Essential

Revision Notes
for MRCP
Third Edition
Contents
Contributors toThird Edition vii
Contributors to Second Edition ix
Preface to theThird Edition xi
CHAPTER
1. Cardiology 1
J Paisey
2. Clinical Pharmacology,Toxicology and Poisoning 53
S Waring
3. Dermatology 73
H Robertshaw
4. Endocrinology 91
C Dayan
5. Epidemiology 125
G Whitlock
6. Gastroenterology 139
J Ramesh
7. Genetics 179
E Burkitt Wright
8. Genito-urinary Medicine and AIDS 197
B Goorney
9. Haematology 211
K Patterson
10. Immunology 249
M J McMahon
11. Infectious Diseases andTropical Medicine 265
C van Halsema
12. Maternal Medicine 291
L Byrd
13. Metabolic Diseases 317
Smeeta Sinha
v
14. Molecular Medicine 353
K Siddals
15. Nephrology 389
P Kalra
16. Neurology 447
G Rees
17. Ophthalmology 483
K Smyth
18. Psychiatry 501
E Sampson
19. Respiratory Medicine 527
D Wales
20. Rheumatology 569
M J McMahon
21. Statistics 593
A Wade
Index 607
Contents
vi
Chapter 1
Cardiology
CONTENTS
1.1 Clinical examination
1.1.1 Jugular venous pulse (JVP)
1.1.2 Arterial pulse associations
1.1.3 Cardiac apex
1.1.4 Heart sounds
1.2 Cardiac investigations
1.2.1 Electrocardiography (ECG)
1.2.2 Echocardiography
1.2.3 Nuclear cardiology: myocardial
perfusion imaging (MPI)
1.2.4 Cardiac catheterisation
1.2.5 Exercise stress testing
1.2.6 24-hour ambulatory blood
pressure monitoring
1.2.7 Computed tomography (CT)
1.2.8 Magnetic resonance imaging
(MRI)
1.3 Valvular disease and
endocarditis
1.3.1 Murmurs
1.3.2 Mitral stenosis
1.3.3 Mitral regurgitation (MR)
1.3.4 Aortic regurgitation (AR)
1.3.5 Aortic stenosis (AS)
1.3.6 Tricuspid regurgitation (TR)
1.3.7 Prosthetic valves
1.3.8 Infective endocarditis
1.4 Congenital heart disease
1.4.1 Atrial septal defect (ASD)
1.4.2 Ventricular septal defect (VSD)
1.4.3 Patent ductus arteriosus (PDA)
1.4.4 Coarctation of the aorta
1.4.5 Eisenmenger syndrome
1.4.6 Tetralogy of Fallot
1.4.7 Important post-surgical
circulation
1.5 Arrhythmias and pacing
1.5.1 Bradyarrhythmias
1.5.2 Supraventricular tachycardias
1.5.3 Atrial arrhythmias
1.5.4 Ventricular arrhythmias and
channelopathies
1.5.5 Pacing and ablation procedures
1.6 Ischaemic heart disease
1.6.1 Angina
1.6.2 Myocardial infarction
1.6.3 Medical therapy for myocardial
infarction
1.6.4 Coronary artery interventional
procedures
1
1.7 Other myocardial diseases
1.7.1 Cardiac failure
1.7.2 Hypertrophic cardiomyopathy
(HCM)
1.7.3 Dilated cardiomyopathy (DCM)
1.7.4 Restrictive cardiomyopathy
1.7.5 Myocarditis
1.7.6 Cardiac tumours
1.7.7 Alcohol and the heart
1.7.8 Cardiac transplantation
1.8 Pericardial disease
1.8.1 Constrictive pericarditis
1.8.2 Pericardial effusion
1.8.3 Cardiac tamponade
1.9 Disorders of major vessels
1.9.1 Pulmonary hypertension
1.9.2 Venous thrombosis and
pulmonary embolism
1.9.3 Systemic hypertension
1.9.4 Aortic dissection
Appendix I
Normal cardiac physiological values
Appendix II
Summary of further trials in cardiology
Essential Revision Notes for MRCP
2
Cardiology
1.1 CLINICAL EXAMINATION
1.1.1 Jugular venous pulse (JVP)
This reects the right atrial pressure (normal to 3 cm
above the clavicle with the subject at 458). This
should fall with inspiration, which increases venous
return by a suction effect of the lungs, and with
expansion of the pulmonary beds. However, if the
neck veins are distended by inspiration this implies
that the right heart chambers cannot increase in size
due to restriction by uid or pericardium: Kuss-
mauls sign. Non-pulsatile JVP elevation occurs with
superior vena caval obstruction.
Normal waves in the JVP
a wave
Due to atrial contraction active push up superior
vena cava (SVC) and into the right ventricle (may
cause an audible S4).
c wave
An invisible icker in the x descent due to closure
of the tricuspid valve, before the start of ventricular
systole.
x descent
Downward movement of the heart causes atrial
stretch and a drop in pressure.
v wave
Due to passive lling of blood into the atrium
against a closed tricuspid valve.
y descent
Opening of the tricuspid valve with passive move-
ment of blood from the right atrium to the right
ventricle (causing an S3 when audible).
Pathological waves in the JVP
a waves
Lost in atrial brillation, giant in tricuspid stenosis
or in pulmonary hypertension with sinus rhythm
(atrial septal defect (ASD) will exaggerate the natur-
al a and v waves in sinus rhythm).
Giant v(s) waves
Merging of the a and v waves into a large wave
(with a rapid y descent) as pressure continues to
increase due to ventricular systole in patients with
tricuspid regurgitation.
Steep x descents
Occur in states where there is atrial lling only due
to ventricular systole and downward movement of
the base of the heart, ie compressed atrial states
with tamponade or constrictive pericarditis.
Rapid y descent
Occurs in states where high ow occurs with tricus-
pid valve opening (eg tricuspid regurgitation (high
atrial load) or constrictive pericarditis) vacuum
effect. A slow y descent indicates tricuspid stenosis.
Cannon a waves
Atrial contractions against a closed tricuspid valve
due to a nodal rhythm, a ventricular tachycardia,
ventricular-paced rhythm (regular), complete heart
block or ventricular extrasystoles (irregular). They
occur regularly but not consistently in type 1
second-degree heart block.
1.1.2 Arterial pulse associations
Collapsing: aortic regurgitation, arteriovenous
stula, patent ductus arteriosus or other large
extra-cardiac shunt
Slow rising: aortic stenosis (delayed percussion
wave)
Bisferiens: a double shudder due to mixed
aortic valve disease with signicant
regurgitation (tidal wave second impulse)
Jerky: hypertrophic obstructive cardiomyopathy
Alternans: severe left ventricular failure
Cardiology
3
Paradoxical (pulsus paradoxus): an excessive
reduction in the pulse with inspiration (drop in
systolic BP .10 mmHg) occurs with left
ventricular compression, tamponade,
constrictive pericarditis or severe asthma as
venous return is compromised
Causes of an absent radial pulse
Dissection of the aorta with subclavian
involvement
Iatrogenic: post-catheterisation
Peripheral arterial embolus
Takayasus arteritis
Trauma
1.1.3 Cardiac apex
An absent apical impulse
The apex may be impalpable in the following situa-
tions:
Obesity/emphysema
Right pneumonectomy with displacement
Pericardial effusion or constriction
Dextrocardia (palpable on right side of chest)
Apex associations
Palpation of the apex beat (reecting counter-clock-
wise ventricular movement striking the chest wall
during isovolumic contractions) can detect the fol-
lowing pathological states:
Heaving: left ventricular hypertrophy (LVH) (and
all its causes), sometimes associated with
palpable fourth heart sound
Thrusting/hyperdynamic: high left ventricular
volume (eg in mitral regurgitation, aortic
regurgitation, patent ductus arteriosus (PDA),
ventricular septal defect)
Tapping: palpable rst heart sound in mitral
stenosis
Displaced and diffuse/dyskinetic: left
ventricular impairment and dilatation (eg dilated
cardiomyopathy, myocardial infarction (MI))
Double impulse: with dyskinesia is due to left
ventricular aneurysm; without dyskinesia in
hypertrophic cardiomyopathy (HCM)
Pericardial knock: constrictive pericarditis
Parasternal heave: due to right ventricular
hypertrophy (eg ASD, pulmonary hypertension,
chronic obstructive pulmonary disease (COPD),
pulmonary stenosis)
Palpable third heart sound: due to heart failure
and severe mitral regurgitation
1.1.4 Heart sounds
Abnormalities of rst heart sounds are given in
Table 1.1 and of second heart sounds are given in
Table 1.2.
Table 1.1. Abnormalities of the rst heart sound (S1): closure of mitral and tricuspid valves
Loud Soft Split Variable
Mobile mitral stenosis Immobile mitral stenosis RBBB Atrial brillation
Hyperdynamic states Hypodynamic states LBBB Complete heart block
Tachycardic states Mitral regurgitation VT
Left-to-right shunts Poor ventricular function Inspiration
Short PR interval Long PR interval Ebsteins anomaly
LBBB, left bundle branch block; RBBB, right bundle branch block; VT, ventricular tachycardia
Essential Revision Notes for MRCP
4
Third heart sound (S3)
Due to the passive lling of the ventricles on open-
ing of the AV valves, audible in normal children
and young adults. Pathological in cases of rapid left
ventricular lling (eg mitral regurgitation, ventricular
septal defect (VSD), congestive cardiac failure and
constrictive pericarditis).
Fourth heart sound (S4)
Due to the atrial contraction that lls a stiff left
ventricle, such as in LVH, amyloid, HCM and left
ventricular ischaemia. It is absent in atrial brilla-
tion.
Causes of valvular clicks
Aortic ejection: aortic stenosis, bicuspid aortic
valve
Pulmonary ejection: pulmonary stenosis
Mid-systolic: mitral valve prolapse
Opening snap (OS)
In mitral stenosis an OS can be present and occurs
after S2 in early diastole. The closer it is to S2 the
greater the severity of mitral stenosis. It is absent
when the mitral cusps become immobile due to
calcication, as in very severe mitral stenosis.
1.2 CARDIAC INVESTIGATIONS
1.2.1 Electrocardiography (ECG)
Both the axis and sizes of QRS vectors give impor-
tant information. Axes are dened:
308 to +908: normal
308 to 908: left axis
+908 to +1808: right axis
908 to 1808: indeterminate
Tip if the QRS is positive in leads 1 and aVF the
axis is normal.
The causes of common abnormalities are given in
the box on p. 7. ECG strips illustrating typical
changes in common disease states are shown in
Figure 1.1.
Table 1.2. Abnormalities of the second heart sound (S2): closure of aortic then pulmonary valves
(,0.05 s apart)
Intensity Splitting
Loud: Fixed: Single S2:
Systemic hypertension (loud A2)
Pulmonary hypertension (loud P2)
ASD Severe pulmonary stenosis/aortic stenosis
Hypertension
Tachycardic states Widely split: Large VSD
ASD (loud P2) RBBB Tetralogy of Fallot
Pulmonary stenosis Eisenmenger syndrome
Soft or absent: Deep inspiration Pulmonary atresia
Severe aortic stenosis Mitral regurgitation Elderly
Reversed split S2:
LBBB
Right ventricular pacing
PDA
Aortic stenosis
A2, aortic second sound; ASD, atrial septal defect; LBBB, left bundle branch block; P2, pulmonary second sound;
PDA, patent ductus arteriosus; RBBB, right bundle branch block; VSD, ventricular septal defect
Cardiology
5
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Essential Revision Notes for MRCP
6
Causes of common abnormalities in the
ECG
Causes of left axis deviation
Left bundle branch block (LBBB)
Left anterior hemi-block (LAHB)
LVH
Primum ASD
Cardiomyopathies
Tricuspid atresia
Low-voltage ECG
Pulmonary emphysema
Pericardial effusion
Myxoedema
Severe obesity
Incorrect calibration
Cardiomyopathies
Global ischaemia
Amyloid
Causes of right axis deviation
Infancy
Right bundle branch block (RBBB)
Right ventricular hypertrophy (eg lung
disease, pulmonary embolism, large
secundum ASD, severe pulmonary
stenosis, tetralogy of Fallot)
Abnormalities of ECGs in athletes
Sinus arrhythmia
Sinus bradycardia
First-degree heart block
Wenckebach phenomenon
Junctional rhythm
Clinical diagnoses which can be made from
the ECGof an asymptomatic patient
Atrial brillation
Complete heart block
HCM
ASDs (with RBBB)
Long QT and Brugada syndromes
Wolff ParkinsonWhite (WPW) syndrome
(delta waves)
Arrhythmogenic right ventricular dysplasia
(cardiomyopathy)
Short PRinterval
This is rarely less than 0.12 s; the most common
causes are those of pre-excitation involving acces-
sory pathways or of tracts bypassing the slow region
of the atrioventricular (AV) node; other causes do
exist.
Pre-excitation
WPW syndrome
LownGanongLevine syndrome (short
PR syndrome)
Other
Ventricular extrasystole falling after
P wave
AV junctional rhythm (but P wave will
usually be negative)
Low atrial rhythm
Coronary sinus escape rhythm
Normal variant (especially in the young)
Causes of tall Rwaves inV1
It is easy to spot tall R waves in V1. This lead largely
faces the posterior wall of the left ventricle (LV) and
the mass of the right ventricle. As the overall vector
is predominantly towards the bulkier LV in normal
situations, the QRS is usually negative in V1. This
balance can be reversed in the following situations:
Right ventricular hypertrophy (myriad causes)
RBBB
Posterior infarction
Dextrocardia
WPW syndrome with left ventricular pathway
insertion (often referred to as type A)
HCM (septal mass greater than posterior wall)
Bundle branch block and ST-segment
abnormalities
Complete bundle branch block is a failure or delay
of impulse conduction to one ventricle from the AV
node, requiring conduction via the other bundle,
and then transmission within the ventricular myo-
cardium; this results in abnormal prolongation of
QRS duration (>120 ms) and abnormalities of the
Cardiology
7
normally isoelectric ST segment. In contrast to
RBBB, LBBB is always pathological.
Causes of LBBB
Ischaemic heart disease (recent or old
MI)
Hypertension
LVH
Aortic valve disease
Cardiomyopathy
Myocarditis
Post-valve replacement
Right ventricular pacemaker
Tachycardia with aberrancy or
concealed conduction
Ventricular ectopy
Causes of RBBB
Normal in the young
Right ventricular strain (eg pulmonary
embolus)
ASD
Ischaemic heart disease
Myocarditis
Idiopathic
Tachycardia with aberrancy or
concealed conduction
Ventricular ectopy
Causes of ST elevation
Early repolarisation
Acute MI
Pericarditis (saddle-shaped)
Ventricular aneurysm
Coronary artery spasm
During angioplasty
Non-standard ECG acquisition settings
(eg on monitor)
Other ST-T wave changes (not elevation)
Ischaemia: ST depression,
T inversion and
peaking
Digoxin therapy: downsloping
ST depression
Hypertrophy: ST depression,
T inversion
Post-tachycardia: ST depression,
T inversion
Hyperventilation: ST depression,
T inversion and
peaking
Oesophageal/upper abdominal
irritation:
ST depression,
T inversion
Cardiac contusion: ST depression,
T inversion
Mitral valve prolapse:
T wave inversion
Acute cerebral event
(eg subarachnoid haemorrhage):
ST depression,
T inversion
Electrolyte abnormalities
Q waves can be permanent (reecting myocardial
necrosis) or transient (suggesting failure of myocar-
dial function, but not necrosis).
Permanent Q waves
Transmural infarction
LBBB
WPW syndrome
HCM
Idiopathic cardiomyopathy
Amyloid heart disease
Neoplastic inltration
Friedreichs ataxia
Dextrocardia
Sarcoidosis
Progressive muscular dystrophy
Myocarditis (may resolve)
Transient Q waves
Coronary spasm
Hypoxia
Hyperkalaemia
Cardiac contusion
Hypothermia
Essential Revision Notes for MRCP
8
Potassiumand ECG changes
There is a reasonable correlation between plasma
potassium and ECG changes.
Hyperkalaemia
Tall T waves
Prolonged PR interval
Flattened/absent P waves
Very severe hyperkalaemia
Wide QRS
Sine wave pattern
Ventricular tachycardia/ventricular
brillation/asystole
Hypokalaemia
Flat T waves, occasionally inverted
Prolonged PR interval
ST depression
Tall U waves
ECG changes following coronary artery
bypass surgery
U waves (hypothermia)
Saddle-shaped ST elevation (pericarditis)
PR-segment depression (pericarditis)
Low-voltage ECG in chest leads (pericardial
effusion)
Changing electrical alternans (alternating ECG
axis cardiac tamponade)
S1Q3T3 (pulmonary embolus)
Atrial brillation
Q waves
ST-segment and T-wave changes
Electrocardiographic techniques for
prolonged monitoring
Holter monitoring: the ECG is monitored in one
or more leads for 2472 h. The patient is
encouraged to keep a diary in order to correlate
symptoms with ECG changes
External recorders: the patient keeps a monitor
with them for a period of days or weeks. At the
onset of symptoms the monitor is placed to the
chest and this records the ECG
Wearable loop recorders: the patient wears a
monitor for several days or weeks. The device
records the ECG constantly on a self-erasing
loop. At the time of symptoms, the patient
activates the recorder and a trace spanning
some several seconds before a period of
symptoms to several minutes afterwards is
stored
Implantable loop recorders: a loop recorder is
implanted subcutaneously in the pre-pectoral
region. The recorder is activated by the patient
or according to pre-programmed parameters.
Again the ECG data from several seconds before
symptoms to several minutes after are stored;
data are uploaded by telemetry. The battery life
of the implantable loop recorder is approx-
imately 18 months
1.2.2 Echocardiography
Principles of the technique
Sound waves emitted by a transducer are reected
back differentially by tissues of variable acoustic
properties. Moving structures (including uid struc-
tures) reect sound back as a function of their own
velocity. The signal-to-noise ratio is improved by
minimising the distance and number of acoustic
structures between the transducer and the object
being recorded.
A longitudinal beam differentiating structures by
reectivity plotted against time gives an M-mode
image. Allows accurate measurement of dimen-
sions, eg LA size, end-diastolic dimension.
A longitudinal beam measuring velocities gives a
Doppler velocity a continuous wave picks up the
greatest velocity along the line, a pulsed wave
focuses on a specic point and tissue Doppler on a
xed point of myocardium. Velocities can be used
to calculate pressure gradients. Used to measure
valve gradients and wall motion parameters.
A broad beam gives a two-dimensional moving
image that can be processed into a three-
dimensional image with appropriate echo probe
and processing software. The standard windows
permit imaging of the cardiac chambers to assess
structural abnormalities and function.
Cardiology
9
Sampling multiple velocities within a two-dimen-
sional image and assigning colours to the positive
and negative velocities gives a visual image of
colour ow mapping. Ideal for assessing valvular
regurgitation.
Diagnostic uses of echocardiography
Conventional echocardiography is used in the diag-
nosis of:
Pericardial effusion and tamponade
Valvular disease (including large vegetations)
HCM, dilated cardiomyopathy, LV mass and
function
Cardiac tumours and intracardiac thrombus
Congenital heart disease (eg PDA; coarctation of
the aorta)
Right ventricular function and pressure
Stress echo is used in the diagnosis of myocardial
viability and ischaemia.
Standard contrast echo is used in the diagnosis of
right-to-left shunts, especially ASD/VSD.
Transpulmonary contrast echo is used to improve
discrimination between the blood pool and the
endocardium to improve denition in those subjects
whose characteristics lead to poor image quality. It
is also used to diagnose LV thrombus and other
specic conditions (eg the congenital failure of
muscle bre alignment (known as non-compaction)
and apical hypertrophy).
Tissue Doppler imaging is used to improve the
accuracy of LV wall motion assessments.
Three-dimensional echo is used to investigate con-
genital heart disease and in valve studies; it also has
research applications.
Transoesophageal echocardiography (TOE) is indi-
cated in the diagnosis of aortic dissection, suspected
atrial thrombus, the assessment of vegetations or
abscesses in endocarditis, prosthetic valve dysfunc-
tion or leakage, intraoperative assessment of LV
function, and where there is a technically sub-
optimal transthoracic echocardiogram.
Intravascular ultrasound gives high-resolution
images of coronary arteries; it is useful in assessing
plaque size and in stent deployment.
Intracardiac ultrasound images the heart chambers
from within; it is used mainly in those with congeni-
tal heart disease and in electrophysiological proce-
dures.
Classic M-mode patterns
Due to improvements in real-time image quality M-
mode imaging is now used less in clinical practice;
it does, however, allow interpretable traces to be
printed as still images, and these still occasionally
feature in exams. Particular M-mode patterns that
have been used in past MRCP exams include:
Aortic regurgitation: uttering of the anterior
mitral leaet is seen
HCM: systolic anterior motion (SAM) of the
mitral valve leaets and asymmetrical septal
hypertrophy (see Figure 1.2)
Mitral valve prolapse: one or both leaets
prolapse during systole
Mitral stenosis: the opening prole of the cusps
is at and multiple echoes are seen when there
is calcication of the cusps
1.2.3 Nuclear cardiology: myocardial
perfusion imaging (MPI)
Perfusion tracers such as thallium or technetium can
be used to gauge myocardial blood ow, both at
rest and during exercise- or drug-induced stress.
Tracer uptake is detected using tomograms and
displayed in a colour scale in standard views.
Lack of uptake may be:
Physiological: due to lung or breast tissue
absorption
Pathological: reecting ischaemia, infarction or
other conditions in which perfusion
abnormalities also occur (eg HCM or
amyloidosis)
Pathological perfusion defects are categorised as
xed (scar) and reversible (viable but ischaemic
tissue).
Essential Revision Notes for MRCP
10
MPI can be used to:
Detect infarction
Investigate atypical chest pains
Assess ventricular function
Determine prognosis and detect myocardium
that may be re-awakened from hibernation
with an improved blood supply (eg after
coronary artery bypass grafting (CABG))
1.2.4 Cardiac catheterisation
Coronary and ventricular angiography
Direct injection of radio-opaque contrast into the
coronary arteries allows high-resolution assessment
of restrictive lesions and demonstrates any anoma-
lies. Left ventriculography provides a measure of
ventricular systolic function.
Aortography in cardiac diagnoses
Improved availability and resolution of cross-
sectional imaging techniques have greatly reduced
the need for diagnostic aortography.
The following can be identied with an aortogram:
AR
Coarctation of the aorta
Aortic dissection
PDA
Aberrant subclavian arteries
Aortic root abscess
Coronary artery anomalies
Paraprosthetic AR
Bypass grafts
Aortic root dilatation (eg Marfan syndrome)
Right heart catheterisation
Catheterisation of the right heart chambers and
pulmonary artery (PA) can be undertaken as a ward
investigation using a SwanGanz otation catheter
or as part of an X-ray-uoroscopy-guided cathlab
study.
It allows right ventricular and PA angiography, and
direct pressure and saturation measurements of the
right atrium (RA), right ventricle (RV) and PA. Wed-
ging the catheter in small arteries prevents forward
pressure from being transmitted, so the transducer
measures the pressure of the pulmonary capillary
bed, which is equal to pulmonary venous pressure.
In the cathlab initial manoeuvres such as simultane-
ous LV catheterisation and contrast injection add to
the diagnostic value of the procedure: a gradient
between pulmonary wedge (PV) pressure and left
ventricular end-diastolic pressure (LVEDP) quanties
mitral stenosis (usually previously diagnosed by
Figure 1.2 Classic valvular disease patterns seen with M-mode echocardiography
Cardiology
11
echocardiography) and direct pulmonary angio-
graphy can be performed. Direct pulmonary angio-
graphy has now been largely replaced by CT
angiography.
Complications of cardiac catheterisation
Complications are uncommon (approximately 5%,
including minor complications); these include con-
trast allergy, local haemorrhage from puncture sites
with subsequent occurrence of thrombosis, false
aneurysm or arteriovenous (AV) malformation. Vaso-
vagal reactions are common. Other complications
are:
Coronary dissection (particularly the right
coronary artery in women) and aortic dissection
or ventricular perforation
Air or atheroma embolism: in the coronary or
other arterial circulations, with consequent
ischaemia or strokes
Ventricular dysrhythmias: can even cause death
in the setting of left main stem disease
Mistaken cannulation and contrast injection into
the conus branch of the right coronary artery
can cause ventricular brillation
Overall mortality rates are quoted at ,1/1000
cases
1.2.5 Exercise stress testing
This is used in the investigation of coronary artery
disease, in exertion-induced arrhythmias, and in the
assessment of cardiac workload and conduction
abnormalities. Exercise tests also give diagnostic
and prognostic information post-infarction, and gen-
erate patient condence in rehabilitation after MI.
Diagnostic sensitivity is improved if the test is con-
ducted with the patient having discontinued anti-
anginal (especially rate-limiting) medication.
The main contraindications to exercise testing in-
clude those conditions where fatal ischaemia or
arrhythmias may be provoked, or where exertion
may severely and acutely impair cardiac function.
These include the following:
Severe aortic stenosis or HCM with marked
outow obstruction
Acute myocarditis or pericarditis
Pyrexial or coryzal illness
Severe left main stem disease
Untreated congestive cardiac failure
Unstable angina
Dissecting aneurysm
Ongoing tachy- or bradyarrhythmias
Untreated severe hypertension
Indicators of a positive exercise test result
The presence of each factor is additive in the overall
positive prediction of coronary artery disease:
Development of anginal symptoms
A fall in BP of .15 mmHg or failure to increase
BP with exercise
Arrhythmia development (particularly
ventricular)
Poor workload capacity (may indicate poor left
ventricular function)
Failure to achieve target heart rate (allowing for
-blockers)
.1 mm down-sloping or planar ST-segment
depression, 80 ms after the J point
ST-segment elevation
Failure to achieve 9 min of the Bruce protocol
due to any of the points listed
Exercise tests have low specicity in the following
situations (often as a result of resting ST-segment
abnormalities):
Ischaemia in young women with atypical chest
pains
Atrial brillation
LBBB
WPW syndrome
LVH
Digoxin or -blocker therapy
Anaemia
Hyperventilation
Biochemical abnormalities such as
hypokalaemia
Essential Revision Notes for MRCP
12
1.2.6 24-hour ambulatory blood
pressure monitoring
The limited availability and relative expense of
ambulatory blood pressure monitoring prevents its
use in all hypertensive patients. Specic areas of
usefulness include the following situations:
Assessing for white coat hypertension
Borderline hypertensive cases that may not need
treatment
Evaluation of hypotensive symptoms
Identifying episodic hypertension (eg in
phaeochromocytoma)
Assessing drug compliance and effects
(particularly in resistant cases)
Nocturnal blood pressure dipper status (non-
dippers are at higher risk)
1.2.7 Computed tomography (CT)
CT has theoretical capability in both anatomical
(coronary arteries, chamber dimension, pericar-
dium) and functional (contractility, ischaemia, viabi-
lity) assessments of the heart. It is the gold standard
investigation for:
Pulmonary thromboembolic disease
Anatomical assessment of the pericardium (eg in
suspected constriction)
Anomalous coronary artery origins (reliable
imaging of the proximal third of major coronary
arteries)
Extramyocardial mediastinal masses
Other indications include assessment of:
Chamber dimensions
Myocardial function, perfusion and ischaemia
1.2.8 Magnetic resonance imaging
(MRI)
Cardiac MRI is the gold standard technique for
assessment of myocardial function, ischaemia, per-
fusion and viability, cardiac chamber anatomy and
imaging of the great vessels. It has a useful adjunc-
tive role in pericardial/mediastinal imaging. Major
drawbacks are its contraindication in patients with
certain implanted devices (eg pacemakers) and
time (consequently also cost), as a full functional
study can take about 45 minutes. The contrast used
(gadolinium), while not directly nephrotoxic, is sub-
ject to increased risk of metabolic toxicity in renally
impaired individuals.
Chief indications of cardiac MRI:
Myocardial ischaemia and viability assessment
Differential diagnosis of structural heart disease
(congenital and acquired)
Chamber anatomy denition
Initial diagnosis and serial follow-up of great
vessel pathology (especially aortopathy)
Pericardial and mediastinal structural assessment
1.3 VALVULAR DISEASE AND
ENDOCARDITIS
1.3.1 Murmurs
Benign ow murmurs: soft, short systolic murmurs
heard along the left sternal edge to the pulmonary
area, without any other cardiac auscultatory, ECG
or chest X-ray abnormalities. Thirty per cent of
children may have an innocent ow murmur.
Cervical venous hum: continuous when upright and
is reduced by lying; occurs with a hyperdynamic
circulation or with jugular vein compression.
Large AV stula of the arm: may cause a harsh ow
murmur across the upper mediastinum.
Effect of posture on murmurs: standing signicantly
increases the murmurs of mitral valve prolapse and
HCM only. Squatting and passive leg raising in-
crease cardiac afterload and therefore decrease the
murmur of HCM and mitral valve prolapse, whilst
increasing most other murmurs such as ventricular
septal defect, aortic, mitral and pulmonary regurgi-
tation, and aortic stenosis.
Effect of respiration on murmurs: inspiration ac-
centuates right-sided murmurs by increasing venous
return, whereas held expiration accentuates left-
sided murmurs. The strain phase of a Valsalva
manoeuvre reduces venous return, stroke volume
Cardiology
13
and arterial pressure, decreasing all valvular mur-
murs but increasing the murmur of HCM and mitral
valve prolapse.
Classication of murmurs
Mid-/late systolic murmurs
Innocent murmur
Aortic stenosis or sclerosis
Coarctation of the aorta
Pulmonary stenosis
HCM
Papillary muscle dysfunction
ASD (due to high pulmonary ow)
Mitral valve prolapse
Mid-diastolic murmurs
Mitral stenosis or Austin Flint due to
aortic regurgitant jet
Carey Coombs (rheumatic fever)
High AV ow states (ASD, VSD, PDA,
anaemia, mitral regurgitation, tricuspid
regurgitation)
Atrial tumours (particularly if causing
AV ow disturbance)
Continuous murmurs
PDA
Ruptured sinus of Valsalva aneurysm
ASD
Large AV stula
Anomalous left coronary artery
Intercostal AV stula
ASD with mitral stenosis
Bronchial collaterals
1.3.2 Mitral stenosis
Two-thirds of patients presenting with this are
women. The most common cause remains chronic
rheumatic heart disease; rarer causes include
congenital disease, carcinoid, systemic lupus
erythematosus (SLE) and mucopolysaccharidoses
(glycoprotein deposits on cusps). Stenosis may oc-
cur at the cusp, commissure or chordal level.
Anticoagulation for atrial brillation protects
from 173 increased risk of thromboembolism
Features of severe mitral stenosis
Symptoms
Dyspnoea with minimal activity
Haemoptysis
Dysphagia (due to left atrium
enlargement)
Palpitations due to atrial brillation
Chest X-ray
Left atrial or right ventricular
enlargement
Splaying of subcarinal angle (.908)
Pulmonary congestion or hypertension
Pulmonary haemosiderosis
Echo
Doming of leaets
Heavily calcied cusps
Direct orice area ,1.0 cm
2
Signs
Low pulse pressure
Soft rst heart sound
Long diastolic murmur and apical thrill
(rare)
Very early opening snap, ie closer to S2
(lost if valves immobile)
Right ventricular heave or loud P2
Pulmonary regurgitation (Graham Steell
murmur)
Tricuspid regurgitation
Cardiac catheterisation
Pulmonary capillary wedge end diastole
to left ventricular end-diastolic pressure
(LVEDP) gradient .15 mmHg
Left atrium (LA) pressures .25 mmHg
Elevated RV and PA pressures
High pulmonary vascular resistance
Cardiac output ,2.5 l min
1
m
2
with
exercise
Essential Revision Notes for MRCP
14
Mitral balloonvalvuloplasty
Valvuloplasty using an Inoue balloon requires either
a trans-septal or a retrograde approach and is used
only in suitable cases where echo shows that:
The mitral leaet tips and valvular chordae are
not heavily thickened, distorted or calcied
The mitral cusps are mobile at the base
There is minimal or no mitral regurgitation
There is no left atrial thrombus seen on TOE
1.3.3 Mitral regurgitation (MR)
The full structure of the mitral valve includes the
annulus, cusps, chordae and papillary musculature,
and abnormalities of any of these can cause regur-
gitation. The presence of symptoms and increasing
left ventricular dilatation are indicators for surgery
in the chronic setting. Operative mortalities are
2%7% for valvular replacements in patients with
NYHA grade II III symptoms. Various techniques
have revolutionised mitral valve surgery, transform-
ing outcomes from being no better than medical
therapy with replacement to almost normal with
repair. In skilled surgical hands the repair is tailored
to the precise anatomical abnormality.
Functional MR is a term used to describe MR that is
due to stretching of the annulus secondary to ven-
tricular dilatation.
Main causes of MR
Myxomatous degeneration
Functional, secondary to ventricular
dilatation
Mitral valve prolapse
Ischaemic papillary muscle rupture
Congenital heart diseases
Collagen disorders
Rheumatic heart disease
Endocarditis
Indicators of the severity of MR
Small-volume pulse
Left ventricular enlargement due to overload
Presence of S3
Atrial brillation
Mid-diastolic ow murmur
Precordial thrill, signs of pulmonary
hypertension or congestion (cardiac failure)
Signs of predominant MRin mixedmitral
valve disease
Soft S1; S3 present
Displaced and hyperdynamic apex (left
ventricular enlargement)
ECG showing LVH and left axis deviation
Mitral valve prolapse
This condition occurs in 5% of the population and
is commonly over-diagnosed (depending on the
echocardiography criteria applied). The patients are
usually female and may present with chest pains,
palpitations or fatigue, although it is often detected
incidentally in asymptomatic patients. Squatting in-
creases the click and standing increases the mur-
mur, but the condition may be diagnosed in the
absence of the murmur by echo. Often there is
myxomatous degeneration and redundant valve
tissue due to deposition of acid mucopolysacchar-
ide material. Antibiotic prophylaxis before dental
or surgical interventions should be recommended
for those with a murmur. Mitral valve prolapse is
usually eminently suitable for mitral valve repair
although this should only be undertaken if the
severity of the regurgitation associated with the
condition justies it (see above). Several conditions
are associated with mitral valve prolapse (see over-
leaf), and patients with the condition are prone to
certain sequelae.
Sequelae of mitral valve prolapse:
Embolic phenomena
Rupture of mitral valve chordae
Dysrhythmias with QT prolongation
Sudden death
Cardiac neurosis
Cardiology
15
Conditions associated with mitral valve
prolapse
Coronary artery disease
Polycystic kidney disease
Cardiomyopathy dilated cardiomyopathy/
HCM
Secundum ASD
WPW syndrome
PDA
Marfan syndrome
Pseudoxanthoma elasticum
Osteogenesis imperfecta
Myocarditis
SLE; polyarteritis nodosa
Muscular dystrophy
Left atrial myxoma
1.3.4 Aortic regurgitation (AR)
Patients with severe chronic aortic regurgitation (AR)
have the largest end-diastolic volumes of those with
any form of heart disease and also have a greater
number of non-cardiac signs. AR may occur acutely
(as in dissection or endocarditis) or chronically
when the left ventricle has time to accommodate.
Causes of AR
Valve inammation
Chronic rheumatic
Infective endocarditis
Rheumatoid arthritis; SLE
Hurler syndrome
Aortitis
Syphilis
Ankylosing spondylitis
Reiter syndrome
Psoriatic arthropathy
Aortic dissection/trauma
Hypertension
Bicuspid aortic valve
Ruptured sinus of Valsalva aneurysm
VSD with prolapse of (R) coronary cusp
Disorders of collagen
Marfan syndrome (aortic aneurysm)
Hurler syndrome
Pseudoxanthoma elasticum
Eponymous signs associated with AR
Quinckes sign nail-bed uctuation of
capillary ow
Corrigans pulse (waterhammer);
collapsing radial pulse
Corrigans sign visible carotid pulsation
De Mussets sign head nodding with each
systole
Duroziezs sign audible femoral bruits
with diastolic ow (indicating moderate
severity)
Traubes sign pistol shots (systolic
auscultatory nding of the femoral arteries)
Austin Flint murmur functional mitral
diastolic ow murmur
Argyll Robertson pupils aetiological
connection with syphilitic aortitis
Mu llers sign pulsation of the uvula
Indications for surgery
Acute severe AR will not be tolerated for long by a
normal ventricle and therefore requires prompt sur-
gery, except in the case of infection, where delay
for antibiotic therapy is preferable (if haemodynamic
stability allows). At 10 years, 50% of patients with
moderate chronic AR are alive, but once symptoms
occur deterioration is rapid.
Essential Revision Notes for MRCP
16
Features of AR indicative of the need
for surgery
Symptoms of dyspnoea/left ventricular
failure
Reducing exercise tolerance
Rupture of sinus of Valsalva aneurysm
Infective endocarditis not responsive to
medical treatment
Enlarging aortic root diameter in Marfan
syndrome with AR
Enlarging heart
End-systolic diameter .55 mm at echo
Pulse pressure .100 mmHg
Diastolic pressure ,40 mmHg
Lengthening diastolic murmur
ECG: lateral lead T-wave inversion
1.3.5 Aortic stenosis (AS)
Patients often present with the classic triad of symp-
toms: angina, dyspnoea and syncope. Echo and
cardiac catheterisation gradients of .60 mmHg are
considered severe and are associated with a valve
area ,0.5 cm
2
. The gradient may be reduced in the
presence of deteriorating left ventricular function or
mitral stenosis, or signicant AR.
Causes of AS: may be congenital bicuspid valve,
degenerative calcication (common in the
elderly) and post-rheumatic disease
Subvalvular: causes of aortic gradients include
HCM and subaortic membranous stenosis, while
supravalvular stenosis is due to aortic
coarctation, or Williams syndrome (with eln
facies, mental retardation, hypercalcaemia)
Sudden death: may occur in AS or in
subvalvular stenosis due to ventricular
tachycardia. The vulnerability to ventricular
tachycardia is due to LVH
Complete heart block: may be due to
calcication involving the upper ventricular
septal tissue housing the conducting tissue. This
can also occur post-operatively (after valve
replacement) due to trauma
Calcied emboli: can arise in severe calcic AS.
All symptomatic patients should be considered
for surgery: operative mortality for AS is
predominantly related to the absence (2%8%)
or presence (10%25%) of left ventricular
failure
Indicators of severe AS
Symptoms of syncope or left ventricular
failure
Signs of left ventricular failure
Absent A2
Paradoxically split A2
Presence of precordial thrill
S4
Slow-rising pulse with narrow pulse
pressure
Late peaking of long murmur
Valve area ,0.5 cm
2
on echocardiography
1.3.6 Tricuspid regurgitation (TR)
Causes of severe TR include the following:
Functional, due to right ventricular dilatation
(commonly co-exists with signicant MR)
Infection. The tricuspid valve is vulnerable to
infection introduced by venous cannulation
(iatrogenic or through intravenous drug abuse)
Carcinoid (nodular hepatomegaly and
telangiectasia)
Post-rheumatic
Ebsteins anomaly: tricuspid valve dysplasia with
a more apical position to the valve. Patients
have cyanosis and there is an association with
pulmonary atresia or ASD and, less commonly,
congenitally corrected transposition
1.3.7 Prosthetic valves
Valve prostheses may be metal or tissue (biopros-
thetic). Mechanical valves are more durable but
tissue valves do not require full lifelong anti-
coagulation. All prostheses must be covered with
Cardiology
17
antibiotic therapy for dental and surgical proce-
dures; they have a residual transvalvular gradient
across them.
Mechanical valves
StarrEdwards: ball and cage ejection systolic
murmur (ESM) in the aortic area and an opening
sound in the mitral position are normal
BjorkShiley: single tilt disc audible clicks
without stethoscope
St Jude (Carbomedics): double tilting discs with
clicks
Tissue valves
Allografts: porcine or bovine three-cusp valve
3 months anticoagulation sometimes
recommended until tissue endothelialisation. No
need for long-term anticoagulation if patient is
in sinus rhythm
Homografts: usually cadaveric and, again, need
no long-term anticoagulation
Infection of prosthetic valves
Mortality is still as high as 60% depending on
the organism
Within 6 months of implantation, it is usually
due to colonisation by Staphylococcus
epidermidis
Septal abscesses may cause PR-interval
lengthening
Valvular sounds may be mufed by vegetations;
new murmurs may occur
Mild haemolysis can occur, and is detected by
the presence of urobilinogen in the urine
Dehiscence is an ominous feature requiring
urgent intervention
Anticoagulation in pregnancy
Warfarin may cause fetal haemorrhage and has a
teratogenicity risk of 5%30%. This risk is dose-
dependent and abnormalities include chondrodys-
plasia, mental impairment, optic atrophy and nasal
hypoplasia. The risk of spontaneous abortion may
be increased. There is no agreed consensus on the
ideal strategy: warfarin, unfractionated heparin and
low-molecular-weight heparin all have advocates
and detractors.
1.3.8 Infective endocarditis
Clinical presentation
Commonly presents with non-specic symptoms of
malaise, tiredness and infective-type symptoms.
Heart failure secondary to valvular regurgitation or
heart block may also occur as may an incidental
presentation in the context of another primary infec-
tion.
Signs of infective endocarditis
As well as cardiac murmurs detected at ausculta-
tion, there are several other characteristic features of
infective endocarditis:
Systemic signs of fever and arthropathy
Hands and feet: splinter haemorrhages, Osler
nodes (painful), Janeway lesions (painless) and
clubbing (late); needle-track signs may occur in
arm or groin
Retinopathy: Roth spots
Hepatosplenomegaly
Signs of arterial embolisation (eg stroke or
digital ischaemia)
Vasculitic rash
Streptococcus viridans (-haemolytic group) are
still the most common organisms, occurring in
50% of cases
Marantic (metastatic-related) and SLE-related
(LibmanSacks) endocarditis are causes of non-
infective endocarditis
Almost any pathogenic organism may be
implicated, particularly in the
immunocompromised patient
See also Section 1.3.7 on Prosthetic valves and
Table 1.3.
Essential Revision Notes for MRCP
18
Management of infective endocarditis
The aim of treatment is to sterilise the valve medi-
cally (usually 46 weeks of IV antibiotics) then
assess whether the valvular damage sustained (eg
degree of incompetance) or the risk of recurrence
(eg if prosthetic valves) mandates surgical replace-
ment. Earlier operations are only undertaken if
clincally necessary as outcomes are poorer.
Poor prognostic factors in endocarditis
Prosthetic valve
Staphylococcus aureus infection
Culture-negative endocarditis
Depletion of complement levels
Indications for surgery
Cardiac failure or haemodynamic
compromise
Extensive valve incompetence
Large vegetations
Septic emboli
Septal abscess
Fungal infection
Antibiotic-resistant endocarditis
Failure to respond to medical therapy
Antibiotic prophylaxis
The conditions listed in the next box are associated
with an increased risk of endocarditis.
Acquired valvular heart disease with
stenosis or regurgitation
Valve replacement
Structural congenital heart disease,
including surgically corrected or palliated
structural conditions, but excluding isolated
ASD, fully repaired VSD or fully repaired
PDA, and closure devices that are judged
to be endothelialised
Previous infective endocarditis
HCM
Antibiotic and chlorhexidine mouthwash prophy-
laxis is no longer recommended for dental proce-
dures, endoscopies or obstetric procedures.
Patients should be made aware of non-medical risk-
prone activities (eg IV drug use, piercings) and the
symptoms of possible endocarditis.
1.4 CONGENITAL HEART DISEASE
Causes of congenital acyanotic heart
disease*
With shunts
Aortic coarctation (with VSD or PDA)
VSD
ASD
PDA
Partial anomalous venous drainage (with
ASD)
Without shunts
Congenital AS
Aortic coarctation
*Associated shunts
Table 1.3. Infective endocarditis
Groups affected by
endocarditis
% of all cases of
endocarditis
Chronic rheumatic disease 30
No previous valve disease 40
Intravenous drug abuse 10
Congenital defects 10
Prosthetic 10
Cardiology
19
Causes of cyanotic heart disease
With shunts
Tetralogy of Fallot (VSD)
Severe Ebsteins anomaly (ASD)
Complete transposition of great vessels
(ASD VSD/PDA)
Without shunts
Tricuspid atresia
Severe pulmonary stenosis
Pulmonary atresia
Hypoplastic left heart
1.4.1 Atrial septal defect (ASD)
ASDs are the most common congenital defects
found in adulthood. Rarely, they may present as
stroke in young people, due to paradoxical embolus
that originated in the venous system and reached
the cerebral circulation via right-to-left shunting.
Fixed splitting of the second heart sound is the
hallmark of an uncorrected ASD. There may be a
left parasternal heave and a pulmonary ESM due to
increased blood ow. There are three main sub-
types:
Secundum (70%): central fossa ovalis defects
often associated with mitral valve prolapse
(10%20% of cases). ECG shows incomplete or
complete RBBB with right axis deviation. Note
that a patent foramen ovale (slit-like deciency
in the fossa ovalis) occurs in up to 25% of the
population, but this does not allow equalisation
of atrial pressures, unlike ASD
Primum (15%): sited above the AV valves, often
associated with varying degrees of mitral and
tricuspid regurgitation and occasionally a VSD,
and thus usually picked up earlier in childhood.
ECG shows RBBB, left axis deviation, rst-
degree heart block. Associated with Down
syndrome, Klinefelter syndrome and Noonan
syndrome
Sinus venosus (15%): defect in the upper
septum, often associated with anomalous
pulmonary venous drainage directly into the
right atrium
Operative closure is recommended with pulmonary-
to-systolic ow ratios above 1.5:1. Closure of secun-
dum defects may be performed via cardiac catheter-
isation.
HoltOram syndrome: (triphalangeal thumb with
ASD) is a rare syndrome (autosomal dominant with
incomplete penetration). It is associated with ab-
sence (or reduction anomalies) of the upper arm.
Lutembacher syndrome: a rare combination of an
ASD with mitral stenosis (the latter is probably
rheumatic in origin).
Investigations for ASDs
Right atrial and right ventricular dilatation may be
seen on any imaging technique as may pulmonary
artery conus enlargement. Other characteristic fea-
tures are:
Chest X-ray: pulmonary plethora
Echo: paradoxical septal motion, septal defect
and right-to-left ow of contrast during venous
injection with Valsalva manoeuvre
Catheterisation: pulmonary hypertension
raised right ventricular pressures and step-up in
oxygen saturation between various parts of the
right circulation (eg SVC to high right atrium)
Treatment of ASD
There is no specic medical therapy for ASDs; they
are managed by either closure (percutaneous or
surgical) or clinical and echocardiographic follow-
up.
Indications for closure:
Symptoms (dyspnoea)
Systemic embolism
Chamber dilatation
Elevated right heart pressures
Signicant left-to-right shunt
Essential Revision Notes for MRCP
20
1.4.2 Ventricular septal defect (VSD)
VSDs are the most common isolated congenital
defect (2/1000 births; around 30% of all congenital
defects); spontaneous closure occurs in 30%50%
of cases (usually muscular or membranous types).
As with ASDs, closure may be performed via cardi-
otomy or percutaneously.
Indications for closure
Signicant left-to-right shunt
Associated with other defect requiring
cardiotomy
Elevated right heart pressure
Endocarditis
Irreversible pulmonary changes may occur from
1 year of age, with vascular hypertrophy and
pulmonary arteriolar thrombosis, leading to
Eisenmenger syndrome
Parasternal thrill and pansystolic murmur are
present. The murmur may be ejection systolic in
very small or very large defects. With large
defects the aortic component of the second
sound is obscured, or even a single/palpable S2
is heard; a mitral diastolic murmur may occur.
The apex beat is typically hyperdynamic
Once the Eisenmenger complex develops, the thrill
and left sternal edge (LSE) murmur abate and signs
are of pulmonary hypertension regurgitation and
right ventricular failure. Surgery should occur earlier
to avoid this situation; otherwise a combined heart/
lung transplant would be required.
Other cardiac associations of VSD
PDA (10%)
AR (5%)
Pulmonary stenosis
ASD
Tetralogy of Fallot
Coarctation of the aorta
Types of VSD
Muscular
Membranous
AV defect
Infundibular
Into the right atrium (Gerbode defect)
1.4.3 Patent ductus arteriosus (PDA)
PDA is common in premature babies, particularly
female infants born at high altitude; also if maternal
rubella occurs in the rst trimester. The connection
occurs between the pulmonary trunk and the des-
cending aorta, usually just distal to the origin of the
left subclavian artery. PDA often occurs with other
abnormalities.
Key features of PDA
A characteristic left subclavicular thrill
Enlarged left heart and apical heave
Continuous machinery murmur
Wide pulse pressure and bounding pulse
Signs of pulmonary hypertension and Eisenmenger
syndrome develop in about 5% of cases. Indo-
metacin closes the duct in about 90% of babies
while intravenous prostaglandin E
1
may reverse the
natural closure (useful when PDA is associated with
coarctation, hypoplastic left heart syndrome and in
complete transposition of the great vessels, as it will
help to maintain ow between the systemic and
pulmonary circulations). The PDA may also be
closed thoracoscopically or percutaneously.
1.4.4 Coarctation of the aorta
Coarctation can present in infancy with heart failure
or in adulthood (third decade) with hypertension,
exertional breathlessness or leg weakness. This
shelf-like obstruction of the aortic arch, usually
distal to the left subclavian artery, is 25 times more
common in males and is responsible for about 7%
of congenital heart defects.
Cardiology
21
Treatment is by surgical resection, preferably with
end-to-end aortic anastomosis, or by balloon angio-
plasty for recurrence after surgery (which occurs in
5%10% of cases). Complications may occur de-
spite resection/repair and these include hyper-
tension, heart failure, berry aneurysm rupture,
premature coronary artery disease and aortic dissec-
tion (in the third or fourth decade of life).
Associations of coarctation
Cardiac
Bicuspid aortic valve (and thus AS
AR) in 10%20%
PDA
VSD
Mitral valve disease
Non-cardiac
Berry aneurysms (circle of Willis)
Turner syndrome
Renal abnormalities
Signs of coarctation
Hypertension
Radiofemoral delay of arterial pulse
Absent femoral pulses
Mid-systolic or continuous murmur
(infraclavicular)
Subscapular bruits
Rib notching on chest X-ray
Post-stenotic aortic dilatation on chest
X-ray
1.4.5 Eisenmenger syndrome
Reversal of left-to-right shunt, due to massive irre-
versible pulmonary hypertension (usually due to
congenital cardiovascular malformations), leads to
Eisenmenger syndrome. Signs of development in-
clude:
Decrease of original pansystolic (left-to-right)
murmur
Decreasing intensity of tricuspid/pulmonary ow
murmurs
Single S2 with louder intensity, palpable P2;
right ventricular heave
Appearance of Graham Steell murmur due to
pulmonary regurgitation
PSM and v waves due to tricuspid regurgitation
(TR)
Clubbing and central cyanosis
Eisenmenger syndrome
Causes
VSD (the Eisenmenger complex)
ASD
PDA
Complications of Eisenmenger syndrome
Right ventricular failure
Massive haemoptysis
Cerebral embolism/abscess
Infective endocarditis (rare)
1.4.6 Tetralogy of Fallot
The most common cause of cyanotic congenital
heart disease (10%), usually presenting after age
6 months (as the condition may worsen after birth).
Key features
Pulmonary stenosis (causes the systolic
murmur)
Right ventricular hypertrophy
VSD
Overriding of the aorta
Right-sided aortic knuckle (25%)
Clinical features
Cyanotic attacks (pulmonary infundibular
spasm)
Clubbing
Parasternal heave
Systolic thrill
Palpable A2
Soft ejection systolic murmur (inversely
related to pulmonary gradient)
Single S2 (inaudible pulmonary closure)
ECG features of right ventricular
hypertrophy
Essential Revision Notes for MRCP
22
Possible complications of Fallots
Endocarditis
Polycythaemia
Coagulopathy
Paradoxical embolism
Cerebral abscess
Ventricular arrhythmias
Cyanotic attacks worsen with catecholamines,
hypoxia and acidosis. The murmur lessens or
disappears as the right ventricular outow
gradient increases
Squatting reduces the right-to-left shunt by
increasing systemic vascular resistance; it also
reduces venous return of acidotic blood from
lower extremities, and hence reduces
infundibular spasm
The presence of a systolic thrill and an intense
pulmonary murmur differentiates the condition
from Eisenmenger syndrome
A Blalock shunt operation results in weaker
pulses in the arm from which the subclavian
artery is diverted to the pulmonary artery
1.4.7 Important post-surgical
circulations
Systemic right ventricle
Transposition of the great vessels and similar condi-
tions in which the right ventricle supplies the aorta
and the left ventricle supplies the pulmonary artery
are now treated by arterial switch. Effectively this is
a complete correction.
Prior to the development of the arterial switch
procedure, treatment was by venous redirection
the vena cavae redirected via the atria to the left
ventricle and the pulmonary veins to the right
ventricle via the atria, with the morphological right
ventricle then pumping oxygenated blood into the
aorta. However, there was a high risk of ventricular
dysfunction, valve regurgitation and ventricular ar-
rhythmias in these patients and decompensation
would be provoked by development of atrial ar-
rhythmias.
Single ventricular circulation
Individuals born with only one functional ventricle
are treated by redirecting the vena cavae directly
into the pulmonary arteries (total cavopulmonary
correction) and now do very well. Early versions of
this operation (the classic Fontan) used the right
atrium between the vena cavae, but this often led to
atrial dilatation and then brillation with a risk of
decompensation.
Common congenital circulations
Common congenital circulations are summarised in
Table 1.4 overleaf.
1.5 ARRHYTHMIAS AND PACING
Atrial brillation (AF) remains the most common
cardiac arrhythmia, with incidence increasing with
age (Framingham data indicate a prevalence of 76/
1000 males and 63/1000 females aged 8594
years). Atrial utter frequently co-exists with atrial
brillation, and although it has a different immedi-
ate causal mechanism it is a reection of the same
underlying disease. These arrhythmias assume parti-
cular signicance because of the stroke risk asso-
ciated with them.
SVT is the term usually used to indicate a pre-
sumed re-entry tachycardia involving the AV node
or an accessory pathway.
Ventricular tachycardia and ventricular brillation
are life-threatening conditions, but there is a clear
evidence base for the use of implantable cardiover-
ter debrillators in both primary and secondary
prevention (see Appendix II). Anti-arrhythmic drugs
or catheter ablation may be useful adjuncts to treat-
ment or, in some cases, they can be used as
alternatives to debrillators.
1.5.1 Bradyarrhythmias
Any heart rate below 60 beats per minute is a
bradycardia. A bradyarrhythmia is a pathological
bradycardia. Bradyarrhythmias are considered ac-
cording to their prognostic signicance and sympto-
Cardiology
23
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Essential Revision Notes for MRCP
24
matic impact. High-grade AV block (Mobitz 2 or
complete) is associated with sudden death and
patients should be paced urgently even if asympto-
matic. Permanent pacing is very effective in redu-
cing symptoms in most bradyarrhythmias; the
exception is neurocardiogenic syncope where the
results are disappointing.
Common bradyarrhythmias and associated
conditions
Neurocardiogenic symptoms
An exaggerated vasodepressor (hypotension), cardi-
oinhibitory (bradycardic) or mixed reex may cause
syncope or presyncope. Various drugs have been
tried as treatment, with limited success. In patients
with a predominant cardioinhibitory component,
dual chamber pacing may reduce the severity and
frequency of syncopal episodes but results are often
disappointing.
Sinus node disease
Sinus bradycardia and sinus pauses can cause
syncope, presyncope or non-specic symptoms.
Thyroid function and electrolytes should be
checked on presentation and corrected prior to con-
sidering pacemaker therapy. Pacing is only indi-
cated in signicantly symptomatic cases (as there is
no prognostic benet of pacing in sinus node
disease).
First-degree AV block
A PR interval of .200 ms is abnormal but usually
requires no treatment. The combinations of rst-
degree AV block with (1) LBBB, (2) RBBB with axis
deviation or (3) with alternating LBBB and RBBB is
interpreted as trifascicular block (more accurately
block in two fascicles and delay in the third). If
associated with syncope, trifascicular block repre-
sents an indication for pacing on both prognostic
and symptomatic grounds.
Second-degree Mobitz 1 (Wenckebach) AV
block
Progressive prolongation and then block of the PR
interval is categorised as Mobitz 1. It may be
normal during sleep and in young, physically t
individuals (who have high vagal tone). If it occurs
when the patient is awake and is associated with
symptoms in older people, pacing may be indicated
on symptomatic grounds.
High-grade AV block (second-degree Mobitz 2
block and third-degree complete heart block)
Bradycardias with more than one P wave per QRS
complex (second-degree Mobitz 2) or with AV
dissociation are grouped together as high-grade AV
block. Untreated, they are associated with mortality
that may exceed 50% at 1 year, particularly in
patients aged over 80 years and in those with non-
rheumatic structural heart disease. Pacing is indi-
cated on prognostic grounds even in the asympto-
matic.
Complete heart block is the most common
reason for permanent pacing
When related to an infarction, high-grade AV
block occurs mostly with right coronary artery
occlusion, as the AV nodal branch is usually
one of the distal branches of the right coronary
artery
In patients with an anterior infarct, high-grade
AV block is a poor prognostic feature, indicating
extensive ischaemia
Congenital cases may be related to connective
tissue diseases; however, in patients with normal
exercise capacities, recent studies show that the
prognosis is not as benign as was previously
thought and pacing is therefore recommended
in a wide range of circumstances (see ESC
guidelines by Vardas et al. Eur Heart J, 2007;
28:225695)
Tachyarrhythmias
Tachyarrhythmias are caused by re-entry, triggered
activity or automaticity:
Re-entry the arrhythmia is anatomically
dependent and usually the primary problem as
opposed to sequelae of another reversible state
Automaticity arrhythmia is often secondary to
a systemic cause (eg electrolyte imbalance,
sepsis, adrenergic drive) and is multifocal
Cardiology
25
Triggered activity shares features of both
mechanisms and is seen in both primary
arrhythmias and in drug toxicity
1.5.2 Supraventricular tachycardias
There are two major groups of re-entrant tachycar-
dias often described as SVT:
AV nodal re-entry tachycardia (AVNRT):
involves a re-entry circuit in and around the AV
node
AV re-entry tachycardia (AVRT): this involves
an accessory pathway between the atria and
ventricles some distance from the AV node (eg
WPW syndrome and related conditions)
AVnodal re-entry tachycardia
Differential conduction in tissue around the AV
node allows a micro re-entry circuit to be main-
tained, resulting in a regular tachycardia.
Accessory pathways
An accessory pathway that connects the atrium and
ventricle mediates the tachycardia by enabling ret-
rograde conduction from ventricle to atrium. More
seriously, the accessory pathway may predispose to
unrestricted conduction of AF from atria to ventri-
cles as a result of anterograde conduction through
the pathway. This may lead to ventricular brilla-
tion.
WPW is said to be present when a delta wave
(partial pathway-mediated pre-excitation) is present
on the resting ECG. Associations with WPW
include: Ebsteins anomaly (may have multiple
pathways), HCM, mitral valve prolapse and thyro-
toxicosis; it is more common in men.
Some accessory pathways are not manifest by a
delta wave on the resting ECG but are still able to
participate in a tachycardia circuit.
Atrial tachycardias, including utter, AF, sinus tachy-
cardia and fascicular ventricular tachycardia may all
be mistaken for SVT.
1.5.3 Atrial arrhythmias
Atrial utter
The atrial rate is usually between 250 and 350
beats/min and is often seen with a ventricular re-
sponse of 150 beats/min (2:1 block). The block may
vary between a 1:1 ratio and a 1:4 or even a 1:5
ratio. Isolated atrial utter (without atrial brillation)
has a lower association with thromboembolism;
however, recommendations for anticoagulation are
the same as for AF.
The ventricular response may be slowed by
increasing the vagal block of the AV node (eg
carotid sinus massage) or by adenosine, which
uncovers the utter waves on ECG
This is the most likely arrhythmia to respond to
DC cardioversion with low energies (eg 25 volts)
Amiodarone and sotalol may chemically
cardiovert, slow the ventricular response or act
as prophylactic agents
Radiofrequency ablation is curative in up to
95% of cases
Atrial utter is described as typical when associated
with a sawtooth atrial pattern in the inferior leads
and positive utter waves in V1. Atypical utters
tend to occur in congenital heart disease or after
surgery or prior ablation.
Atrial brillation (AF)
This arrhythmia is due to multiple wavelet propaga-
tion in different directions. The source of the ar-
rhythmia may be myocardial tissue in the openings
of the four pulmonary veins, which enter into the
posterior aspect of the left atrium, and this is parti-
cularly the case in younger patients with paroxys-
mal AF. AF may be paroxysmal, persistent (but
cardiovertable) or permanent, and in all three
states is a risk factor for strokes. Treatment is aimed
at ventricular rate control, cardioversion, recurrence
prevention and anticoagulation. Catheter ablation is
indicated in symptomatic individuals who are resis-
tant to, or intolerant of, medical therapy.
With AF a major decision is whether to control rate
Essential Revision Notes for MRCP
26
or alter the rhythm:
Surprisingly, rhythm control does not reduce the
risk of stroke (indeed paroxysmal AF carries the
same stroke risk as chronic AF) and therefore
does not affect the indications for
anticoagulation
Cardioversions, multiple drugs and ablations are
all used to alter rhythm
In asymptomatic individuals rate control is
recommended
Associations with atrial brillation
Ischaemic heart disease
Pericarditis
Mitral valve disease
Pulmonary embolus
Hypertension
Atrial myxomas
Thyroid disease
LVH
Acute alcohol excess/chronic alcoholic
cardiomyopathy
ASD
Post-coronary artery bypass graft (CABG)
Caffeine excess
Dilated left atrium (.4.5 cm)
Pneumonia
WPW syndrome
Bronchial malignancy
The overall risk of systemic emboli is 5%7%
annually (higher with rheumatic valve disease); this
falls to 1.6% with anticoagulation. Transoesopha-
geal echocardiography (TOE) may exclude atrial
appendage thrombus but cannot predict the
development of a thrombus in the early stages post-
cardioversion; anticoagulation is therefore always
recommended post-cardioversion.
Risk factors for stroke with non-valvular AF
Previous history of cerebrovascular
accident or transient ischaemic attack
(risk 322.5)
Diabetes (31.7)
Hypertension (31.6)
Heart failure
Risk factors for recurrence of AF after
cardioversion
Long duration (.13 years)
Rheumatic mitral valve disease
Left atrium size .5.5 cm
Older age (.75 years)
Left ventricular impairment
The CHADS 2 score can be used for stratifying
thromboembolic risk in AF:
1 point is awarded for each of: congestive
heart failure, hypertension, age over 75,
diabetes
2 points are awarded for systemic emboli
A score of 3 indicates a high risk of
thrombus formation and is a strong
indication for anticoagulation
Scores of 1 and 2 are intermediate values
(anticoagulation is given at the discretion of
the physician)
The score has the virtue of simplicity but is
quite conservative, probably
underestimating the risk associated with
prior stroke/transient ischaemic attack
1.5.4 Ventricular arrhythmias and
channelopathies
Ventricular tachycardia (monomorphic)
Ventricular tachycardia (VT) has a poor prognosis
when left ventricular function is impaired. After the
exclusion of reversible causes such patients may
Cardiology
27
need implantable debrillators and anti-arrhythmic
therapy.
Ventricular rate is usually 120260 beats/min
Patients should be DC cardioverted when there
is haemodynamic compromise; overdrive
pacing may also terminate VT
Amiodarone, sotalol, ecainide and lidocaine
may be therapeutic adjuncts or prophylactic
agents; magnesium may also be useful
Associations of ventricular tachycardia
Myocardial ischaemia
Hypokalaemia or severe hyperkalaemia
Long QT syndrome (see below)
Digoxin toxicity (VT may arise from either
ventricle, especially with associated
hypokalaemia)
Cardiomyopathies
Congenital abnormalities of the right
ventricular outow tract (VT with LBBB and
right axis deviation pattern)
Features favouring ventricular tachycardia in
broad-complex tachycardia
It is often difcult to distinguish VT from SVT with
aberration (disordered ventricular propagation of a
supraventricular impulse); VT remains the most
common cause of a broad-complex tachycardia,
especially with a previous history of MI. The follow-
ing ECG observations favour VT:
Capture beats: intermittent SA node complexes
transmitted to ventricle
Fusion beats: combination QRS from SA node
and VT focus meeting and fusing (causes
cannon waves)
RBBB with left axis deviation
Very wide QRS .140 ms
Altered QRS compared to sinus rhythm
V lead concordance with all QRS vectors,
positive or negative
Dissociated P waves: marching through the VT
History of ischaemic heart disease: very good
predictor
Variable S1
Heart rate ,170 beats/min with no effect of
carotid sinus massage
Note: none of the above has as high a positive
predictive value for VT diagnosis as a history of
structural heart disease (especially MI).
Ventricular tachycardia (polymorphic) ^
torsades de pointes
Anti-arrhythmic agents (particularly class III) may
predispose to torsades as the arrhythmia is often
initiated during bradycardia. The VT is polymorphic
(QRS complexes of different amplitudes twist
around the isoelectric line), with QT prolongation
when the patient is in sinus rhythm.
Intravenous magnesium and K

channel
openers may control the arrhythmia, whereas
isoprenaline and temporary pacing may prevent
bradycardia and hence the predisposition to VT
May be due to QT prolongation of any cause
(see later)
Proarrhythmic channelopathies
Abnormally prolonged QT intervals may be familial
or acquired, and are associated with syncope and
sudden death, due to ventricular tachycardia (espe-
cially torsades de pointes). Mortality in the un-
treated symptomatic patient with a congenital
abnormality is high but some patients may reach
the age of 5060 years despite repeated attacks.
Causes and associations are shown below.
Essential Revision Notes for MRCP
28
Proarrhythmic causes of abnormal
repolarisation (ST-T changes)
Familial
Long QT syndromes 15
Brugada syndrome
Short QT syndrome
Arrhythmogenic right ventricular
dysplasia
Drugs
Quinidine
Erythromycin
Amiodarone
Tricyclic antidepressants
Phenothiazines
Probucol
Non-sedating antihistamines
(eg terfenadine)
Ischaemic heart disease
Metabolic
Hypocalcaemia
Hypothyroidism
Hypothermia
Hypokalaemia
Rheumatic carditis
Long QT syndromes: The corrected QT is .540 ms
(normal 380460 ms). Ninety per cent are famil-
ial, with chromosome 11 defects being common
(RomanoWard syndrome has autosomal dominant
inheritance; Jervell Lange-Nielsen syndrome is
autosomal recessive and associated with congenital
deafness). Arrhythmias may be reduced by a combi-
nation of -blockers and pacing.
Cardiac causes of electromechanical
dissociation
When faced with a cardiac arrest situation it is
important to appreciate the list of causes of electro-
mechanical dissociation (EMD):
Hypoxia
Hypovolaemia
Hypokalaemia/hyperkalaemia
Hypothermia
Tension pneumothorax
Tamponade
Toxic/therapeutic disturbance
Thromboembolic/mechanical obstruction
1.5.5 Pacing and ablation procedures
Temporary pacing
The ECG will show LBBB morphology (unless there
is septal perforation, when it is RBBB). Pacing may
be ventricular (right ventricle apex) or AV (atrial
appendage and right ventricle apex) for optimised
cardiac output.
Complications include:
Crossing the tricuspid valve during insertion,
which causes ventricular ectopics, as does
irritating the outow tract
Atrial or right ventricular perforation and
pericardial effusion
Pneumothorax: internal jugular route is
preferable to the subclavian one, as it minimises
this risk and also allows control after inadvertent
arterial punctures
Permanent pacing
More complex permanent pacing systems include
rate-responsive models, which use movement sen-
sors or physiological triggers (respiratory rate or QT
interval) to increase heart rates. Although more
expensive they avoid causing pacemaker syndrome
and they act more physiologically for optimal left
ventricular function.
Cardiology
29
Indications for temporary pacing
Asystole
Haemodynamically compromised
bradycardia
Prophylaxis of MI complicated by
second-degree or complete heart block
Prior to high-risk cardiac interventions
or pacemaker replacement
Prevention of some tachyarrhythmias
(eg torsades)
Overdrive termination of various
arrhythmias (eg atrial utter, VT)
Indications for permanent pacing
Chronic AV block
Sick sinus syndrome with symptoms
(including chronotropic incompetence
the inability to appropriately increase
the heart rate with activity)
Post-AV nodal ablation for arrhythmias
(elective or inadvertent)
Neurocardiogenic syncope
HCM
Dilated cardiomyopathy (may pace
more than two chambers)
Long QT syndrome
Prevention of atrial brillation
Post-cardiac transplantation
Pacing in heart failure
There are several synonymous terms for pacing in
patients with cardiac failure. These include cardiac
resynchronisation therapy, biventricular pacing
and multisite pacing. In heart failure pacing is
indicated when all of the following are present:
NYHA IIIIV heart failure
QRS duration .130 ms or other clear evidence
of dyssynchrony
Left ventricular ejection fraction ,35% with
dilated ventricle and patient on optimal medical
therapy (diuretics, angiotensin-converting
enzyme (ACE) inhibitors and -blockers)
The atria and right ventricle are paced in the usual
fashion and in addition to this a pacing electrode is
placed in a tributary of the coronary sinus on the
lateral aspect of the left ventricle. The two ventricles
are paced simultaneously or near-simultaneously
with a short AV delay. The aim is to optimise AV
delay and reduce inter- and intraventricular asyn-
chrony. This therapy is known to reduce mortality,
to improve exercise capacity, to improve quality of
life and to reduce hospital admissions.
Implantable cardioverter debrillators (ICD)
ICDs are devices that are able to detect life-threa-
tening tachyarrhythmias and to terminate them by
overdrive pacing or a counter-shock. They are im-
planted in a similar manner to permanent pace-
makers. Current evidence supports their use in both
secondary prevention of cardiac arrest and also as
targeted primary prevention (eg for individuals with
left ventricular impairment and those with familial
syndromes such as arrhythmogenic right ventricular
dysplasia, Brugada syndrome, long QT variants).
Radiofrequency ablation
Radiofrequency ablation is resistive, heat-mediated
(658C) protein membrane disruption causing cell
lysis. Using cardiac catheterisation (with electrodes
in right- or left-sided chambers) it interrupts electri-
cal pathways in cardiac structures. Excellent results
are obtained in the treatment of accessory pathways
and atrial utter, and with complete AV nodal abla-
tion or AV node modication. Ventricular tachycar-
dia is technically more difcult to treat (ventricular
myocardium is much thicker than atrial myocar-
dium).
Isolation of the pulmonary veins by ablation therapy
is now an established technique to treat atrial bril-
lation. Current cure rates are around 85%, but more
than one procedure is required in half the cases.
Complete heart block and pericardial effusions are
rare complications of radiofrequency ablation.
Indications to refer to an electrophysiologist
Indications for referral to an electrophysiologist are
given in Table 1.5.
Essential Revision Notes for MRCP
30
1.6 ISCHAEMIC HEART DISEASE
In 1990 coronary artery disease became the leading
worldwide cause of death, currently claiming 7.2
million lives per year.
Risk factors for coronary artery disease
Primary
Hypercholesterolaemia (LDL*)
Hypertension
Smoking
Unclear
Low bre intake
Hard water
High plasma brinogen levels
Raised Lp(a) levels
Raised factor VII levels
Protective factors
Exercise
Moderate amounts of alcohol
Low cholesterol diet
Increased HDL:LDL**
Secondary
Reduced HDL cholesterol
Obesity
Insulin-dependent diabetes mellitus
Non-insulin-dependent diabetes
Family history of coronary artery disease
Physical inactivity
Stress and personality type
Gout and hyperuricaemia
Race (Asians)
Low weight at 1 year of age
Male sex
Chronic renal failure
Increasing age
Low social class
Increased homocystine levels and
homocystinuria
*Low-density lipoprotein
**Ratio of high-density lipoprotein to LDL
Table 1.5. Indications for referral to an electrophysiologist
Condition When to refer Potential treatment
SVT More than one episode Radiofrequency ablation
Atrial utter More than one episode Radiofrequency ablation
Atrial brillation Highly symptomatic, refractory to
or intolerant of drug therapy
Radiofrequency ablation
Ventricular brillation Unless there is an obvious
reversible cause, eg ST-segment
elevation MI (STEMI)
ICD
Ventricular tachycardia Unless obvious reversible cause Radiofrequency ablation or ICD
Ischaemic cardiomyopathy Ejection fraction ,30% on
optimal medical therapy
Primary prevention ICD
NYHA class III IV heart failure, QRS
.130 ms, ejection fraction ,35%
On optimal medical therapy Heart failure pacing
Cardiology
31
Smoking and its relationship to
cardiovascular disease
Smokers have an increased incidence of the follow-
ing cardiovascular complications:
Coronary artery disease
Malignant hypertension
Ischaemic stroke
Morbidity from peripheral vascular disease
Sudden death
Subarachnoid haemorrhage
Mortality due to aortic aneurysm
Thromboembolism in patients taking oral
contraceptives
Both active and passive smoking increase the risk of
coronary atherosclerosis by a number of mechan-
isms. These include:
Increased platelet adhesion/aggregation and
whole-blood viscosity
Increased heart rate; increased catecholamine
sensitivity/release
Increased carboxyhaemoglobin level and, as a
result, increased haematocrit
Decreased HDL cholesterol and vascular
compliance
Decreased threshold for ventricular brillation
1.6.1 Angina
Other than the usual forms of stable and unstable
angina, those worthy of specic mention include:
Decubitus: usually on lying down due to an
increase in LVEDP or associated with dreaming,
cold sheets, or coronary spasm during rapid eye
movement (REM) sleep
Variant (Prinzmetal): unpredictable, at rest, with
transient ST elevation on ECG. Due to coronary
spasm, with or without underlying
arteriosclerotic lesions
Syndrome X: this refers to a heterogeneous
group of patients who have ST-segment
depression on exercise testing but
angiographically normal coronary arteries. The
patients may have very-small-vessel disease and/
or abnormal ventricular function. It is
commonly described in middle-aged females
and oestrogen deciency has been suggested to
be an aetiological factor
Vincent angina: nothing to do with cardiology;
infection of the pharyngeal and tonsillar space!
Causes of non-anginal chest pains
Pericardial pain
Aortic dissection
Mediastinitis
Associated with trauma, pneumothorax
or diving
Pleural
Usually with breathlessness in pleurisy,
pneumonia, pneumothorax or a large
peripheral pulmonary embolus
Musculoskeletal
Gastrointestinal
Including oesophageal, gastric,
gallbladder, pancreatic
Hyperventilation/anxiety
Reproduction of sharp inframammary
pains on forced hyperventilation is a
reliable test
Mitral valve prolapse
May be spontaneous, sharp, supercial,
short-lived pain
Symptomatic assessment of angina
The Canadian cardiovascular assessment of chest
pain is useful for grading the severity of angina:
Grade I: angina only on strenuous or prolonged
exertion
Grade II: angina climbing two ights of stairs
Grade III: angina walking one block on the
level (indication for intervention)
Grade IV: angina at rest (indication for urgent
intervention)
1.6.2 Myocardial infarction
Conservative estimates suggest there are 113 000
myocardial infarctions per year in the UK with
signicant pre-hospital mortality, and 5%6% in-
hospital mortality and 6%7% 30-day mortality for
Essential Revision Notes for MRCP
32
those surviving to hospital admission. Overall 19%
of UK deaths are directly attributable to coronary
disease.
Diagnosis of MI
Acute, evolving or recent MI
Either one of the following criteria satises the diag-
nosis for an acute, evolving or recent MI:
Typical rise and gradual fall (troponin) or more
rapid rise and fall (CK-MB) of biochemical
markers of myocardial necrosis with at least one
of the following:
Ischaemic symptoms
Development of pathological Q waves on
the ECG
ECG changes indicative of ischaemia (ST-
segment elevation or depression)
Pathological nding of an acute MI (eg at post-
mortem)
Established MI
Any one of the following criteria satises the diag-
nosis of an established MI:
Development of new pathological Q waves on
serial ECGs. The patient may or may not
remember previous symptoms. Biochemical
markers of myocardial necrosis may have
normalised, depending on the length of time
that has passed since the infarct developed
Pathological nding of a healed or healing MI
Previous MI is also suggested when coronary
artery disease and a regional ventricular wall
motion abnormality are seen, or characteristic
myocardial scars are observed with MRI
Distinction between ST-segment elevation MI
(STEMI) and non-STEMI (NSTEMI)
An acute MI should be classied as STEMI when
there is:
ST-segment elevation (2 mm in two or more
chest leads, or 1 mm in two or more limb leads)
A chronic MI with Q-wave formation
Pathological or imaging evidence of a full-
thickness scar
Other MIs that do not meet these criteria should be
classied as NSTEMI.
Cardiac enzymes
The widespread use of troponin assays has both
simplied and lowered the bar for the diagnosis of
MI. A number of markers of cardiac damage are
now available. Table 1.6 is a guide to the timing of
the initial rise, peak and return to normality.
Troponin assays in patients with renal failure
The troponin level may be elevated simply because
a patient has renal failure. In patients with renal
failure who present with chest pain it is helpful to
assess the troponin level at baseline as well as at
12 h after the onset of symptoms, and sometimes at
later time points. In these circumstances only a
rising troponin level would be suggestive of ischae-
mic myocardial damage.
Complications of MI
Since the advent of thrombolysis, complication rates
have been reduced (eg halved for pericarditis, con-
duction defects, ventricular thrombus, fever, Dress-
ler syndrome). All complications may be seen with
any type of infarction, but the following are the
most common associations.
Complications of anterior infarctions
Late VT/VF
Left ventricular aneurysm
Left ventricular thrombus and systemic
embolism (usually 13 weeks post-MI)*
Complete heart block (rare)
Ischaemic mitral regurgitation
Congestive cardiac failure
Cardiac rupture usually at days 410
with EMD
VSD with septal rupture
Pericarditis and pericardial effusion
(Dressler syndrome with high
erythrocyte sedimentation rate (ESR),
fever, anaemia, pleural effusions and
anti-cardiac muscle antibodies is seen
occasionally)
Cardiology
33
Complications of inferior infarctions
Higher re-infarction rate
Inferior aneurysm with mitral
regurgitation (rare)
Pulmonary embolism (rare)
Complete heart block and other degrees
of heart block
Papillary muscle dysfunction and mitral
regurgitation
Right ventricular infarcts need high
lling pressures (particularly if posterior
extension)
*Although warfarin provides no general benet, it may
reduce the overall CVA rate (1.5%3.6%) in those
patients with echocardiographically demonstrable mural
left ventricular thrombus after a large anterior MI, so
recommended for up to 6 months after the infarction
Heart block and pacing after myocardial
infarction
Temporary pacing is indicated in anterior MI
complicated by complete heart block. This
presentation is associated with high mortality
due to the extensive myocardial damage. The
decision as whether to temporarily pace a
patient with inferior infarction and complete
heart block is primarily dictated by the patients
haemodynamic status. Atropine and
isoprenaline can also be tried. Narrow-complex
escape rhythms are more stable. An
observational period of 7 days post-MI is
appropriate to allow the return of sinus rhythm
before considering permanent pacing
The right coronary artery is the dominant vessel
(over left circumex) in 85% of patients. As this
gives off branches to SA and AV nodes, heart
Table 1.6. Guide to the timing of changes in cardiac enzymes
Marker Initial
rise
Peak Return to
normal
Notes
Creatine phosphokinase* 48 h 18 h 23 days CPK-MB is main cardiac isoenzyme
Myoglobin 14 h 67 h 24 h Low specicity from skeletal muscle damage
Troponin** 312 h 24 h 310 days Troponins I and T are the most sensitive and
specic markers of myocardial damage
available
Lactate dehydrogenase
(LDH)
10 h 2448 h 14 days Cardiac muscle mainly contains LDH
* Creatine phosphokinase has three isoenzymes, of which the CPK-MB isoenzyme is most cardiac-specic,
although numerous other organs possess the enzyme in small quantities. A CPK-MB of .2.5% of the total CPK has
been suggested as very specic for MI in the context of chest pain. This is inaccurate in situations of signicant
acute or chronic skeletal injury, where CPK levels will be high
** Troponin interpretation is specic to the assay used and local guidelines should be consulted. A level greater
than the 99th centile for the assay is regarded as positive. Assays may be read only, semi-quantitative or
quantitative. Positives occur in all conditions where myocardial damage occurs, including pulmonary embolus,
myocarditis, extreme bradycardia or tachycardia, sepsis, renal impairment and uncontrolled diabetes mellitus
Essential Revision Notes for MRCP
34
block might be observed if a dominant right
coronary artery is occluded
1.6.3 Medical therapy for myocardial
infarction
Thrombolysis is benecial up to 6 h after pain onset
but may be given for up to 12 hours in the context
of continuing pain or deteriorating condition. Reca-
nalisation occurs in 70% of patients after thrombo-
lysis (compared with a 15% recanalisation rate
without thrombolysis) and results in a higher, earlier
creatine phosphokinase (CPK) rise (but a lower total
CPK release). Reperfusion arrhythmias are common
within the rst 2 hours after thrombolysis.
Primary angioplasty is superior to thrombolysis for
acute MI; the same ECG criteria apply to case
selection.
Tissue plasminogen activator and similar recombi-
nant agents are accompanied by a prothrombotic
phase lasting about 48 hours and this period should
be covered with heparin.
Contraindications to thrombolysis
Although there are numerous relative contraindica-
tions where the risk/benet considerations are indi-
vidual to the patient, there are several absolute
contraindications to thrombolysis.
Contraindications to thrombolysis
Absolute contraindications
Active internal bleeding or
uncontrollable external bleeding
Suspected aortic dissection
Recent head trauma (,2 weeks)
Intracranial neoplasms
History of proved haemorrhagic stroke
or cerebral infarction ,2 months earlier
Uncontrolled high BP (.200/120
mmHg)
Pregnancy
Relative contraindications
Traumatic prolonged cardiopulmonary
resuscitation
Bleeding disorders
Recent surgery
Probable intracardiac thrombus (eg AF
with mitral stenosis)
Active diabetic haemorrhagic
retinopathy
Anticoagulation or INR .1.8
Groups particularly beneting from thrombolysis
(determined by the GUSTO, ISIS 2 and ISIS 3 trials)
include:
Those with large anterior infarction
Those with pronounced ST elevation
Elderly (.75 years)
Those with poor left ventricular function or
LBBB, or systolic BP ,100 mmHg
Those who have early administration: within 1 h
of pain onset
Posterior infarction (a tall R wave in V1 with ST
depression in leads V1V3): no clear benet of
thrombolysis has been shown as few such patients
have been enrolled into major trials (ECG interpreta-
tion is often difcult when the presentation is not
with inferior infarct). However, the general consen-
sus would still be to give thrombolysis. Sixty per
cent of posterior MIs are due to right coronary artery
disease.
NSTEMI: have not been shown to benet from
thrombolysis. They have a low in-patient but high
(65%) untreated 1-year mortality (compared to 34%
for STEMI infarcts) and they should be investigated
early and aggressively.
There is now a good evidence base for a range of
pharmacological treatments in patients presenting
with acute coronary syndromes (See Table 1.7).
These are aimed at dispersing clot (aspirin, clopido-
grel, heparin), preventing arrhythmias (-blockers),
stabilising plaque (statins) and preventing adverse
remodelling.
Cardiology
35
Table 1.7. Summary of clinical trials in patients with acute MI*
Agents used for acute MI Mortality in
treated group (%)
Mortality in
control subjects
(%)
Number treated
to save 1 life
Trials involved
Aspirin 9.4 (at 5 weeks) 11.8 42 ISIS 2
Clopidogrel 11.4 9.3 Composite
endpoint
CURE
Thrombolytics 10.7

(at 21 days) 13.0

43

GISSI 1

, ISIS 2,
TIMI II, GUSTO
-Blockers 3.9 (at 7 days) 4.6 143 ISIS 1
ACE inhibitors 35.2

(after 39-
month mean
follow-up)
39.7

22

SAVE, SOLVD

, AIRE
Lipid-lowering therapy
(patients with average
cholesterol)
10.2 (after 5 years) 13.2 33 CARE (note endpoints
included second non-
fatal MI and cardiac
deaths)
Heparin with aspirin and
any form of thrombolysis
8.6 9.1 200 Meta-analysis of
68 000 patients
Magnesium: contradictory data but no mortality reduction LIMIT 1, 2, ISIS 4
Nitrates: no clear benet ISIS 4, GISSI 3
Warfarin: no proved benet above aspirin after thrombolysis
* See also Appendix II: Summary of further trials in cardiology

Data from that particular trial

Essential Revision Notes for MRCP
36
1.6.4 Coronary artery interventional
procedures
Percutaneous coronary intervention (PCI)
After coronary angioplasty the recurrence or re-
stenosis rate is 30% within 3 months and 40%
60% for total occlusions that are successfully
dilated as treatment of acute MI. These gures have
been greatly reduced, rst by bare metal stents and
then further by drug-eluting stents. Drug-eluting
stents are covered by an antimitotic agent to prevent
smooth muscle/brous tissue proliferation. Unfortu-
nately, they also inhibit endothelialisation so in-
creasing the risk of thrombosis and so dual
antiplatelet therapy (aspirin and clopidogrel) is man-
datory for 12 months after the intervention and
lifelong single antiplatelet therapy is required there-
after.
Lesions particularly amenable to PCI include
those that are discrete, proximal, non-calcied,
unoccluded, that are away from side branches
and that occur in patients with a short history of
angina. While there is a small acute occlusion
rate, these can usually be managed successfully
with intra-coronary stenting, such that the need
for emergency CABG has fallen to under 1%
More challenging lesions include those within
grafts, at bifurcations, calcied or long lesions
and those within small vessels. Diabetics have
poorer outcomes compared with non-diabetics
Almost any lesion can be stented including left
main stem disease, three-vessel disease and
even chronic total occlusions but careful
evaluation and discussion with the patient are
necessary, as in many situations bypass grafting
has a better evidence base
Coronary artery bypass grafting (CABG)
CABG has clear benets in specic groups of pa-
tients with chronic coronary artery disease (when
compared with medical therapy alone). Analysis has
previously been limited because randomised trials
included small numbers and were performed sev-
eral decades ago; patients studied were usually
males aged ,65 years. The population now receiv-
ing CABG has changed, but so has medical therapy.
Prognostic benets are shown for symptomatic,
signicant left main stem disease (Veterans
Study), symptomatic proximal three-vessel
disease and in two-vessel disease which
includes the proximal left anterior descending
artery (CASS data)
Patients with moderately impaired left
ventricular function show greater benet, but
those with poor left ventricular function have
greater operative mortality. Overall mortality is
,2%, rising to between 5% and 10% for a
second procedure. Eighty per cent of patients
gain symptom relief
Peri-operative graft occlusion is around 10% for
vein grafts, which otherwise last 810 years.
Arterial grafts (internal mammary, free radial,
gastro-epiploic) have a higher initial patency
rate but long-term outcomes are disappointing
with the exception of internal mammary grafts,
which are clearly superior to vein grafts
A Dressler-like syndrome may occur up to
6 months post-surgery
Minimally invasive CABG involves the
redirection of internal mammary arteries to
coronary vessels without the need for cardiac
bypass and full sternotomy incisions (often
termed off pump coronary revascularisation).
Recovery times following this procedure are
shorter than for conventional surgery but the
procedures are technically more challenging
Post-MI rehabilitation
After MI patients are kept in hospital for 5 days,
should take 2 months off work and have 1 months
abstinence from sexual intercourse and driving (see
following text). Cardiac rehabilitation is particularly
important for patient condence. Depression occurs
in 30% of patients. Patients who are fully revascu-
larised or invasively investigated and found to have
no ongoing ischaemic focus may be discharged
after 3 days and be rehabilitated more rapidly.
Fitness to drive
The DVLA provides extensive guidelines for coron-
ary disease and interventions. Their website
(www.dvla.gov.uk) should be consulted, especially
Cardiology
37
with regard to class 2 licences (for vehicles over
3500 kg, minibuses and buses) but the essential
points are given in Table 1.8.
1.7 OTHER MYOCARDIAL DISEASES
1.7.1 Cardiac failure
Cardiac failure can be dened as the pumping
action of the heart being insufcient to meet the
circulatory demands of the body (in the absence of
mechanical obstructions). A broad echocardio-
graphic denition is of an ejection fraction (EF)
,40% (as in the SAVE trial, which enrolled patients
for ACE inhibitors post-MI). Overall 5-year survival
is 65% with EF ,40%, compared to 95% in those
with EF .50%.
The most common single cause of cardiac failure in
the Western world is ischaemic heart disease (IHD).
Hypertension is also a very frequent cause
either acting alone or in combination with IHD
Diastolic heart failure is increasingly recognised
although difcult to diagnose as an isolated
condition. It describes impaired ventricular
lling that elevates pulmonary and/or systemic
venous pressure with activation of the
neurohormonal system as seen in systolic heart
failure
All patients with systolic heart failure have a
degree of diastolic dysfunction some believe
that isolated diastolic dysfunction may be an
early step prior to development of systolic heart
failure
EF is only a guide to cardiac function, which also
depends on other factors including pre-load, after-
Table 1.8. Fitness to drive
Condition Driving restriction Notes
Unexplained syncope 6 months from last
episode or until effective
treatment is given
Clear vasovagal events that occur only
when the patient is erect do not preclude
driving
Cardiac catheter procedure (including
angiography, percutaneous coronary
intervention, electrophysiological
studies/ablation)
1 week Should be able to perform emergency stop
unhindered
Myocardial infarction 1 month
Permanent pacemaker 1 month Only 1 week if the patient has never been
syncopal
Prophylactic ICD 1 month No clinical arrhythmia or syncope
Secondary prevention ICD 6 months DVLA must be informed
ICD shock therapy 6 months Unless an inappropriate shock is
preventable by reprogramming or
intervention, eg a change in the detection
or therapy programming to avoid shocks
for sinus tachycardia or atrial arrhythmias
Essential Revision Notes for MRCP
38