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CHAPTER9 Cardiology and vascular disease
Prevention ofcardiovasculardisease
1 in 3 deaths result from heart disease; in England alone, there are 732,000
stroke- related deaths each year in England.
Risk factors forcardiovascular disease Table 9.5
Primary prevention Aims to stop cardiovascular disease developing.
Population strategy Inuences factors that i CHD risk in an entire popula-
tion, e.g. anti- smoking campaigns. GPs can do this by displaying health education posters/ literature (e.g. in waiting room, practice leaet).
Health checks for the over40s There is a national screening programme
for people aged 40– 74y in the UK to identify CVD, DM, and cancer earlier
through health checks every 5y. The check provides:
• Lifestyle advice (E p. 223)
• Information about cancer screening programmes available in the UK
• CVD risk assessment— including demographic information, FH, smoking
status, alcohol consumption, BMI, BP, and lipid prole
• DM risk stratication— E p. 315
High- risk strategy Most CVD occurs in individuals of medium risk as that is
the largest group. However, individuals at high risk have the most to gain
from risk reduction. This strategy aims to identify individuals at high risk
through opportunistic screening and health checks and d their risk through
lifestyle modication ± medication. High- risk groups:
• All people aged >85y
• All patients with a familial dyslipidaemia— E p. 225
• People with eGFR <60 mL/ min/ 1.73m2 and/ or albuminuria
• People with type 1 DM who are >40y or have had DM for >10y or have
established nephropathy or other CVD risk factors
• People with 10y CVD risk of ≥10% using the QRisk3 calculator
(Mhttps:// qrisk.org/ three/ )
0 Current risk estimation tools give 10y CVD risk; the Joint British
Societies tool provides an estimate of lifetime risk (M www.jbs3risk.com).
This is particularly useful when discussing CVD risk with younger patients as
their 10y risk is often very low regardless of risk factors.
Factors used inthe QRisk3 cardiovascular riskcalculation
• Age
• Gender
• Ethnicity
• Socioeconomic status
• BMI
• Cholesterol levels
• Smoking
• Diabetes
• FH of CVD
• AF
• BP
• BP medication
• CKD
• RA
• SLE
• Severe mental illness
• Antipsychotic medication
• Steroid medication
0 If the risk score is near the threshold for intervention, consider other
factors that may predispose to CVD and cause risk underestimation, e.g.:
• Has the person recently stopped smoking?
• Is the patient already taking lipid- lowering therapy?
• Does the patient have raised triglycerides?
• Are other conditions present that i risk (e.g. psoriasis, HIV, other
systemic inammatory disorder, taking immunosuppressant medication)?
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PREVENTION OFCARDIOVASCULARDISEASE
Secondary prevention Aims to stop progression of symptomatic car-
diovascular disease. 46% people who die from MI are already known to
have CHD. There is strong evidence that targeting patients with CVD for
risk- factor modication is eective in d risk of recurrent CVD.
Table9.5 Risk factors forcardiovascular disease
Non-modiable Modiable (proven benet) Modiable (unproven
Age—i with age
Sex—♂ > ♀ in those
< 65y
Ethnic origin—in
the UK people who
originate from the
Indian subcontinent
have i risk, AfroCaribbeans have d risk
Socioeconomic
*
position
Personal history of
CVD
Family history of
CVD—<55y ♂;
<65y ♀
Low birth weight
(IUGR)
*
These 9 factors account for 90% of risk for acute MI.
Smoking*—E p. 156
Hyperlipidaemia—E p. 222
Hypertension*—E p. 218
DM*—E p. 326
Diet*—E p. 148
Obesity (particularly waist-hip
ratio)*—E p. 152
Physical inactivity*—E p. 154
Alcohol consumption*—E p. 158
Left ventricular dysfunction/
heart failure (2° prevention)—E
p. 234
Coronary prone behaviour—
competitiveness, aggression
and feeling under time pressure
(2° prevention)—behaviour
modication is associated with
d risk
benet)
Haemostatic
factors—i plasma
brinogen
Apolipoproteins—
ilipoprotein(a)
Homocysteine—i
blood homocysteine
Vitamin levels—d
blood folate, vitamins
B12 and B
Depression
*
6
The GP’s role GPs have a role in:
• Identication of patients who would benet from primary prevention
• Ensuring patients at high risk of atherosclerotic disease have ongoing
follow- up through disease registers, routine recall, and follow- up
• Promoting lifestyle modication in at-risk patients (E p. 223)
• Ensuring current best care guidelines are followed and treatment
regimens are updated as policies change; this is a major challenge for
primary care as guidelines change frequently and often conict
• Checking the process through audit
Further information
NICE (2014, updated 2016)Cardiovascular risk assessment and the modication of blood lipids for the primary and secondary prevention of cardiovascular disease. M www.nice.org.uk/ guidance/ cg181
SIGN (2017) Risk estimation and the prevention of cardiovascular disease.
M https:// www.sign.ac.uk/ sign- 149- risk- estimation- and- the- preventionof- cardiovascular- disease.html
Patient information
British Heart Foundation F 0300 330 3311 M www.bhf.org.uk
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CHAPTER9 Cardiology and vascular disease
Blood pressuremeasurement
Taking bloodpressure
• Use a validated sphygmomanometer— a list is available on the British
Hypertension Society website (M www.bhsoc.org)
• Regularly maintain and calibrate your sphygmomanometer
• Use a cu of correct bladder size:most adults— 12 × 26cm; large adults
(arm circumference >33cm)— 12 × 40cm; thin adults and children with
arm circumference ≤26cm— 10 × 18cm
• Seat the patient comfortably with arm outstretched and supported at
the level of the heart
• Measure BP to the nearest 2mmHg; measure diastolic BP when heart
sounds completely disappear (K5)— only use the pressure at which they
suddenly mue (K4) when K5 cannot be determined
• Measure BP in both arms— if the dierence in systolic BP is >10mmHg
between the 2 arms, repeat the measurement. Aconsistent dierence
of >10mmHg is an independent risk factor for CVD and all- cause
mortality; treat identied CVD risk factors. Use the higher of the 2
readings when considering further management of BP
0 Automated devices may not measure BP accurately if there is pulse irregularity (e.g. AF). Check the radial or brachial pulse before checking BP
and measure BP manually using direct auscultation over the brachial artery
if pulse is irregular.
‘White coat’ hypertension Prevalence 10%. Some patients’ BP increases in
response to having their BP checked
If BP is ≥140/ 90mmHg intheconsultation
• Take a 2nd measurement— if that measurement is substantially dierent
from the 1st measurement, take a 3rd measurement; record the lower
of these measurements as the BP
• If BP on repeat testing is ≥140/ 90mmHg and not known to be
hypertensive, oer ambulatory BP monitoring (ABPM) or home BP
monitoring to conrm the diagnosis; consider ABPM or home BP
monitoring (HBPM) for people on antihypertensive medication who are
known to have ‘white coat’ hypertension
• If hypertension is not conrmed on ABPM/ HBPM, measure BP every
5y or more frequently if close to 140/ 90mmHg
• If the person has severe hypertension (systolic BP ≥180mmHg or diastolic BP ≥110mmHg), consider starting antihypertensive treatment immediately without waiting for the result of ABPM/ HBPM.
Refer for same- day specialist assessment if suspected:
• Accelerated hypertension (BP>180/ 110mmHg ± papilloedema ±
retinal haemorrhage) or
• Phaeochromocytoma (labile/ postural hypotension, headache,
palpitations, pallor, and excessive sweating)
Ambulatory BP monitoring (ABPM) A BP measuring device is worn
on the body for 24h. It takes BP every 20min in the day time and less frequently
(usually hourly) at night. i BP readings on ABPM are more strongly correlated
to end- organ damage than one- o measurements. ABPM is used for:
• The diagnosis of hypertension (E p. 218)
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BLOOD PRESSUREMEASUREMENT
• Diagnosis or exclusion of ‘white coat’ hypertension
• Monitoring of response to treatment
• Assessing medication- related postural hypotension
Interpretation ABPM is considered abnormal if
• Average day- time ABPM is ≥135/ 85mmHg
• Average night- time ABPM is ≥120/ 70mmHg
0 NICE bases the diagnosis of hypertension on average day- time ABPM
only (minimum 14 readings).
Night- time ABPM BP falls at night in normotensive individuals. Some hypertensive patients are described as ‘non- dippers’. This means that their BP
does not fall at night and is associated with i risk of target end- organ
damage. Conversely, some hypertensive patients have excessive dips in
their BP at night (>10%); this is associated with i CVD events.
Home BP monitoring (HBPM) Useful:
• If ABPM facilities are not available within a reasonable time frame for
diagnosis of hypertension
• For patients who cannot tolerate ABPM
• For monitoring of antihypertensive treatment
Instructions Patients should use a validated and calibrated BP machine.
• Measure BP on at least 4— and preferably 7— consecutive days
• Measure BP 2×/ d (morning and evening) when seated; take 2 readings
>1min apart
• Discard the readings taken on day 1 and take an average value of all the
remaining measurements
Interpretation HBPM is abnormal if average is ≥135/ 85mmHg.
Hypertension E p. 218 Cardiogenic shock E p. 1065
Postural hypotension BP drops on moving from supine or sitting pos-
ition to standing position. Presents with falls, postural dizziness, and/ or
light- headedness. Measure BP supine or seated and then ask the patient
to stand up. Re- measure BP after 1min standing. Standing usually causes
a slight d in the systolic BP (<20mmHg) and a slight i in the diastolic BP
(<10mmHg). In postural hypotension there is usually a marked d in both
systolic (>20mmHg) and diastolic BP.
• Review medication Stop any non- essential medication contributing to
symptoms, e.g. night sedation, unnecessary diuretics
• Optimize treatment of intercurrent heart disease, Parkinson’s
disease, or DM
• Advise patients to take care when standing— especially if getting up
from their beds or out of a hot bath/ shower, and after meals
Measure subsequent BP with the patient standing. Consider specialist referral if symptoms persist despite GP management.
Further information
Clark CE, etal. (2012) The dierence in blood pressure readings between
arms and survival:primary care cohort study. BMJ 344:e1327.
NICE (2011, updated 2016)Hypertension in adults:diagnosis and management. M www.nice.org.uk/ guidance/ cg127
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CHAPTER9 Cardiology and vascular disease
Hypertension
Hypertension is a major risk factor for CVD. It is normally symptomless
until it causes organ damage. Prevalence i with age; 25% of all adults and
>50% of people aged >60y have hypertension. Management aims to detect
and treat i BP before damage occurs.
Causes
• Unknown (‘essential’)— 95%; alcohol (10%) or obesity may be
contributory factors
• Endocrine disease— Cushing’s (both syndrome and 2° to steroids); Conn’s
syndrome; phaeochromocytoma; acromegaly; hyperparathyroidism; DM
• Renal disease • Pregnancy
• Coarctation of the aorta— E p. 252
Presentation
• Usually asymptomatic and found during routine BP screening or
incidentally. Occasionally headache or visual disturbance
• May be symptoms of end- organ damage— LVH, TIAs, previous CVA/
MI, angina, renal impairment, PVD
Measurement ofblood pressure E p. 216
Diagnosis ofhypertension BP is a normally distributed continuous vari-
able; each 2mmHg i in systolic BP is associated with a 7% i risk of mortality
from IHD and a 10% i risk of mortality from stroke. There is no gure above
which hypertension can be diagnosed denitively. Criteria currently in useN:
• Stage 1 hypertension Clinic BP ≥140/ 90mmHg and subsequent daytime
average ABPM/ HBPM ≥135/ 85mmHg
• Stage 2 hypertension Clinic BP ≥160/ 100mmHg and subsequent
daytime average ABPM/ HBPM ≥150/ 95mmHg
• Severe hypertension Clinic systolic BP ≥180mmHg or clinic diastolic BP
≥110mmHg
• If the person has severe hypertension (systolic BP ≥180mmHg or
diastolic BP ≥110mmHg), consider starting antihypertensive treatment
immediately without waiting for the result of ABPM/ HBPM.
Refer for same day specialist assessment if suspected:
• Accelerated hypertension (BP >180/ 110mmHg ± papilloedema
±retinal haemorrhage) or
• Phaeochromocytoma (labile/ postural hypotension, headache,
palpitations, pallor, and excessive sweating)
Isolated systolic hypertension Systolic BP ≥160mmHg— oer the
same treatment as people with i systolic and diastolic BP.
Further assessment Aims to identify target organ damage:
• Examination Check heart size, heart sounds, and for heart failure;
examine the fundi, looking for silver wiring, AV nipping, ame
haemorrhages and cotton wool spots
• Blood tests Creatinine, electrolytes, eGFR, glucose/ HbA1c, lipid
prole, consider GGT if excess alcohol is a possibility
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HYPERTENSION
• Urine Dipstick for RBCs and protein; laboratory sample for
albumin:creatinine ratio
• Cardiovascular risk estimation E p. 214
• ECG ± Echo (if LVH is suspected)
0 If i BP is not diagnosed but there is evidence of target organ damage
(e.g. LVH, proteinuria), look for alternative causes.
Education Patients will not take tablets regularly, be motivated to change
lifestyle, or turn up for regular checks if they do not understand why treating
their i BP is important. Conversely, some patients who were t and well
prior to their diagnosis will assume a sick role unless it is explained that they
are well and treatment is designed to stop illness developing. Back- up verbal
information with written information that patients can take home; reinforce
information at follow- up and oer opportunities for discussion. Do not
forget to warn patients about possible side eects of any medications.
Lifestyle advice Oer lifestyle advice to all patients with a diagnosis of
hypertension and those with FH of i BP. Reinforce advice with written
information:
• Oer smoking cessation advice and help (E p. 156)
• d weight to optimum for height (E p. 152)
• Encourage regular exercise— dynamic is best, e.g. walking, swimming,
cycling (E p. 154)
• d alcohol to <14U/ wk for ♂ and ♀ (E p. 158)
• d dietary salt intake (aim for <6g salt/ d)
• i dietary fruit and vegetable intake— aim for >5 portions/ d
• d excess coee consumption and other caeine- rich products
• Encourage relaxation and stress management
• Do not oer Ca2+, Mg2+, or K+ supplements as a method to d BP
Statin (E p. 224). Prescribe:
• If hypertension complicated by CVD irrespective of baseline cholesterol
or LDL levels or
• For primary prevention in patients >40y with hypertension and 10y
CVD risk ≥10%
Initiating antihypertensive drugtreatment
Stage 1 hypertension Oer drug treatment if <80y of age and ≥1 of:
• Target organ damage
• Established CVD
• Renal disease
Stage 2 hypertension Oer drug treatment to all patients.
0 If aged <40y, stage 1 hypertension, and no evidence of target organ
damage, CVD, renal disease, or DM, consider specialist referral to exclude
2°causes of hypertension and for detailed estimation of CVD risk.
• DM
• 10y CVD risk ≥10%
General rules forantihypertensive drugtreatment
• If a drug is not tolerated Stop; move to the next line of therapy
• If a drug is tolerated but the BP target is not met Add in the next line
of therapy
• Where possible Recommend treatment with drugs taken only once a
day and prescribe non- proprietary drugs which minimize cost
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CHAPTER9 Cardiology and vascular disease
Choice of antihypertensive drug(s) Figure 9.1 0 Side eects
of drug treatment for hypertension are common. 40– 50% started on an
antihypertensive drug discontinue regardless of which class of drug is used.
80% of side eects are seen in 1st year of treatment.
Treatmenttargets
Non- diabetic patients withoutCKD
• Clinic BP <140/ 90mmHg (<150/ 90mmHg if aged ≥80y)
• ABPM/ HBPM (e.g. for patients with white coat hypertension) average
daytime BP <135/ 85mmHg (<145/ 85mmHg if aged ≥80y)
Patients withdiabetes (E p. 326)
• <140/ 80mmHg— uncomplicated type 2 DM
• <135/ 85mmHg— uncomplicated type 1 DM
• <130/ 80mmHg— if any renal, foot, eye or cardiovascular complications
of type 1 or type 2 DM
CKD Aim for BP <140/ 90mmHg; <130/ 80mmHg if CKD + DM or
CKD+ ACR of ≥70mg/ mmol (E p. 415).
History ofstroke/ TIA Aim for systolic BP <130mmHg unless carotid stenosis
when target is 140– 150mmHg.
Follow- up Regular review of patients with i BP is essential.
Review interval Depends on stability of BP:
• After starting treatment Review after 1mo
• If BP is controlled Review after a further 3mo, then every 3– 6 mo
• If BP is not controlled Bring the patient back to repeat the BP reading
and/ or ask for ABPM/ HBPM. Do not alter medication on the strength
of a single BP reading. If i BP is sustained, alter medication. Review in
the same way monthly until BP is controlled
Format ofthe annualreview
• Check BP and look for signs of end- organ failure— including annual urine
test for proteinuria
• Discuss symptoms and medication
• Assess and treat other modiable risk factors for CHD/ CVA
• Reinforce lifestyle advice
Referral tocardiology/ generalmedicine
E=Emergency admission; U=Urgent; S=Soon; R=Routine.
• Accelerated hypertension— E
• Renal impairment— U/ S/ R
• Suspected secondary hypertension— U/ S/ R
• Patients <40y or BP dicult to treat (step 4)— R
• Pregnancy— to obstetrician— urgency depends on stage of pregnancy
and clinical features— E p. 804
Reducing or stopping treatment d BP too far (<120/ 80mmHg)
may i morbidity (e.g. as a result of postural hypotension and falls)—
particularly in the elderly:
• Do not stop medication if high CVD risk or end- organ damage
• If diastolic BP <80mmHg and systolic BP <140mmHg consistently,
consider d or stopping medication; 1– 2y after withdrawal of medication
50% are normotensive and 40% stay o drug therapy permanently
• Continue BP follow- up lifelong even if o medication
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Figure9.1 Choice of antihypertensive drug
HYPERTENSION
221
hypertension. Exceptions:
• Younger women of child- bearing potential
• Patients with hypertension and evidence of i sympathetic drive
• Patients intolerant of or with contraindications to ACE inhibitors/ ARBs
If initial therapy is with a β- blocker and a second drug is required, add a
non- rate- limiting calcium channel blocker to d risk of DM.
Management ofhypertension inpregnancy E p. 804
Further information
NICE (2011, updated 2016)Hypertension in adults:diagnosis and management. M www.nice.org.uk/ guidance/ cg127
NICE (2014, updated 2016)Cardiovascular risk assessment and the modication of blood lipids for the primary and secondary prevention of cardiovascular disease. M www.nice.org.uk/ guidance/ cg181
Patient information
British Heart Foundation F 0300 330 3311 M www.bhf.org.uk
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CHAPTER9 Cardiology and vascular disease
Hyperlipidaemia
Average cholesterol level in a population is a predictor of CVD risk and dependent on diet but, on an individual level, it is a much poorer predictor—
only 42% who develop CVD have i cholesterol. However, lowering LDL
and raising HDL is thought to reduce progression of coronary atherosclerosis, whatever the age of the patient, and is a valuable tool for both primary
and secondary prevention of CVD.
Cholesterol testing Cholesterol is a fatty substance manufactured by
the body (mainly liver) which plays a vital role in functioning of cell membranes. Cholesterol levels are checked with a non- fasting blood sampleN.
Alipid prole includes:
• HDL (high- density lipoprotein) cholesterol— low levels are associated
with i risk CVD
• Non- HDL cholesterol— low- density lipoprotein (LDL) + very low-
density lipoprotein (VLDL). High levels are associated with i CVD risk
• Triglycerides (TGs)— independent risk factor for CVD
• Ratio of total cholesterol:HDL— used to predict risk. No threshold—
the higher the ratio the greater the risk. High risk if ≤6
0 Consider familial dyslipidaemia (E p. 225) in any patient if total cholesterol >7.5mmol/ L and FH of premature CVD. Refer for specialist assessment if total cholesterol >9.0mmol/ L or non- HDL cholesterol >7.5mmol/
L, regardless of FHN.
Management ofraised triglycerides
• If TGs >20mmol/ L— refer for urgent specialist review if not a result of
excess alcohol or poor glycaemic control
• If TGs 10– 20mmol/L— repeat the triglyceride measurement with a
fasting test (after an interval of ≥5d, but in <2wk). Review for potential
secondary causes of hyperlipidaemia (Box 9.1) and seek specialist advice
if TGs remain ≥10mmol/ L
• If TGs 4.5– 9.9mmol/ L— CVD risk may be underestimated by risk
assessment tools. Optimize management of other CVD risk factors.
Seek specialist advice i TGs + non- HDL cholesterol >7.5mmol/ L
Lipid screening In the UK, the NHS provides health checks every 5y
for those aged 40– 74y (E p. 214). These include a lipid prole. Potential
problems with this strategy:
• Those most needing a health check are least likely to attend
• There may be less inclination to eat a healthy diet if cholesterol levels
are known to be normal
• Those with i cholesterol levels may assume a sick role
Blood cholesterol concentration is also not steady over time. 1 in 4 icholes-
terol levels are normal on repeat testing. If lipid levels are high on screening,
repeat with attention to diet; only treat with a statin if lipids remain high
despite low- cholesterol diet and 10y CVD risk is ≥10%.
Opportunistic screening Oer if other risk factors for CVD or signs of
icholesterol (e.g. corneal arcus <50y, xanthelasma, xanthomata).
Calculating cardiovascular disease (CVD) risk Always consider cholesterol in
the context of other risk factors for CVD— E p. 215.
Secondary hyperlipidaemia High lipid levels as a consequence of an-
other condition— Box 9.1.
N
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HYPERLIPIDAEMIA
Box 9.1 Secondary causes ofhyperlipidaemia
Drugs:
•
Steroids
•
β- blockers
•
Thiazides
•
COC pill
•
Isotretinoin
•
Antipsychotics
•
Tamoxifen
•
Antiretrovirals
a
Treatment of hyperglycaemia in DM d secondary h yperlipidaemia.
b
Patients with hypothyroidism should receive adequate thyroid replacement before assessing
need for lipid- lowering treatment. Correction of hypothyroidism may resolve the lipid abnormality and untreated hypothyroidism i risk of myositis with statins.
Obesity
DM (E p. 314)
Excess alcohol
Smoking (lowers HDL)
Pregnancy
Hypothyroidism
Renal failure
Nephrotic syndrome
RA/ SLE
a
b
HIV
Cholestasis
Cushing’s syndrome
Porphyria
Myeloma
Lipodystrophies
Glycogen storage disease
Non- drug therapy Oer to all patients with i cholesterol, i CVD risk,
and those with DM or personal/ family history of CHD/ CVD. Reinforce
advice with written information.
• d intake of fats to <30% of total energy intake (saturated fats <7%)
and d cholesterol intake to <300 mg/ d. Replace saturated fats with
monounsaturated/ polyunsaturated fats. If cholesterol level >5mmol/ L,
low- cholesterol diets result in d in cholesterol of 8.5% at 3mo
• Eat ≥5 portions of fruit or vegetables/ d, 4– 5 portions unsalted nuts,
seeds, or legumes/ wk, and ≥2 portions of sh/ wk (including 1 of
oily sh— maximum 2 portions of oily sh/ wk if pregnant); choose
wholegrains; reduce sugar
• d alcohol intake to ≤14U/ wk; <3– 4U/ d (♂) or <2– 3U/ d (♀) maximum
• Weight d— in patients with BMI ≥30kg/ m2, weight d of 10kg l 7% d in
non- HDL and 13% i in HDL cholesterol
• i physical activity— enhances cholesterol- lowering eects of diet and
weight d. Advise 150min moderate (or 75min vigorous) exercise/ wk +
muscle strengthening exercises2×/ wk
• Stop smoking (E p. 156)
0 Plant sterol/ stanol esters inhibit cholesterol absorption and can d serum
cholesterol with average diet by 10%. d eect if already on a low- fat diet.
Avoid if on lipid- lowering medications, DM (type 1 or 2)or CKD.
Who should be treated witha statin? Consider statin therapy for:
Primary prevention If:
• >85y (if appropriate) • 10y CVD risk ≥10%
• eGFR <60mL/ min/ 1.73m2 and/ or albuminuria
• Type 1 DM + >40y or DM for >10y or established nephropathy or
other CVD risk factors
Start treatment after optimizing lifestyle intervention, and treatment of
other modiable risk factors/ secondary causes of dyslipidaemia.
Secondary prevention If history of CVD— start treatment immediately irrespective of initial cholesterol levels
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