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

ESC <strong>Guidelines</strong> 3societies and translated into the local language, whennecessary.All in all, the task of writing <strong>Guidelines</strong> or ExpertConsensus Document covers not only the integration of themost recent research but also the creation of educationaltools and implementation programmes for the recommendations.The loop between clinical research, writing ofguidelines, and implementing them into clinical practicecan then only be completed if surveys and registries areorganized to verify that actual clinical practice is inkeeping with what is recommended in the guidelines. Suchsurveys and registries also make it possible to check theimpact of strict implementation of the guidelines onpatient outcome.Classes of RecommendationsClass IClass IIClass IIaClass IIbClass IIIEvidence and/or general agreement that a givendiagnostic procedure/treatment is beneficial,useful, and effectiveConflicting evidence and/or a divergence of opinionabout the usefulness/efficacy of the treatmentor procedureWeight of evidence/opinion is in favour ofusefulness/efficacyUsefulness/efficacy is less well established byevidence/opinionEvidence or general agreement that the treatmentor procedure is not useful/effective and, in somecases, may be harmfulLevel of evidence A Data derived from multiple randomizedclinical trials or meta-analysesLevel of evidence B Data derived from a single randomizedclinical trial or large non-randomizedstudiesLevel of evidence C Consensus of opinion of the experts and/orsmall studies, retrospective studies, andregistriesIntroductionStable angina pectoris is a common and disabling disorder.However, the management of stable angina has not beensubjected to the same scrutiny by large randomized trialsas has, for example, that of acute coronary syndromes(ACS) including unstable angina and myocardial infarction(MI). The optimal strategy of investigation and treatmentis difficult to define, and the development of new tools forthe diagnostic and prognostic assessment of patients,along with the continually evolving evidence base forvarious treatment strategies, mandates that the existingguidelines be revised and updated. The Task Force hastherefore obtained opinions from a wide variety of expertsand has tried to achieve agreement on the best contemporaryapproaches to the care of stable angina pectoris, bearingin mind not only the efficacy and safety of treatments butalso the cost and the availability of resources. The TaskForce has taken the view that these guidelines shouldreflect the pathophysiology and management of angina pectoris,namely myocardial ischaemia due to coronary arterydisease (CAD), usually macrovascular, i.e. involving largecoronary arteries, but also microvascular in some of thepatients. Furthermore, this Task Force does not deal withprimary prevention, which has already been covered inother recently published guidelines 1 and has limited its discussionon secondary prevention. Recently published guidelinesand consensus statements that overlap to aconsiderable extent with the remit of this document arelisted in Table 1.Definition and pathophysiologyStable angina is a clinical syndrome characterized bydiscomfort in the chest, jaw, shoulder, back, or arms, typicallyelicited by exertion or emotional stress and relievedby rest or nitroglycerin. Less typically, discomfort mayoccur in the epigastric area. William Heberden first introducedthe term ‘angina pectoris’ in 1772 2 to characterizea syndrome in which there was ‘a sense of strangling andanxiety’ in the chest, especially associated with exercise,although its pathological aetiology was not recognizeduntil some years later. 3 It is now usual to confine theterm to cases in which the syndrome can be attributed tomyocardial ischaemia, although essentially similar symptomscan be caused by disorders of the oesophagus,lungs, or chest wall. Although the most common cause ofmyocardial ischaemia is atherosclerotic CAD, demonstrablemyocardial ischaemia may be induced in the abscence byhypertrophic or dilated cardiomyopathy, aortic stenosis,or other rare cardiac conditions in the absence of obstructiveatheromatous coronary disease, which are notconsidered in this document.Myocardial ischaemia is caused by an imbalance betweenmyocardial oxygen supply and myocardial oxygen consumption.Myocardial oxygen supply is determined by arterialoxygen saturation and myocardial oxygen extraction,which are relatively fixed under normal circumstances,and coronary flow, which is dependent on the luminal crosssectionalarea of the coronary artery and coronary arteriolartone. Both cross-sectional area and arterioloar tone may bedramatically altered by the presence of atheroscleroticplaque within the vessel wall, leading to imbalancebetween supply and demand when myocardial oxygendemands increase, as during exertion, related to increasesin heart rate, myocardial contractility, and wall stress.Ischaemia-induced sympathetic activation can furtherincrease the severity of ischaemia through a variety ofmechanisms including a further increase of myocardialoxygen consumption and coronary vasoconstriction. Theischaemic cascade is characterized by a sequence ofevents, resulting in metabolic abnormalities, perfusion mismatch,regional and then global diastolic and systolic dysfunction,electrocardiographic (ECG) changes, and angina.Adenosine released by ischaemic myocardium appears tobe the main mediator of angina (chest pain) through stimulationof A1 receptors located on cardiac nerve endings. 4Ischaemia is followed by reversible contractile dysfunctionknown as ‘stunning’. Recurrent episodes of ischaemia and