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111
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mm (Sokolow–
35
mm in women (Cornell criteria).
is greater than
5
20
V
wave in
R
3 Cardiovascular medicine
and
1
mm in men or >
V
28
>
3
V
wave in
S
wave in
S
mm (Sokolow– Lyon criteria) or if the
11
≥
VL
Left ventricular hypertrophy— this is from a patient with malignant hypertension— note the sum of the
25
.
3
Fig
wave in a
R
Lyon criteria). Other criteria include the presence of an
3 Cardiovascular medicine
Angina pectoris
ECG
CXR
PRN
CABG
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112
If
ACS
is a possible diagnosis (including unstable angina), see pp
Angina
22
is symptomatic reversible myocardial ischaemia. Features:
1
Constricting/ heavy discomfort to the chest, jaw, neck, shoulders, or arms.
2
Symptoms brought on by exertion.
3
Symptoms relieved within 5min by rest or glyceryl trinitrate (
All
3
features = typical angina; 2 features = atypical angina; 0– 1 features = non-
anginal chest pain
.
Other precipitants: emotion, cold weather, and heavy meals. Associated symptoms:
dyspnoea, nausea, sweatiness, faintness. Fea tures that make an gina less likel y: pain
that is continuous, pleuritic, or worse with swallowing; pain associated with palpitations, dizziness or tingling.
Causes Atheroma. Rarely: anaemia; coronary artery spasm; AS; tachyarrhythmias;
HCM
; arteritis/ small vessel disease (microvascular angina/ cardiac syndrome X).
Types of angina Stable angina Induced by eort, relieved by rest. Good prognosis.
Unstable angina (Crescendo angina.) Angina of increasing frequency or severity;
occurs on minimal exertion or at rest; associated with risk of
Precipitated by lying flat. Variant (Prinzmetal) angina (
gina
gina’) Caused by coronary artery spasm (rare; may coexist with fixed stenoses).
Te st s
usually normal, but may show ST depression; flat or inverted T waves; signs of
MI
. Blood tests
past
are usual ly nec essar y to co nfirm a n
tions
FBC, U&E, TFT
Management
Address exacerbating factors
Secondary prevention of cardiovascular disease
• Stop smoking; exercise; dietary advice; optimize hypertension and diabetes control.
• 75mg aspirin daily if not contraindicated.
• Address hyperlipidaemia— see p
• Consider
dose if the pain has not gone after
present
ACE
- i, especially if hypertensive or diabetic.
symptom relief
5
min after the second dose. SE: headaches, BP.
Anti- anginal medication (p
do not combine - blockers with non- dihydropyridine calcium antagonists). If these
(
fail to control symptoms or are not tolerated, trial other agents.
• β- blockers: eg atenolol 50mg BD or bisoprolol 5– 10mg OD.
• Calcium antagonists: amlodipine— start at 5mg OD; diltiazem— dose depends on
formulation.
• Long- acting nitrates: eg isosorbide mononitrate— starting regimen depends on
formulation. Alternatives:
• Ranolazine: inhibits late Na+ current. Start at
elderly, weight <
• Ivabradine: reduces heart rate with minimal impact on BP. Patient must be in sinus
rhythm. Start with
• Nicorandil: a K+ channel activator. Start with 5– 10mg BD. CI: acute pulmonary oe-
60
dema, severe hypotension, hypovolaemia,
Revascularization Considered when optimal medical therapy proves inadequate or
if likely to derive survival benefit, eg left main or triple vessel disease.
• Percutaneous coronary intervention (PCI) (p
stenosed vessel to open the lumen. A stent is usually inserted to reduce the risk
of re- stenosis. Dual antiplatelet therapy (
recommended for at least
in- stent thrombosis. Seek specialist advice regarding antiplatelets if the patient
has a high bleeding risk or requires surgery.
•
(p
119
) compared to
peat revascularization and those with multivessel disease can expect better outcomes. However, recovery is slower.
114–17
.
GTN
).
MI
. Decubitus an-
BOX
‘Vasospastic an-
S, lipids, Hb
A1
c. Consider echo and
IHD
dia gnosi s— see
. Furt her inv est iga -
BOX
‘In vesti gatin g pati ents’ .
Anaemia, tachycardia (eg fast AF), thyrotoxicosis.
682
.
GTN
spray or sublingual tabs. Advise the patient to repeat the
5
min and to call an ambulance if the pain is still
106
) First line: - blocker and/ or calcium channel blocker
GTN
skin patches. SE: headaches, BP.
375
mg BD. Caution if heart failure,
kg, or prolonged QT interval.
5
mg BD. Only consider if clinical HF also present.
LV
failure.
104
): a balloon is inflated inside the
DAPT
12
months after stent insertion to reduce the risk of
PCI
, patients undergoing
; usually aspirin and clopidogrel) is
CABG
are less likely to need re-
Investigating patients with possible stable angina
IHD
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Investigations for ischaemic heart disease (
• Exercis e
ECG
• Angiography— either using cardiac CT with contrast, or transcatheter angiography
(more invasive but can be combined with stenting,
• Fun ctio nal im agin g ( p
— assess for ischaemic
102
): myocardial perfusion scintigraphy, stress echo (echo
whilst undergoing exercise or receiving dobutamine), cardiac
NICE
recommends the following investigations when considering stable angina.
Typ i ca l an gi na i n a p a ti en t wi th pr eviousl y pro ven
ECG
IHD
cha nges.
) include:
p
104
).
MRI
.
Treat as stable angina; if further confirmation is required, use non- invasive
ECG
testing, eg exercise
. Oer non- invasive functional testing when there is uncer-
tainty about whether chest pain is caused by myocardial ischaemia.
Typ i ca l an d at yp ic al a ng i na
CT
angiography, fig
transcatheter angiography as
3.26
. If inconclusive, use functional imaging as 2nd line and
3
rd line.
Non- anginal chest pain
Does the patient have ischaemic changes on 12- lead
• Yes : in ve st i ga te a s p e r t yp i ca l an d at yp ic al a ng in a .
• No: no further investigations for
IHD
for o ther re asons— discuss with a specialist). Ensure alternative chest pain diag-
IHD
at this point (unless high clinical suspicion of
ECG
?
noses are adequately explored.
Fur ther inv esti gati ons
If the patient has typical angina but few risk factors for
IHD
, be sure to look
for possible precipitating or exacerbating factors, eg severe anaemia or
cardiomyopathy.
If anginal symptoms not adequately controlled with optimal medical therapy
Oer transcatheter angiography. Additional non- invasive or invasive functional
testing may be required to evaluate angiographic findings and guide decisions.
Fig 3.
26
CT angiogram data has been used
3D
to construct this
points to an obstruction of the right coronary artery.
Reprinted from Journal of the American
College of Cardiology,
et al., Noninvasive Evaluation With Multislice
Computed Tomography in Suspected Acute
image. The white arrow
Coronary Syndrome,
permission from Elsevier.
52(3
), MM Henneman
216– 22, 2008
, with
113
23
3 Cardiovascular medicine
Vasospastic angina (Prinzmetal angina)
Angina due to epicardial coronary artery spasm, which can occur even in normal
coronary arteries. The pain usually occurs during rest (often at night) and resolves rapidly with short- acting nitrates (eg
ST
- segment elevation or depression.
Risks and triggers Smoking increases risk but hypertension and hypercholester-
olaemia do not. Probable triggers include cocaine, amphetamine, marijuana, low
magnesium, and artery instrumentation (eg during angiography).
Treatment Avoid triggers. Correct low magnesium. Stop smoking.
Calcium channel blockers
aspirin, and triptans. Prognosis is usually very good.
GTN
spray).
ECG
during pain shows
±
long- acting nitrates. Avoid non- selective - blockers,
PRN GTN
.
3 Cardiovascular medicine
Acute coronary syndromes (
ACS
STEM I
NSTEMI
ECG
STEMI
NSTEMI
CXR
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114
Definitions
a common underlying pathology— plaque rupture, thrombosis, and inflammation.
However,
includes unstable angina and myocardial infarction (MI). These share
ACS
may rarely be due to emboli, coronary spasm, or vasculitis (p
normal coronary arteries. Myocardial infarction means there is myocardial cell death,
releasing troponin (see
Unstable angina refers to the presence of ischaemic symptoms suggestive of
death.
an ACS without elevation in biomarkers with or without
chaemia. An
in
without
MI
V
7
may be a
–
V
if posterior
9
ST
- segment elevation— the
STEMI
non- specific changes, or be normal
and significant necrosis can occur without
Risk factors Non- modifiable Age, sex, family history of
55
relative <
yrs). Modifiable Smoking, hypertension, DM, hyperlipidaemia, obesity,
sedentary lifestyle, cocaine use.
Incidence >
100 000
Diagnosis An increase in cardiac biomarkers (eg troponin) and either: symptoms
ECG
of ischaemia,
changes of new ischaemia, development of pathological Q waves,
new loss of myocardium, or regional wall motion abnormalities on imaging.
Symptoms Acute central chest pain, lasting >20min, often associated with nausea,
sweatiness, dyspnoea, palpitations.
seen in elderly and diabetic patients. Can also present as a cardiac arrest (early
angiography better in this setting if suggestive
sent with: syncope, pulmonary oedema, epigastric pain and vomiting, post- operative
hypotension or oliguria, acute confusional state, stroke, and diabetic hyperglycaemic
MI
S are a lso mo re like ly to be under- diagnosed in women ( mortality).
states.
Signs Distress, anxiety, pallor, sweatiness, pulse or , BP or , 4th heart sound.
There may be signs of heart failure (
pansystolic murmur (papillary muscle dysfunction/ rupture,
may be present. Later, a pericardial friction rub or peripheral oedema may develop.
Tests
(See fig
LBBB
new
hours to days (
specific changes, or normal.
ECG
S and
and may hinder
in these cases, clinical assessment and troponin levels are especially important.
Look for cardiomegaly, pulmonary oedema, or a widened mediastinum. Don’t
routinely delay treatment whilst waiting for a
cardiac enzymes.
3.27
occur within hours. T- wave inversion and pathological Q waves follow over
p90).
ECG
S with chronic bundle branch block are unhelpful for diagnosing
STEMI
Cardiac enzymes (See
(cTnT and cInI) are the most sensitive and specific markers of myocardial necrosis.
Dierent hospitals use dierent assays: check the required timing of troponin blood
samples where you work (eg two samples
assays, most patients can be diagnosed within
indicated if initial −ve test and suggestive presentation. Acute
most patients by
picion of an ACS, a
6
h, but the guidelines suggest that if there is a high degree of sus-
12
sitive but less specific and not frequently used.
Dierential diagnosis (p86.) Stable angina, pericarditis, myocarditis, Takotsubo
p
cardiomyopathy (
139
pneumothorax, musculoskeletal pain, pancreatitis.
Management See p
Mortality 50% of deaths occur within 2h of onset of symptoms. Up to 7% die be-
fore discharge. Worse prognosis if: elderly,
ACS
)
554
BOX
'Troponin'). Ischaemia means a lack of blood supply, ± cell
ECG
—
ACS
with ST- segment elevation (may only be present
) or new- onset
LBBB
; or an
ECG
may show ST depression, T- wave inversion,
.
The degree of irreversible myocyte death varies,
ST
elevati on.
admissions per annum (UK) due to
ACS
without chest pain is called ‘silent’; mostly
JVP
, 3rd heart sound, basal crepitations) or a
.)
: classically, hyperacute (tall) T waves, ST elevation, or
changes indicative of is-
— troponin- positive
IHD (MI
in 1st- degree
MI
S.
ECG
changes). Silent MIs may pre-
VSD
). Low- grade fever
/ unstable angina: ST depression, T- wave inversion, non-
In 20% of
diagnosis (see
MI
S, the
ECG
may be normal initially. Paced
BOX
'Modified Sgarbossa's criteria', p93);
CXR
. Blood
FBC, U&E
BOX
‘Troponin’.) Cardiac troponin levels
3
h apart). With highly sensitive troponin
2– 3
h of presentation. Serial testing is
, glucose, lipids,
MI
can be excluded in
NSTEMI
h sample should be obtained. Other cardiac enzymes are sen-
Echo Regional wall abnormalities.
), aortic dissection (p
116
, pp
780– 83
.
647
), PE, oesophageal reflux/ spasm,
LV
failure, and ST changes.
) in
ACS
S
Normal Hours Days Weeks Months
Fig 3.
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27
Sequential
ECG
changes following acute MI.
Myocardial injury vs infarction
• Myocardial injury ('troponin leak') Elevated cTn with at least one value above the
99
th percentile. Considered acute if there is a rise and/ or fall of cTn values. No signs/
symptoms suggestive of myocardial ischaemia.
• Myocardial infarction (MI) Acute myocardial injury with clinical evidence of acute
myocardial ischaemia (ie ≥
• Typ e 1 MI Caused by acute atherothrombotic
1
of sy mptom s,
ECG
or i magin g chan ges).
CAD
and usually precipitated by atherosclerotic plaque disruption (rupture or erosion). Also includes coronary artery
dissection.
• Typ e 2 MI Caused by an imbalance between myocardial oxygen supply and demand
unrelated to acute atherothrombosis, eg sustained tachyarrhythmia, severe anaemia, shock, respiratory failure, coronary spasm, emboli.
• Typ e 3 MI Sud den un expec ted ca rdiac death with s ympto ms/
cardial ischaemia.
• Typ e 4 MI MI ass ociated w ith
• Typ e 5 MI MI ass ociated w ith car diac s urgery.
PCI
or s tent/ scaold thrombosis.
24
ECG
sug gesti ve of m yo-
Troponin
Troponins are proteins involved in cardiac and skeletal muscle contraction
fig
3.28
). When myocardial cells are damaged, troponins are released and enter
(
the bloodstream. The levels of troponin in the blood can therefore help with
diagnosing myocardial damage. Troponins
Cardiac troponin is a highly sensitive biomarker of myocardial cell damage (injury),
which is often, but not always, due to
cell release, it is not specific for
ACS
I
and T are most specific to the heart.
CAD
. While it is highly specific for myocardial
as the cause. Injury to myocardial cells can arise
from conditions such as myocarditis, pericarditis, infiltrative conditions, or other noncardiac mechanisms such as following preload- induced mechanical stretch (eg heart
failure), oxygen supply– demand mismatch (eg tachyarrhythmia), haemodynamic
stress (eg right ventricular strain due to a massive
otherwise normal hearts (eg sepsis). With these conditions, the troponin levels are
likely to change little hour by hour as the insults are ongoing. Troponin levels can also
be raised iatrogenically, eg following
A common cause of consistently elevated troponin is
myocardial injury or other underlying structural heart disease rather than epicar-
CAD
. Hence, when measuring troponin in
dial
change in level is often more important than the level itself.
CPR, DC
and be mindful of the clinical context in which it was checked. However, although
troponin has a lower sensitivity, specificity and
levels are still associated with worse
CV
outcomes.
PE
), or physiological stresses in
ca rdiov ers ion, abla tio n the rapy.
CKD
, likely due to chronic
CKD
or dialysis- dependent patients,
Check old values
PPV
for type 1 MI in
CKD
25
, elevated
115
3 Cardiovascular medicine
Fig 3.
28
Diagram of myocardial contraction unit. The troponin complex controls when the
myosin heads can bind to the actin chain, shortening the muscle fibre.
Reproduced from Barnard et al., Cardiac Anaesthesia,
with permission from Oxford University Press.
2010
,
3 Cardiovascular medicine
Management of
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116
ACS
management depends on whether the
1
ST elevation myocardial infarction (
elevation on
MI
s (fig
3.29
Urgent revascularization is essential.
2
ACS
without ST elevation: serial troponins are needed to dierentiate non- ST
elevation
MI
After the immediate actions described on
ACS
ACS
is ‘ST elevation’ or not:
STEMI
ECG
(fig
3.12
) but also
): this category includes
ACS
with new
LBBB
(fig
3.10
) where ST elevation may only be seen with extra leads (
p
780
.
S (
NSTEMI
S) (trop rise) from unstable angina (no trop rise). p
pp
780– 83
, treatment of
on managing symptoms, secondary prevention of further cardiovascular disease,
revascularization (if not already undertaken), and addressing complications.
Symptom control Manage chest pain with
if very severe). If this proves insucient, consider a
if recent sildenafil use). If patient is deteriorating or if pain worsening, seek senior
help. Manage symptomatic heart failure,
p
PRN GTN
and opiates (IV morphine only
GTN
infusion (monitor
136
.
Modify risk factors
• Patients should be strongly advised, and helped, to stop smoking (p85).
• Identify and treat diabetes, hypertension, hyperlipidaemia, and
• Advise a diet high in oily fish, fruit, vegetables, & fibre, and low in saturated fats.
• Encourage daily exercise. Refer to a cardiac rehab programme.
• Mental health: flag to the patient’s GP if depression or anxiety are present— these
CKD
are independently associated with poor cardiovascular outcomes.
Optimize cardioprotective medications
• Antiplatelets: aspirin (75mg OD) and a second antiplatelet agent (eg ticagrelor) for
12
months to vascular events (eg MI, stroke). Consider adding a
at least
lansoprazole) for gastric protection. If already taking
• Anticoagulate, eg with enoxaparin 1mg/ kg BD (OD if
• - blockade reduces myocardial oxygen demand. Start low and increase slowly,
monitoring pulse and
•
ACE
- i (or
ARB
• High- dose statin, eg atorvastatin 80mg.
• Do an echo to assess LV function. Add
BP
. If contraindicated, consider verapamil or diltiazem.
) in all patients. Monitor renal function.
MRA
(eg spironolactone) if LV function <40%.
DOAC
, see
GFR
BOX
<30mL/ min), until discharge.
Revascularization
•
STEMI
patients and very high- risk
should receive immediate angiography
GRACE
score >
140
109– 140
• Patients wi th mult ivessel dis ease may be c onside red for
) should have angiography within 24h; intermediate risk (eg
) within 3d; low- risk patients may be considered for non- invasive testing.
Manage complications See p
NSTEMI
patients (eg haemodynamically unstable)
±
PCI. NSTEMI
patients who are high risk (eg
118
.
CABG
instead of
Discharge Address any questions the patient has. Discuss ‘red flag’ symptoms and
where to seek medical advice should they arise. Ensure the management plan is
communicated to the patient’s
GP.
Book clinic and cardiac rehab appointments.
General advice
• Driving26 Drivers with group 1 licences (car and motorcycle) can resume driving
1
wk after successful angioplasty, or 4wks after
40
plasty, if their ejection fraction is >
DVLA
of their
ACS
they may be able to restart after
• Work How soon a patient can return to work will depend on their clinical progress
and the nature of their work. They should be encouraged to discuss speed of re-
±
changes in duties (eg to lighter work if manual labour) with their employer.
turn
Some occupations cannot be restarted post-
and stop driving; depending on the results of functional tests,
%. Group 2 licence holders must inform the
6
wks.
ACS
without successful angio-
MI
: eg airline pilots & air trac controllers. Drivers of public service or heavy goods vehicles will have to undergo
functional testing (eg exercise test), as mentioned previously.
ACS
with ST
); and posterior
V
–
V
7
782
ACS
focuses
BP,
omit
.
PPI
(eg
'Triple thera py'.
GRACE
PCI
(p
119
).
9
.
).
suggests
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6
V
waves) and
Q
elevation in
ST
. The
90
waves (‘upside- down’ pathological
R
elevation pattern, see p
ST
: dominant
3
–
1
V
), we would see the classic
9
–
7
V
117
3 Cardiovascular medicine
Triple therapy
For patients post-
PCI
with stenting who also have an indication for long- term
anticoagulation, eg pre- existing
taking into account both the thrombotic and bleeding risk. Seek expert cardiology advice.
safest combination where necessary.
DOAC
(rather than warfarin) + clopidogrel monotherapy may be the
The posterior infarct is evidenced by the reciprocal changes seen in
MI.
Acute posterolateral
29
.
Fig
AF
, decision- making needs to be individualized,
27
elevation). If extra chest leads were added (
ST
depression (‘upside- down’
ST
lateral infarction. A blockage in the circumflex coronary artery could explain both the posterior and lateral changes.
3 Cardiovascular medicine
Complications of
AV
SVT
AF
PVCS
RVF
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118
Cardiac arrest (See p
Cardiogenic shock (See p
Left ventricular failure (ischaemic cardiomyopathy) (See p
Bradyarrhythmias Sinus bradycardia See p
suer atropine- unresponsive bradycardia due to infarction of nodal tissue.
block Most commonly seen in inferior MI. Observe closely as ~40%
degree
develop higher degrees of
- blockers should be stopped).
require pacing unless poorly tolerated.
developing sudden complete
resolves within a few days. Insert pacemaker (may not be necessary after inferior
MI
if narrow
MI
complicated by trifascicular block or non- adjacent bifascicular disease (p
QRS,
reasonably stable and pulse 40– 50). Bundle branch block Pace
Tachyarrhythmias
and should be corrected.
(pain, hypoxia, sepsis, etc.) and add - blocker if not contraindicated.
or flutter If compromised, DC cardioversion. Otherwise, medical therapy as per
p
126
. Frequent
3
consecutive
(≥
PVC
S >
are associated with increased risk of sudden death. Correct hypokalaemia and
hypomagnesaemia and ensure the patient is on - blockers, if not contraindicated
Sustained VT (Consecutive
DC
shock (if no pulse, treat as per advanced life support algorithm, see p
ized
3
). Use anti- arrhythmics only if VT recurrent and not controlled with shocks.
fig A
Consider ablation &/ or
occurring after
p
(see
48
878
, fig A3), consider
h usually indicates pump failure or cardiogenic shock. : DC shock
Right ventricular failure (
JVP
. Fluid is key; avoid vasodilators (eg nitrates) and diuretics. Inotropes are re-
quired in some cases.
Pericarditis Central chest pain, relieved by sitting forwards.
fig
elevation, see
3.45
Systemic embolism May arise from LV mural thrombus. After large anterior MI,
consider anticoagulation with
Cardiac tamponade (p
Kussmaul’s sign,
2
mued heart sounds. Diagnosis: echo. Treatment: pericardial as-
piration (provides temporary relief,
Mitral regurgitation May be mild (minor papillary muscle dysfunction) or severe
(chordal or papillary muscle rupture secondary to ischaemia). Presentation: pulmonary oedema. Treat
LV free wall or interventricular septum rupture New holosystolic murmur
VSD
in the case of
. Can lead to cardiogenic shock, tamponade, and sudden death.
Diagnosis: echo, pericardiocentesis. Treatment: surgery.
Late malignant ventricular arrhythmias Occur 1– 3wks post- MI and are the
cardiologist’s nightmare. Avoid hypokalaemia, the most easily avoidable cause.
24
h
ECG
Consider
Dressler’s syndrome (p
aemia, and
Left ventricular aneurysm This occurs late (4– 6wks post- MI), and presents with
LVF
, angina, recurrent
monitoring prior to discharge if large MI.
ESR
1– 3wks post- MI. Treatment: consider
tion. Treatment: anticoagulate, consider excision.
2
JVP
rises during inspiration. Adolf Kussmaul was a prominent 19th- century physician and the first to attempt gastroscopy. Inspired by a sword swallower he passed a rigid tube into the stomach; however, light
technology was limited and it was not until years later that gastroscopists could visualize the stomach.
MI
878
, fig A3.)
786
.)
792
. Patients with inferior MIs may
AV
block (in which case calcium channel blockers and
136
, p
784
, p
786
.)
1
st-
Wenckebach phenomenon (Mobitz type I) Does not
Mobitz type II block Carries a high risk of
AV
block; should be paced. Complete AV block Usually
128
NB:
K+ , hypoxia, and acidosis all predispose to arrhythmias
).
Sinus tachycardia Myocardial O2 demand, treat causes
See p
122
(premature ventricular complexes) and non- sustained VT
100
bpm and lasting <30s) are common after acute MI and
PVC
S >
100
bpm and lasting >30s.) Treat with synchron-
878
ICD
. Ventricular fibrillation 80% occurs within 12h. VF
ICD
.
)/ infarction Presents with low cardiac output and
ECG
, p
133
. Treatment:
786
LVF
(p
133
VT,
or systemic embolism.
NSAID
S. Echo to check for eusion.
DOAC
or warfarin for 3 months.
) Presents with low cardiac output, pulsus paradoxus,
see p
757
for technique), surgery.
784
) and consider valve replacement.
) Recurrent pericarditis, pleural eusions, fever, an-
NSAID
ECG
: persistent ST- segment eleva-
: saddle- shaped ST
50
% mortality in first week.
S; steroids if severe.
.
,
Coronary artery bypass graft (
CABG
CABG
CABG
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CABG
is performed in left main stem disease; multivessel disease; multiple severe
CABG
)
stenoses; patients unsuitable for angioplasty; failed angioplasty; refractory angina.
Indications for
— to improve survival
• Left main stem disease.
• Triple- vessel disease involving proximal part of the left anterior descending.
Indications for
— to relieve symptoms
• Angina unresponsive to drugs.
• Unstable angina (sometimes).
• If angioplasty is unsuccessful.
NB:
when
CABG
and percutaneous coronary intervention (
NICE
both clinically valid options,
technology should push the decision towards
vessel coronary artery disease and normal
those with triple- vessel disease and abnormal
CABG
. Compared with
patient stay. Recent
RCT
survival rates are similar after
recommends that the availability of new stent
PCI
LV
PCI, CABG
results in longer recovery time and length of in-
S indicate that early procedural mortality rates and
PCI
and
CABG
. Compared with
function usually undergo
PCI
, eg angioplasty) are
. In practice, patients with single-
PCI
LV
function more often undergo
PCI, CABG
, and
5
- year
probably
provides more complete long- term relief of angina in patients, and less repeated
revascularization.
Procedure The heart is usually stopped and blood pumped artificially by a ma-
chine outside the body (cardiac bypass). Minimally invasive thoracotomies not requiring this are well described,
saphenous vein or internal mammary artery is used as the graft. Several grafts
may be placed. >
this). Internal mammary artery grafts last longer.
50
% of vein grafts close in 10yrs (low- dose aspirin helps prevent
28
but randomized trials are few. The patient’s own
Complications Bleeding, stroke, cognitive dysfunction, sternal wound infection,
AKI
mediastinitis,
, peri- op MI, early graft occlusion, arrhythmias, vasoplegic shock,
pericarditis, pericardial eusion/ tamponade.
On- pump or o- pump O- pump refers to
monary bypass. Similar short- term outcomes to on- pump surgery but higher
rates of revascularization at
unless high risk of stroke from aortic manipulation.
After
If angina persists or recurs (from poor graft run- o, distal disease,
1
year with o- pump.29 On- pump generally preferable
CABG
without the use of cardiopul-
new atheroma, or graft occlusion) restart anti- anginal drugs, and consider angioplasty. Ensure optimal management of hypertension, diabetes, and hyperlipidaemia, and that smoking is addressed. Continue aspirin
consider clopidogrel if aspirin contraindicated. Mood, sex, and intellectual prob-
30
are common early. Rehabilitation helps:
lems
• Exercise: walkcycleswimjog.
• Drive at 1 month: no need to tell
• Return to work, eg at 3 months.
DVLA
if non-
HGV
licences, p
75
mg OD indefinitely;
150
.
119
3 Cardiovascular medicine
‘We’ is more important than ‘I’
René Gerónimo Favaloro, an Argentinian surgeon, is known as the father of
surgery. Prior to this, he spent years trying to improve the health of local farming
communities in his home country, educating them about preventative medicine,
creating blood banks, building operating theatres, and training new doctors. In
1967
, after joining the Cleveland Clinic, he performed the first successful bypass
surgery. Shortly after this, he returned to Argentina where he established the
Favaloro Foundation dedicated to medical research and teaching for the people of
Latin America. Reminding us all of the great collective eort of past, present, and
future colleagues, he once wrote humbly, ‘In medicine, the advances are always
the result of many eorts accumulated over the years.’
CABG
3 Cardiovascular medicine
Arrhythmias— overview
https://t.me/med1917
120
Disturbances of cardiac rhythm (arrhythmias) are:
• Common.
• Often benign (but may reflect underlying heart disease).
• Often intermittent, causing diagnostic diculty; see
• Occasionally severe, causing cardiac compromise which may be fatal.
Emergency management: pp
Causes Cardiac Ischaemic heart disease (
tation secondary to mitral regurgitation; cardiomyopathy; pericarditis; myocarditis;
aberrant conduction pathways.
- agonists, digoxin, tricyclics, doxorubicin); metabolic imbalance (K+ , Ca
drugs (
2
2
+
, hypoxia, hypercapnia, acidosis, thyroid disease); and phaeochromocytoma.
Mg
Presentation Palpitations, chest pain, presyncope/ syncope, hypotension, or pul-
monary oedema. Some arrhythmias may be asymptomatic, incidental findings, eg
History Take a detailed history of palpitations (p36). Ask about precipitating fac-
tors, onset/ oset, nature (fast or slow, regular or irregular), duration, associated
symptoms (chest pain, dyspnoea, collapse). Review drug history. Ask about past
medical history and family history of cardiac disease and sudden death. Syncope
occurring during exercise is always concerning; the patient may have a condition
predisposing them to sudden cardiac death (eg long
Tests
FBC, U&E
WPW
(
(hypokalaemia).
‘Continuous
stenosis,
, glucose, Ca
syndrome), long QT interval (metabolic imbalance, drugs, congenital), U waves
24
h
ECG
monitoring’). Echo to look for structural heart disease, eg mitral
HCM
. Provocation tests: exercise
physiological studies may be needed.
Narrow complex tachycardias See pp
Atrial fibrillation and flutter See pp
Broad complex tachycardias See pp
Bradycardia See p
(heart block). Intermittent, self- resolving bradycardic episodes can cause significant problems (eg recurrent syncope). Continuous
ECG
monitoring’) will be needed to assist the diagnosis ± specialist tests (eg tilt
table testing for reflex syncope). Seek out reversible causes, eg hypothyroidism or
medications such as - blockers. In some cases, no reversible cause is found and the
intermittent bradycardia is suciently dangerous to warrant a permanent pace-
p
128
). See
maker (
Management Some arrhythmias can be managed conservatively, eg by reducing
alcohol intake. Many arrhythmias respond to
BOX
tablets or a ‘pill in the pocket’.
(
p
128
), ablation (eg of accessory pathways or arrhythmogenic foci), or implantable
cardioverter defibrillators (
MI
and in those with congenital arrhythmogenic conditions (p
Screening athletes The incidence of
1:100 000
/ yr) but it is a devastating event— likely attributable to a combination of
structural heart disease, inherited arrhythmia syndrome, &
cardiovascular screening of young competitive athletes (those who engage in
6– 8
h/ week of intensive sport since >6 months) is recommended by the
>
should include a detailed personal and family history, physical examination, and
12
- lead
ECG
a
first- degree
.31 Common
AV
block, incomplete
pattern— all of which are likely attributable to training- related changes.
normalities warranting further investigation include ventricular pre- excitation, epsilon waves, complete
inversion.
BOX
788– 93
‘C ont in uou s
.
IHD
); structural changes, eg left atrial dila-
ECG
mo nit or ing ’.
Non- cardiac Caeine; smoking; alcohol; pneumonia;
QT
2
+
2
+
, Mg
,
TSH, ECG
: look for signs of
ECG
monitoring or other continuous
ECG
790– 1
790– 1
788– 9
792
(causes and management of acute bradycardia) and p90
syndrome).
IHD, AF
, short PR interval
ECG
monitoring (see
, cardiac catheterization ± electro-
, p
126
.
, p
126
.
, p
128
.
ECG
monitoring (
BOX
‘Continuous
, ‘Sinus node dysfunction’.
medical management with regular
Interventional management may include pacemakers
ICD
S), eg in patients with ventricular arrhythmias post-
SCD
among young athletes is low (1:50
ECG
variants found in athletes include sinus bradycardia,
RBBB
, isolated electrical
LBBB
, pathological Q waves, ST depression, long QTc, T- wave
148
).
CAD
. Pre- participation
LVH
, early repolarization
ESC
ECG
AF.
BOX
000
and
ab-
2
+
,
–
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