Guidelines on the Management of Stable Angina Pectoris ... - Cardio

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46 ESC <strong>Guidelines</strong>was addressed in a Report from the ESC Joint Study Group onthe Treatment of Refractory Angina, published in 2002. 660Chronic stable refractory angina can be defined as a clinicaldiagnosis based on the presence of symptoms of stableangina, thought to be caused by ischaemia due to advancedcoronary disease and which are not controllable by a combinationof maximal medical therapy, bypass surgery and percutaneousintervention. Non-cardiac causes of chest painshould be excluded, and where appropriate, cognitive behaviouraltherapy, psychological assessment, and/or psychiatricconsultation may be considered.According to the previously mentioned report from theJoint Study Group, we have no accurate figures on theoccurrence and frequency of refractory angina. A Swedishsurvey of patients referred for coronary arteriographybecause of stable angina pectoris performed in 1994–95showed that nearly 10% of patients were rejected for revascularizationdespite severe symptoms. 661,662The most common reasons that revascularization is notconsidered appropriate are:(1) Unsuitable anatomy(2) One or several previous bypass grafting and/or PTCAprocedures(3) Lack of available graft conduits(4) Extra-cardiac diseases which increase perioperativemorbidity and mortality(5) Advanced age, often in combination with these factorsChronic refractory angina requires an effective optimizationof medical treatment assuring the use of differentdrugs in maximal tolerated doses. This issue is extensivelydeveloped in the original document of the Joint StudyGroup. Within the last few years, new modalities exploringnew concepts of therapy are under extensive evaluation,although not all have been successful: neuromodulationtechniques (transcutaneous electric nerve stimulation andspinal cord stimulation), thoracic epidural anaesthesia,endoscopic thoracic sympathectomy, stellate ganglionblockade, transmyocardial or percutaneous laser revascularization,angiogenesis, enhanced external counterpulsation,heart transplantation, and drugs that modulate metabolism.Transcutaneous electrical stimulation and spinal cordstimulation are well-established methods used in severalcentres for the management of refractory angina with positiveeffects on symptoms and a favourable side-effectprofile. 663–665 These techniques have a favourable analgesiceffect even without any improvement in myocardial ischaemia.A significant increase in the average exercise time ontreadmill testing has however been observed. The numberof published reports and the number of patients enrolledin clinical trials are small, and the long-term effects ofthese techniques are unknown.Enhanced external counterpulsation (EECP) is an interestingnon-pharmacological technique, which has also beeninvestigated largely in the USA. Two multi-centre registrieshave evaluated the safety and effectiveness of EECP. 666–668The technique is very well tolerated when used over aperiod of 35 hours of active counterpulsation during4–7-week period. Anginal symptoms were improved in75–80% of patients.Transmyocardial revascularization has been comparedwith medical therapy in several studies. In one study (in275 patients with CCS class IV symptoms), 76% of patientswho had undergone transmyocardial revascularizationimproved two or more functional classes after 1 year offollow-up, as compared with 32% (P , 0.001) of the patientswho received medical therapy alone. 669 Mortality did notdiffer significantly between the two groups. Other studiesof transmyocardial revascularization (either surgically or percutaneously)have been unable to confirm this benefit. 670,671In particular, a recent randomized controlled trial of 298patients showed that treatment with percutaneous myocardiallaser provides no benefit beyond that of a similar shamprocedure in patients blinded to their treatment. 672Furthermore, measurement of regional myocardial bloodflow and coronary flow reserve by means of PET has failedto show imporved perfusion following this procedure. 673International studies and registries are urgently requiredto clarify the epidemiology of this condition and furtherresearch is encouraged to definitely establish the roles ofexisting and novel alternative techniques to manage thesepatients.Conclusions and Recommendations(1) Angina pectoris due to coronary atherosclerosis is acommon and disabling disorder. Although compatiblewith longevity, there is an increased risk of progressionto MI and/or death. With proper management, thesymptoms can usually be controlled and the prognosissubstantially improved.(2) Every patient with suspected stable angina requiresprompt and appropriate cardiological investigation toensure that the diagnosis is correct and that the prognosisis evaluated. As a minimum, each patient shouldhave a carefully taken history and physical examination,a comprehensive risk factor evaluation, and aresting ECG.(3) To confirm the diagnosis and plan further management,an initial non-invasive strategy, using exercise ECG,stress echo, or myocardial perfusion scintigraphy ismost appropriate. This allows an assessment of thelikelihood of and the severity of CHD in patients withmild-to-moderate symptoms and effective risk stratification.In many patients, coronary arteriography mayfollow, but an initial invasive strategy without priorfunctional testing is rarely indicated, and may onlybe considered for patients with new onset severe oruncontrolled symptoms.(4) The exercise ECG should be interpreted with attentionto haemodynamic response, workload achieved, andclinical features of the individual as well as symptomsand ST-segment response. Alternative investigationsare needed when exercise is not possible or the ECG isnot interpretable, or in addition to exercise testingwhen the diagnosis remains uncertain or functionalassessment is inadequate.(5) In addition to their role in intial assessment of stableangina symptoms, myocardial perfusion scintigraphyand stress echocardiography are of particular value indemonstrating the extent and localization of myocardialischaemia.(6) Echocardiography and other non-invasive imaging modalities,such as magnetic resonance, are helpful in evaluatingventricular function.
ESC <strong>Guidelines</strong> 47(7) The interpretation of chest pain is particularly difficultin young and middle-aged women. The classicalsymptom complex of chronic stable angina, which is areliable indicator of obstructive coronary disease inmen, is not so in younger women. This problem is compoundedby the higher prevalence of coronary arteryspasm and ‘Syndrome X’ in women with chest painand by the frequency of ‘false-positive’ exercisetests. However, these complexities should not preventappropriate investigation and treatment of women,particularly the use of non-invasive investigations forthe purposes of risk stratification and use of secondarypreventative therapies.(8) After initial risk evaluation, risk-factor correction bylife-style modification should be implemented inaddition to pharmacological intervention as necessary.Strict diabetic control and weight control alongwith smoking cessation strategies are strongly advisedin all patients with coronary disease, and bloodpressure control is extremely important. Successfulrisk-factor management may modify the initial riskassessment.(9) In terms of specific pharmacological therapy, shortactingnitrates, when tolerated, may be used toprovide acute symtomatic relief. In the absence of contraindicationsor intolerance, patients with stableangina pectoris should be treated with aspirin(75 mg/day) and statin therapy. A beta-blocker shouldbe used first line or, alternatively, a calcium-channelblocker or long-acting nitrate may be used to provideanti-anginal effects, as described earlier, withadditional therapy as necessary. ACE-inhibition is indicatedin patients with co-existing ventricular dysfunction,hypertension, or diabetes and should be stronglyconsidered in patients with other high-risk features.Beta-blockers should be recommended in all post-MIpatients and in patients with LV dysfunction, unlesscontraindicated.(10) Anti-anginal drug treatment should be tailored to theneeds of the individual patient and should be monitoredindividually. The dosing of one drug should beoptimized before adding another one, and it is adviseableto switch drug combinations before attempting athree drug regimen.(11) If not undertaken for further prognostic evaluation,coronary arteriography should be undertaken whensymptoms are not satisfactorily controlled by medicalmeans, with a view to revascularization.(12) PCI is an effective treatment for stable angina pectorisand is indicated for patients with angina not satisfactorilycontrolled by medical treatment when thereare anatomically suitable lesions. Restenosis continuesto be a problem, which has been diminished byadvances in stenting technology. There is no evidencethat PCI reduces the risk of death in patients withstable angina compared with medical or surgicaltherapy.(13) CABG is highly effective in relieving the symptoms ofstable angina and reduces the risk of death over longtermfollow-up in particular subgroups of patients,such as those with LM stem stenosis, proximal LADstenosis, and three-vessel disease, especially if LVfunction is impaired.(14) There is evidence 674,675 that some gaps remainbetween best practice and usual care in the managementof stable angina. Specifically, many individualswith stable angina are not referred for functionaltesting to confirm the diagnosis and determine prognosis.Furthermore, there is worrying variability in ratesof prescription of statins and aspirin. Because of thewide variations in the quality of care afforded to sufferersfrom angina, there is a strong case for auditingseveral components of the management of the condition.As is the practice in some countries, local,regional, or national registers of the outcome of PCIand surgery should be created and maintained.References1. De Backer G, Ambrosioni E, Borch-Johnsen K, Brotons C, Cifkova R,Dallongeville J et al. European guidelines on cardiovascular diseaseprevention in clinical practice: third joint task force of European andother societies on cardiovascular disease prevention in clinical practice(constituted by representatives of eight societies and by invitedexperts). Eur J Cardiovasc Prev Rehabil 2003;10:S1–S10.2. Heberden. Some account of a disorder of the breast. Med Transact R CollPhys Lond 1772;2:59.3. Parry CH. An inquiry into the symptoms and causes of syncope anginosa,commonly called angina pectoris. Edinburgh, London: Bryce, Murray andCallow;1799.4. Crea F, Gaspardone A. New look to an old symptom: angina pectoris.Circulation 1997;96:3766–3773.5. Tomai F, Crea F, Chiariello L, Gioffre PA. Ischemic preconditioning inhumans: models, mediators, and clinical relevance. Circulation1999;100:559–563.6. Cohn PF, Fox KM, Daly C. Silent myocardial ischemia. Circulation2003;108:1263–1277.7. Gould KL, Kirkeeide RL, Buchi M. Coronary flow reserve as a physiologicmeasure of stenosis severity. J Am Coll Cardiol 1990;15:459–474.8. Gould KL. Effects of coronary stenoses on coronary flow reserve andresistance. Am J Cardiol 1974;34:48–55.9. Mohlenkamp S, Hort W, Ge J, Erbel R. Update on myocardial bridging.Circulation 2002;106:2616–2622.10. Pupita G, Maseri A, Kaski JC, Galassi AR, Gavrielides S, Davies G et al.Myocardial ischemia caused by distal coronary-artery constriction instable angina pectoris. N Engl J Med 1990;323:514–520.11. Braunwald E. Unstable angina. A classification. Circulation 1989;80:410–414.12. Myocardial infarction redefined–a consensus document of The JointEuropean Society of Cardiology/American College of CardiologyCommittee for the redefinition of myocardial infarction. Eur Heart J2000;21:1502–1513.13. Yamagishi M, Terashima M, Awano K, Kijima M, Nakatani S, Daikoku Set al. Morphology of vulnerable coronary plaque: insights from follow-upof patients examined by intravascular ultrasound before an acute coronarysyndrome. J Am Coll Cardiol 2000;35:106–111.14. Libby P. Molecular bases of the acute coronary syndromes. Circulation1995;91:2844–2850.15. Buffon A, Biasucci LM, Liuzzo G, D’Onofrio G, Crea F, Maseri A.Widespread coronary inflammation in unstable angina. N Engl J Med2002;347:5–12.16. Rose GA, Blackburn H. Cardiovascular survey methods. Monogr SerWorld Health Organ 1968;56:1–188.17. Cook DG, Shaper AG, MacFarlane PW. Using the WHO (Rose) angina questionnairein cardiovascular epidemiology. Int J Epidemiol 1989;18:607–613.18. Lampe FC, Whincup PH, Wannamethee SG, Ebrahim S, Walker M, Shaper AG.Chest pain on questionnaire and prediction of major ischaemic heart diseaseevents in men. Eur Heart J 1998;19:63–73.19. Bulpitt CJ, Shipley MJ, Demirovic J, Ebi-Kryston KL, Markowe HL, Rose G.Predicting death from coronary heart disease using a questionnaire. Int JEpidemiol 1990;19:899–904.20. LaCroix AZ, Guralnik JM, Curb JD, Wallace RB, Ostfeld AM, HennekensCH. Chest pain and coronary heart disease mortality among older menand women in three communities. Circulation 1990;81:437–446.
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Guidelines on the Management of Stable Angina Pectoris ... - Cardio

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