(BQ) Part 1 book Practical cardiology presentation of content: Coronary risk factors, hypertension, an overview of clinical electro cardiography, the patient with chest pain. (BQ) Part 1 book Practical cardiology presentation of content: Coronary risk factors, hypertension, an overview of clinical electro cardiography, the patient with chest pain.
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 Elsevier Australia (a division of Reed International Books Australia Pty Ltd) Tower 1, 475 Victoria Avenue, Chatswood, NSW 2067 ACN 001 002 357 This edition © 2008 Elsevier Australia This publication is copyright Except as expressly provided in the Copyright Act 1968 and the Copyright Amendment (Digital Agenda) Act 2000, no part of this publication may be reproduced, stored in any retrieval system or transmitted by any means (including electronic, mechanical, microcopying, photocopying, recording or otherwise) without prior written permission from the publisher Every attempt has been made to trace and acknowledge copyright, but in some cases this may not have been possible The publisher apologises for any accidental infringement and would welcome any information to redress the situation This publication has been carefully reviewed and checked to ensure that the content is as accurate and current as possible at the time of publication We would recommend, however, that the reader verify any procedures, treatments, drug dosages or legal content described in this book Neither the author, the contributors, nor the publisher assume any liability for injury and/or damage to persons or property arising from any error in or omission from this publication 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 7295 3841 (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 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 • T H E P A T I E N T W I T H C H E S T P A I N 173 Septal rupture It is often possible clinically and usually possible echocardiographically to distinguish septal from papillary muscle rupture In addition, a Swan-Ganz catheter can sample the increased saturation in the right ventricle and the pulmonary artery at the bedside The ventral septal defect (VSD) murmur is louder, harsher and more often associated with a thrill than a papillary rupture Anterior infarcts are associated with apical septal defects and inferior infarcts with rupture of the basal septum If the event is recognised early, surgical repair may be possible Rupture of the ventricular free wall usually (but not always50) causes immediate death It accounts for about 15% of post-infarct sudden deaths Very occasionally, the rupture is contained by an area of adherent pericardium This results in a pseudoaneurysm, which may be diagnosed by echocardiography or left ventriculography (Fig 4.41, video clip 19) and repaired Figure 4.41 Pseudoaneurysm This 59-year-old man had ischaemic chest pain one week before presenting to hospital with an episode of sudden pleuritic chest pain His ECG showed inferior Q waves and some residual ST depression The coronary angiogram showed a culprit lesion in the right coronary artery The left ventriculogram shown here reveals a contained cardiac rupture of the inferior wall (arrow) In the corresponding video clip contrast can be seen entering and leaving the pseudoaneurysm While he was being prepared for urgent surgery this man died suddenly and could not be resuscitated from PEA RV infarction The association of hypotension with an inferior infarct and preserved systolic LV function on echo suggests the possibility of RV infarction Left ventricular output is affected by inadequate 174 PRACTICA L C A R D I O L O G Y filling from the right ventricle, even though in many cases it is compromised in its own right There is usually a positive Kussmaul’s sign The jugular venous pressure (JVP) rises during inspiration because of right ventricular inability to deal with the increased venous return that occurs during inspiration These patients respond to fluid loading and should not be treated with diuretics or inotropes unless there is associated LV failure The prognosis for return of RV systolic function is very good, but the overall outlook for the patient remains adversely affected by RV infarction on presentation.51 All inferior infarcts should have lead V4R on admission ECG; the important evidence of RV infarction contained therein is quite fleeting Pericarditis complicating myocardial infarction Patients who develop more chest pain after an infarct may have developed pericarditis The pain is usually pleuritic and different in character from the pain of the infarct It must be distinguished from that due to further ischaemia The presence of a pericardial rub is a most helpful sign Early (epistenocardiac) pericarditis is due to irritation of the pericardium as a result of infarction affecting the epicardial surface of the heart It is the only clinical sign of the infarction being transmural (ECG Q-wave and non-Q-wave infarctions have a considerable overlap in the subendocardial-transmural stakes) Later pericarditis may be an autoimmune condition called Dressler’s syndrome; for some reason its incidence appears to be diminishing.52 Both conditions can usually be controlled by non-steroidal anti-inflammatory agents Dressler’s may require suppression with steroids but has a tendency to relapse when these are withdrawn The presence of a rub should be investigated with an echocardiogram (Fig 4.42, video clip 18) If a significant pericardial collection is seen, it may be prudent to withdraw anticoagulant treatment with heparin There is a small risk that this treatment may increase the risk of developing a haemorrhagic effusion and cardiac tamponade Figure 4.42 An echocardiogram of a 70-year-old woman who developed pleuritic chest pain followed by increasing dyspnoea 10 days after an anterior infarct The echo shows a large pericardial collection at the apex and between the right ventricular free wall and the chest • T H E P A T I E N T W I T H C H E S T P A I N 175 LV thrombus Up to 20% of patients whose infarcts have not been treated with anticoagulants have been shown to develop mural thrombi This incidence rate rises to 40% for anterior infarcts It is lower in patients who have received thrombolytic treatment and heparin About 10% of mural thrombi result in detectable systemic emboli Mural thrombi are relatively easily diagnosed by echocardiography Certain echo features such as the presence of a mobile area of clot or projection of clot into the LV cavity suggest a higher risk of embolism Treatment is anticoagulation with heparin and then three to six months of treatment with warfarin LV aneurysm The development of a discrete area of LV wall dyskinesis with paradoxical motion and a broad53 but discernible neck may complicate up to 5% of infarcts (especially anterior and late presentation) It is diagnosed by echocardiography, or cardiac catheterisation Electrocardiographically it is suggested by persistent (> months) ST segment elevation It indicates an adverse prognosis Left ventricular geometry and function may be improved if the aneurysm can be resected Recurrent ischaemia This is discussed on p 165 Further investigations The patient’s prognosis and the further treatment that should be recommended depend on the left ventricular ejection fraction and the extent of coronary disease The ejection fraction (for both ventricles) may be calculated by gating images of the heart after injection of an isotope (usually technetium) The scanning camera acquires images of the blood in the heart in a series of gates within the cardiac cycle over 15 minutes or so Ejection fractions obtained in this way are the standard way of comparing infarct sizes Regional wall motion abnormalities can also be assessed An ejection fraction of 55% or more is normal for the left ventricle and 45% or more is normal for the right ventricle A left ventricular ejection fraction of less than 40% suggests significant dysfunction and risk of complications such as remodelling and the development of cardiac failure A reduced ejection fraction is the most reliable indicator of an impaired prognosis Remodelling When an infarcted area of myocardium leads to alterations in left ventricular geometry and then dilatation of the ventricle, this process is called remodelling or negative remodelling It is a maladaptive process that may begin soon after an infarct and progress over many years It is thought that the disturbance to normal left ventricular shape that occurs when a significant part of the cardiac wall does not contract normally leads to changes in the contractile performance of non-infarcted areas Changes in myocyte structure have been demonstrated in areas away from the infarcted zone Remodelling also occurs in response to other stressors such as hypertension and aortic stenosis The left ventricular hypertrophy caused by these conditions can be described as remodelling Reversal (positive remodelling) and prevention of these changes has been shown to be possible with the use of drugs that interrupt the maladaptive neurohormonal changes that occur with heart failure (p 275) ACE inhibitors and beta-blockers have been shown to reverse remodelling, as has treatment of hypertension by any means Early treatment with these drugs for patients with large infarcts improves the prognosis The extent of coronary artery disease can be judged by coronary angiography (p 136) or indirectly by exercise testing The performance of coronary angiography routinely after uncomplicated ST elevation myocardial infarction has not been shown to improve the prognosis It has, however, a number of advantages over non-invasive testing It gives more certainty and 176 PRACTICA L C A R D I O L O G Y reassurance to the patient and makes further management easier; and it may allow earlier discharge from hospital It is now unusual for an ST elevation infarct patient not to be investigated with a coronary angiogram either at the time of the infarct with a view to primary angioplasty or as soon as practical after thrombolysis The alternative is to perform exercise testing five to seven days after infarction for patients with no further ischaemic symptoms or complications and go on to angiography if this test is abnormal The Open Artery Trial (OAT) looked at routine reopening of occluded infarct-related arteries in patients without continuing ischaemia who presented more than three days after an infarct with an occluded artery There was no advantage to the patient in routine angioplasty of these vessels compared with medical treatment Cardiac rehabilitation Although rehabilitation has been a part of the management of patients following a myocardial infarction since the beginning of the last century, ideas have changed radically about the form this should take In the early 1900s Sir Thomas Lewis insisted his patients remain in bed and be ‘guarded by day and night nursing and helped in every way to avoid voluntary movement or effort’ These severe restrictions were continued for at least six to eight weeks The thinking was that complete rest would reduce the risk of aneurysm formation and avoid hypoxia that might cause arrhythmias Even after discharge mild exertion was discouraged for up to a year and return to work was most unusual In the 1970s periods of bed rest of between one and four weeks were enforced and patients remained in hospital for up to four weeks It is now clear that this de-conditioning has many adverse physical and psychological effects Patients with uncomplicated infarcts are now mobilised in hospital within a day or so of admission and are often discharged on the third day if successful primary angioplasty has been performed Many hospitals provide a supervised rehabilitation program for patients who have had an infarct or episode of unstable angina The program begins in hospital as soon as possible after admission It includes a graded exercise regimen and advice about risk factor control Such programs have many benefits for patients to help them to return quickly to normal life, including work and sexual activity The supervised exercise regimen helps restore the patient’s confidence There is clear evidence of the benefits of exercise for patients with ischaemic heart disease.54 Rehabilitation programs have been shown to be cost-effective Well-conducted programs are tailored to individual patients’ needs and are very popular with many patients.55 There are often long-term exercise groups available for people who have completed the formal classes Non-cardiac causes of chest pain Pulmonary embolism This is an important cause of chest pain that requires urgent treatment and must be distinguished from pain due to myocardial ischaemia and pericarditis Patients may have primary risk factors for venous thrombosis, such as factor V Leiden mutation, protein S or C or antithrombin III deficiency, antiphospholipid antibody (lupus anticoagulant), or an already known secondary hypercoagulable state of pregnancy, use of oral contraception, recent surgery, trauma, immobility, malignancy or heart failure Both acute and chronic lung disease can affect the right side of the heart, usually because of the changes in pulmonary vascular resistance that occur as a result of parenchymal lung disease or abnormalities of the pulmonary arteries themselves, for example as a result of pulmonary embolism or idiopathic pulmonary hypertension (p 273) These effects on the heart are called cor pulmonale Acute right ventricular abnormalities occur following large pulmonary emboli • T H E P A T I E N T W I T H C H E S T P A I N 177 Symptoms Patients may present with chest pain or dyspnoea, or both The chest pain is pleuritic and may occur anywhere in the chest Confusion with angina is only likely if the pain happens to be anterior or central Dyspnoea is usually more prominent than pain, and the differential diagnosis is more often with cardiac failure, pneumonia or asthma (p 276) Haemoptysis, until recently mistakenly ascribed to pulmonary infarction, may result from secondary pulmonary haemorrhages The examination This may be normal but a large pulmonary embolism is almost always associated with tachypnoea and tachycardia The patient may appear extremely breathless and signs of obstructive shock may be present with large life-threatening emboli While signs of right ventricular failure may be present, they are often difficult to detect in a collapsed patient Hypoxaemia from ventilation/perfusion mismatch is common, but clinical cyanosis is usually associated with either shock or right-to-left shunt through a patent foramen ovale in the wake of acute pulmonary hypertension Investigations Electrocardiography Minor emboli cause little more than sinus tachycardia; major ones may result in the classical McGinn-White (S1Q3T3) pattern or one of its variants (Fig 4.43), often with a degree of RBBB and ST segment elevation in lead V1 Two caveats should be borne in mind here: any cause of acute cor pulmonale can induce a pattern identical to embolism; and acute and chronic cor pulmonale may be electrocardiographically indistinguishable.56 New right precordial T wave inversion, also a sign of large embolism,57 is a useful sign in that it is less transient than the above patterns Figure 4.43 This breathless 47-year-old man had been treated for an unexplained DVT (deep venous thrombosis) a year previously His ‘room air’ PO2 was 57 mmHg and a chest X-ray showed clear lungs Angiography showed extensive bilateral embolisation and pulmonary artery pressure 80/36 mmHg, implying right ventricular hypertrophy from previous, silent episodes of embolisation Chest X-ray This is useful in two ways: (1) clear lung fields add great support to the diagnosis; and (2) other causes of acute—or chronic—cor pulmonale may be identified A number of 178 PRACTICA L C A R D I O L O G Y non-specific, mostly pleural-based abnormalities develop over time; the more diagnostic signs, such as segmental oligaemia, are so subtle as to be observed only in retrospect Arterial blood gases First, a simple rule: sick patients, who may at any time arrest, should not have arterial blood gases (ABGs) taken on ‘room air’ The latter may look appropriate but this is a dangerous approach for a sick patient The ABGs may be normal; indeed, theoretically, it is hard to see why occlusion of a pulmonary artery branch, per se, should cause hypoxaemia However, most patients eventually diagnosed as having thromboembolism are somewhat hypoxic, presumably through V/Q mismatch The PCO2 may be low (through hyperventilation) or normal; when suddenly high in, for example, a paralysed and ventilated patient, it constitutes excellent evidence for increased dead space ventilation following pulmonary arterial embolisation D-dimer While elevated blood levels are seen with thrombosis as well as a host of other conditions, normal levels help exclude thromboembolism, especially in low-risk accident and emergency patients with normal blood gases V/Q lung scan The lungs are scanned after intravenous injection of technetium (Tc-99) Non-perfused areas of the lung are compared with a scan performed after the patient inhales radioactive xenon gas Typically a pulmonary embolism appears as an area that is ventilated but not perfused A normal study practically excludes thromboembolism, while a ‘high-probability’ scan is almost diagnostic The problem is that many patients have ‘low’ or ‘medium probability’ scans and come to require further studies.58 Angiography Most suspected cases of pulmonary embolism are now investigated with a spiral CT pulmonary angiogram This requires an intravenous bolus of contrast The pulmonary arteries are visible down to the subsegmental branches The test is very sensitive and specific but involves a moderately high dose of radiation and a dose of contrast that may cause deterioration in renal function (contrast nephropathy) (p 137) Conventional angiography, like coronary angiography, is the standard against which other tests are evaluated However, it requires right heart catheterisation, and less-invasive tests have come to replace it in most centres Another analogy is venography in the search of ‘causal’ iliofemoral thrombi, now largely supplanted by Doppler ultrasound Echocardiography An echocardiogram may be useful where a large pulmonary embolus is suspected If there are changes suggesting raised pulmonary artery pressures or right ventricular strain (abnormal movement of the LV septum), the embolus is likely to be very large and the prognosis may be improved with the use of thrombolytic drugs Treatment The quality and timing of the supportive treatment in accident and emergency, radiology, intensive or coronary care is as important as the therapy directed at the embolus It involves pain control, adequate oxygenation (by mechanical ventilation if required), judicious fluid loading and intelligent use of inotropes, usually dobutamine Once the diagnosis is definite or likely, definitive treatment should begin without delay Pulmonary embolism is a life-threatening condition The evidence for the use of thrombolytic drugs does not come from large randomised trials,59 but the current approach is to give thrombolytic treatment to patients who are hypotensive or cyanosed and probably to those with evidence • T H E P A T I E N T W I T H C H E S T P A I N 179 of right ventricular strain The aim of treatment is to prevent death and to reduce the risk of developing chronic pulmonary hypertension (p 269) Most experience is with the use of streptokinase for these patients The usual regimen is a slow bolus of 250,000 units followed by an infusion at 100,000 units per hour The length of treatment and exact doses are still controversial Recombinant tissue plasminogen activator (rTPA) is increasingly used as an alternative, with a 10 mg bolus followed by another 90 mg over two hours Both fibrinolytics are followed by heparin or enoxaparin until warfarin takes over at a therapeutic international normalised ratio of 2.0–3.0 The majority of patients are treated with heparin at first It prevents fresh clot deposition—a form of secondary prevention The existing thrombus stabilises over a few days and becomes much less friable and less likely to embolise Intravenous unfractionated heparin is given as an infusion after a bolus of 5000–10,000 units The initial infusion rate of 1000 units/hour is adjusted according to the APPT Increasingly, fractionated low-molecular weight heparins such as enoxaparin are used instead: mg/kg is given subcutaneously twice a day Patients who are stable can often be discharged after a few days to have enoxaparin at home until the warfarin becomes therapeutic There is no need for adjustments according to clotting measurements (they not work with enoxaparin), but elderly patients and those with renal impairment should be given a lower dose Longer-term anticoagulation with warfarin is indicated for at least three to six months and probably indefinitely for recurrent emboli or persistent original indications for prophylaxis Those who cannot be safely anticoagulated should be offered a temporary or permanent inferior vena caval filter, easily inserted by the radiologist, but not without problems of its own This option is also valid for those with recurrent embolism while adequately anticoagulated In desperate situations, surgical or catheter (endovascular) removal of the thrombus (usually a saddle-embolus across the bifurcation of the pulmonary trunk) is justified If the patient is successfully salvaged, further thought ought to be given to the likely source of the emboli and the aggressive approach can be extended to iliofemoral thrombi.60 Aortic dissection Dissection of the aorta is an uncommon but extremely important cause of chest pain It may be difficult to distinguish from the pain of myocardial infarction, and indeed involvement of one of the coronary artery ostia (usually the right) may result in associated (usually inferior) myocardial infarction The majority of dissections begin with an intimal tear a few centimetres above the sinuses of Valsalva and either stay confined to the ascending aorta or spread to the arch and the descending aorta (Stanford type A).61 Another 30% start just below the origin of the left subclavian artery (type B) and tend to remain confined to the descending and abdominal aorta Symptoms The pain of aortic dissection is usually very severe and of very sudden onset It is of maximum intensity at the start It may have a ‘tearing’ quality and usually radiates to the interscapular region As expected, type A causes more anterior pain and type B more back pain, but the overlap should preclude any firm inferences The examination There may be signs of circulatory collapse—hypotension, cyanosis, dyspnoea—or even syncope due to bleeding into the pericardial sac and tamponade (the most common mechanism of death) or to bleeding into the left pleura or elsewhere Attempts to drain a recognised haemopericardium should be discouraged.62 Aortic regurgitation may cause acute heart failure because of severe disruption of the aortic valve annulus The early diastolic murmur of aortic regurgitation (p 304) may be audible, and if of recent onset is very suggestive of dissection Dissection into the origins of the great vessels may cause loss of pulses in one or both arms 180 PRACTICA L C A R D I O L O G Y Diagnosis Dissection is a medical and often surgical emergency Immediate investigations in hospital are necessary to confirm the diagnosis The chest X-ray may show widening of the mediastinum (Fig 4.44) The aortic knob may be abnormal, sometimes with a specific ‘ring sign’—0.5 cm or greater separation of the calcium in the intima from the outer edge of the aortic silhouette There is still doubt about the single most useful test, but transoesophageal echocardiography, CT scanning of the chest (Fig 4.45), MRI of the chest and aortography are all useful Institutional preferences vary, but in all cases the surgeons’ input into the choice of tests should be sought as early as possible, for obvious reasons Multi-detector CT scanning is used in some accident and emergency departments as a triple rule-out investigation (Fig 4.18(b)) Early experience with 64-slice scanners suggests they can reliably exclude significant coronary disease, pulmonary embolism and aortic dissection with a single scan and one breath hold Treatment All cases need aggressive reduction of the arterial blood pressure, usually to a mean of 60–70 mmHg, or a minimum compatible with cerebral and renal perfusion At the same time, the heart rate should be controlled, reducing the shearing rate of rise of the pressure wave (dp/dt) For this reason, initial therapy involves beta-blockers such as esmolol or metoprolol, or alpha-/beta-blockers such as labetolol, supplemented by direct vasodilators like sodium nitroprusside If beta-blockade is contraindicated, a calcium channel like verapamil can be used Type A dissections usually require surgical repair, sometimes involving Figure 4.44 CXR showing a widened mediastinum from a 75-year-old patient with sudden onset of severe chest pain that radiated to the back (arrow) • T H E P A T I E N T W I T H C H E S T P A I N 181 Figure 4.45 A CT of the chest with contrast injection showing an aortic dissection in a 50-year-old man with Marfan’s syndrome (arrow) aortic valve resuspension Distal, type B, dissections are treated medically or, increasingly, by endovascular stents.63 Pneumothorax This only uncommonly causes confusion with myocardial ischaemia The pain is sharp and of sudden onset, usually pleuritic, and associated with dyspnoea The patient may have had episodes before (spontaneous pneumothorax) or had a recent chest injury Spontaneous pneumothorax is more common in young, thin males There may be reduced or absent breath sounds over one of the upper lobes The chest X-ray will show absence of lung markings above the collapsed lung (Fig 4.46) Tension pneumothorax may cause significant displacement of the heart and mediastinum, often with marked ECG changes Even without tension, pneumothorax—especially left-sided—can mime myocardial infarction.64 Chest wall pain This is usually given as the diagnosis when no other explanation comes to mind The pain tends to be sharp and localised It may be associated with an area of chest wall tenderness There may have been a chest injury or recent exercise involving the chest muscles The cause of chest wall pain may sometimes be mysterious until the rash of herpes zoster appears Reassurance and analgesics may be all that is required, but in cases of doubt exercise testing may be needed to help exclude ischaemia and give reassurance Oesophageal causes Oesophageal reflux and less often oesophageal spasm can cause chest pain difficult to distinguish from that of ischaemia Gastroenterologists usually prefer to have cardiac causes excluded before they begin to investigate for gut causes 182 PRACTICA L C A R D I O L O G Y Figure 4.46 There is a massive right pneumothorax with collapsed lung seen against the hilum (arrow) There is increased translucency because of the absence of vascular shadows The pain of reflux is more often described as burning than dull or heavy; it tends not to be related to exercise There may be an association with meals but remember that angina pectoris may be worse after meals.65 Reflux pain may be helped by antacids but oesophageal spasm can be rapidly and confusingly relieved by sublingual nitrates, down to radiologic resolution of the ‘corkscrew oesophagus’ Chest pain: points to remember ecide whether myocardial ischaemia is a possible or likely cause D If angina seems possible, decide whether it is stable or unstable Unstable angina (ACS) patients should be admitted to hospital If myocardial infarction is a possibility, urgent admission should be arranged Early treatment decisions are based on ECG findings but the cardiac markers provide valuable information for risk stratification Do not label a patient as having ischaemic heart disease without objective evidence (e.g an exercise test), but not withhold treatment while waiting Aspirin and beta-blockers are the drugs of first choice for angina and for patients following a myocardial infarction, unless contraindicated Early intervention improves prognosis for STEMI and NSTEACS patients • T H E P A T I E N T W I T H C H E S T P A I N 183 C a s e - b a se d lear n i ng: is ch aemic hear t disease— a cu t e cor on ary sy nd r o mes Mr AB is a 48-year-old who presents to the accident and emergency department two hours after the onset of crushing retrosternal chest pain associated with sweating and anxiety He was admitted with an acute myocardial infarction (STEMI) and with a history of ‘diet-controlled’ type diabetes He has a significant family history of ischaemic heart disease, smokes 20 cigarettes a day and is overweight (BMI 32, waist measurement 105 cm) There is a history of hypertension but he stopped his anti-hypertensive drugs six months ago when he ran out of them He cannot remember the names of his medications Objectives for the group to understand The group needs to become familiar with the principles of the modern management of acute coronary syndromes Epidemiology and population health The presenter should ask questions about coronary artery disease epidemiology including the important risk factors (Chs and 2), disease prevalence and typical age of onset The importance of combinations of risk factors and previous ischaemic heart disease as a risk factor should be identified The influence of diabetes on risk and on future management must be discussed How have the risks of death and major complications of acute myocardial infarction changed over the last 30 years (p 157)? Presenting symptoms and clinical examination The group should discuss the features of ischaemic chest pain and compare the characteristics of pain due to myocardial infarction and other ACSs with those of angina A differential diagnosis of chest pain should be drawn up by the group (p 176) The common clinical findings associated with myocardial infarction should be mentioned Review of pathophysiology The presenter should ask questions about the difference in pathophysiology of STEMI and non-STEACS What are the common complications of myocardial infarction—early (e.g arrhythmias, cardiogenic shock and sudden death (p 167)) and late (e.g cardiac failure and arrhythmias)— and the risk of these, especially for Mr AB? What are some of the less common complications? The group should consider the aetiology and implications of an infarct-related ventricular septal defect, papillary muscle infarction and mitral regurgitation, LV thrombus and stroke (p 172) The group should discuss the concept of LV remodelling Evidence-based practice relevant to case The group should discuss the role and method of risk stratification using symptoms, ECG changes and cardiac markers for ACS patients What is the evidence supporting the use of ‘reperfusion therapy’ (thrombolysis and primary angioplasty) for non-STEACS versus STEMI? What is the role of anti-platelet therapy (clopidogrel and aspirin, IIb/IIIa inhibitors) for ACSs? What other drug treatment is of proven value for ACSs? The group should be led into a discussion of some of the important ACS trials What is the preferred method of administration for some of these drugs (e.g unfractionated heparin versus fractionated heparin)? What is the evidence for the use of dual anti-platelet therapy? Is there an optimum duration of treatment? 184 PRACTICA L C A R D I O L O G Y The group should understand the important predictors of outcome (e.g LV function) Should a patient be encouraged to join a cardiac rehabilitation program? Is there evidence of such a program’s usefulness (p 176)? Mr AB’s physical examination and initial investigations At this stage the presenter should ask the group what should be done first for Mr AB They should be persuaded that a 12-lead ECG (Fig 4.28) should be performed without delay What other examinations and investigations should be performed? On what is a decision to recommend reperfusion treatment based? What history, what physical examination and investigations? The group should discuss the ECG and suggest immediate management A catheter laboratory is available and Mr AB goes there for an immediate coronary angio graphy How much delay is acceptable for this process? When should thrombolysis be preferred to urgent intervention? The group should discuss the concepts of ‘door to balloon time’ and ‘door to needle time’ What treatment should Mr AB receive in the accident and emergency department while he waits for the catheter laboratory team to arrive? The presenter should ask the group about appropriate assessment of the patient (e.g blood pressure, physical examination) What analgesia should be given if Mr AB is in pain and distressed? What routine treatment is given before intervention is attempted (e.g aspirin, clopidogrel, intravenous heparin, right groin shave)? What blood tests should be performed urgently (blood count, electrolytes, creatinine, blood sugar cardiac markers)? The group should understand how any of these tests should be used to help manage the patient For example, what should be done about an elevated blood sugar or creatinine? Should a decision about treatment wait for the cardiac marker estimations to come back? What information should be given to Mr AB at this stage? Diagnostic pathology The presenter should emphasise the importance of the ECG in planning immediate treatment— ST elevation versus non-ST elevation The group should discuss the important ECG changes of myocardial ischaemia What is the significance of elevation of cardiac markers, and how should they be used to direct treatment? What is the role of exercise testing and sestamibi scanning for patients after an ACS? When should risk factor assessment be made, and what should be measured (e.g serum cholesterol and triglycerides, blood sugar levels)? The group should draw up a list of all the information that can be obtained that will influence the prognosis at the time of presentation and at the time of discharge Mr AB’s test results The only abnormal results were: troponin I 35, CK 2200, blood sugar mmol/L, creatinine 120 μmol/L, total cholesterol 6.2 mmol/L The group should discuss the significance of these results for Mr AB with regard to their significance for prognosis and further management Personal and professional development and medico-legal aspects The group should discuss the place of incentives and legislation in modifying cardiac risk factors in the population, such as smoking cessation, subsidisation of cholesterol-lowering drugs for primary prevention, and restrictions on the advertising of foods with a high saturated fat content What are the legal requirements for obtaining consent from a seriously ill patient for urgent treatment for coronary intervention versus drug treatment? Imaging The presenter should ask the group to outline the role of coronary angiography and echocardiography in ACSs Is there a place for the newer screening tests for coronary artery disease—multi-slice CT coronary angiography, coronary calcium scoring (p 138)—for these patients? • T H E P A T I E N T W I T H C H E S T P A I N 185 Mr AB’s prognosis Mr AB has a successful angioplasty to his left anterior descending coronary artery He is given intravenous abciximab at the start of the case He has TIMI flow at the end of the case and a left ventriculogram shows only mild anterior hypokinesis with an ejection fraction of 55% Left ventricular end-diastolic pressures are normal The group should be asked the significance of these findings for his prognosis What is the role of IIb/IIIa inhibitors in primary angioplasty for acute myocardial infarction? Therapeutics The presenter should ask the group to discuss the management of arrhythmias and acute cardiac failure complicating STEMI They should understand the types of thrombolytic drugs and their risks and side effects What drugs are appropriate as discharge treatment—drugs to control risk factors (secondary prevention versus primary prevention), drugs to prevent LV remodelling, anti-platelet drugs? What is the place of urgent surgery in ACS (p 158)? Psychosocial aspects The presenter should ask for comment on the role of the medical and nursing staff in helping patients to recover their confidence after suffering a life-threatening illness What should be discussed with the patient about the severity of the illness, especially when early treatment and discharge from hospital minimise the apparent severity of the condition? How can patients be helped to become non-smokers? What advice should be given about the timing of return to work and sexual activity? How should the patient’s understanding of the event and reason for continuing treatment be assessed? Mr AB’s long-term management What would be the group’s approach to the long-term management of Mr AB with particular reference to his risk factors—his diabetes, weight, smoking, cholesterol and hypertension? What is his prognosis and risk of a further ischaemic event with and without aggressive risk factor control? Research Are there any aspects of Mr AB’s management that lack an appropriate evidence base? 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Anticoagulation Trial for AF Investigators New Engl J Med 19 90; 323 :15 05 15 11 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