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

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26 ESC <strong>Guidelines</strong>with one fish oil capsule (Omacor) daily was shown to reducethe risk of sudden death in patients (85% men) with a recentMI. 361 A detailed further analysis of the GISSI-Prevenzionetrial 362 showed an early reduction of cardiovascular deathwhich was dependent on fewer sudden deaths. The effectwas attributed to antiarrhythmic effects of omega-3 fattyacid supplementation, in agreement with previous experimentaldata. 362 A meta-analysis of omega-3 fatty acid supplementation363 confirmed the effect on sudden death and showed areduction of mortality, but concluded that reasonably largerisk reduction with such therapy can only be expectedamong high-risk patients, such as patients with a recent MI.A more recent meta-analysis of the effects of lipid-loweringtherapies on mortality also confirmed the beneficial effectof n-3 fatty acids in secondary prevention. 364 Patients withstable angina without high risk features should rarely beconsidered for omega-3 fatty acid supplementation. Dietaryintervention to achieve fish consumption at least onceweekly can, however, be more widely recommended. 365,366Vitamins and antioxidantsVitamin supplementation has not been shown to reducecardiovascular risk in patients with CAD. In contrast to theabove-mentioned findings with dietary intervention,several large studies have failed to find benefits frompharmacological supplementation with antioxidantvitamins. 367–369Hypertension, diabetes, and other disordersConcomitant disorders should be managed appropriately.Particular attention should be given to control of elevatedblood pressure, diabetes mellitus, and other features ofthe metabolic syndrome which increase the risk of progressionof coronary disease. Of particular note, the TaskForce report on CVD prevention 250 suggests considering alower threshold for institution of pharmacological therapyfor hypertension (130/85) for patients with establishedCHD (which would include patients with angina and noninvasiveor invasive confirmation of coronary disease).Patients with concomitant diabetes and/or renal diseaseshould be treated with a blood pressure goal of ,130/80 mm Hg. 286 Diabetes is a strong risk factor for cardiovascularcomplications and should be managed carefully withgood glycaemic control and attention to other riskfactors. 286,370,371Multifactorial intervention in diabetic patients mayindeed reduce both cardiovascular and other diabetic complicationsmarkedly. 372 Recently, the addition of pioglitizoneto other hypoglycaemic medication has been shown toreduce the incidence of death, non-fatal MI, or stroke (asecondary endpoint) in patients with type 2 diabetes andvascular disease by 16%; the primary composite endpoint,which included a number of vascular endpoints, was notsignificantly reduced. 373 Anaemia or hyperthyroidism, ifpresent, should be corrected.Physical activityPhysical activity within the patient’s limitations should beencouraged, as it may increase exercise tolerance, reducesymptoms, and has favourable effects on weight, bloodlipids, blood pressure, glucose tolerance, and insulin sensitivity.Advice on exercise must take into account theindividual’s overall fitness and the severity of symptoms.An exercise test can act as a guide to the level at whichan exercise programme can be initiated. Detailed recommendationson exercise prescription and on recreationaland vocational activities are provided by the ESC WorkingGroup on Cardiac Rehabilitation. 150Psychological factorsAlthough the role of stress in the genesis of CAD is controversial,there is no doubt that psychological factors are importantin provoking attacks of angina. Furthermore, thediagnosis of angina often leads to excessive anxiety.Reasonable reassurance is essential, and patients maybenefit from relaxation techniques and other methods ofstress control. Appropriate programmes may reduce theneed for drugs and surgery. 374 A randomized controlledtrial 375 of a self-management plan showed an apparentimprovement in the psychological, symptomatic, andfunctional status of patients with newly diagnosed angina.Car drivingIn most countries, patients with stable angina are permittedto drive except for commercial public transport or heavyvehicles. Stressful driving conditions should be avoided.Sexual intercourseSexual intercourse may trigger angina. Common sense willdictate that this should not be too physically or emotionallydemanding. Nitroglycerin prior to intercourse may behelpful. Phosphodiesterase (PGE5) inhibitors such as sildenafil,tadafil, and vardenafil, used in the treatment of erectiledysfunction, may bestow benefits in terms of exercise durationand can be safely prescribed to men with CAD butshould not be used in those receiving long-acting nitrates. 376The patient must be informed about the potentially harmfulinteractions between PGE5 inhibitors and nitrates or NO(nitric oxide) donors. 377,378EmploymentAn assessment should always be made of the physical andpsychological factors involved in an affected subject’swork (including housework). Patients should, if possible,be encouraged to continue in their occupation, with appropriatemodifications, if necessary.Pharmacological treatment of stableangina pectorisThe goals of pharmacological treatment of stable anginapectoris are to improve quality of life by reducing the severityand/or frequency of symptoms and to improve the prognosisof the patient. Measures of quality of life reflectdisease severity and carry prognostic information if properlyassessed. 379 When selecting evidence-based strategies forpharmacological prevention of cardiac complications anddeath, one should consider the often benign prognosis ofthe patient with stable angina pectoris. Pharmacotherapyis a viable alternative to invasive strategies for the treatmentof most patients with stable angina pectoris51,290,380,381 and was actually associated with fewercomplications than surgery or PCI during a 1-year follow-upof the MASS-II study. 382 An invasive treatment strategy may
ESC <strong>Guidelines</strong> 27be reserved for patients at high risk or patients with symptomsthat are poorly controlled by medical treatment. 290The intensity of preventive pharmacotherapy should be tailoredto the individual risk of the patient, keeping in mindthe relatively low risk of many patients with stable anginapectoris.Pharmacological therapy to improve prognosisCo-existing disorders such as diabetes and/or hypertensionin patients with stable angina should be well controlled, dyslipidaemiashould be corrected, and smoking cessationattempted (without or with pharmacological support).Statin and angiotensin-converting enzyme (ACE)-inhibitortreatment may provide protection above that which canbe ascribed to their lipid and blood pressure loweringeffects, respectively, and are discussed separately. Inaddition, antiplatelet treatment should always beconsidered for patients with ischaemic heart disease.Levels of evidence based on prognosis and symptom reliefare provided for the recommended treatments for anginain the treatment algorithm illustrated in Figure 7.Antithrombotic drugs. Antiplatelet therapy to preventcoronary thrombosis is indicated, due to a favourable ratiobetween benefit and risk in patients with stable CAD.Low-dose aspirin is the drug of choice in most cases,whereas clopidogrel may be considered for some patients.Because of the evolving story of increased cardiovascularrisks with cyclooxygenase (COX)-2 inhibitor or NSAIDtreatment, as well as interactions between NSAIDs andaspirin, these drugs will also be commented upon from thecardiovascular perspective.Low-dose aspirin. Aspirin remains the cornerstone ofpharmacological prevention of arterial thrombosis and isvery well studied. 383–387 Aspirin acts via irreversible inhibitionof platelet COX-1 and thus thromboxane production,which is normally complete with chronic dosing 75 mg/day. 385 The optimal antithrombotic dosage of aspirinappears to be 75–150 mg/day, as the relative risk reductionafforded by aspirin may decrease both below and above thisdose range. 387 In agreement with this interpretation, anobservational post hoc analysis of the CURE study found anincreased risk of cardiovascular events with an aspirindosage 200 vs. 100 mg per day (HR 1.23; 95% CI1.08–1.39) in patients with acute coronary syndromes. 388Randomized studies comparing different dosages of aspirinare, however, few.Contrary to the antiplatelet effects, the gastrointestinalside-effects of aspirin increase at higher doses. 385 In a wellconductedobservational study, a doubling of peptic ulcerbleeding was observed when the aspirin dose increasedfrom 75 to 160 mg, and another doubling when it increasedto 325 mg/day. 389 However, in a meta-analysis of long-termstudies, 390 there was no clear dose–response relationshipbetween studies regarding the risk of gastrointestinal haemorrhage.The incidence of gastrointestinal haemorrhage was2.30% with aspirin at a dosage below 162.5 mg/day vs.1.45% with placebo, relative risk 1.59 (95% CI 1.40–1.81).The relative risk in trials using higher doses (.162.5 mg)was 1.96 (95% CI 1.58–2.43). In this meta-analysis, thelarge US Physicians Health Study (USPHS) with 325 mg onalternate days dominated the low-dose aspirin group,whereas the The Swedish Angina Pectoris Aspirin Trial(SAPAT) study (75 mg daily) was not included. Variable definitionsand reporting of gastrointestinal bleeds mayconfound between-study comparisons of different dosagesof aspirin. Antiplatelet therapy in patients with upper gastrointestinalbleeding problems is commented upon afterclopidogrel.Intracranial bleeds may increase with all antithromboticdrugs. The relative risk of suffering an intracranial haemorrhageincreases by 30%, 391 but the absolute risk of suchcomplications attributable to antiplatelet drug therapy isless than 1 per 1000 patient-years of treatment with aspirinat doses 75 mg/day. 383,385 There is no evidence for a dosedependenceof the risk of intracranial bleeding with aspirin inthe therapeutically effective dose range. In patients withatherosclerotic vascular disease, where the main aetiologyof stroke is ischaemic, the net effect of aspirin treatmentregarding stroke is clearly beneficial. 383,385 Thus, thedosage of aspirin should be the lowest effective one inorder to optimize the balance between therapeutic gainsand gastrointestinal side effects during chronic therapy.SAPAT showed a 34% reduction of MI or cardiac death, correspondingto an absolute risk reduction (ARR) of 1% peryear, with aspirin 75 mg/day compared with placebo insotalol-treated patients with stable angina pectoris. 47Low-dose aspirin treatment slightly increased the risk ofmajor gastrointestinal haemorrhage (11 vs. 6 cases duringmore than 4000 patient-years of treatment in each group).Treatment was discontinued due to adverse effects in 109aspirin vs. 100 placebo-treated patients. 47 Thus, aspirin75 mg/day is both effective and well tolerated in stableangina pectoris. Treatment of a small subgroup of doctorswith angina pectoris with 325 mg aspirin every other day(compared with placebo) resulted in a significant reductionof non-fatal MI in the USPHS. 392 Low daily dosing of aspirin(75 mg) is thus well documented in stable angina pectorisand is preferred in order to increase compliance (with aregular daily medication routine) and to reduce risks ofside-effects and interactions.COX-2 inhibitors and NSAIDs. COX-2 inhibition reduces theproduction of prostacyclin, which has vasodilatory andplatelet-inhibiting effects. Attenuation of prostacyclin formationmay predispose to elevated blood pressure, acceleratedatherogenesis, and thrombosis upon plaque rupture. 393The recent withdrawal of rofecoxib (Vioxx), a highly selectiveCOX-2 inhibitor, was caused by findings of an increasedrisk of serious coronary events in a placebo-controlled trialof cancer prevention. 394 An increased risk of sufferingfatal or non-fatal MI was also found in a meta-analysis ofother randomized trials with rofecoxib. 395 There is also supportingevidence for harmful effects of COX-2 inhibitionfrom several observational studies. 396 A cancer preventiontrial with celecoxib showed a dose-related increase in therisk of suffering cardiovascular complications, with HRs of2.3 (95% CI 0.9–5.5) and 3.4 (1.4–7.8) for 200 and 400 mgcelecoxib bid, respectively. 397 A placebo-controlled studyof parecoxib/valdecoxib (iv þ oral therapy) for the treatmentof post-operative pain after CABG showed an increasedrisk of suffering cardiovascular events with only 10 days oftreatment with COX-2 inhibition. 398 Thus, there are indicationsfrom studies with several COX-2 inhibitors thatthey may increase the risk of coronary thrombotic eventsin patient populations with different levels of cardiovascular
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