac myocytes and are used as markers in the diagnosis and management of heart failure. B-type natriuretic peptide (BNP) and the N-terminal proBNP (NT-proBNP) are both used for diagnostic purposes. NICE CG108 recommends measurement of natriuretic peptides to diagnose or rule out heart failure

29
Q

Values for the management of chronic heart failure - BNP & NT-proBNP

A

Criteria
BNP
NT-proBNP

Normal values
Less than 100pg/ml
Less than 400pg/ml

Suspect heart failure & refer
100 to 400pg/ml
400-2000pg/ml

High levels – refer/manage urgently
Greater than 400pg/ml
Greater than 2000pg/ml

30
Q

Prognosis - Heart failure

A

Heart failure carries a poor prognosis. Mortality runs at 30-40% for patients diagnosed within the first year, thereafter falling to less than 10% per year. The prognosis for heart failure carries a survival rate of < 50% over five years from diagnosis.
25-50% of cases are sudden deaths, usually from ventricular arrhythmias. There is a better prognosis if the left ventricular systolic function is preserved. In end-stage heart failure there is a need for palliative care. It is important to note that some patients have heart failure with a preserved ejection fraction (HFPEF) however much of the evidence for treatment of heart failure is for heart failure with systolic dysfunction of the left ventricle (LVSD)

31
Q

Underlying causes heart failure

A

Myocardial dysfunction - IHD, diabetes, pregnancy, cardiomyopathies

Volume overload (excessive preload) - Aortic or mitral valve regurgitation

Pressure overload (excessive afterload) - Aortic stenosis, hypertension

Impaired filling - Rheumatic heart disease

Arrhythmias - Atrial fibrillation

High output - Thyrotoxicosis, anaemia

32
Q

The most common cause of heart failure is

A

myocardial dysfunction which is commonly systolic (i.e. reduced left ventricular contraction).

In healthy patients the left ventricular ejection fraction (LVEF) is normally over 50% but in left ventricular systolic dysfunction (LVSD) this is reduced to less than 50%.
Symptoms of heart failure commonly occur when the LVEF is less than 35%. If the LVEF falls to below 10% there is a risk of thrombus formation within the ventricle and so oral
anticoagulation is necessary.

33
Q

Signs and symptoms of heart failure

A
 Shortness of breath
 Swelling of feet and legs
 Chronic lack of energy
 Difficulty sleeping at night (orthopnoea)
 Hepatomegaly caused by congestion leading to ascites (Presents as a swollen or tender abdomen with loss of appetite)
 Cough with frothy sputum
 Increased urination at night
 Confusion and/or impaired memory
 Arrhythmias
 Raised jugular venous pressure (JVP)
 Presence of a third heart sound (S3)
 Reduced exercise tolerance
34
Q

New York Heart Association (NYHA) classification

A

The New York Heart Association (NYHA) classification system is based upon symptoms and exercise capacity. This is a classification used internationally to provide standardisation from which to determine severity of the patient’s condition.

I - No limitations: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations
II - Slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations, dyspnoea or angina pectoris
III - Marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms
IV - Unable to carry out any physical activity without discomfort: symptoms present at rest, increase with any physical activity

35
Q

Any underlying cause of heart failure must be investigated to optimise treatment.
Investigations will primarily include:

A

 Cardiac imaging e.g. transthoracic echocardiogram (2D Doppler)
 Natriuretic peptides measurements
 Electrocardiogram (ECG)
 Clinical assessment of functional capacity (NHYA classification)
 Fluid status
 Urea and electrolytes (U&Es) and serum creatinine
 Estimated glomerular filtration rate (eGFR)
 Pulse oximetry
 Cognitive status
 Nutritional status
 Review of all medications
 Screening for depression

Other:
 Full blood count (FBC)
 Fasting blood glucose and lipids
 Urinalysis
 Thyroid function tests (TFTs)
 Chest X-ray (CXR)
 Peak flow or spirometry
36
Q

There are three strategies for management of heart failure

A

behavioural modification, pharmacological therapy and interventional procedures.

37
Q

Drug therapy heart failure - The main aims of treatment are as follows:

A

 Relieve symptoms such as breathlessness, fluid retention and fatigue
 Improve the patient’s exercise tolerance (see NYHA classification)
 Reduce the incidence of acute exacerbations which often result in hospital admissions
 Reduced mortality associated with the condition

dysfunction (also described in the literature as heart failure with reduced ejection fraction or HFPEF) is a combination of an ACE inhibitor and a beta blocker. If an ACE inhibitor is not tolerated then an angiotensin II receptor antagonist may be used instead.
The drugs should be titrated to a ‘target dose’ which is the optimal dose recommended for heart failure treatment.
Aldosterone antagonists are added to ACE inhibitor and beta blocker therapy in patients who remain symptomatic. Digoxin may be used for worsening or severe heart failure for symptomatic patients already taking an ACE inhibitor plus a beta blocker plus an aldosterone antagonist.
Diuretics may be employed for patients with fluid overload, ensuring intake of fluid and salt restriction as appropriate.
Neprilysin inhibitors are a new class of drug for the management of symptomatic chronic heart failure in patients with moderate to severe symptoms (and ejection fraction of < 35%). Neprilysin inhibitors inhibit the enzyme neprilysin which breaks down natriuretic peptides. A combination product called 'Entresto' containing both sacubitril, a neprilysin inhibitor, and valsartan, an angiotensin II receptor blocker is now available.
Treatment should be initiated by a heart failure specialist.
38
Q

In summary a number of drug/drug classes are employed in the management of heart
failure as indicated in NICE guidance CG 108:

A

 Angiotensin converting enzyme inhibitors (ACEIs)
 Angiotensin II receptor blockers (ARBs)
 Beta blockers
 Aldosterone antagonists (also known as mineralocorticoid receptor antagonists - MRAs)
 Hydralazine (a direct acting vasodilator)
 Nitrates
 Cardiac glycosides (digoxin)
 Loop diuretics
 Thiazide diuretics
 Ivabradine
 Neprilysin inhibitors

39
Q

Lifestyle Interventions
The following measures should be recommended to patients diagnosed with heart failure.
These include:

A
 Avoid excessive alcohol intake. Alcohol is a myocardial depressant. Heavy alcohol use can cause dilated cardiomyopathy these patients should be advised to abstain from alcohol.
 Stop smoking. The effects of smoking in heart failure have not been quantified, but observational data suggests that continued smoking is associated with increased mortality from heart failure and increased hospital admissions. Patients should be offered smoking cessation advice and support.
 Low intensity exercise. This should be recommended in stable heart failure only. Aerobic exercise within the limits dictated by symptoms should be encouraged. Avoid swimming or any exercise based in water if there is NYHA class III or IV.
 Decrease salt intake to <6 g per day. Salt substitutes should be avoided because of the high potassium content.
 Daily weight monitoring. Patients with chronic HF should be encouraged to weigh themselves daily (before dressing, after voiding, before eating) and inform their GP of any weight gain of 1.5-2kg over 2 days
40
Q

The following procedures may be considered for patients with heart failure in whom pharmacological therapy alone does not control cardiac function and symptoms

A

 Cardiac resynchronisation therapy with pacing (CRT-P), also known as biventricular pacing.
 Implantable cardioverter defibrillators (ICDs)

Others:
 Coronary revascularisation (PCI or CABG if refractory angina present)
 Cardiac transplantation (for patients with severe refractory symptoms or refractory cardiogenic shock)
 Assisted ventilation for patients with obstructive sleep apnoea (CPAP)

41
Q

What is hyperlipidaemia?

A

Hyperlipidaemia (dyslipidaemia) describes a condition in which levels of lipids are raised in the blood plasma. The term ‘lipids’ refers to cholesterol and triglycerides. Hyperlipidaemia is considered a risk factor in the pathogenesis and development of cardiovascular disease.

42
Q

Cholesterol – in summary

A

The body obtains cholesterol from the diet where it is absorbed by the gut and transported to the liver. It is also synthesised in the liver, gut and the central nervous system.
Cholesterol is converted into low density lipoproteins (LDL) in the circulation where it is delivered to most tissues facilitated by LDL receptors. Excess cholesterol is removed from tissue by high density lipoproteins (HDL) where it can return to the liver. Cholesterol is also excreted in the bile. Much of the plasma’s cholesterol is present as LDL. Importantly, cholesterol’s role is as a precursor for the formation of steroid hormones and bile acids. It is an essential component of cell membranes

43
Q

What are the causes of hyperlipidaemia?

A

There are a number of causes of hyperlipidaemia which can be categorised as either primary or secondary hyperlipidaemia.
Primary hyperlipidaemia or familial hyperlipidaemia (FH) is an inherited disorder characterised by higher than normal levels of lipids. There is a significantly greater risk of an individual with familial hyperlipidaemia developing cardiovascular disease at a much younger than expected age.
The causes of secondary hyperlipidaemia include a diet high in saturated fats, obesity, renal disease, diabetes and hypothyroidism.

44
Q

Diagnosis - hyperlipidaemia

A

Usually hyperlipidaemia itself is symptomless and is often diagnosed when the patient has a blood test taken revealing raised lipid levels.

Individuals with familial hyperlipidaemia may present with xanthomas (yellow, fatty growths under the skin) around the joints or xanthelasthma (yellow plaques) around the eyelids.

Asking about the following should help determine primary or secondary causes:
 Previous history of cardiovascular disease
 Family history of cardiovascular disease
 Lifestyle: diet and exercise
 Smoking and alcohol history
 Existing medical history
 Existing medication history (consider drugs which can raise lipid levels)

45
Q

Measurement of lipids

A

A number of lipids are measured in clinical practice in order to assess a person’s level of cardiovascular risk and to assess the need for intervention with diet, lifestyle modification and drug therapy.
Measurement of lipids usually includes total cholesterol (TCL), low density lipoproteins (LDL), high density lipoproteins (HDL) and triglycerides.
o Total cholesterol (TCL): A level below 5.00mmol/L is generally desirable. It can be measured at any time of day without the need for fasting.
o Low density lipoproteins (LDL): Known in the literature as ‘bad’ cholesterol. A level below 3.00mmol/L is generally desirable. High levels are considered to be associated
with increased cardiovascular risk.
o High density lipoproteins (HDL): Known in the literature as ‘good cholesterol’. Higher levels are associated with lowering cardiovascular risk. A level of 1.20mmol/L or
more in women and 1.0mmol/L or more in men is considered desirable. It can be measured at any time of day without the need for fasting.
o Triglycerides: High levels are associated with increased cardiovascular risk. A level below 1.7mmol/L is considered desirable.
o Non-HDL cholesterol: this refers to the Total Cholesterol value minus the HDL value and is calculated as part of the full lipid profile measurement in NICE CG 181.
Measurements of LDL, HDL and triglycerides are usually taken after an individual has fasted for around 12-14 hours.

46
Q

Management of dyslipidaemia should begin with lifestyle modification.

A

This includes weight reduction to improve lipid profile and reduce CV risk. Regular exercise should be encouraged (refer to national guidance). Appropriate modifications to alcohol consumption and smoking cessation are recommended.
Modification to diet should aim for the following:
 Reduction of cholesterol and saturated fats
 Increase in insoluble fibre and plant sterols
 Mediterranean-style diet including the consumption of oily fish

47
Q

Lipid-regulating drugs

A

Statins are the drugs of first choice for primary and secondary prevention of cardiovascular disease. They are more effective than other lipid-lowering drugs at reducing LDL cholesterol. Statins have been shown to reduce cardiovascular events and mortality irrespective of the individual’s initial cholesterol reading.
High intensity statins and ezetimibe are used to manage familial hyperlipidaemias usually under the care of a lipid specialist.
Statins have a number of adverse effects including an association with muscle toxicity (myositis, myopathy and rhabdomyolysis). Patients should be counselled to report any adverse effects including muscle aches and pains. Statins can raise liver enzymes and NICE recommends baseline liver function tests before, at 3 months and at 12 months of statin therapy. Statins interact with a number of drugs and checking for potential interactions prior to initiating treatment is essential.
Other lipid lowering drugs used in hyperlipidaemia include fibrates, bile acid sequestrants, nicotinic acid and omega-3 fatty acid compounds (fish oils). Fibrates are not recommended for routine use in primary or secondary prevention. Bile acid sequestrants, nicotinic acid and omega-3 fatty acid compounds are not recommended for either primary or secondary prevention.

48
Q

PCSK9 Inhibitors

A
A new class of drug (introduced 2016) is available for the management of patients with hyperlipidaemia who are at very high risk of MI or stroke. The drugs are known as PCSK9 inhibitors (human monoclonal antibody drugs) and work by inhibiting a protein called PCSK9 which is responsible for regulating the number of LDL receptors in the liver. Reduction of the protein increases the number of LDL receptors leading to a reduction in LDL blood levels.
The two drugs introduced are alirocumab and evolucumab and both must be given by subcutaneous injection at least every two weeks. The PCSK9 inhibitors are indicated when lipid levels are not adequately controlled by statins, other lipid lowering agents or where intolerable side effects occur with existing therapy.
49
Q

Primary prevention of cardiovascular disease

A

In the UK people 40 years and older are reviewed regularly to assess their estimate of cardiovascular risk. At least one lipid profile measurement is taken prior to an individual’s risk assessment.
A validated online assessment tool such as the QRISK2 risk calculator (QRISK3-2017 now available) recommended by NICE is used by doctors and practice nurses to assess individual cardiovascular risk.

50
Q

The QRISK tool is not recommended for the following groups of patients:

A

o Patients with Type 1 diabetes (can be used for type 2 diabetes)
o Patients who have an eGFR of < 60ml/min/ 1.732
and/or albuminuria because they are already at risk of cardiovascular disease
o Patients who already have pre-existing cardiovascular disease
o Patients with familial hyperlipidaemia or other inherited lipid disorders

51
Q

when should statin be offered

A

In any individual for whom the risk outcome (using the risk calculator tool) indicates that they have a 10% or greater risk of developing cardiovascular disease over the next 10 years then statin therapy can be offered. Before a decision is taken to start statin therapy an informed discussion should take place between clinician and patient. Lifestyle changes and risks/benefits of statin therapy should be first discussed. Advice on making lifestyle changes is discussed first before offering a statin. NICE CG 181 guidance recommends that when a statin is offered for primary prevention atorvastatin 20mg daily (= high intensity) should be recommended to individuals whose minimum risk outcome is that indicated above.

52
Q

Secondary prevention of cardiovascular disease

A

Statin therapy forms part of the overall management in preventing recurrence of cardiovascular events such as myocardial infarction, stroke, or complications of
cardiovascular disease in individuals already diagnosed.
NICE recommends treatment with atorvastatin 80mg daily (= high intensity), unless there are contraindications, drug interactions, risk of adverse events necessitating a need to review the drug and/or the dose. Additionally, the individual may have a preference to start on a lower dose.