100 Questions in Cardiology
100 Questions in Cardiology
100 Questions in Cardiology
Cardiology
Diana Holdright
BMJ Books
Edited by
Diana Holdright
Consultant Cardiologist, Department of Cardiology,
UCL Hospitals, London, UK
and
Hugh Montgomery
Honorary Consultant, UCL Hospitals Intensive Care Unit,
and
Lecturer in Cardiovascular Genetics, UCL Hospitals,
The Middlesex Hospital, London, UK
BMJ
Books
Contents
Contributors
Introduction
1
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5
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8
9
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xii
xvii
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105
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137
Contents
66
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ix
139
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x
82
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208
Contents
100 Which patients should undergo preoperative
non-invasive investigations or coronary
angiography?
101 Which factors predict cardiac risk from general
surgery and what is the magnitude of the risks
associated with each factor?
Index
xi
210
212
216
Contributors
Prithwish Banerjee
Specialist Registrar in Cardiology, Hull and East Yorkshire
Hospitals, Hull Royal Infirmary, Hull, UK
Matthew Barnard
Consultant Anaesthetist, UCL Hospitals, The Middlesex Hospital,
London,UK
J Benhorin
Associate Chief, The Heiden Department of Cardiology, Bikur
Cholim Hospital and The Hebrew University, Jerusalem, Israel
John Betteridge
Professor of Endocrinology and Metabolism, UCL Hospitals, The
Middlesex Hospital, London, UK
Kieran Bhagat
Regional Facilitator (Cardiovascular Programme), World Health
Organisation and Honorary Professor of Clinical Pharmacology,
Medical School, University of Zimbabwe, Harare, Zimbabwe
Aidan Bolger
Clinical Research Fellow, Department of Cardiac Medicine,
National Heart and Lung Institute, London, UK
David J Brull
British Heart Foundation Junior Fellow, UCL Cardiovascular
Genetics, Rayne Institute, London, UK
R Cesnjevar
Cardiothoracic Surgeon, Great Ormond Street Hospital for
Children NHS Trust, London, UK
Peter Clifton
Director Clinical Research Unit, CSIRO Health Sciences and
Nutrition, Adelaide, Australia
John Cockcroft
General Practitioner, CAA Authorised Medical Examiner, Billericay
Health Centre, Billericay, Essex, UK
Martin Cowie
Senior Lecturer in Cardiology and Honorary Consultant
Cardiologist, University of Aberdeen and Grampian University
Hospitals Trust, Department of Cardiology, Aberdeen Royal
Infirmary, Aberdeen, UK
xii
Contributors
xiii
Seamus Cullen
Senior Lecturer, Department of Grown Up Congenital Cardiology,
UCL Hospitals, The Middlesex Hospital, London, UK
Vincent S DeGeare
Lecturer, Great Ormond Street Hospital for Children NHS Trust,
London, UK
Vic Froelicher
Consultant Cardiologist, Cardiology Division, Veterans Affairs
Palo Alto Health Care System, Stanford University, California, USA
Anthony Gershlick
Professor of Medicine, Department of Academic Cardiology,
University of Leicester, UK
Cindy L Grines
Director of the Cardiac Catheterization Laboratories, Division of
Cardiology, William Beaumont Hospital, Royal Oak, Michigan,
USA
Suzanna Hardman
Senior Lecturer in Cardiology with an interest in Community
Cardiology, University College London Medical School, and
Honorary Consultant Cardiologist, the UCL and Whittington
Hospitals
Address for correspondence: UCLMS (Whittington campus),
Academic & Clinical Department of Cardiovascular Medicine,
Whittington Hospital, London, UK
Martin Paul Hayward
Cardiothoracic Surgeon, The Austin and Repatriation Medical
Centre, Melbourne, Australia
Daniel E Hillman
Professor and Chair, Department of Pharmacy Practice, Creighton
University, Omaha, Nebraska, USA
Aroon Hingorani
Senior Lecturer in Clinical Pharmacology and Therapeutics,
British Heart Foundation Intermediate Fellow, Centre for Clinical
Pharmacology, UCL, Rayne Institute, London, UK
Diana Holdright
Consultant Cardiologist, Department of Cardiology, UCL
Hospitals, The Middlesex Hospital, London, UK
xiv
Rachael James
Cardiology SpR, The Royal Sussex County Hospital Brighton,
Brighton, UK
Roy M John
Associate Director, Cardiac Electrophysiology Laboratory, Lahey
Clinic Medical Center, Burlington, MA, USA
Robin Kanagasabay
SpR Cardiothoracic Surgery, St Georges Hospital Medical School,
London, UK
RA Kenny
Head of Department of Medicine (Geriatric), University of
Newcastle Upon Tyne, Institute for Health of the Elderly, Royal
Victoria Infirmary, Newcastle Upon Tyne, UK
Brendan Madden
Consultant Cardiothoracic and Transplant Surgeon, Cardiothoracic
Transplant Unit, St Georges Hospital, London, UK
Kenneth W Mahaffey
Assistant Professor of Medicine, Duke Clinical Research Institute,
Durham, NC, USA
Niall G Mahon
Specialist Registrar in Cardiology, St Georges Hospital Medical
School, London, UK
Joseph F Malouf
Associate Professor, Mayo Medical School, and Consultant, Division
of Cardiovascular Diseases and Internal Medicine, Mayo Clinic,
Rochester, Minnesota, USA
Richard Mansfield
Lecturer in Cardiology, Cardiovascular Repair and Remodeling
Group, Middlesex Hospital, London, UK
W McKenna
Registrar in Cardiology, St Georges Hospital Medical School,
London, UK
Hugh Montgomery
Honorary Consultant, UCL Hospitals Intensive Care Unit, and
Lecturer in Cardiovascular Genetics, UCL Hospitals, London, UK
Contributors
xv
Marc R Moon
Assistant Professor of Cardiothoracic Society Department of
Cardiothoracic Surgery, Washington University School of
Medicine, St Louis, Missouri, USA
Stan Newman
Professor of Psychology, Deptartment of Psychological Medicine,
UCL Hospitals, The Middlesex Hospital, London, UK
Petros Nihoyannopoulos
Senior Lecturer and Consultant Cardiologist, Cardiology
Department, Imperial College School of Medicine, National Heart
and Lung Institute, Hammersmith Hospital, London, UK
Michael S Norrell
Consultant Cardiologist, Hull and East Yorkshire Hospitals, Hull
Royal Infirmary, Hull, UK
Lionel H Opie
Co-Director, Cape Heart Centre and Medical Research Council,
Inter-University Cape Heart Group, University of Cape Town,
and Consultant Physician, Groote Schuur Hospital, Cape Town,
South Africa
Diarmuid OShea
Consultant Physician, Department of Geriatric Medicine, St
Vincents University Hospital, Dublin, Ireland
Krishna Prasad
Specialist Registrar in Cardiology, Department of Cardiology,
University of Wales College of Medicine, Cardiff, UK
Liz Prvulovich
Consultant Physician in Nuclear Medicine, Institute of Nuclear
Medicine, Middlesex Hospital, London, UK
Henry Purcell
Senior Fellow in Cardiology, Royal Brompton and Harefield NHS
Trust, London, UK
Michael Schachter
Senior Lecturer in Clinical Pharmacology, Department of Clinical
Pharmacology, Imperial College School of Medicine, and
Honorary Consultant Physician, St Marys Hospital, London, UK
Rakesh Sharma
Clinical Research Fellow, Department of Cardiac Medicine,
National Heart and Lung Institute, London, UK
xvi
Alistair Slade
Consultant Cardiologist, Royal Cornwall Hospitals Trust, Treliske
Hospital, Truro, Cornwall, UK
Simon Sporton
Specialist Registrar in Cardiology, Department of Cardiology, St
Bartholomews Hospital, London, UK
Mark Squirrell
Senior Technician, Department of Cardiology, UCL Hospitals, The
Middlesex Hospital, London, UK
Matthew Streetly
Specialist Registrar in Haematology, Department of Haematology,
University College Hospital, London, UK
Jan Stygall
Clinical Psychologist, The Middlesex Hospital, London, UK
DP Taggart
Consultant Cardiothoracic Surgeon, John Radcliffe Hospital,
Oxford, UK
Sara Thorne
Consultant Cardiologist, Department of Cardiology, Queen
Elizabeth Hospital, Birmingham
Adam D Timmis
Consultant Cardiologist, Department of Cardiology, London
Chest Hospital, London, UK
Tom Treasure
Consultant Cardiothoracic Surgeon, Department of Cardiothoracic
Surgery, St Georges Hospital, London, UK
Victor T Tsang
Consultant Cardiothoracic Surgeon, Great Ormond Street Hospital
for Children NHS Trust, London, UK
Jonathan Unsworth-White
Consultant Cardiothoracic Surgeon, Department of Cardiothoracic
Surgery, Derriford Hospital, Plymouth, Devon, UK
Peter Wilson
Consultant Microbiologist, Department of Clinical Microbiology,
University College Hospital, London, UK
Introduction
This book differs from most other available cardiology texts. We
have designed it to provide didactic answers to specific questions,
wherever possible. Some are everyday questions. Others deal
with less common situations, where an answer is often not
readily found. The book is suitable for all grades of doctor,
cardiologist and physician alike.
Responses have been kept as brief as possible and practical. A
few important topics defied our editorial culling and were given
more space. The aim was not to review the entire literature, but
rather to present the conclusions which that author has reached
from such evaluation, combined with experience. Where helpful
or necessary, a few relevant references have been provided with
the answer.
We hope that the text can be read in several ways to suit the
reader in one go, referred to on the wards or in clinic or dipped
into for pleasure and education. The short question and answer
format should permit such an approach.
We have tried to produce a selection of topics spanning most
aspects of cardiovascular disease but there will, of course, be
obvious questions which we have not posed. Please write to us
c/o BMJ Books, BMA House, Tavistock Square, London WC1H
9JR, with any suggestions for questions you would like to see
answered in a future edition. Finally, because the answers given
are personal to each author, you may disagree with some
responses. Please feel free to do so. This is not a set of guidelines
set in stone.
Diana Holdright and Hugh Montgomery
Acknowledgement
We would like to acknowledge Dr Chris Newman whose initial
suggestion led to this book.
xvii
Difference in usual
SBP (mmHg)
DBP (mmHg)
% increase in risk of
Stroke
CHD
9
14
19
34
46
56
5
7.5
10
21
29
37
3540
2025
3145
823
Further reading
McMahon S. Blood pressure and risks of cardiovascular disease. In: Swales
JD, ed. Textbook of hypertension. Oxford: Blackwell Scientific,1994:46.
Collins R, Peto R. Antihypertensive drug therapy. Effects on stroke and
coronary heart disease. In: Swales JD, ed. Textbook of hypertension. Oxford:
Blackwell Scientific, 1994:1156.
Further testing
If routine testing reveals abnormalities or the patient has been
referred for resistant hypertension then further investigations
are justified. These should be determined by clinical suspicion
(for example, symptoms or signs of phaeochromocytoma,
Cushingoid appearance etc.) and the outcome of routine investigations (for example proteinuria, haematuria, hypokalaemia etc.).
Urinalysis. 24 hour quantification of protein, electrolytes, and
creatinine clearance.
Radiological. Initially, ultrasound examination of the abdomen
screens renal size, anatomy and pelvicalyceal disease.
Computerised tomography of the abdomen scan has greater
sensitivity for adrenal tumours and phaeochromocytomas.
MIBG scanning will help identify extra-adrenal phaeochromocytoma. Renal angiography will identify renal artery
stenosis.
Renal biopsy should be performed if microscopy or plasma
immunological screening is suggestive of systemic
inflammatory or renovascular disease.
Young patients
Since age is a major determinant of absolute risk, treatment
thresholds based on absolute risk levels will tend to postpone
treatment to older ages. However, younger patients with elevated
BP who have a low absolute risk of stroke and CHD exhibit
greatly elevated relative risks of these events compared to their
normotensive age-matched peers. Deciding on the optimal age of
treatment in such individuals presents some difficulty and the
correct strategy has yet to be determined.
Elderly patients
The absolute risk of CHD and stroke in elderly hypertensive
patients is high and, consequently, the absolute benefit from
treatment is much greater than in younger patients. Decisions to
treat based on absolute risk are therefore usually straightforward.
However, there is little in the way of firm trial evidence for the
benefits of treatment in individuals aged more than 80. In these
patients, decisions could be made on a case-by-case basis taking
into account biological age.
References
1 New Zealand guidelines and tables available at http: //www.nzgg.org.nz
2 Hingorani AD, Vallance P. A simple computer programme for guiding
management of cardiovascular risk factors and prescribing. BMJ
318: 1015
1999;3
3 Hansson L, Zanchetti A, Carruthers SG et al. Effects of intensive blood
pressure lowering and low-dose aspirin in patients with hypertension:
351: 175562.
principal results of the HOT trial. Lancet 1998;3
Further reading
Ramsay LE et al. British Hypertension Society guidelines for hyper319: 6305.
tension management 1999: summary. BMJ 1999;3
10
11
12
13
3 Cavis BR, Cutler JA, Gordon DJ et al. Rationale and design for the antihypertensive and lipid lowering treatment to prevent heart attack trial
(ALLHAT). Am J Hypertens 1996; 9: 34260.
14
REVIEW
Adequacy of treatment: BP and cholesterol target
Side effects from treatment
Lifestyle modifications
*
Sitting position. Mean of 2-3 measurements over 46 weeks unless severity of BP dictates
earlier treatment.
** Abnormalities identified from history, examination or baseline screen dictate further investigation to confirm/exclude renal parenchymal, renovascular, endocrine or other secondary
causes of hypertension.
*** The presence of hypertensive retinopathy or LVH is an indication for BP lowering irrespective
of the absolute BP level.
****For references to risk calculators see Qu4, page 7.
Reference: Vallance P. CME Cardiology II. Hypertension, J Roy Coll Phys Lon 1999; 33: 119-23
15
16
17
18
19
20
21
by 1020%. Fibrates also lower LDL cholesterol in primary hypercholesterolaemia (type IIa hyperlipidaemia) by 1525%. They are
first line treatment for severe hypertriglyceridaemia and (in
combination with statins) in severe mixed lipaemia. They are
second line drugs in patients intolerant of statins for hypercholesterolaemia and mixed lipaemia. Data from end point clinical
trials are not extensive and concerns over fibrate safety have
remained since the original WHO clofibrate trial which was associated with increased non-CHD deaths. However the Helsinki
Heart Study showed a positive outcome and the recent VA HIT
trial, again with gemfibrozil, was positive. However the recent
secondary BIP prevention study with bezafibrate was negative.
High dose fish oil capsules have a role in the treatment of
severe hypertriglyceridaemia. They reduce hepatic VLDL output.
In practice they are used in combination with fibrates and
occasionally statins. The author has also used them in rare
patients with familial hypertriglyceridaemia during pregnancy to
protect against pancreatitis.
Further reading
Betteridge DJ, Morrell JM. Clinicians guide to lipids and coronary heart
disease. London: Chapman & Hall Medical, 1998.
Betteridge DJ, Illingworth DR, Shepherd J, eds. Lipoproteins in health and
disease. London: Edward Arnold, 1999.
22
Statins
These are generally well tolerated. In the major end point trials,
adverse events were little different from placebo.
Myositis, defined as painful, tender muscles with a high CPK, is
rare, occurring with a frequency of lower than 1 in 10,000
patient years. Routine CPK measurement is not recommended
as modest elevations (generally secondary to physical activity)
are quite common even in patients on placebo treatment. It is
important to remember that black patients have higher CPKs
than whites, and that hypothyroidism is an important cause of
raised CPK. Patients should be warned to stop the drugs if
severe muscle pain is experienced.
Liver function should be checked prior to statin therapy as
abnormal hepatic function and high alcohol intake are relative
contraindications for these drugs which are metabolised
principally through the liver. Approximately one in 400 patients
will develop greater than 3-fold transaminase increases which
revert to normal with dose reduction or stopping of the drug. They
can be used in moderate renal impairment. It is good practice to
check liver function tests periodically during statin therapy.
Fibrates
These are also generally well tolerated but can also cause myositis
and hepatic dysfunction. Clofibrate (in the WHO trial) was
associated with increased gallstone formation through increased
biliary cholesterol content. This drug is now redundant and the
newer fibrates have less impact on biliary composition. Doubt
remains concerning long term safety with the fibrate class in
terms of non-cardiac mortality. However the WHO clofibrate trial
was the major contributor to this concern. The recent VA HIT
study (reported at the AHA meeting in Dallas, November 1998)
showed that gemfibrozil reduced risk by approximately a quarter
23
Drug interactions
Care should be exercised when statins are combined with fibrates
or used in patients taking cyclosporin (e.g. transplant patients) as
the risk of side effects (particularly myositis) is increased. Dosage
should be limited in transplant patients taking cyclosporin as
drug levels are increased. Care should also be exercised when
used in combination with drugs metabolised through the
cytochrome P450 pathway (e.g. antifungals, erythromycin) as
there is a potential for interactions. There is a theoretical potential
for interaction with warfarin but the author has not found this a
problem in practice.
Resins
The resins are associated with a high frequency of gastrointestinal
side effects which limit their use. They may interfere with the
absorption of other drugs so should be taken either one hour
before or four hours after other therapeutic agents. The resins
theoretically may interfere with the absorption of fat soluble
vitamins and folic acid but this is not a major problem in practice.
However, perhaps with increasing indication of the role of homocysteine as a risk factor, folic acid supplements might be
recommended in patients on resins.
24
25
26
27
28
Table 15.1
Absolute
Acute myocardial infarction (within 3 to 5 days)
Unstable angina
Uncontrolled cardiac arrhythmias causing symptoms of
haemodynamic compromise
Active endocarditis
Symptomatic severe aortic stenosis
Uncontrolled symptomatic heart failure
Acute pulmonary embolus or pulmonary infarction
Acute non-cardiac disorder that may affect exercise
performance or be aggravated by exercise (e.g. infection, renal
failure, thyrotoxicosis)
Acute myocarditis or pericarditis
Physical disability that would preclude safe and adequate test
performance
Thrombosis of lower extremity
Relative
Left main coronary stenosis or its equivalent
Moderate stenotic valvular heart disease
Electrolyte abnormalities
Significant arterial or pulmonary hypertension
Tachyarrhythmias or bradyarrhythmias
Hypertrophic cardiomyopathy
Mental impairment leading to inability to cooperate
High degree atrioventricular block
*Relative contraindications can be superseded if benefits outweigh risks of
exercise.
From Fletcher GF, Balady G, Froelicher VF et al. Exercise standards: a statement
for Healthcare Professionals from the American Heart Association Writing
9: 580615. (Reproduced by permission.)
Group. Circulation 1995;9
References
1. Gibbons RJ, Chatterjee K, Daley J et al. ACC/AHA/ACP-ASIM guidelines for the management of patients with chronic stable angina: a
report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines. J Am Coll Cardiol
33: 2092197.
1999;3
29
30
31
32
33
34
35
Beta blockers
In the absence of contraindications, beta blockers are preferred as
initial therapy for angina.1 Evidence for this is strongest for
patients with prior MI. Long term trials show that there is a 23%
reduction in the odds of death among MI survivors randomised to
beta blockers.2
Calcium antagonists
Calcium antagonists (especially those which reduce heart rate)
are suitable as initial therapy when beta blockers are contraindicated or poorly tolerated. Outcome trials are underway but
there is currently little evidence to suggest they improve prognosis post-MI, although diltiazem and verapamil may reduce the
risk of reinfarction in patients without heart failure,3 and
amlodipine may benefit certain patients with heart failure.
Other agents
Nicorandil, a potassium channel opener with a nitrate moiety,
and the metabolic agent, trimetazidine, may also be useful, but
these have not been tested in outcome studies.
Many patients with exertional symptoms may need a
combination of anti-anginals, but there is little evidence to
support the use of triple therapy. Patients requiring this should
be assessed for revascularisation. There are no important differences in the effectiveness of the principal classes of anti-anginal
36
37
38
Risk stratification
The initial step in risk stratification is an ECG. Patients with
acute ST elevation are considered to have an acute MI and
require reperfusion therapy according to local protocols.
Individuals with ST depression are also at high risk and require
admission for further evaluation. The presence of a positive
troponin T in this group further confirms them as high risk. In
situations where patients present either with a normal ECG or
with T wave changes only, the value of a positive troponin T is
vital in risk stratification. All patients who are troponin T
positive should be considered as high risk, whilst in contrast, a
negative troponin T 12 hours or more after the onset of
symptoms puts the individual in a low risk group. If the result
of a negative troponin T test taken 12 hours or more after the
onset of chest pain is taken in conjunction with a pre-discharge
exercise test, this further reduces the chance of an inappropriate
discharge.4 Figure 20.1 illustrates one possible management
algorithm.
39
ST elevation
ST depression
Acute MI
High-risk
Admit
Troponin T
Positive
High-risk
Admit
Negative
Positive
High-risk
Admit
Negative
Low-risk
40
Conclusion
Troponin T has a vital role in the triage of patients presenting
with chest pain. A positive test identifies high-risk individuals
who may benefit from aggressive anti-platelet therapy or early
intervention, whilst negative troponin T tests 12 or more hours
after the onset of symptoms identify those at low risk who can be
considered for early hospital discharge.
References
1 Hamm CW, Goldmann BU, Heeschen C et al. Emergency room triage of
patients with acute chest pain by means of rapid testing for cardiac
troponin T or troponin I. N Engl J Med 1997; 337: 164853.
2 Lindahl B, Venge P, Wallentin L, for the FRISC Study Group. Relation
between troponin T and the risk of subsequent cardiac events in
93: 165157.
unstable coronary artery disease. Circulation 1996;9
3 Ohman EM, Armstrong PW, Christensen RH et al. for the GUSTO IIa
Investigators. Cardiac troponin T levels for risk stratification in acute
335: 133341.
myocardial ischemia. N Engl J Med 1996;3
4 Lindahl B, Andren B, Ohlsson J et al. Risk stratification in unstable
coronary artery disease. Additive value of troponin T determinations
18: 76270.
and pre-discharge exercise tests. Eur Heart J 1997;1
41
42
References
1 Van Miltenburg AJ, Simoons ML, Veerhoek RJ et al. Incidence and
follow-up of Braunwald subgroups in unstable angina pectoris. J Am
25: 128692.
Coll Cardiol 1995;2
2 Yusuf S, Flather M, Pogue J et al. for the OASIS (Organisation to
Assess Strategies for Ischaemic Syndromes) Registry Investigators.
Variations between countries in invasive cardiac procedures and
outcomes in patients with suspected unstable angina or myocardial
352: 50714.
infarction without initial ST elevation. Lancet 1998;3
3 Boden WE, ORourke RA, Crawford MH et al. for the Veterans Affairs
Non-Q Wave Infarction Strategies in Hospital (VANQWISH) Trial
Investigators. Outcomes in patients with acute non-Q-wave
myocardial infarction randomly assigned to an invasive as compared
338 :
with a conservative management strategy. N Engl J Med 1998;3
178592.
43
Anti-ischaemic therapy
Nitrates relieve ischaemic pain but there is no evidence of
prognostic benefit from their use.
Calcium antagonists are effective anti-ischaemic and vasodilator
drugs. However, in the absence of beta blockade, nifedipine
should be avoided due to reflex tachycardia. Verapamil and
diltiazem have useful rate-lowering properties, but should be
used cautiously in patients with ventricular dysfunction and
patients already taking beta blockers.
Beta-adrenoceptor blockers are an important treatment in unstable
angina, not only relieving symptoms but also reducing the
likelihood of progression to infarction and cardiac death. There is
no evidence to favour one class of beta blocker over another.
Antithrombotic therapy
Aspirin has an important and undisputed role in the treatment of
unstable angina, reducing the risk of fatal/non-fatal MI by 70%
acutely, by 60% at 3 months and by 52% at 2 years.1 A first dose of
160-325mg should be followed by a maintenance dose of 75mg
daily.
Ticlopidine and clopidogrel, antagonists of ADP-mediated platelet
aggregation, are possible alternatives in patients unable to take
aspirin, although ticlopidine has important side effects and trials
using clopidogrel have yet to be completed (e.g. CURE study).
44
45
46
47
48
Pharmacological approaches
To date no pharmacological agent has had a significant effect on
reducing the incidence of restenosis. There are a number of
reasons for this including the lack of correlation between animal
models and the situation in man, the drug doses used or the
power of some of the trials. Recent interest has focused on the use
of antiproliferative agents such as paclitaxel and tranilast.
The antioxidant Probucol has been shown to be effective in
limiting restenosis after balloon angioplasty. However, lack of
licensing in some countries, limited data on the clinical impact of
treatment, and the fact that pre-treatment for 4 weeks is required,
may all be factors in limiting its use.
Gene therapy involves the transfer of DNA into host cells with
the aim of inducing specific biological effects. Vectors for gene
delivery include plasmid DNA-liposome complexes and viral
vectors such as the replication deficient recombinant adenovirus.
Design of appropriate delivery devices has taken a number of
directions including double balloon catheters and perforated
balloons allowing high pressure injection through radial pores.
Various approaches have been used to limit experimental
restenosis by inducing cell death (e.g. fas ligand gene to induce
apoptosis), inhibiting smooth muscle cell migration (e.g. overexpression of TIMP-1 and eNOS) or by inhibiting cell cycle
regulators of smooth muscle cell proliferation (e.g. antisense
49
Brachytherapy
Over the last few years there has been considerable interest in
intravascular brachytherapy (radiation therapy). The ability of
ionising radiation to halt cell growth by damaging the DNA of
dividing cells, and the view that neointimal hyperplasia
represented a benign proliferative condition led to its application
in vascular disease. A variety of catheter based delivery systems
and radioactive stents are available using either beta (e.g. 32P) or
gamma (e.g. 192Ir) sources. A number of studies have shown
impressive results on reducing restenosis rates and many more
are underway but enthusiasm for the technique should be
tempered because there are concerns about long term safety.
Indeed there are very recent reports of unexpected late thrombotic
occlusion.
Photodynamic therapy (PTD) involves the local activation of a
systemically administered photosensitising agent by nonionising radiation in the form of non-thermal laser light. Many of
the sensitising agents that have been studied have been products
of porphyrin metabolism such as 5-aminolaevulinic acid. Much
of the work in this field to date has been in the treatment of cancer
but there is an accumulation of small and large animal data
showing a reduction in neointimal hyperplasia after balloon
injury. Favourable vessel wall remodelling has also been
observed in a pig model of balloon coronary and iliac angioplasty.
Reports of the clinical application of photodynamic therapy are
limited but a clinical pilot study of adjuvant PDT in superficial
femoral angioplasty showed it to be a safe and effective
technique. Further work needs to be done to establish its role in
coronary disease.
Further reading
Jenkins MP, Buonaccorsi GA et al. Reduction in the response to coronary
and iliac artery injury with photodynamic therapy using 5-amino45: 47885.
laevulinic acid. Cardiovasc Res 2000;4
Kullo IJ, Simari RD, Schwartz RS. Vascular gene transfer; from bench to
19: 196207.
bedside. Arterioscler Thromb Vasc Biol 1999;1
50
Landzberg BR, Frishman WH, Lerrick K. Pathophysiology and pharmacological approaches for prevention of coronary artery restenosis
following coronary artery balloon angioplasty and related procedures.
34: 36198.
Prog Cardiovasc Dis 1997;3
Weinberger J, Simon AD. Intracoronary irradiation for the prevention of
12: 46874.
restenosis. Current Opin Cardiol 1997;1
Yokoi H, Daida H, Kuwabara Y et al. Effectiveness of an antioxidant in
preventing restenosis after percutaneous transluminal coronary angioplasty: the Probucol Angioplasty Restenosis Trial. J Am Coll Cardiol
30: 85562.
1997;3
51
52
53
What to give
Currently, the choice of thrombolytic varies by country and
depends especially on the type of health care system and funding
in place. In many countries, in the absence of previous
administration the first line thrombolytic is SK (1.5 million units
in 100 mls 5% dextrose/0.9% NaCl over 3060 minutes).
Alternatively, tPA is given as a 15mg bolus followed by 50mg
over 60 minutes, then 35mg over a further 30 minutes. Based on
the GUSTO study a case can be made for tPA in those presenting
very early (<4 hours with large anterior infarcts). New plas minogen activators such as recombinant plasminogen activator (rPA) and prourokinase are currently the subject of a number of
clinical studies. Reteplase (rPA), is a nonglycosylated deletion
mutant of wild type tPA. It is the first member of the third generation thrombolytics, has a longer half life and is given as a double
bolus (10IU + 10IU). Equivalence trials comparing tPA and
reteplase have demonstrated no difference in outcome and
currently these two drugs are interchangeable, with decisions
about use being based on availability and price.6 Lanoteplase has
been withdrawn prior to launch because of patent issues and
TNK-tPA is being trialled against tPA (ASSENT 2).7 Bleeding
with this new agent was between 2.8% and 7.4% dependent on
dose (ASSENT 1).8 Data suggest that there may be a role for
rescue angioplasty in patients who fail to show electrocardiographic evidence of reperfusion.9 However, results of randomised
trials addressing this issue are awaited.
References
1 Fibrinolytic Therapy Trialists (FTT) Collaborative Group. Indications
for fibrinolytic therapy in suspected acute myocardial infarction:
collaborative overview of early mortality and major morbidity from all
343: 31122.
randomised trials of more than 1000 patients. Lancet 1994;3
2 Feldman M, Cryer B. Aspirin absorption rates and platelet inhibition
times with 325mg buffered aspirin tablets (chewed or swallowed
84 :
whole) and with buffered aspirin solution. Am J Cardiol 1999;8
4049.
3 LATE Study Group. Late assessment of thrombolytic efficiency (LATE)
study with alteplase 624 hours after onset of acute myocardial
342: 75966.
infarction. Lancet 1993;3
4 The European Myocardial Infarction Project Group. Pre-hospital
thrombolytic therapy in patients with suspected acute myocardial
329: 3839.
infarction. N Engl J Med 1993;3
54
55
56
57
58
59
60
61
62
63
Aspirin
Aspirin at low to medium doses (75325mg daily) reduces
mortality, reinfarction and particularly stroke by 1045% after
myocardial infarction. It has been estimated that there is about
one serious haemorrhage, gastrointestinal or intracerebral, for
every event prevented. At the moment there is no comparable
evidence for dipyridamole, ticlopidine or clopidogrel.
Beta blockers
There is overwhelming evidence for the beneficial effect of beta
blockers, both within the first few hours of myocardial infarction
and for up to three years afterwards. Reduction in mortality
ranges from 15 to 45%, almost all of it accounted for by fewer
instances of sudden death. All beta blockers appear equally
suitable, except those with partial agonist activity. The contraindications are controversial, but most would include asthma, severe
heart block and otherwise untreated heart failure, but patients
with poor left ventricular function benefit most. In asthmatic
patients, particularly, heart rate limiting calcium channel blockers
(verapamil or diltiazem) may be useful alternatives to beta
blockers in the absence of uncontrolled heart failure.
Lipid-lowering drugs
The large secondary prevention trials with simvastatin and pravastatin (4S, CARE, LIPID) have demonstrated unequivocally the
64
ACE inhibitors
These drugs would of course be used in patients with
symptomatic heart failure but should also be used in asymptomatic
patients with ejection fractions <40%. This is associated with
significant decreases in mortality (2030%) and in sudden death,
as well as in reinfarction. All ACE inhibitors so far tested share
these effects. Treatment should be started within 12 days of the
infarct and should be continued indefinitely. Whether all patients
should be given these drugs post-infarction, in the absence of
contraindications, is a more difficult issue. In unselected
populations the benefits of treatment are much less clear cut.
However, data from the recent HOPE trial1 suggest substantial risk
reduction for higher risk vascular patients which may include a
large proportion of patients who have suffered a myocardial
infarction. Other ongoing trials (such as EUROPA, using
Perindopril) may help clarify this issue.
Other action
In addition to these relatively specific measures, diabetes and
hypertension must of course be treated as required, and smoking
discouraged. Some have advocated the use of fish oils especially
in dyslipidaemic patients, either as supplements or as fish. The
use of warfarin has been controversial for many years. It is highly
effective in preventing cardiovascular events, particularly stroke,
but at the cost of more adverse effects than aspirin and the
inconvenience of monitoring. It is therefore not recommended for
first-line use by most cardiologists.
65
66
67
68
69
70
71
72
73
74
The patients who gain most from surgery are those most at risk
from dying with medical therapy alone. Pertinent high-risk
characteristics included left main stem (LMS) disease, triple
vessel disease or double vessel disease that included a proximal
LAD lesion, and triple vessel disease associated with impaired LV
function. The VA study at 18 years2 demonstrated superior
surgical survival throughout the 18 years, but was only
significant overall at 7 years (med. vs surg. survival 53% vs 79%
p = 0.007); benefit was much greater in the high risk group with
LMS stenosis >50%, single or double vessel disease with
impaired LV function, and triple vessel disease with LV EF <40%.
In 1988 ECSS3 reported 12 year results demonstrating significantly higher cumulative survival in the surgical group, notably
again in patients with 3 vessel disease (med. vs surg. survival
82% vs 94% (p = 0.0002) at 5 years and 68% vs 78% (p = 0.01) at
10 years). Proximal LAD disease >95% in two or three vessel
disease was an outstanding anatomical predictor of survival
(med. vs surg. survival at 10 years 65% vs 77% (p = 0.007)), again
with significant crossover into the surgery group. The CASS
study4 demonstrated no difference in survival for any subset at 5
years, but did not include any patients with poor LV function,
LMS disease, angina greater than class 2, co-morbid disease or
unstable angina. It is therefore difficult to extrapolate data from
this trial to modern patient populations.
Combining results from seven of these early randomised trials
led to the publication of survival figures for 5, 7 and 10 years.5
Medical vs surgical mortality for all patients was 15.8% vs 10.2%
(p = 0.0001) at 5 years, with attenuation of this benefit to a
mortality of 30.5% (med.) and 26.4% (surg.) (p = 0.03) at 10
years. Extension of life for all patients having surgery was 4.3
months at 10 years. High-risk patients once again benefited the
most from surgery, but in lower risk groups, a survival extension
for those with proximal LAD disease (14 months), triple vessel
disease (7 months) or LMS disease (19 months) was identified.
This survival benefit was independent of degree of LV
impairment or abnormal stress testing. Median survival for
patients with LMS disease was 13.1 years in the surgical group
and 6.2 years for those treated medically. The superior patency of
the LIMA graft compared with saphenous vein grafts has been
established beyond any doubt and additional survival benefit, up
to 18 years, has been demonstrated.6
75
References
1 Edwards FH, Clark RE, Schwarz M. Coronary artery bypass grafting:
Society of Thoracic Surgeons National Database experience. Ann Thorac
57;1219.
Surg 1994;5
2 The Veterans Administration Coronary Artery Bypass Surgery
Cooperative Study Group. Eighteen year follow up in the Veterans
Affairs Cooperative study of coronary artery bypass surgery for
86: 1216.
unstable angina. Circulation 1992;8
3 The European Coronary Surgery Study Group. Twelve year follow up
of survival in the Randomised European Coronary Surgery Study.
319: 3327.
N Engl J Med 1988;3
4 CASS principle investigators. Myocardial infarction and mortality in
the Coronary Artery Study (CASS) randomised trial. N Engl J Med
310: 7508.
1984;3
5 Yusuf S, Peduzzi P, Fisher LD et al. Effect of CABG surgery on survival:
overview of 10 year results from randomised trials by the CABG
344: 56370.
surgery triallists collaborations. Lancet 1994;3
6 Boylan MJ, Lytle BW, Loop FD et al. Surgical treatment of isolated left
anterior descending coronary stenosis comparison of LIMA and
venous autografts at 1820 years follow up. J Thorac Cardiovasc Surg
107: 65762.
1994;1
76
77
78
3 Lytle BW, Blackstone EH, Loop FD et al. Two internal thoracic artery
117: 85572.
grafts are better than one. J Thorac Cardiovasc Surg 1999;1
4 Taggart DP. The radial artery as a conduit for coronary artery bypass
82: 40910.
grafting. Heart 1999;8
79
80
81
Further reading
Arrowsmith JE, Harrison MJG, Newman SP et al. Neuroprotection of the
brain during cardiopulmonary bypass. A randomized trial of
Remacemide during coronary artery bypass in 171 patients. Stroke
29: 235762.
1998;2
Murkin JM, Newman SP, Stump DA et al. Statement of consensus on
assessment of neurobehavioral outcomes after cardiac surgery. Ann Thorac
59: 128995.
Surg 1995;5
Murkin JM, Stump DA, Blumenthal JA et al. Defining dysfunction:
group means versus incidence analysis: a statement of consensus. Ann
64: 9045.
Thorac Surg 1997;6
Newman SP, Harrison MJG, eds. The brain and cardiac surgery. London;
Harwood Academic, 2000.
82
83
Further reading
Brady PA, Terzic A. The sulphonylurea controversy: more questions from
31: 9506.
the heart. J Am Coll Cardiol 1998;3
Smits P, Thien T. Cardiovascular effects of sulphonylurea derivatives.
38: 11621.
Implications for the treatment of NIDDM? Diabetologia 1995;3
84
85
86
87
88
Further reading
Schlant RC. Timing of surgery for nonischemic severe mitral re99: 3389.
gurgitation. Circulation 1999;9
Treasure T. Timing of surgery in chronic mitral regurgitation: In: Wells
FC, Shapiro LM. Mitral valve disease. Oxford: Butterworth Heinemann,
1996: 187200.
Tribouilloy CM, Enriquez-Sarano M, Schaff HV et al. Impact of preoperative symptoms on survival after surgical correction of mitral re99: 4005.
gurgitation. Circulation 1999;9
89
90
91
3 Lee EM, Shapiro LM, Wells FC. Superiority of mitral valve repair in
18 :
surgery for degenerative mitral regurgitation. Eur Heart J 1997;1
65563.
4 Gillinov AM, Cosgrove DM, Lytle BW et al. Reoperation for failure of
113 : 46773;
mitral valve repair. J Thorac Cardiovasc Surg 1997;1
discussion 4735.
5 Barlow CW, Imber CJ, Sharples LD et al. Cost implications of mitral
valve replacement versus repair in mitral regurgitation. Circulation
96(9 suppl): II903; discussion II945.
1997;9
92
93
after the Ross procedure. More than 90% of all patients are free of
any complications (death, degeneration, valve failure, endocarditis) after ten years. However, the subpulmonary homograft
may need replacement in the future. The Ross procedure is
technically demanding. It is the method of choice for aortic valve
replacement in the young, with excellent early postoperative
haemodynamic results and good mid-term results. Long term
results of the Ross procedure using current techniques are awaited.
Further reading
Elkins RC. The Ross operation: a twelve year experience. Ann Thorac Surg
68(suppl 3): S1418.
1999;6
Ross DN. Replacement of aortic and mitral valve with a pulmonary autograft. Lancet 1967;iii: 9568.
94
Mechanical mitral
Mechanical aortic
Tissue mitral
Tissue aortic
Stroke
TIA
Events
2.4
1.0
0
1.8
4.2
1.3
2.5
0.7
380
870
600
80
6.5
2.0
2.5
1.5
95
96
97
98
99
100
101
History
The investigation should begin with the taking of a detailed history.
This should include the construction of a family tree with at least
three generations.
Descriptive investigations
Electrocardiography. In the majority of patients, the 12-lead electrocardiogram (ECG) shows abnormalities such as voltage criteria
for left ventricular hypertrophy (LVH), minor intraventricular
conduction defects or bundle branch blocks. Only rarely (<5% of
cases) is the ECG completely normal.
Echocardiography. The mainstay of diagnosis is the echocardiographic demonstration of left ventricular hypertrophy (LVH),
with either the interventricular septum or the free wall measuring
15mm. A very detailed study by an experienced operator is
often necessary as hypertrophy may involve any part of LV. It is
important to note that for adults with family history of HCM,
modified diagnostic criteria apply.
102
103
Treatment of symptoms
Typical symptoms include dyspnoea, palpitations and chest pain.
Dyspnoea is usually due to left ventricular diastolic dysfunction
while chest pain is frequently due to myocardial ischaemia. The
pain may however be atypical and occur in the absence of
demonstrable epicardial coronary disease. The treatment chosen
will depend on whether there is significant outflow tract
obstruction (outflow gradient 30mmHg). In those without
obstruction, the choice is between either a beta blocker or a calcium
antagonist, such as high dose verapamil (up to 480mg/day). In
those with obstruction a beta blocker with or without disopyramide
is usually the first choice for those patients with outflow obstruction
(~25% of patients). Both drugs reduce the outflow gradient and
improve diastolic function by their negative inotropism. Verapamil
should only be used with caution as it may worsen the outflow
obstruction (through the increased vasodilatation and consequent
ventricular emptying with contraction). Palpitations may be due to
supraventricular or ventricular arrhythmias. Supraventricular
arrhythmias including atrial fibrillation may be controlled with
beta blockers, verapamil or amiodarone.
Patients with refractory symptoms may be candidates for
invasive treatment modalities such as dual chamber pacing with a
short AV delay, alcohol septal ablation or surgical myectomy.
Surgical septal myectomy is long established and can be
combined with mitral valve replacement in patients with
associated significant mitral regurgitation. When patients present
with progressive ventricular dilatation and reduced systolic
function, cardiac transplantation may need to be considered.
104
105
106
Minor
Echocardiography
Left ventricular wall thickness
13mm in the anterior septum
or 15mm in the posterior
septum or free wall
Deep S in V2 (>25mm)
Unexplained syncope, chest pain
dyspnoea
Source McKenna WJ, Spirito P, Desnos M et al. Experience from clinical genetics
in hypertrophic cardiomyopathy. Proposal for new diagnostic criteria in adult
77: 1302.
members of affected families. Heart 1997;7
107
108
109
110
Further reading
Dec GW, Fuster V. Idiopathic dilated cardiomyopathy (review). N Engl J
331: 156475.
Med 1994;3
111
Symptomatic patients
All patients with clinically diagnosed heart failure should receive
an ACE inhibitor. The survival advantages are consistent
(mortality reduction of about 20%) and far outweigh the
relatively small risk of serious side effects. In post-infarct
clinically diagnosed heart failure, ACE inhibition reduced
mortality by 27% at an average follow up of 15 months, and 36%
with a mean follow up of nearly 5 years.1
112
113
5 Topol E. ACE inhibitors still the drug of choice for heart failure and
354: 1797.
more. Lancet 1999;3
6 Pitt B, Zannad F, Remme WJ et al. The effect of spironolactone on
morbidity and mortality in patients with severe heart failure.
Randomized Aldactone Evaluation Study Investigators. N Engl J Med
341: 70917.
1999;3
114
Nitrates alone
Nitrates on their own can be used intermittently for relief of
dyspnoea not well documented, but logical to try. For example,
intermittent sublingual or oral nitrates may benefit a patient
already on high doses of loop diuretics and an ACE inhibitor, but
who still has severe exertional or nocturnal dyspnoea, and needs
relief. The continuous use of nitrates does, however, run the risk
of nitrate tolerance, which in turn may be lessened by
combination with hydralazine.1
115
116
117
118
119
120
121
II
III
IV
Functional capacity
Patients with cardiac disease, but without resulting
limitation of physical activity. Ordinary physical activity
does not cause undue fatigue, palpitation, dyspnea, or
anginal pain.
Patients with cardiac disease resulting in slight
limitation of physical activity. They are comfortable at
rest. Ordinary physical activity results in fatigue,
palpitation, dyspnea, or anginal pain.
Patients with marked limitation of physical activity.
They are comfortable at rest. Less than ordinary activity
causes fatigue, palpitation, dyspnea, or anginal pain.
Patients with cardiac disease resulting in inability to
carry on any physical activity without discomfort.
Symptoms of heart failure or of the anginal syndrome
may be present even at rest. If any physical activity is
undertaken, discomfort is increased.
References
1 The Criteria Committee of the New York Heart Association. Criteria for
diagnosis and treatment of heart disease, 9th edition, Little, Brown and
Company, 1994.
2 Keogh AM, Baron DW, Hickie JB. Prognostic guides in patients with
idiopathic or ischemic dilated cardiomyopathy assessed for cardiac
65: 9038.
transplantation. Am J Cardiol 1990;6
122
123
124
Further reading
Elbeery JR, Owen CH, Savitt MA et al. Effects of the left ventricular
assist device on right ventricular function. J Thorac Cardiovasc Surg
99: 80916.
1990;9
Kormos RL, Borovetz HS, Gasior T et al. Experience with univentricular
support in mortally ill cardiac transplant candidates. Ann Thorac Surg
49: 26172.
1990;4
125
126
127
128
129
130
131
132
Further reading
Grant SCD, Brooks NH. Accelerated graft atherosclerosis after heart
69: 46970.
transplantation. Br Heart J 1993;6
Madden B, Shenoy V, Dalrymple-Hay M et al. Absence of bradycardic
response to apnoea and hypoxia in cardiac transplant recipients with
16: 3947.
obstructive sleep apnoea. J Heart Lung Transplant 1997;1
Mann J. Graft vascular disease in heart transplant patients. Br Heart J
68: 2534.
1992;6
133
134
135
136
References
1 Hart RG. Warfarin in atrial fibrillation: underused in the elderly, often
82: 53940.
inappropriately used in the young. Heart 1999;8
Further reading
Stroke Prevention in Atrial Fibrillation Investigators. Adjusted dose
warfarin versus low-intensity, fixed dose warfarin plus aspirin for
high-risk patients with atrial fibrillation: stroke prevention in atrial
348: 6338.
fibrillation III. Lancet 1996;3
Stroke Prevention In Atrial Fibrillation Investigators. Stroke Prevention
84: 52739.
in Atrial Fibrillation Study. Final results. Circulation 1991;8
Hardman SM, Cowie M. Fortnightly review(:) anticoagulation in heart
318: 23844 (website version at www.bmj.com).
disease. BMJ: 1999;3
Petersen P, Botsen G, Godfredsen J et al. Placebo-controlled, randomised
trial for prevention of thromboembolic complications in chronic atrial
fibrillation. The Copenhagen AFASAK Study. Lancet 1989;ii: 1759.
137
138
139
140
Further reading
Falk RH. Proarrhythmic responses to atrial antiarrhythmic therapy. In:
Falk RH, Podrid PJ, eds. Atrial fibrillation mechanisms and management, 2nd
edition. Philadelphia: Lippincott and Raven, 1997: 371379.
Janse MJ, Allessie MA. Experimental observations on atrial fibrillation.
In: Falk RH, Podrid PJ, eds. Atrial fibrillation mechanisms and management.
2nd edition. Philadelphia: Lippincott and Raven, 1997: 5373.
Nattel S, Courtemarche, Wang Z. Functional and ionic mechanisms of
antiarrhythmic drugs in atrial fibrillation. In: Falk RH, Podrid PJ, eds.
Atrial fibrillation mechanisms and management, 2nd edition. Philadelphia:
Lippincott and Raven, 1997: 7590.
141
142
143
144
145
146
147
148
149
150
Further reading
Hardman SMC, Cowie M. Fortnightly review: anticoagulation in heart
318: 238244 (website version at www.bmj.com.)
disease. BMJ 1999;3
The Stroke Prevention in Atrial Fibrillation Investigators. Predictors of
thromboembolism in atrial fibrillation I. Clinical features of thrombo116: 15.
embolism in atrial fibrillation. Ann Intern Med 1992;1
The Stroke Prevention in Atrial Fibrillation Investigators. Predictors of
thromboembolism in atrial fibrillation II. Echocardiographic features of
116: 612.
patients at risk. Ann Intern Med 1992;1
151
152
Further reading
Aschenberg W, Schiuter M, Kremer P et al. Transoesophageal twodimensional echocardiography for the detection of left atrial appendage
7: 1636.
thrombus. J Am Coll Cardiol 1986;7
Manning WJ, Weintraub RM, Waksmonski CA et al. Accuracy of transoesophageal echocardiography for identifying left atrial thrombi. A
123: 81722.
prospective intraoperative study. Ann Intern Med 1995;1
Omran H, Jung W, Rabahieh R et al. Imaging of thrombi and assessment of
left atrial appendage function: a prospective study comparing trans81: 1928.
thoracic and transoesophageal echocardiography. Heart 1999;8
Schweizer P, Bardos P, Erbel R et al. Detection of left atrial thrombi by
45: 14856.
echocardiography. Br Heart J 1981;4
153
154
155
156
157
ECG
24 hour ECG
24 hour BP
Carotid sinus massage supine and erect (only if negative
supine)
External loop recorder
Electrophysiological studies
Head up tilt test
CT head and EEG if appropriate
Implantable loop recorder
158
Table 75.1
Diagnostic consideration
Neurally mediated
Carotid sinus syncope
Vasovagal syncope
Situational
Orthostatic
Post-prandial
Cardiogenic
Structural heart disease aortic
and mitral stenosis
Ischaemic heart disease
Non-cardiovascular
Seizures
Cerebrovascular disease
Subclavian steal
Symptom or finding
Syncope with head rotation
After pain, unpleasant sight or
sound
Prolonged standing
Athlete after exertion
Micturition, cough, swallow,
defecation
On standing
After meals
Syncope on exertion
Witness fitting
Associated with vertigo, dysarthria,
diplopia or other motor and sensory
symptoms of brain stem ischaemia
Syncope with arm exercise
Modified from Kenny RA ed., Syncope in the older patient. Chapman and Hall
Medical 1996.
159
160
Still symptomatic
< 170mmol/L
> 170mmol/L
Salt loading
Still symptomatic
Still symptomatic
Blocker/SSRI
Still symptomatic/
cannot tolerate/
contraindicated
Fludrocortisone
and/or Midodrine
Algorithm 75.1
Still symptomatic
161
162
163
164
165
166
167
168
Electric fences
Nobody should touch an electric fence but should electric shock
occur it would be wise to have the system checked by formal
interrogation in case electrical mode reversion has occurred.
Mobile phones
Mobile phones have been extensively investigated in terms of
interaction with implanted devices. Analogue phones do not interact
with implanted devices but more modern digital devices have the
potential to interfere with pacing systems when utilised within a
field of 1015 cm. Pacemaker patients with mobile phones are
therefore advised to carry mobile telephones on the opposite side
169
of the body from the site of the device implant and should hold the
device to the opposite ear.
Further reading
Gimbel JR, Johnson D, Levine PA et al. Safe performance of magnetic
resonance imaging on five patients with permanent cardiac pacemakers.
19: 91319.
Pacing Clin Electrophysiol 1996;1
Hayes DL, Wang PJ, Reynolds DW et al. Interference with cardiac pace336: 14739.
makers by cellular telephones. N Engl J Med 1997;3
170
171
172
173
174
175
176
177
% of cases
51
17
9
5
4
3
3
2
2
27:
From Basilico FC. Cardiovascular disease in athletes. Am J Sports Med 1999;2
10821.
178
179
180
Pulmonary
Hepatic
Thyroid
Bradycardia
Neurologic
Skin
Eye
Gastrointestinal
Drug
Discontinuation
ATMI* meta-analysis1
Low-dose meta-analysis2
Amiodarone
Placebo
OR
Amiodarone
Placebo
OR
1.6
1.0
8.4
2.4
0.5
NR
NR
NR
0.5
0.4
1.6
0.8
0.2
NR
NR
NR
3.1
2.7
4.9
2.6
2.8
NR
NR
NR
1.9
1.2
3.7
3.3
4.6
2.3
1.5
4.2
0.7
0.8
0.4
1.4
1.9
0.7
0.1
3.3
2.2
1.2
4.2
2.2
2.0
2.5
3.4
1.1
41
27
NR
23
15
NR
References
1 Amiodarone Trials Meta-Analysis Investigators. Effect of prophylactic
amiodarone on mortality after acute myocardial infarction and in
congestive heart failure: meta-analysis of individual data from 6500
350: 141724.
patients in randomized trials. Lancet 1997;3
2 Vorperian VR, Harighurst TC, Miller S et al. Adverse effects of low dose
30: 7918.
amiodarone: a meta-analysis. J Am Coll Cardiol 1997;3
3 Gleadhill IC, Wise RA, Schonfeld S et al. Serial lung function testing in
patients treated with amiodarone: a prospective study. Am J Med 1989
86: 410.
;8
181
182
183
184
185
that the ICD should be reserved for those with the worst LV
function. Unfortunately, such patients have competing causes for
mortality such as pump failure and electromechanical
dissociation that are responsible for 50% of deaths. On the other
hand, patients with little or no impairment of LV function and a
single tachyarrhythmic event usually have late and rare recurrence leading to sudden death. An ICD can potentially restore
them to near normal life expectancy in the absence of ongoing
myopathic process. The long term studies requiring more than
one life span of an ICD are not available to define the true value of
ICD therapy in such patients.
Although the ability of the implantable cardioverter defibrillator (ICD) to terminate potentially lethal ventricular
arrhythmias is well acknowledged there is less consensus as to
whom should receive an ICD. A good place to start is the
American College of Cardiology/American Heart Association
Practice Guidelines for Arrhythmia Devices.1 There are three
classes of indications: class one, where there is evidence and/or
general agreement that the treatment is beneficial, useful and
effective; class two, where there is conflicting evidence or a divergence of opinion; and class three, where there is evidence and
general agreement that a treatment is not useful or effective.
The class one indications for ICD implantation are:
1 Cardiac arrest due to VF or VT not due to a transient or reversible
cause.
2 Spontaneous sustained VT.
3 Syncope of undetermined origin with clinically relevant,
haemodynamically significant sustained VT or VF induced at
electrophysiological study when drug therapy is ineffective,
not tolerated or not preferred.
4 Non-sustained VT with coronary disease, prior MI, LV
dysfunction, and inducible VF or sustained VT at electrophysiological study that is not suppressible by a class I antiarrhythmic drug.
The class two indications for ICD implantation are:
1 Cardiac arrest presumed to be due to VF when electrophysiological testing is precluded by other medical conditions.
2 Severe symptoms attributable to sustained ventricular
arrhythmias while awaiting cardiac transplantation.
186
3 Familial or inherited conditions with a high risk for lifethreatening ventricular tachyarrhythmia such as long QT
syndrome or hypertrophic cardiomyopathy.
4 Non-sustained VT with coronary artery disease, prior MI, and
LV dysfunction, and inducible sustained VT or VF at electrophysiological study.
5 Recurrent syncope of undetermined aetiology in the presence
of ventricular dysfunction and inducible ventricular
arrhythmias at electrophysiological study when other causes of
syncope have been excluded.
The size of the risk reduction to patients and the degree of life
prolongation are only moderate in the trials showing benefit of
ICD over antiarrhythmic therapy. The cost per life year saved is
also wildly different in these trials giving us conflicting
information, e.g. $22,800 (MADIT) and $114,917 (AVID).
There is a wide variation in implant rates across the world
(Table 87.1).
Table 87.1
countries1
Country
USA
Germany
France
Italy
Netherlands
UK
1997
23,407
1975
210
280
150
240
34,121
3556
420
950
220
410
120
45
10
16
9
7
187
188
189
190
191
5 Minimise the risk of complications occurring both from inappropriate therapy delivered to the patient and those associated
with wound and pocket infection.1
6 Anticipate the elective replacement of the device and plan for
this eventuality.
7 Provide a support structure for the patient and their family
including advice, counselling and education. Some centres
provide a formal patient support group; there are both positive
and negative views on this practice.2,3
References
1 Troup P, Chapman P, Wetherbee J et al. Clinical features of AICD
78:155.
system infections. Circulation 1988;7
2 Badger JM, Morris PLP. Observations of a support group for automatic
implantable cardioverter defibrillator recipients and their spouses.
18: 23843.
Heart Lung 1989;1
3 Teplitz L, Egenes KJ, Brask L. Life after sudden death: the
development of a support group for automatic implantable
4: 2032.
cardioverter defibrillator patients. J Cardiovasc Nurs 1990;4
192
193
Sinus tachycardia
Lead fracture
Diaphragmatic muscle sensing
Electromagnetic interference.
References
1 Nunain SO, Roelke M, Trouton T et al. Limitations and late complications
of third-generation automatic cardioverter-defibrillators. Circulation
91: 220413.
1995;9
2 Pacifico A, Hohnloser SH, Williams JH et al. Prevention of implantable340:
defibrillator shocks by treatment with sotalol. N Engl J Med 1999;3
185562.
194
Maternal risk
This relates to the degree of ventricular dysfunction and the
ability to adapt to altered haemodynamics. Risk and management
can therefore be discussed in relation to New York Heart
Association (NYHA) functional class:
NYHA I-II
Should manage pregnancy without difficulty (maternal
mortality 0.4%)
May require admission for rest and diuretic therapy
Venous thrombosis prophylaxis with heparin for patients on
bedrest
NYHA III
At significant risk (maternal mortality for NYHA III-IV 6.8%)
Planned hospital admission for rest, treatment of heart failure
and monitoring
Risk of deterioration in ventricular function which may not
improve post-partum.
Early delivery if heart failure progressive despite optimal inpatient management
NYHA IV
Should be advised not to become pregnant. Therapeutic
abortion should be considered.
195
Fetal risk
Fetal risk should be considered in terms of two factors:
1 Factors which put the mother at risk
2 Adverse effects from maternal drugs:
ACE inhibitors should be discontinued prior to conception
because of the risk of embryopathy
Limited or unfavourable data on fetal effects of many antiarryhthmics
Beta blockers may be associated with maternal hypotension,
and hence reduce placental perfusion. They may thus
contribute to premature labour
Warfarin see Q93 (page 196) and Q95 (page 202).
Note that digoxin and verapamil are safe to use.
Further reading
Oakley CM. Management of pre-existing disorders in pregnancy: heart
37: 10211.
disease. Presc J 1997;3
Salazar E, Izaguirre R, Verdejo J et al. Failure of adjusted doses of subcutaneous doses of heparin to prevent thromboembolic phenomena in
pregnant patients with mechanical cardiac valve prostheses. J Am Coll
27: 1698703.
Cardiol 1996;2
196
Mechanical valves
Anticoagulation is the issue here: in particular, the risk of
warfarin embryopathy vs risk of valve thrombosis.
The choice lies between:
1 Warfarin throughout pregnancy, stopping it for a minimal
length of time for delivery
2 Convert to heparin during the first trimester with hospital
admission and meticulous control of APTT. Return to warfarin
for the second trimester and reinstate heparin at ~34/40.
197
Note:
1 Mitral tilting disc prostheses at particular risk: fatal thrombotic
occlusion of these valves in pregnant women described despite
well-controlled heparin anticoagulation
2 Risk of significant warfarin embryopathy not as high as
previously thought, especially if the mother achieves adequate
anticoagulation on <5mg warfarin.
3 No data on low molecular weight heparin in this situation, so
its use cannot be recommended.
The patient must be fully informed, and involved in deciding
her mode of anticoagulation (medicolegal implications).
Further reading
Salazar E, Izaguirre R, Verdejo J et al. Failure of adjusted doses of subcutaneous doses of heparin to prevent thromboembolic phenomena in
pregnant patients with mechanical cardiac valve prostheses. J Am Coll
27: 1698703.
Cardiol 1996;2
198
199
200
201
Management
Women who do not wish to continue warfarin throughout pregnancy can be reassured that conceiving on warfarin appears safe
but conversion to heparin, to avoid the risk of embryopathy,
needs to be carried out by 6 weeks. Breast-feeding on either
warfarin or heparin is safe. Possible regimes include:
Warfarin throughout pregnancy until near term and then
conversion to unfractionated heparin.
Unfractionated heparin for the first trimester. Warfarin until
near term and then resumption of heparin.
References
74: 10711.
1 Oakley CM. Anticoagulants in pregnancy. Br Heart J 1995;7
2 Cotrufo M, de Luca TSL, Calabro R et al. Coumarin anticoagulation
during pregnancy in patients with mechanical valve prostheses. Eur J
5: 3005.
Cardiothorac Surg 1991;5
3 Maternal and Neonatal Haemostasis Working Party of the Haemostasis
and Thrombosis Task Force. Guidelines on the prevention, investigation and management of thrombosis associated with pregnancy. J
46: 48996.
Clin Pathol 1993;4
4 Ginsberg JS, Hirsh J. Use of antithrombotic agents during pregnancy.
108(suppl 4): 305S11S.
Chest 1995;1
5 Salazar E, Izaguirre R, Verdejo J et al. Failure of adjusted doses of
subcutaneous heparin to prevent thromboembolic phenomena in
pregnant patients with mechanical cardiac valve prostheses. J Am Coll
27: 1698703.
Cardiol 1996;2
6 Hirsh J. Low-molecular weight heparin for the treatment of venous
135(suppl 6): S33642.
thromboembolism. Am Heart J 1998;1
202
203
204
2. Persistent sepsis
This is defined as failure to achieve bloodstream sterility after 35
days of appropriate antibiotic therapy or a lack of clinical
improvement after one week.
205
4. Extravalvular extension
Annular abscesses are more common with aortic (25-50%) than
mitral (1-5%) infections; in either case, surgical intervention is
preferred (survival: 25% medical, 60-80% surgical). Conduction
disturbances are a typical manifestation.
5. Peripheral embolisation
This is common (30-40%), but the incidence falls dramatically
following initiation of antibiotic therapy. Medical therapy is
appropriate for asymptomatic aortic or small vegetations. Surgical
therapy is indicated for recurrent or multiple embolisation, large
mobile mitral vegetations or vegetations that increase in size
despite appropriate medical therapy.
6. Cerebral embolisation
Operation within 24 hours of an infarct carries a 50% exacerbation
and 67% mortality rate, but the risk falls after two weeks (exacerbation <10%, mortality <20%). Following a bland infarct, it is
ideal to wait 23 weeks unless haemodynamic compromise
obligates early surgical intervention. Following a haemorrhagic
infarct, operation should be postponed as long as possible (46
weeks).
Further reading
Moon MR, Stinson EB, Miller DC. Surgical treatment of endocarditis.
40: 23964.
Prog Cardiovasc Dis 1997;4
206
207
208
209
210
211
Step 9
All patients have now been assigned to surgery, angiography or
non-invasive testing. The results of non-invasive tests must
incorporate both the absolute result (positive or negative) and
quantification of the result (e.g. magnitude and regional location
of ischaemic area). These results will determine which patients
should proceed to angiography. Significant abnormalities require
further assessment by angiography. Minor and intermediate
abnormalities only require further assessment in the presence of
low functional capacity or major surgical risk.
It should be noted that, at least in high-risk patients undergoing vascular surgery, beta blockade is the only medical intervention proven to have major impact on outcome.2
Reference
1 ACC/AHA guidelines for perioperative cardiovascular evaluation for
93: 12801317.
noncardiac surgery. Circulation 1996;9
2 Poldermans D, Boersma E, Bax JJ et al. The effect of bisoprolol on perioperative mortality and myocardial infarction in high-risk patients
undergoing vascular surgery. Dutch Echocardiographic Cardiac Risk.
341: 178994.
N Engl J Med 1999;3
212
Clinical predictors
Functional status
Surgical magnitude
Results of non-invasive investigations.
213
Points
Detsky
Points
Eagle**
Points
Age
MI or Q wave
Angina
>70
<6 months
5
10
1
1
1
S3 or raised
JVP
11
5
10
10
20
10
>70
Q wave
Angina
LV
dysfunction
Arrhythmia
Non sinus
>70
< 6 months
CCS class 3
CCS class 4
Pulmonary
oedema
<1 week
Non sinus
Other heart
disease
Other
Important
Aortic Stenosis
PO2<60
pCO2>50
K<3
Urea >50
Creatinine >200
20
Surgery
Emergency,
Intrathoracic,
Abdominal
4
3
Critical aortic
Stenosis
PO2<60
PCO2>50
K<3
Urea >50
Creatinine >260
Bedridden
Emergency
Ventricular 1
ectopy
Diabetes
10
*Modified from Mangano DT, Golman L. Preoperative assessment of patients with known
333: 17506.
or suspected coronary artery disease. N Engl J Med 1995;3
**Designed for patients undergoing vascular surgery
Table 101.2
Class
Points
Goldman
Class 1
Class 2
Class 3
Class 4
05
612
1325
>25
18
330
1438
30100
Detsky
Class 1
Class 2
Class 3
015
2030
>30
5
27
60
Eagle
Class 1
Class 2
Class 3
0
12
>3
03
616
2950
*Modified from Palda VA, Detsky AS. Perioperative assessment and management
127: 31328.
of risk from coronary artery disease. Ann Intern Med 1997;1
214
Table 101.3
Major
Unstable coronary syndromes
Recent MI
Unstable angina
Decompensated heart failure
Significant arrhythmias
High grade atrioventricular block
Symptomatic ventricular arrhythmias or supraventricular
arryhthmias in presence of underlying heart disease or with
uncontrolled ventricular rate
Severe valvular disease
Intermediate
Mild stable angina
Prior MI
Compensated or previous heart failure
Diabetes
Minor
Advanced age
Abnormal ECG
Rhythm other than sinus
Low functional capacity
History of stroke
Uncontrolled systemic hypertension
*Modified from ACC/AHA guidelines for perioperative cardiovascular
93: 1280317.
evaluation for noncardiac surgery. Circulation 1996;9
Table 101.4
215
High
Emergent major operations
Aortic and other vascular surgery
Anticipated prolonged surgery associated with large fluid shifts
Intermediate
Carotid endarterectomy
Head and neck
Intraperitoneal and intrathoracic
Orthopaedic
Prostate
Low
Endoscopic procedures
Superficial procedures
Breast
*Modified from ACC/AHA guidelines for perioperative cardiovascular
93: 1280317.
evaluation for noncardiac surgery. Circulation 1996;9
References
1 Mangano DT, Browner WS, Hollenberg M et al. Association of perioperative myocardial ischemia with cardiac morbidity and mortality in
men undergoing noncardiac surgery. The Study of Perioperative
323: 17818.
Ischemia Research Group. N Engl J Med 1990;3
2 Mangano DT, Golman L. Preoperative assessment of patients with known
333: 17506.
or suspected coronary artery disease. N Engl J Med 1995;3
3 Palda VA, Detsky AS. Perioperative assessment and management of
127: 31328.
risk from coronary artery disease. Ann Intern Med 1997;1
4 ACC/AHA guidelines for perioperative cardiovascular evaluation for
93: 1280317.
noncardiac surgery. Circulation 1996;9
5 LItalien GJ, Paul DS, Hendel RC et al. Development and validation of
a Bayesian model for perioperative cardiac risk assessment in a cohort
27: 77986.
of 1081 vascular surgical candidates. J Am Coll Cardiol 1996;2
Index
Main topics of questions are indicated by page references in bold
abciximab 44
ACE inhibitors
contraindication, malignant
hypertension 15
patients with impaired ventricles
11113
secondary prevention of acute
myocardial infarction 64
use in pregnancy 195
adenovirus titre, dilated
cardiomyopathy investigation
108
AFCAPS/TEXCAPS study 17
airport metal detectors, pacemaker
patients and 168
aldactone, RALES study 116
ALLHAT trial 12
amiodarone
adverse effects 17981
atrial fibrillation cardioversion 139
hypertrophic cardiomyopathy 103,
104
ICD patients 189
paroxysmal atrial fibrillation 133
amlodipine
angina 35
chronic heart failure 11415
amrinone 115
angina
cardiac transplant patients 1312
stable, choice of antianginal agent 356
unstable
medical treatments 434
PTCA and CABG in 457
risks of myocardial infarction and
death 412
angiography, coronary
dilated cardiomyopathy 108
pre-operative 21011
angiotensin-converting inhibitors see
ACE inhibitors
angiotensin-receptor blockers, heart
failure 112
anion-exchange resins
dyslipidaemia 20
side effects 23
Antiarrhytmics versus Implantable
Defibrillators (AVID) Trial 184
anticoagulation therapy
cardioversion
atrial flutter 147
DC cardioversion of atrial
fibrillation 1412, 145
elective surgery, mechanical heart
valve patients 2023
paroxysmal and chronic atrial
fibrillation 1356
pregnancy 2001
valve disease 1967
see also heparin; warfarin
antihypertensive therapy
blood pressure thresholds and 79
effect on cardiovascular risk 1
efficacy in terms of survival 1011
encephalopathy 1516
malignant hypertension 1516
24-hour blood pressure monitoring 3
antioxidant vitamins, prescription to
coronary heart disease patients
24
anti-thymocyte globulin, transplant
patients 129
aortic coarctation, follow up after
repair 99100
aortic stenosis, pregnancy 196
aortic valve replacement, Ross
procedure 923
arrhythmias
supraventricular, radiofrequency
ablation 1378
see also names of specific arrhythmias
aspirin
acute myocardial infarction 51
secondary prevention 63
atrial fibrillation patients 1356
stopping before cardiac surgery 86
unstable angina 43
ASSENT trials 53
assist devices 1234
ATBC study 24
atenolol, hypertension, effect on
mortality 10
atrial fibrillation (AF)
anticoagulation therapy 1356
cardioversion
anticoagulation in 1412, 145
chemical and DC 13940
elective 1434, 1456
CVA/TIA risk in chronic and
paroxysmal AF 14950
paroxysmal, drug treatment/role for
digoxin 1334
216
Index
atrial flutter, cardioversion,
embolisation/anticoagulation
and 1478
atrial septal defects, treatment in
adults 978
azathioprine, transplant patients
12930
beta blockers
angina 35
unstable 43
heart failure 116, 11819
hypertension
effect on mortality 10
malignant 15
hypertrophic cardiomyopathy 103
long QT syndrome 175
paroxysmal atrial fibrillation 133
role in atrial fibrillation
cardioversion 139
secondary prevention of acute
myocardial infarction 63
use in pregnancy 195
bezafibrate 21
biopsy, endomyocardial, dilated
cardiomyopathy 109
bisoprolol, CIBIS II study 116, 118
Biventricular Assist Devices
(BIVADS) 1234
block, trifascicular, pacing in 1645
blood pressure
ambulatory monitoring
hypertrophic cardiomyopathy 102
24-hour 34
lowering
malignant hypertension 15
treatment decisions 79
see also antihypertensive therapy
night time readings (dippers/nondippers) 4
see also hypertension
brachytherapy, prevention of
restenosis following PTCA 49
Braumwald classification 37, 41
bypass surgery see coronary artery
bypass graft
CABG see coronary artery bypass graft
Caesarean section, elective 1989
calcium channel blockers
angina 35
unstable 43
hypertension treatment
cardiovascular risk 1213
effect on mortality 10
hypertrophic cardiomyopathy 103
paroxysmal atrial fibrillation 133
217
role in atrial fibrillation
cardioversion 139
secondary prevention of acute
myocardial infarction 63
captopril, heart failure 112
cardiac arrest, torsade de pointes at
1734
Cardiac Insufficiency Bisoprolol Study
II (CIBIS II) 116, 118
cardiogenic shock, myocardial
infarction and 689, 956
cardiomyopathy
dilated
investigation 10810
pregnancy 1945
hypertrophic see hypertrophic
cardiomyopathy
cardiopulmonary bypass,
neuropsychological
complications 7981
cardioversion
atrial fibrillation
anticoagulation in 1412, 145
chemical cardioversion, drugs for
13940
DC cardioversion 139, 1412,
1456
elective cardioversion 1434,
1456
atrial flutter, embolisation/
anticoagulation and 1478
pacemaker patients 170
CARE, statin trial 18
carvedilol, congestive heart failure 118
cerebrovascular accident see stroke
CHAOS study 24
chest pain
acute, troponin T in diagnosis and
stratification 3740
hypertrophic cardiomyopathy 103
see also angina
cholesterol
lowering, drug choice/monitoring
201
target levels
asymptomatic
hypercholesterolaemia 17
coronary heart disease patients 18
clofibrate 21
side effects 22
clopidogrel, unstable angina 43
cognitive dysfunction following
cardiopulmonary bypass 7981
collapse see syncope
coronary artery bypass graft (CABG)
effect of recent myocardial infarction
on perioperative risks 845
218
myocardial infarction complicated
by cardiogenic shock 68, 69
patients with unstable angina 457
risk of death 70
survival following 735
switch from sulphonylureas to
insulin after 823
total arterial revascularisation 768
Coronary Artery Study (CASS) 74
coronary heart disease (CHD)
antioxidant vitamins and 24
lipid-lowering therapy 18
preventative 17
post-transplant 131
risk
blood pressure lowering and 78
hypertension and 1
Coxsackie titre, dilated
cardiomyopathy investigation
108
cyclophosphamide, transplant patients
129
cyclosporin-A, transplant patients
129, 130
dalteparin 44
death, sudden see sudden death
defibrillator, implantable see
implantable cardioverter
defibrillator
diabetic retinopathy, thrombolytic
therapy and 578
digoxin
heart failure patients 11617
paroxysmal atrial fibrillation 1334
use in pregnancy 195
dihydropyridines
long-acting, chronic heart failure
11415
short-acting, hypertension treatment,
cardiovascular risks 12
diltiazem
angina 35
unstable 43
role in atrial fibrillation
cardioversion 139
disopyramide, paroxysmal atrial
fibrillation 133
driving after myocardial infarction
667
DUKE study/score 29
dyslipidaemia drug therapy, choice
and monitoring 201
echocardiography
assessment of myocardial viability
334
Index
dilated cardiomyopathy 108
dobutamine stress 33, 34, 210, 212
hypertrophic cardiomyopathy 101
relatives of patients 106, 107
myocardial contrast 33
transthoracic and transoesophageal
thrombus detection in left atrium
1512
TIA and stroke patients 1534
Eisenmenger syndrome 95, 96, 125
electric fences, pacemaker patients
and 168
electrocardiography (ECG)
dilated cardiomyopathy 108
exercise see exercise tests
hypertrophic cardiomyopathy 101
relatives of patients 106, 107
implantable loop recorder 162
syncope monitoring 1612
ELITE II trial 112
encephalopathy, hypertensive 15
endocarditis, infective
antibiotic prophylaxis 2089
blood cultures 207
indications for surgical management
2045
risk
following valve replacement 94,
100
ventricular septal defect and 95
Ross procedure for aortic valve
replacement 92
enoxaparin 44
eptifibatide 44
European Coronary Surgery Study
(ECSS) 74
exercise tests
after myocardial infarction 5960
angina patients, disease prediction
2930
contraindications 278
diagnostic characteristics 256
dilated cardiomyopathy 108
effect of drugs on 27
guidelines 27
hypertrophic cardiomyopathy 102
predictive value 256
angina patients 2930
risks 278
familial hypercholesterolaemia, drug
treatment 20, 21
felodipine, chronic heart failure 11415
fibrates
drug interactions 23
dyslipidaemia 201
side effects 223
Index
fish oil capsules, high dose 21
flecainide
atrial fibrillation cardioversion 139
ICD patients 189
paroxysmal atrial fibrillation 133
flying after myocardial infarction 667
foramen ovale, patent, reference for
closure 1556
Fragmin During Instability in
Coronary Artery Disease
(FRISC) trial 38, 45
Framingham Heart Study, mortality
data 1201
gemfibrozil 21, 223
gene therapy, prevention of restenosis
following PTCA 489
GISSI-2 study 52
glibenclamide 82
glycaemia, control following CABG
823
glyceryl trinitrate (GTN), sublingual 35
glycoprotein IIb/IIIa inhibitors,
unstable angina 44
GUSTO trials 52, 53
GUSTO IIa 38
GUSTO IIb angioplasty substudy 55
heart failure
ACE inhibitors and AT1-receptor
blockers 11113
beta blockers 116, 11819
chronic, role of vasodilators 11415
congestive, endocarditis in 204
digoxin in 11617
morbidity and mortality 2067
prognosis, NYHA functional
capacity score and 1202
Heart Outcomes Prevention
Evaluation (HOPE) study 64
heparin
elective surgery in mechanical heart
valve patients 2023
unstable angina 44
use in pregnancy 196, 197, 198,
2001
hydralazine, malignant hypertension 15
hypercholesterolaemia
familial, drug treatment 20, 21
lipid-lowering therapy 20, 21
asymptomatic patients 17
hypertension
after aortic coarctation repair 99100
cardiovascular risks 12, 8
blood pressure lowering and 7
essential, management plan 14
malignant, management 1516
219
pulmonary, pregnancy and 198, 199
secondary causes, screening for 56
treatment
decisions 79
see also antihypertensive therapy
24-hour monitoring 34
white coat 4
Hypertension Optimal Treatment
(HOT) study 8
hypertensive encephalopathy 15
hyperthyroidism, amiodaroneinduced 17980
hypertrophic cardiomyopathy (HCM)
investigation/diagnosis 1012
children 107
relatives of patients 1067
sudden death and 177, 178
risk factors 1012, 104
treatment 1034
pacing 105
hypothyroidism, amiodarone-induced
180
immunosuppressive therapy,
transplant patients 12930
implantable cardioverter defibrillator
(ICD)
follow-up of patients 1901
hypertrophic cardiomyopathy 104
indications for 1857
VT stimulation studies 182, 183
interaction with drugs 189
long QT syndrome 175
multiple shocks from 1923
non-sustained ventricular
tachycardia 1712
patient management 1889
survival benefits 1845
implantable loop recorder (ILR) 162
insulin, following CABG 823
internal mammary artery grafts 767
ISIS-3 study 52
isosorbide dinitrate (ISDN) 35
isosorbide mononitrate (ISMN) 35
labetalol, hypertensive
encephalopathy 1516
lanoteplase 53
Late Assessment of Thrombolytic
Efficiency (LATE) study 51
Left Ventricular Assist Device (LVAD)
1234
left ventricular function, impaired,
ACE-inhibitor treatment 111
lipid-lowering therapy
asymptomatic
hypercholesterolaemia 17
220
coronary heart disease patients 18
drug choice/monitoring 201
drug interactions 23
secondary prevention of acute
myocardial infarction 634
side effects 223
LIPID study 18
liver function, effect of lipid-lowering
therapy 22
long QT syndrome 1756, 177
Long-Term Intervention with
Pravastatin in Ischaemic
Disease (LIPID) Study 18
losartan, heart failure 112
magnesium sulphate, intravenous,
hypertensive encephalopathy in
pre-eclampsia 16
magnetic resonance imaging (MRI),
pacemaker patients 168
methyldopa, malignant hypertension
15
methylprednisolone, transplant
patients 129
Metoprolol CR/XL Randomised
Intervention Trial in Heart
Failure (MERIT-HF) 118
milrinone 115
mitral regurgitation, surgery for 878,
89
mitral stenosis, pregnancy 196
mitral valve repair 8991
mycophenolate mofetil, transplant
patients 12930
myocardial infarction (MI)
ACE-inhibitor treatment of impaired
ventricular function 11112
angioplasty in 556
cardiogenic shock and 689, 956
driving and flying after 667
effect of recent MI on perioperative
risks of CABG 845
exercise testing after 5960
risk, at time of cardiac surgery 701
risks of recurrent ischaemic events
612
secondary prevention after 635
septal rupture following 72
thrombolytic therapy 514
contraindications 578
unstable angina and 412
ventricular septal defect following
956
myocardial perfusion imaging (MPI)
312
myocardium, hibernating/stunned
334
Index
myositis, lipid-lowering therapy and
22, 23
neuropsychological complications,
cardiopulmonary bypass 7981
New York Heart Association
functional capacity score, heart
failure prognosis 1202
nicorandil, angina 35
nifedipine
contraindication 43
malignant hypertension 15
hypertension treatment,
cardiovascular risks 12
nimodipine, malignant hypertension
16
nitrates
angina 35
unstable 43
chronic heart failure 114
OKT3, transplant patients 129
Organisation to Assess Strategies for
Ischaemic Syndromes (OASIS)
Registry 41, 456
pacemakers
and cardioversion 170
external magnetic interference 1689
insertion risks 1667
VVI/dual chamber, prescription
gudelines 1667
pacing
hypertrophic cardiomyopathy 105
trifascicular disease 1645
paclitaxel 48
PAMI trial 55
percutaneous transluminal coronary
angioplasty (PTCA)
myocardial infarction 556
complicated by cardiogenic shock
68, 69
restenosis prevention following
4850
unstable angina patients 457
phones, mobile, pacemaker patients
1689
photodynamic therapy (PTD),
prevention of restenosis
following PTCA 49
plasminogen activator, recombinant
(r-PA) 53
positron emission tomography (PET),
assessment of myocardial
viability 334
PRAISE studies 114
pravastatin, LIPID study 18
Index
pregnancy
contraindications 198
dilated cardiomyopathy 1945
valve disease 1967
Primary Angioplasty in Myocardial
Infarction (PAMI) trial 55
Probucol 48
propafenone, paroxysmal atrial
fibrillation 133
propranolol, hypertension, effect on
mortality 10
prourokinase 53
PTCA see percutaneous transluminal
coronary angioplasty
pulmonary autograft (Ross) procedure
923
QT intervals: long QT syndrome
1756, 177
radial artery grafts 77
RADIANCE Study 116
radiofrequency ablation,
supraventricular tachycardia
1378
Randomized Aldactone Evaluation
Study (RALES) 116
resins see anion-exchange resins
reteplase (rPA) 53
retinopathy, diabetic, thrombolytic
therapy and 578
RomanoWard syndrome 175
Ross procedure 923
SAVE study 11112
Scandinavian Simvastatin Survival
Study (4S) 18
screening
long QT syndrome 175
secondary causes of hypertension 56
serology, dilated cardiomyopathy
investigation 109
SHOCK trial 68
single-photon emission computed
tomography, 201T1 (T1SPECT),
assessment of
myocardial viability 334
sodium nitroprusside, hypertensive
encephalopathy 1516
SOLVD prevention trial 111
sotalol, paroxysmal atrial fibrillation
133
spironolactone, heart failure 112
statins
coronary heart disease
prevention 17
treatment 18
221
drug interactions 23
dyslipidaemia 20
myocardial infarction patients 64
side effects 22
streptokinase (SK) 51
acute myocardial infarction 523
stroke
patent foramen ovale and 155
prevention, atrial fibrillation
patients 135
risk
assessment in atrial fibrillation
patient 14950
blood pressure lowering and 78
cardiac surgery 701
following valve replacement 94
hypertension and 1
thrombolytic therapy and 57
transthoracic and transoesophageal
echocardiography 1534
sudden death
hypertrophic cardiomyopathy, risk
factors 1012, 104
prevention using implantable
cardiac defibrillator 184
VT stimulation studies 1823
young athletes 177
investigation of relatives 1778
sulphonylureas, following CABG 823
supraventricular tachycardia (SVT),
radiofrequency ablation 1378
surgery
bypass see coronary artery bypass
graft
cardiac
myocardial infarction risk 701
stopping aspirin before 86
elective, anticoagulation of
mechanical heart valve patient
2023
non-cardiac
cardiac risk factors 21215
pre-operative investigations
21011
syncope
investigation 15760
implantable loop recorder 162
tilt test 160
24-hour ambulatory monitoring
1613
vasovagal, management 159, 160
tacrolimus, transplant patients 129,
130
thallium scanning 312, 210, 212
Thrombolysis in Myocardial
Infarction (TIMI) IIIB trial 45
222
thrombolytic therapy 51
acute myocardial infarction 514
comparison with angioplasty
556
contraindications 578
contraindications
myocardial infarction 578
unstable angina 44
unstable angina 44
thrombus
detection in left atrium,
transthoracic and
transoesophageal
echocardiography 1512
risk in atrial fibrillation
anticoagulation therapy and 135,
141
assessment 14950
cardioversion and 141, 145
risk in atrial flutter, cardioversion
and 147
venous, patent foramen ovale/stroke
patients 155
thyroid function, effects of
amiodarone therapy 17980
ticlopidine, unstable angina 43
tilt test 160
TIMI IIIB trial 45
tirofiban 44
tissue plasminogen activator (tPA) 51
acute myocardial infarction 523
TNK 53
torsade de pointes
at a cardiac arrest 1734
non-sustained ventricular
tachycardia 171
tranilast 48
transient ischaemic attack (TIA)
risks, atrial fibrillation and 14950
transthoracic and transoesophageal
echocardiography 1534
transplantation, heart/heart-lung
angina following 1312
eligibility and suitability 1257
immunosuppressive therapy
12930
survival following 128
trifascicular disease, pacing 1645
trimentazidine, angina 35
Index
troponin T, diagnosis and risk
stratification of acute coronary
syndromes 3740
valve disease, management in
pregnancy 1967
valve replacement
risk of death 70
stroke and endocarditis risk 94
valves, mechanical, anticoagulation
elective surgery and 2023
pregnancy/delivery 1967, 198
vasodilators, chronic heart failure
11415
ventricular arrhythmia, recurrent 192
ventricular septal defect
closure in adults 956
post-infarct 72, 956
ventricular tachycardia (VT)
non-sustained 171
VT stimulation studies 1823
verapamil
angina 35
unstable 43
hypertrophic cardiomyopathy 103
role in atrial fibrillation
cardioversion 139
use in pregnancy 195
Veterans Affairs Non-Q Wave
Infarction Strategies in Hospital
(VANQWISH) Trial 41, 46
vitamin E, prescription in coronary
heart disease patients 24
warfarin
atrial fibrillation patients 1356
elective surgery in mechanical heart
valve patients 2023
embryopathy 196, 197, 200
secondary prevention of acute
myocardial infarction 64
use in pregnancy 2001
valve disease/mechanical valves
196, 197, 198
West of Scotland Coronary Prevention
Study (WOSCOPS) 17
WHO MONICA project 61
Wolff Parkinson White syndrome,
radiofrequency ablation 1378
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