Ebook Practical cardiology (2nd edition) Part 1

Practical
Cardiology
An Approach to the Management of
Problems in Cardiology

Tracey Baker
MB BS, FRACGP, Dip. RACOG

General Practitioner, Canberra

George Nikolic´, OAM
FRACP, FACC, FCCP, FCSANZ, FJFICM

Senior Specialist, Intensive Care Unit,
Consultant Physician in Cardiology,
The Canberra Hospital

Simon O’Connor
FRACP, DDU, FCSANZ

Cardiologist, The Canberra Hospital

Sydney Edinburgh London New York Philadelphia St Louis Toronto


Churchill Livingstone
is an imprint of Elsevier
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National Library of Australia Cataloguing-in-Publication Data
___________________________________________________________________
Baker, Tracey.
Practical cardiology : an approach to the management of problems in cardiology
Tracey Baker ; George Nikolić ; Simon O’Connor.
2nd ed.
Chatswood, N.S.W. : Elsevier Australia, 2008.
ISBN: 978 0 7295 3841 1 (pbk.)
Includes index.
Bibliography.
Cardiology
Heart--Diseases--Diagnosis.
Heart--Diseases--Treatment.
Heart--Diseases--Patients--Hospital care.
Nikolić, George.

O’Connor, Simon.
616.12
___________________________________________________________________
Publisher: Sophie Kaliniecki
Developmental Editor: Sunalie Silva
Publishing Services Manager: Helena Klijn
Edited by Caroline Hunter, Burrumundi Pty Ltd
Proofread by Tim Learner
Cover and internal design by DiZign
Index by Michael Ferreira
Typeset by TnQ Books and Journals Pvt Ltd
Printed in Hong Kong by 1010 Printing International Ltd


Preface

There have been many changes in cardiology—that most rapidly developing speciality—since
1999 when the first edition of this book was published. This edition, with a new publisher and
a third author (George Nikolić), aims to bring the subject right up to date. Much has changed.
Some previous recommendations such as hormone replacement therapy to reduce cardio­
vascular risk have been reversed, and important new concepts such as total cardiovascular 
risk have been introduced.
No medical specialty has been so affected by the results of randomised trials. Some of the
more important trials have been listed and their results summarised. References have been
provided throughout the book for important management recommendations. Students and
medical staff are now expected to be able to back up their practice with evidence. We hope this
book will make that task easier.
There is a new chapter devoted to electrocardiography. There are many basic books available for those beginning to learn about ECG interpretation. We have not tried to reproduce
these but rather to provide a text for those with some basic knowledge that puts ECGs into
their clinical context.

Other cardiac investigations are dealt with throughout the book and a DVD has been 
provided to enable readers to see them in the way they are interpreted—as video images.
Case-based learning sections have been provided for each area of cardiology to help students
to understand the principles of this teaching method.
We hope this modern problem- and evidence-based cardiology text will be helpful to 
­doctors and students.

Tracey Baker
George Nikolić
Simon O’Connor
Canberra, April 2008

ix


Some important cardiology
trials

The number of possible cardiology trials is limited only by the number of possible trial
acronyms.
ACADEMIC: Azithromycin in Coronary Artery Disease Elimination of Myocardial Infection
with Chlamydia. Anderson JL, et al. Circulation 1999; 99:1540–1547. In this trial 302 patients
with known coronary artery disease were treated with either azithromycin, an antibiotic active
against Chlamydia, or a placebo for three months. There was no difference in coronary events
between the two groups over the following two years.
AFFIRM: Atrial Fibrillation Follow-up Investigation of Rhythm Management. Olshansky B,
Rosenfeld LE, Warner AL, et al. J Am Coll Cardiol 2004; 43:1201–1208. This trial assessed the
efficacy of rate control for patients with AF, comparing beta-blockers and calcium channel
blockers in 2027 patients. Beta-blockers were more effective.
APSIS: Angina Prognosis Study in Stockholm. Forslund L, Hjemdahl P, Held C, et al. 

Eur Heart J 2000; 21:901–910. In this study patients with angina (n = 731) and a positive
exercise test were randomised to treatment with verapamil or a beta-blocker and then
performed another exercise test. The maximal ST depression and the exercise duration were
independent predictors of outcome over the following 40 months.
ARTS: Arterial Revascularisation Therapy Study. Serruys P, et al. N Engl J Med 2001; 344: 
1117–1124. This trial studied the effectiveness of CABG compared with angioplasty and bare
metal stenting for diabetics with multi-vessel coronary disease. Diabetics in the CABG arm
had a better outcome than those having angioplasty.
ASSENT-2: Assessment of the Safety and Efficacy of a New Thrombolytic–2. ASSENT-2
investigators. Lancet 1999; 354:716–722. This trial compared tenectoplase and alteplase for
16,949 patients with acute myocardial infarction. There was no difference in mortality at 
30 days and one year between the two groups.
BAATAF: Boston Area Anticoagulation Trial for Atrial Fibrillation. The Boston Area
Anticoagulation Trial for AF Investigators. New Engl J Med 1990; 323:1505–1511. Warfarin
with a target INR of 1.5–2.7 was effective in preventing stroke in 212 AF patients compared
with 208 AF patients treated with aspirin or nothing. The risk reduction was 86%.
CAPRIE: Clopidogrel vs Aspirin in Patients at Risk of Ischaemic Events. CAPRIE Steering
committee. Lancet 1996; 348:1329–1339. The combined risk of stroke, infarction or vascular
death was compared for 19,185 patients with vascular disease on treatment with aspirin or
clopidogrel. There was a reduction in combined risk for the clopidogrel group, who also had
a lower risk of gastrointestinal side effects.
CARE-HF: Cardiac Resynchronisation-Heart Failure. Cleland JG, Daubert JC, Erdmann E, et al.
Cardiac Resynchronisation-Heart Failure Investigators. The effect of cardiac resynchronisation
on morbidity and mortality in heart failure. N Engl J Med 2005; 352:1539–1549. Patients
with severe heart failure were randomised to optimal conventional heart failure treatment
or optimal treatment and CRT. CRT improved symptoms, and reduced the frequency of
hospital admissions and mortality.

xi

xii

Some im p o r t a n t c a r d i o l o g y t r i a l s

CASS: Coronary Artery Surgery Study. CASS Investigators. New Engl J Med 1984; 310:750–758.
This open label study looked at 780 randomised patients with mild angina or who were
asymptomatic after infarction to CABG or medical treatment for six years. There was no
difference in the survival rate.
CHARM—Alternative: Candesartan in Heart Failure; Assessment of Reduction in Mortality
and Morbidity—Alternative. Granger CB, McMurray JJV, Yusef S, et al. Lancet 2003; 362:
772–776. This angiotensin receptor antagonist was successful in reducing morbidity and
cardiovascular mortality in patients with chronic heart failure who were intolerant of ACE
inhibitors.
CHARM—Added: Candesartan in Heart Failure; Assessment of Reduction in Mortality
and Morbidity—Added. McMurray JJV, Ostergren J, Swedberg J, et al. Lancet 2003; 362: 
767–771. The addition of candesartan to an ACE inhibitor in patients with heart failure causes
a further reduction in cardiovascular events.
CHARM—Preserved: Candesartan in Heart Failure; Assessment of Reduction in Mortality
and Morbidity—Preserved. Yusuf S, Pfeffer MA, Swedberg K, et al. Lancet 2003; 362: 
777–781. Candesartan has a moderate effect on the prevention of hospitalisation for patients
with chronic heart failure but with an ejection fraction of greater than 40%.
CIBIS II: Cardiac Insufficiency Bisoprolol Study II. The CIBIS scientific committee. Lancet
1999; 353:9–13. In this study of the treatment of heart failure with bisoprolol, 2647 patients
were treated with the drug or a placebo for a period of one to three years. All-cause mortality
was 11.8% in the treated group and 17% in the placebo group (P < 0.0006).
CIBIS III: Cardiac Insufficiency Bisoprolol Study III. Willenheimer R, et al. Circulation
2005;112:2426–2435. In this heart failure trial, initiation of treatment with bisoprolol
followed by enalapril was compared with the opposite (conventional) sequence. There were 
505 patients in each group and outcomes were the same at 1.22 years.

CLARITY–TIMI 28: Clopidogrel as Adjunctive Reperfusion Therapy. Sabatine MS, et al. 
Am Heart J 2005; 149:222–233. In this trial, 3491 patients with an acute ST elevation myocardial
infarction and having standard reperfusion treatment were given a 300 mg loading dose of
clopidogrel and then 75 mg a day in addition to aspirin or a placebo and aspirin. At 30 days
the clopidogrel group had a significantly lower risk of death or re-infarction (CI 0.21–0.65).
CLARITY: Clopidogrel as Adjunctive Reperfusion Therapy-Thrombolysis in Myocardial
Infarction. Sabatine MS, Cannon CP, Gobson M, et al. N Engl J Med 2005; 352. In this study
the addition of clopidogrel to aspirin and fibrinolytic therapy for patients with an acute ST
elevation infarct improved the patency rate and reduced ischaemic complications.
COBRA: Association Between Erectile Dysfunction and Coronary Artery Disease. Role of
Clinical Presentation and Extent of Coronary Vessels Involvement: The Cobra Trial.
Montorosi P, Ravagnani PM, Galli S, et al. Eur Heart J 2006; 27:2632–2639. Erectile
dysfunction as assessed by a questionnaire was present some years before clinical coronary
disease in these patients.
COMPANION: Comparison of Medical Therapy, Pacing and Defibrillation in Chronic Heart
Failure. Bristow MR, Feldman AM, Saxon LA, et al. N Engl J Med 2004; 350:2140. This study
looked at cardiac resynchronisation therapy with or without an implantable defibrillator in
advanced chronic heart failure. Resynchronisation treatment in these heart failure patients reduced
mortality and the frequency of hospital admissions compared with normal pacing. Patients whose
resynchronisation pacemaker was also a defibrillator had a lower mortality again.
CONSENSUS: Cooperative North Scandinavian Enalapril Survival Study. N Engl J Med
1987; 316:1429–1435; Circulation 1990; 82:1730–1736; Am J Cardiol 1990; 66:40D–45D;
Am J Cardiol 1992; 69:103–107. This trial of enalapril in severe heart failure showed a 27%
reduction in mortality at 12 months compared with the placebo.


Some important cardiology trials

xiii

DASH: Dietary Approaches to Stop Hypertension. Moore TJ, Volmer WM, Appel LJ, et al.
Hypertension 1999; 34:472–477. In this study a combination diet rich in vegetables and lowfat dairy products significantly reduced blood pressure in hypertensive patients compared
with a control diet low in fruit and vegetables and high in dairy fats.
DAVITT II: Danish Verapamil Infarction Trial II. The Danish Study Group on Myocardial
Infarction. Am J Cardiol 1990; 66:779–785. This study showed long-term treatment with
verapamil reduced major ischaemic events after myocardial infarction.
DIG: Digitalis Investigation Group Trial. Rich MW, McSherry F, Williford WO, et al. J Am
Coll Cardiol 2001; 38:806–813. This trial of heart failure randomised 7788 patients with heart
failure to digoxin or a placebo and usual treatment. The treated group had a 27% reduction
in admission for heart failure and a 7% overall reduction in hospital admission. There was
no difference in mortality.
EAFT: European Atrial Fibrillation Trial. EAFT Study Group. Lancet 1993; 342:1255–1262. This
study compared aspirin and warfarin for the prevention of recurrent stroke in patients with
non-rheumatic AF. The risk of stroke was reduced from 12% to 4% per year with warfarin.
EPHESUS: Eplerenone Post-AMI Heart Failure Efficacy and Survival Study. Pitt B, Remme W, 
Zannad F, et al. Eplerenone, a selective aldosterone blocker, in patients’ left ventricular
dysfunction after myocardial infarction. N Engl J Med 2003; 348:1309–1321. This study
showed improved outcomes for patients treated with eplerenone shortly after extensive
myocardial infarction.
Four S: Scandinavian Simvastatin Survival Study. Scandinavian Simvastatin Survival Study
Group. Lancet 1994; 344:1383–1389. This important trial with 4444 patients showed a survival
advantage for patients with coronary artery disease who were treated with a statin.
FRISC: I FRagmin and Fast Revascularisation During Instability in Coronary Artery Disease
Study. FRISC-I Investigators. Lancet 1999; 354:708–715. FRISC II 1 year: FRagmin and Fast
Revascularisation During Instability in Coronary artery Disease Study. FRISC Investigators.
Lancet 2000; 356:9–16. These studies showed a significant reduction in death, recurrent
infarction and hospital readmission for patients with unstable angina when they were treated
with early intervention.
GUSTO V Global Utilisation of Streptokinase and t-Pa for Occluded coronary arteries V.
Topol EJ. The GUSTO Investigators. Lancet 2001; 357:1905–1914. In this trial of ST elevation

infarction patients, reduced dose fibrinolytic treatment combined with glycoprotein IIb/IIIa
inhibition was compared with standard fibrinolytic treatment. There was no difference in
30-day mortality.
Heart Protection Study. Heart Protection Study Collaborative Group. Lancet 2002; 360:7–22. In
this study high-risk patients (previous IHD or multiple risk factors) up to the age of 80 were
treated with simvastatin. Patients with average cholesterol levels were included. There was a
25% reduction in events over five years regardless of initial cholesterol level, age or sex.
HERS II Heart and Estrogen/progestogen Replacement Study. Shlipak MG, Chaput LA,
Vittinghoff E, et al. Am Heart J 2003; 146:870–875. In this part of the HERS studies, changes
in lipid levels associated with HRT were not predictive of cardiovascular outcome.
HOT: Hypertension Optimal Treatment Study. Zanchetti A, Hansson L, Menard J, et al. Risk
assessment and treatment benefit in intensively treated hypertensive patients of the Hypertension
Optimal Treatment (HOT) study for the HOT study group. J Hypertens 2001; 19:819–825. In
this study, maximum reduction in cardiovascular mortality occurred at blood pressures of about
139/87. However, there was no increase in mortality at blood pressure levels below this.
IONA: Impact of Nicorandil in Angina. The IONA Study Group. Lancet 2002; 359:1269–1275.
In this study of 5126 patients with stable angina, in the group treated with nicorandil there
was a significant improvement in the composite endpoint of death, non-fatal infarction and
hospital admission with angina.


xiv

Some im p o r t a n t c a r d i o l o g y t r i a l s

LIFE: Losartan Intervention for Endpoint Reduction Study. Daholf B, Devereux RB,
Kjeildsen SE, et al. Lancet 2002; 359:995–1003. In this trial more than 9000 hypertensive
patients with LVH were treated with losartan (an ARA) or atenolol (a beta-blocker). There
was similar reduction in blood pressure but the losartan group had fewer non-fatal strokes
and a 25% reduction in the new onset of diabetes.

LIPID: Long-Term Intervention with Pravastatin in Ischaemic Disease Study. LIPID
Investigators. Am J Cardiol 1995; 76:474–479; N Engl J Med 1998; 339:1349–1357. In
this study 9000 patients with recent infarction of an acute coronary syndrome and a total
cholesterol level of 4–7 mmol/L were randomised to treatment with this statin or dietary
advice. There was a relative risk reduction in death of 24%, as well as a significant reduction
in further ischaemic episodes, for those patients treated with the statin.
MADIT II: Multi-centre Automatic Defibrillator Implantation Trial II. Moss AJ, Zareba W,
Hall WJ, et al. New Engl J Med 2002; 346:877–883. In this trial 1232 patients with previous
infarction and an ejection fraction of less than 30% were randomised to medical treatment or
a defibrillator. There was a 4.5% relative risk reduction in death for the defibrillator group at
20 months. These were patients who had not had documented ventricular arrhythmias.
MERIT-HF: Metoprolol CR/XL Randomised Intervention Trial in Heart Failure. The MERITHF study group. JAMA 2000; 283:1295–1302. In this trial, 3991 patients with heart failure
(NYHA class II–IV) were treated with slow-release metoprolol or a placebo in addition to
conventional treatment. The trial was ended after one year because of a significant reduction
in all-cause mortality (7.2% vs 11% per patient year). This was a relative risk reduction of
0.60.
MUSTT: Multi-centre Unsustained Tachycardia Trial. Buxton AE, Lee AL, Fisher JD, et al.
A randomised study of the prevention of sudden death in patients with coronary artery
disease. N Engl J Med 1999; 341:1883–1890. In this trial patients with inducible VT, coronary
artery disease and an ejection fraction less than 40% were randomised to EPS-guided
drug treatment or no treatment. Patients who had inducible arrhythmias had a small but
significantly different decrease in overall mortality and arrhythmic death when treated with
anti-arrhythmic drugs guided by EPS.
PEP-CHF: The Perindopril in Elderly People with Chronic Heart Failure. PEP investigators.
Eur Heart J 2006; 27:2338–2345. This trial of an ACE inhibitor in patients with heart failure
and a preserved ejection fraction showed improved exercise tolerance and fewer admissions to
hospital for treated patients, but was not sufficiently powered to show a mortality benefit.
PROGRESS: Perindopril Protection Against Recurrent Stroke Study. PROGRESS Collaborative
Study Group. Lancet 2001; 358:1033–1041. This randomised trial of a perindopril-based
blood pressure-lowering regimen among 6108 individuals with previous stroke or transient

ischaemic attack showed a significant reduction in stroke recurrence in treated patients.
SAVE: Survival and Ventricular Enlargement Study. Rutherford JD, Pfeffer MA, Moye LA, et al.
Circulation 1994; 90:1731–1738. In this study, patients with asymptomatic left ventricular
dysfunction had a better prognosis when treated with captopril than the placebo.
SCD-HeFT: Sudden Death in Heart Failure Trial. Bardy GH, Lee KL, Mark DB, et al. New
Engl J Med 2005; 352:225–237. This trial compared the anti-arrhythmic drug amiodarone,
a placebo and an ICD for patients with an ejection fraction of less than 35%. Follow-up was
for 45 months. ICD treatment reduced mortality by 23%; amiodarone was no different from
the placebo.
SOLVD: Studies of Left Ventricular Dysfunction. SOLVD Investigators. N Engl J Med 1991;
325:293–302. This study looked at the effect on survival of enalapril in patients with a reduced
left ventricular ejection fraction (< 35%) and congestive heart failure. In the treatment arm
of the trial there was a 16% relative risk reduction of death.


Some important cardiology trials

xv

SPAF I: Stroke Prevention in Atrial Fibrillation. SPAF Investigators. Circulation 1991; 83: 
527–539. This study compared a placebo, aspirin and dose-adjusted warfarin for primary
prevention of stroke or thromboembolism in patients with non-rheumatic atrial fibrillation.
Follow-up was for three years. Warfarin reduced the risk by 67% compared with the placebo,
and aspirin reduced it by 42%. Annual event rates were 2.3%, 3.6% and 7%, respectively, for
warfarin, aspirin and the placebo.
SPAF II: Stroke Prevention in Atrial Fibrillation. SPAF Investigators. Lancet 1994; 343:687–691.
This trial compared aspirin and warfarin for the prevention of embolic events in patients with
AF. Warfarin reduced the absolute event rate by 0.7% a year.
SPORTIF V: Stroke Prevention Using an Oral Thrombin Inhibitor in Atrial Fibrillation V.
SPORTIF Investigators. JAMA 2005; 293:690–698. The oral thrombin inhibitor ximelagatran

was compared with warfarin in this high-risk AF group. Ximelagatran was as effective as
warfarin in preventing stroke. However, the drug has been withdrawn by the manufacturer
because of concerns about hepato-toxicity.
STAF: Strategies of Treatment of Atrial Fibrillation. Carlson J, Miketic S, Windeler J, et al.
J Am Coll Cardiol 2003; 41:1690–1696. This trial compared rate control with rhythm control
for patients with AF. There was no difference between the groups in risk of death, stroke or
embolic event.
TIBET: Total Ischaemic Burden European Trial. Fox KM, Mulcahy D, Findlay I, et al. Eur Heart J 
1996; 17:96–103. In this trial patients with mild chronic angina were treated with atenolol,
nifedipine or both (c. 200 patients in each arm). Combination treatment was more effective
than either drug alone in improving exercise capacity.
TNT: Treating to New Targets Trial. Waters DD, Guyton JR, Herrington DM, et al. Does
lowering low density lipoprotein in cholesterol levels below currently recommended guidelines
yield incremental clinical benefits? Am J Cardiol 2004; 183:154. This trial was positive for
patients with a high risk of further cardiac events.
UKPDS: UK Prospective Diabetes Study. UKPDS Group. Lancet 1998; 352:837–853. This
important trial compared macrovascular and microvascular complications of diabetes in
patients randomised to intensive blood glucose control and those with usual treatment.
Those in the intensive group had a reduction in microvascular complications of 25% over
10 years but there was not a significant reduction in macrovascular complications though the
reduction in risk of myocardial infarction came close to being significant.
ValHeFT: Valsartan Heart Failure Trial. Cohn JN, Tognoni G. N Engl J Med 2001; 345: 
1667–1675. In this trial valsartan, an ARA, was compared with usual treatment for heart failure
in patients with NYHA class II–IV heart failure. There was no difference in mortality overall
between the groups but when compared against those patients not on an ACE inhibitor or
beta-blocker there was an improvement in the valsartan group.


Abbreviations

ABGs
ABI
ABLS
ABPM
ACC
ACE
ACLS
ACS
ACT
AEB
AED
AF
AHA
AICD
AIVR
AMI
ANP
AP
APPT
ARA
ASD
ASH
ATP
AV
AV block
BMI
BMS
BNP
BPEG
CABG

CCF
CCU
CHD
COPD
COX
CPAP
CPR
CRP
CRT
CSANZ
CTPA
CVD
CW
CXR
DC

arterial blood gases
ankle brachial index
adult basic life support
ambulatory blood pressure measurement
American College of Cardiology
angiotensin-converting enzyme
advanced cardiac life support
acute coronary syndrome
activated clotting time
atrial ectopic beat
automatic external defibrillator
atrial fibrillation
American Heart Association
automatic implanted cardioverter defibrillator

accelerated idioventricular rhythm
acute myocardial infarction
A-type natriuretic peptide
anteroposterior
activated partial thromboplastin time
angiotensin receptor antagonist
atrial septal defect
asymmetrical septal hypertrophy
adenosine-triphosphate
atrioventricular
atrioventricular block (ECG)
body mass index
bare metal stent
B-type natriuretic peptide
British Pacing and Electrophysiology Group
coronary artery bypass grafting
congestive cardiac failure
coronary care unit
coronary heart disease
chronic obstructive pulmonary disease
cyclo-oxygenase
continuous positive airways pressure
cardiopulmonary resuscitation
C-reactive protein
cardiac resynchronisation therapy
Cardiac Society of Australia and New Zealand
CT pulmonary angiogram
cardiovascular disease
continuous wave
chest X-ray

direct current
xvii


xviii

Abbre via t i o n s

DES
DTS
DVD
ECG
EF
EPS
ESC
ESR
FBC
FDG
FFA
FS
HCM
HDL
HF-PEF
HITS
HRT
hsCRP
ICD
IDL
IGT
IHD

IMT
INR
IO
IPAH
IPH
IVCD
IVUS
JVP
LA
LAA
LAD
LAD
LAHB
LAX
LBBB
LDL
LFT
LGL
LIMA
LV
LVEDD
LVEF
LVESD
LVH
LVOT
MDCT
MRI
MVP
NASPE
NHF

drug-eluting stent
Duke treadmill score
deep venous thrombosis
electrocardiogram
ejection fraction
electrophysiological studies
European Society of Cardiology
erythrocyte sedimentation rate
full blood count
fluorodeoxyglucose
free fatty acids
fractional shortening
hypertrophic cardiomyopathy
high-density lipoprotein
heart failure with a preserved ejection fraction
heparin-induced thrombocytopenia
hormone replacement therapy
high-sensitivity C reactive protein
implanted cardioverter defibrillator
intermediate-density lipoprotein
impaired glucose tolerance
ischaemic heart disease
intima-media thickness
international normalised ratio
intraosseous
idiopathic pulmonary arterial hypertension
idiopathic pulmonary hypertension
intraventricular conduction defect
intravascular ultrasound

jugular venous pressure
left atrium
left atrial abnormality
left anterior descending (coronary artery)
left-axis deviation (ECG)
left anterior hemiblock (ECG)
long-axis view (echocardiograph)
left bundle branch block (ECG)
low-density lipoprotein
liver function test
Lown-Ganong-Levine
left internal mammary artery
left ventricle
left ventricular end-diastolic dimension
left ventricular ejection fraction
left ventricular end-systolic dimension
left ventricular hypertrophy
left ventricular outflow tract
multi-detector computerised tomography
magnetic resonance imaging
mitral valve prolapse
North American Society of Pacing and Electrophysiology
National Heart Foundation


A b b r ev i a t i o n s

NO
NSAIDs
NSTEACS

NSTEMI
NYHA
PA
PA
PAOP
PAP
PCI
PCKD
PCWP
PE
PEA
PET
PICC
PIH
POBA
PTF
PVARP
RAA
RA
RBBB
RCA
RCT
RIMA
ROSC
rTPA
RV
RVOT
SAM
SAX
SCORE

SDS
SLE
SPECT
ST
STEMI
SVG
SVT
TG
TGA
TIA
TIMI
TOE
TPA
UEC
VEB
VF
VSD
VT
WPW

nitric oxide
non-steroidal anti-inflammatory drugs
non-ST elevation acute coronary syndrome
non-ST elevation MI
New York Heart Association
posteroanterior
pulmonary artery
pulmonary artery occlusion pressure
pulmonary artery pressure
percutaneous coronary intervention

polycystic kidney disease
pulmonary capillary wedge pressure
pulmonary embolism
pulseless electrical activity
positron emission tomography
peripherally inserted central catheter
pregnancy-induced hypertension
plain old balloon angioplasty
P-terminal force
post-ventricular atrial refractory period
right atrial abnormality
right atrium
right bundle branch block (ECG)
right coronary artery
randomised controlled trial
right internal mammary artery
return of spontaneous circulation
recombinant tissue plasminogen activator
right ventricle
right ventricular outflow tract
systolic anterior movement
short-axis view (ECG)
systematic coronary risk evaluation
sudden death syndrome
systemic lupus erythematosus
single-photon emission computed tomography
sinus tachycardia
ST elevation myocardial infarction
saphenous vein graft
supraventricular tachycardia

triglycerides
transposition of the great arteries
transient ischaemic attack
thrombolysis in myocardial infarction
transoesophageal echocardiogram
tissue plasminogen activator
urea, electrolytes and creatinine
ventricular ectopic beat
ventricular fibrillation
ventricular septal defect
ventricular tachycardia
Wolff-Parkinson-White

xix


Notes on case-based
learning

Many medical schools have adopted an integrated approach to aspects of teaching, whereby a
patient with an important medical problem is chosen as a way of teaching different aspects of a
disease process and its effect on the patient and society. A single case can be used for the teaching
of anatomy, pathophysiology, history taking, physical examination, appropriate investigations
and management of the condition. Students are also expected to understand the epidemiology,
as well as ethical implications of the disease and its management.
The usual approach is for a student to be chosen to lead the discussion and prepare the
topic. A tutor is present to help keep the discussion directed, but most of the questioning of
the group is done by the nominated student. The whole group is given the topic in advance and
should prepare for the tutorial.
In the clinical years the tutorial is based on a patient who has been seen by the nominated

student. The student takes a detailed history and examines the patient. Access to the patient’s
test results is usually permitted and relevant results (e.g. blood tests, X-rays and reports) are
brought to the tutorial for discussion.
We have included examples of case-based learning presentations in important areas of
cardiology. The aspects of the condition that need discussion are outlined. Not all the answers
are provided, but areas that need research are indicated. Our hope is that these sections will
help both student presenters and the rest of the group to profit from this important learning
exercise.

xxi


Levels of evidence and grades
of recommendation    

ESC
Recommendations
Class I
Class II
Class IIa
Class IIb
Levels of evidence
Level of evidence A
Level of evidence B
Level of evidence C

Evidence or general agreement or both that a given treatment or
procedure is beneficial, useful and effective.
Conflicting evidence or divergence of opinion or both about the
usefulness/efficacy of a treatment or procedure.

Weight of evidence/opinion is in favour of usefulness/efficacy.
Usefulness/efficacy is less well established by evidence/opinion
Data derived from multiple randomised clinical trials or metaanalyses
Data derived from a single randomised clinical trial or large nonrandomised studies
Consensus of opinion of the experts and small studies, retrospective
studies, registries

NHF
Grades of recommendation
Grade A
Rich body of quality randomised controlled trials (RCT)
Grade B
Limited body of RCT data or high-quality non-RCT data
Grade C
Limited evidence
Grade D
No evidence available—panel consensus judgement
Levels of evidence (grade of recommendation)
Level I (A)
RCTs
Level II (B)
At least one RCT
Level III-1 (B)
Well designed pseudo-randomised trials (e.g. alternate allo­cation)
Level III-2 (B)
Comparative studies, cohort studies, case-controlled studies
Level III-3 (C)
Comparative studies with historical control, two or more single arm
studies
Level IV (C)

Case series

xxiii


1
CORONARY RISK
FACTORS
CHAPTER

Introduction
Cardiovascular disease (CVD) is the largest single cause of preventable death in most western
countries and is increasingly a cause of death in the rest of the world. Identification and control
of risk factors have the potential to prevent much of this mortality.
Although the precise cause of coronary artery disease is not known, researchers have
identified a number of risk factors that increase a person’s chance of developing symptomatic
ischaemic heart disease (IHD). These risk factors have been identified on the basis of epidemiological research and, in most cases, probable or definite mechanisms of action have been
demonstrated for these effects. The concept of risk factors did not exist until the 1960s when
data from the Framingham study began to emerge.
An assessment of a patient’s risk factors for coronary disease is an important part of the
management of cardiac symptoms. The presence of risk factors makes symptoms suggestive
of coronary disease more significant. However, risk factors do not predict acute ischaemia.1
Furthermore, the classic risk factors accounted for only 50% of the overall risk in the original
Framingham cohort.2 More recent evaluation using additional factors may have increased the
predictive value of risk factors.3
Everyone should at some stage have his or her cardiac risk factors assessed. Patients presenting with or without cardiac symptoms need periodic re-evaluation of their risk factors.
Much of this can be done by brief history taking and some simple investigations. This provides
an opportunity to make a decision about the overall or total risk for the patient and to give
appropriate advice and treatment.

The causes of coronary symptoms
The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion
that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing
is most often the result of atherosclerosis. Other much less common causes include:
1 coronary artery spasm (p. 146) (often in an already diseased segment of artery but sometimes
as a result of the use of cocaine)
2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment)
3 embolism (e.g. from an infected aortic valve)
4 congenital coronary abnormality
5 vasculitis.
Numerous other cardiac symptoms and problems can be the eventual result of atheromatous
coronary disease. These include myocardial infarction (Ch 4), cardiac failure (Ch 7), cardiac
arrhythmias (Ch 6) and some cardiac valve problems.

Risk factor mechanisms of action
Atherosclerosis is thought to result primarily from a disturbance of the vascular endothelium.
The final common pathway for the effects of endothelial dysfunction is largely through abnormalities of nitric oxide (NO) production. This chemical, released by a healthy endothelium, is
a potent vasodilator and has anti-inflammatory and other favourable actions on the arteries.
1




PRACTICA L C A R D I O L O G Y

Causes of this disturbance can be:

n m
 echanical (hypertension)
n chemical (oxidised lipids, components of cigarette smoke, hyperinsulinaemia) or

n due to immunological injury.
The damaged endothelium attracts inflammatory mediators, platelets and circulating lipids
and promotes fibroblast and smooth muscle proliferation. This results in the formation of a
plaque, which may narrow the arterial lumen.
Plaques can remain stable (or sometimes regress), enlarge, rupture or erode (more common
in diabetics). Most acute ischaemic events (acute coronary syndromes or acute myocardial
infarctions) are thought to be the result of further luminal narrowing caused by the formation
of partly or fully occlusive thrombus on a ruptured or eroded plaque. Coronary risk factors
may therefore operate because they are atherogenic or thrombogenic.

Plaque rupture
Plaque rupture may be at least partly an inflammatory process involving inflammatory cells,
cytokines and even bacteria. This may explain the association between inflammatory markers
such as high-sensitivity C reactive protein (hsCRP) and a risk of acute coronary events. Although
this association seems well established, there is still uncertainty about its role in overall risk
assessment (p. 21).4
Plaques at risk of rupture are called vulnerable plaques. They typically have a thin fibrous
cap. The shoulder regions (Fig 1.2 on p. 6) of these caps are at risk of rupturing and allowing material from within the plaque to come in contact with the blood stream. This material
is intensely thrombogenic. Stable fibrous plaques are much less likely to rupture in this way.
Efforts are underway to develop tests that can identify vulnerable plaques. This is not yet possible, but multi-slice CT scanning and possibly MRI angiography may increasingly be able to
provide information about plaque composition.

Risk factors
A risk factor is a demographic characteristic associated with an increased risk of ischaemic
heart disease when other variables have been controlled. The presence of a risk factor in
an individual increases his or her relative risk of a coronary event (angina, infarction or
death). The absolute risk of a coronary event depends on the individual’s total number
of risk factors and theirseverity (total risk). Important coronary risk factors are shown in
Table 1.1.
Risk assessment charts have been developed to estimate a patient’s cardiac risk over a

number of years using easily identified risk factors. There are charts for different populations.
The charts can be used to predict cardiovascular events or mortality (as in the NHF chart in
Fig 1.1 on p. 4) or cardiac risk (systematic coronary risk evaluation system or SCORE charts).
These charts can be very helpful in deciding when intervention to reduce risk is warranted; for
example, when anti-hypertensive treatment should be commenced for a patient with mild blood
pressure elevation.
Risk factor reduction involves assessing the presence, severity and importance of risk factors
for a patient, and modifying these where possible. Because the risk factors have a multiplicative
effect, modest reduction in a large number of factors may lower the risk more than aggressive
lowering of one factor. Put another way, someone with a number of mild risk factors may be
at more risk than someone with one moderate risk factor. For example, a man with a systolic
blood pressure of 180 mmHg, a cholesterol of 5 mmol/L and who smokes has a 10% 10-year
mortality risk on the SCORE risk chart published by the European Society of Cardiology (ESC),5
whereas a non-smoking man with a blood pressure of 140 mmHg and a cholesterol of 7 mmol/L
has a 5% 10-year mortality risk. Such charts may help convince patients of the need to control
multiple risk factors.


1 • C O R O N A R Y R I S K F A C T O R S



Table 1.1  Important coronary risk factors
1  Existing vascular disease (coronary, cerebral or peripheral)
2  Age
3  Dyslipidaemia
4  Smoking
5  Family history
6  Hypertension
7  Male sex/hormonal factors

8  Diabetes
9  Renal impairment
10  Obesity
11  Inactivity
12  Thrombogenic factors
13  Other dietary factors
14  Homocystinaemia
15  Psychological factors
16  Elevated hsCRP
17  Abnormal CT calcium score/coronary angiogram
18  Left ventricular hypertrophy (hypertensive patients)
19  Abnormal carotid intima-media thickness

It must be remembered that the strongest risk factor for ischaemic coronary events is known
coronary disease. Thus the absolute benefits of risk reduction are greatest for a patient with
coronary disease (secondary prevention) (Table 1.2). Asymptomatic individuals with risk factors
are the targets for attempts at primary prevention. Some risk factors are unalterable, such as age,
sex and family history.
The importance of risk factor control can be seen in the estimates of reduction in coronary
events shown in Table 1.3.

Existing vascular disease
A history of previous myocardial infarction, angina, cerebrovascular disease or peripheral arterial (vascular) disease is the major risk factor for future coronary events. Risk factor control is
of the utmost importance for such patients who have, on average, a 20% risk of further events
in the following 10 years.

Age
Eighty per cent of fatal myocardial infarcts occur in patients over the age of 65. Age alone is
therefore not a reason to ignore other risk factors, although obviously the patient’s likely life
expectancy may influence treatment. Not all interventional trials have included elderly patients,

but those that do have shown benefit. The prognosis for elderly patients who have a significant
ischaemic event is worse than for younger patients and they therefore have more to gain from
treatment that may reduce the incidence of these events.

Family history
A family history of coronary heart disease (CHD) is an independent risk factor when other factors
such as dyslipidaemia and hypertension are excluded. Coronary heart disease in a first-degree




PRACTICA L C A R D I O L O G Y

Figure 1.1  NHF risk assessment chart

relative (sibling or parent) under the age of 65 for a female relative or 55 for a male relative confers
a 2.5 times relative risk. It is important to find out what relatives were affected, their age and how
definite the diagnosis was. A possible stroke in a 90-year-old uncle is not especially important.

Dyslipidaemia
Many trials have shown that the risk of coronary artery disease is proportional to the total
serum cholesterol and low-density lipoprotein (LDL) levels and inversely proportional to the
high-density lipoprotein (HDL) levels. A raised triglyceride level is, on its own, only a modest
risk factor but becomes more important when associated with high serum cholesterol.


1 • C O R O N A R Y R I S K F A C T O R S



Table 1.2  Treatment priorities
1  People with established vascular disease
2  Asymptomatic people at high risk
(a) People with multiple risk factors: > 5% 10-year mortality risk
(b) People with severely abnormal single risk factors: cholesterol > 8 mmol/L, low-density
lipoprotein > 6, blood pressure > 180/110 mmHg
(c)  People with diabetes
3  People with adverse family history
4  All other patients seen in routine practice

Table 1.3  Average reductions in coronary events (benefits are greatest in patients
with highest total risk)
1  Smoking cessation: 50% reduction in coronary events6
2  Low-dose aspirin in high-risk patients: 25% reduction in coronary events7
3 20% reduction in total cholesterol with statin treatment: 30% reduction in coronary
events8
4  Treatment with pravastatin after acute coronary events: 22% reduction in mortality9
5 5–6 mmHg reduction in blood pressure: 15% reduction in coronary events
(40% risk reduction for stroke)10
6  30 minutes of moderate exercise a day: 18% reduction in coronary events11

In general, studies such as the 4S Trial have shown that a 10% reduction in total cholesterol
over three years confers a 20% reduction in ischaemic events and that the benefit increases with
the duration of treatment.12 This benefit occurs in both symptomatic (secondary prevention)
and asymptomatic (primary prevention) patients. The lipid trials show a greater reduction in
ischaemic events when cholesterol is lowered than when hypertension is controlled. The converse
is true for cerebrovascular disease.
Cholesterol lowering slows the progression of atheroma and may be associated with regression
of atheromatous lesions. However, the reduction in the occurrence of ischaemic events is greater
and occurs earlier than would be expected from the relatively minor changes in the angiographic

appearances of the coronary plaques of treated patients. The most likely explanation of this benefit
is that a lower serum cholesterol changes the lipid content of atheromatous plaques and makes
them more stable. This means they are less likely to rupture and attract thrombus (Fig 1.2).
Improvement in endothelial function and vascular reactivity has also been demonstrated
after cholesterol lowering.
Total cholesterol and LDL seem to have a weaker association with coronary artery disease
in women than in men, and even then only up to the age of 65. The benefit of treatment has
been shown for patients at least to the age of 80 and includes men and women. Patients in all
age groups who have a high total risk (i.e. other risk factors) benefit, even if they have not had
an ischaemic event (primary prevention).13
Some early trials conducted before the availability of statins appeared to show an association
between treatment and increased mortality from non-cardiac causes, but this seems not to be causative and the association has not been seen in the later very large cholesterol lowering trials.




PRACTICA L C A R D I O L O G Y

a

Lumen

Lipid-rich core

Thick fibrous cap
composed of collagen
and smooth muscle

Shoulder region

b
Lumen

Large lipid core

Thin fibrous cap with
inflammatory cells

Shoulder region

c

Lumen
Lipid core

Thrombus projecting
into the lumen

Rupture at the shoulder
of the thin fibrous cap

Figure 1.2  Arterial plaque showing lipid core and fibrous cap: (a) stable plaque, (b) unstable
plaque and (c) plaque rupture

An overview of lipid metabolism
As shown in Figure 1.3, the function of serum lipoproteins is to transport dietary and endogenous triglycerides and cholesterol. Dietary triglycerides and cholesterol are incorporated into
chylomicrons in the intestinal epithelium. From here, they are sent to peripheral tissues, are
acted on by the enzyme lipoprotein lipase and the triglycerides are broken down to release
fatty acids that are used by adipose and muscle cells. The remaining lipoprotein fragment, the
chylomicron, enters the circulation and contains mainly cholesterol. It is delivered to the liver

where the cholesterol is either converted to bile acids, excreted directly in bile or redistributed
to other tissues.


1 • C O R O N A R Y R I S K F A C T O R S



Endogenous lipid production
Excess carbohydrate is used to make triglycerides in the liver. These are secreted as very low­density lipoproteins (VLDL) and are acted on by lipoprotein lipase in peripheral tissues to
remove the triglycerides, leaving cholesterol-rich low-density lipoproteins. LDL carries cholesterol to peripheral tissues where it is used for membrane synthesis, steroid synthesis and bile acid
production in the liver itself. As cell membranes and lipoproteins break down, the cholesterol
is released into plasma and carried on HDL.

Low-density lipoproteins
Sixty to seventy per cent of total cholesterol is transported as LDL, and total cholesterol
measurements usually reflect LDL levels. In both males and females, coronary heart disease
risk is proportional to LDL and total cholesterol. As seen above, LDL supplies cholesterol to
peripheral tissues. High concentrations of LDL in the serum accelerate atheroma by interacting
with damaged endothelium. Oxidation of LDL accelerates this process.
A total cholesterol of 5.5 mmol/L, or LDL of 3.5 mmol/L, is usually considered the upper
limit of normal but even these levels seem to be responsible for an increased population risk of
atheroma. Populations with lower average levels than these have less coronary disease. Lower
levels are beneficial for patients with established coronary disease or multiple risk factors.
It is not yet clear whether the lowering of total cholesterol to less than 4.0 (LDL 2.0) provides
further benefit or whether a target level is indeed the correct approach. Trials of more aggressive
cholesterol lowering are underway.14 Although a reduced HDL level (< 1) is associated with
increased risk, there is no evidence as yet that raising HDL has beneficial effects. An elevation of
triglyceride levels (> 1.7) is also considered a marker of increased risk, but there is no evidence
to what level they should be reduced.

Exogenous

Dietary TG
& Chol.

Endogenous

Carries 3/4 of
total chol.

Intestinal cell

Chylom.
(TG & Chol.)

LDL

Endogenous
chol.

LDL
receptor
tissues

LIVER
VLDL
Endothelium
(Lipoprotein lipase)

FFA

Monog.
Chylomic.
remnant (Chol.)

to adipose tissue and muscles

Endothelium
(Lipoprotein lipase)

HDL
and
FFA
Plasma LCAT

FFA

IDL

to adipose tissue and muscles

Figure 1.3  Lipid metabolism
Chol = cholesterol; FFA = free fatty acids; HDL = high-density lipoprotein; IDL = intermediate-density
lipoprotein; LCAT = lecithin cholesterol acyltransferase; monog. = monoglyceride; TG = triglycerides;
VLDL = very low-density lipoprotein.




PRACTICA L C A R D I O L O G Y

Total cholesterol and LDL levels can be affected by many factors (Table 1.4).
Very high LDL and total cholesterol levels can be associated with clinical signs such as tendon
xanthomas (often on the dorsum of the hands), eruptive xanthomata (on the elbows and knees)
and xanthelasma (fatty deposits around the eyes) (Fig 1.4).
Acute illness, such as myocardial infarction or an intervention such as coronary artery
bypass grafting, can be associated with reduced cholesterol levels for 1–2 months. LDL and total
cholesterol levels are not affected by fasting.
Table 1.4  Factors that affect LDL levels
Factors that increase LDL levels

Factors that decrease LDL levels

1  High intake of saturated fat
2 High intake of dietary cholesterol (less
important than saturated fat intake)
3  Diuretics
4  Cyclosporine
5  Some progestogens
6 Secondary causes: anorexia nervosa,
hypothyroidism, Cushing’s syndrome,
porphyria, primary biliary cirrhosis

1 High intake of omega-3 fatty acids (fish,
olive oil, canola)
2 High intake of soluble dietary fibres
(legumes)
3 High intake of dietary anti-oxidant
nutrients (oxidation may make existing

LDL more atherogenic)
4  Plant sterols

Figure 1.4  Xanthelasmata

LDL levels are calculated according to the following formula: LDL = total cholesterol –
HDL  –  (0.45 × triglycerides). This formula is not accurate when triglycerides are greater than
4 mmol/L.
Cholesterol levels are physiologically increased in pregnancy, and their measurement during
pregnancy is not useful.


1 • C O R O N A R Y R I S K F A C T O R S



High-density lipoproteins
HDL levels have an inverse relationship to coronary events in both men and women. Those
patients with an HDL level less than 0.9 have an eightfold increase in coronary events over those
patients with a level greater than 1.5 mmol/L, when other factors are controlled. HDL levels
reflect the breakdown of triglycerides and LDL, and HDL levels are usually inversely related to
triglyceride levels.
The ratio of total cholesterol to HDL is important, especially when total cholesterol is in the
‘equivocal’ range of 5.5–6.5 mmol/L. Total cholesterol/HDL should be less than 5. This ratio
has been incorporated into a number of risk assessment tables, such as SCORE.
A low HDL suggests the need to lower LDL and correct those factors that lower HDL
(Table 1.5).
Table 1.5  Factors that affect HDL levels
Factors that increase HDL levels

Factors that reduce HDL levels

1  Oestrogen
2  Exercise
3 Small amounts of alcohol (10–20 g
per day in men)

1  Smoking
2  Obesity
3  Inactivity
4  Hypothyroidism
5  Postmenopausal state
6  Beta-blockers

Triglycerides
The independent effect of triglyceride levels is weak, and high triglyceride levels are often associated with other risk factors (e.g. low HDLs). Secondary causes of high triglycerides (Table 1.6)
are common and confuse the picture, as does the fact that serum levels can vary greatly with
fasting and recent alcohol intake.
The combination of high triglycerides and elevated LDL (combined dyslipidaemia) is associated with a marked increase in coronary disease risk. Isolated extremely high triglycerides
(greater than 15 mmol/L) are a risk factor for pancreatitis rather than vascular disease.
Modest elevations of triglycerides can usually be managed by weight control, a reduction in
alcohol consumption and changes in medication.

Table 1.6  Factors that increase triglyceride levels
1  Obesity
2  Alcohol
3  Diabetes
4  Oestrogen (including HRT in 20% of users)
5  Diuretics
6  Beta-blockers

7  Secondary causes:
•  Cushing’s syndrome
•  acromegaly
•  uraemia
•  acute hepatitis
8  High triglycerides and low HDLs are associated with insulin resistance.


10

PRACTICA L C A R D I O L O G Y

Patterns of dyslipidaemia
Dyslipidaemia can be:
n sporadic (the most common cause)
n inherited (Table 1.7)
n secondary (Table 1.8).
There are different patterns of dyslipidaemia classified according to the lipoprotein abnormality
and which lipids are abnormal. These are not as important for management as they once were, but
the choice of treatment may still be influenced by the pattern of the abnormality (Table 1.7).
Secondary causes of dyslipidaemia should be considered if the dyslipidaemia is severe and
does not respond to dietary measures (Table 1.9).
Table 1.7  Patterns of dyslipidaemia
Pattern

Elevated
lipoprotein

Elevated lipid

Frequency

I
IIa
IIb
III
IV
V

Chylomicrons
LDL
LDL, VLDL
Chylomicrons, IDL
VLDL
VLDL, chylomicrons

Trig
Chol.
Chol., trig.
Trig., chol.
Trig.
Trig., chol.

Very rare
10%
40%
Very rare
45%
Rare

Table 1.8  The genetic dyslipidaemias
Disorder

Defect

Familial
chylomicronaemia

Lipoprotein
lipase defect

Familial
chylomicronaemia
Familial type III
(dysbetalipo­
proteinaemia)

Apolipoprotein
CII deficiency
Apolipoprotein
BIE receptor
deficiency

Familial hyper­
cholestrolaemia
(AUTO DOM
1:1500)
Familial hypertri­
glyceridaemia
Multiple

lipoprotein
hyperlipidaemia

Lipoprotein
elevation

Clinical
findings

Chylomicrons

Drug
Pattern treatment

Eruptive
xanthomata
Pancreatitis
Chylomicrons, Pancreatitis
VLDL
Chylomicron Eruptive
remnants
xanthomata
Atherosclerosis

I

None

I, V

None

III
IIa, IIb
IV

Deficient LDL
receptor

LDL

Xanthomata
Atherosclerosis

IIa

Fibrates
Statins
Nicotinic
acid
Resin
Statins

Defect
unknown

VLDL

Xanthomata

IV

Defect
unknown

LDL, VLDL

Atherosclerosis

IIa, IIb
IV

Fibrates
Nicotinic
acid
Fibrates
Nicotinic
acid
Statins

AUTO DOM = autosomal dominant inheritance; LDL = low-density lipoproteins; VLDL = very low-density
lipoproteins.


1 • C O R O N A R Y R I S K F A C T O R S

11

Table 1.9  Secondary causes of dyslipidaemia
System

Disorder

Lipoprotein elevated

Pattern

Endocrine

Diabetes
Cushing’s syndrome
Acromegaly
Hypothyroidism
Anorexia nervosa
Porphyria
Alcohol
Oestrogen-containing
contraceptive pill
Glucocorticoids
Uraemia
Nephrotic syndrome
Primary biliary cirrhosis
Acute hepatitis
Systemic lupus
erythematosus (SLE)
Monoclonal gammopathy
Burns, acute myocardial
infarction (AMI)

VLDL, chylomicrons

VLDL
VLDL
LDL
LDL
LDL
Chylomicrons, VLDL
Chylomicrons, VLDL

IV
IV
IV
IIa
IIa
IIa
IV
IV

Drugs

Renal
Hepatic
Immune

Injury

LDL, VLDL
VLDL
LDL, VLDL
LDL
VLDL

Chylomicrons

IV

Chylomicrons, VLDL
LDL

Treatment of dyslipidaemia
The important components of a treatment program for dyslipidaemia are as follows:
1 calculate the patient’s total risk
2 reduce the patient’s weight (reduces triglycerides, cholesterol)
3 increase the patient’s exercise activity (increases HDL, aids weight management)
4 modify the patient’s diet, as follows:
• ensure maximum of 30% kJ from fat
• ensure maximum of 30% fat as saturated fat
• increase plant and fish sources of fat
• increase anti-oxidant nutrients from food
• reduce alcohol intake if triglyceride level or blood pressure is high
5 treat secondary causes (drugs, diabetes, hypothyroidism)
6 modify other risk factors (e.g. smoking) to reduce overall risk
7 consider drug treatment.
By ranking patients according to their risk of future coronary events it is possible to tailor treatment (especially drug treatment) appropriately. This is the basis for the current re­commendations
for lipid management in the Pharmaceutical Benefits Schedule. This rather complicated schedule
tries to take into account the importance of combinations of risk factors (Table 1.10).
Drug treatment should be delayed in most patients without existing coronary disease until after
six weeks to three months of dietary and lifestyle intervention, with the possible ­exception of those
at very high risk. At present, the following drugs are used in the treatment of dyslipidaemia:
n statins (HMGcoA reductase inhibitors)
n absorption inhibitors
n resins