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

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24 ESC <strong>Guidelines</strong>emphasized and the patient should be informed and reassuredabout the benign course of the condition.Recommendations for investigation in patients withclassical triad of Syndrome XClass I(1) Resting echocardiogram in patients with angina andnormal or non-obstructed coronary arteries to assessfor presence of ventricular hypertrophy and/or diastolicdysfunction (level of evidence C)Class IIb(1) Intracoronary acetylcholine during coronary arteriography,if the arteriogram is visually normal, to assessendothelium-dependent coronary flow reserve, andexclude vasospasm (level of evidence C)(2) Intracoronary ultrasound, coronary flow reserve, or FFRmeasurement to exclude missed obstructive lesions, ifangiographic appearances are suggestive of a nonobstructivelesion rather than completely normal, andstress imaging techniques identify an extensive areaof ischaemia (level of evidence C)Vasospastic/variant anginaClinical picture. Patients with variant or vasospastic anginapresent with typically located pain, which occurs at rest,but does not, or only occasionally, occurs with exertion.Such pain characteristics are often caused by coronaryartery spasm, especially when the pain occurs at night andin the early morning hours. 311 If the chest pain is severe,this may lead to hospital admission. Nitrates usually relievethe pain within minutes. The terms vasospastic or variantangina may be used to describe such symptoms, although‘Prinzmetal angina’ 312 has also been used. This term wasinitially used to describe patients with clearly documentedST-elevation during chest pain due to coronary spasm.Angina at rest with preserved exercise tolerance may alsobe associated with significant obstructive coronary diseasewithout demonstrable vasospasm, and management is as outlinedfor typical symptoms. In the case of chest pain withoutsignificant coronary disease or coronary spasm, and no demonstrableischaemia, non-cardiac causes of pain should be consideredand conventional primary prevention adhered to.Asubstantialproportion ofpatients withahistorysuggestiveof vasospastic angina have obstructive coronary disease 313 andin such patients vasospastic angina may co-exist with typicalexertional angina due to fixed coronary lesions. Nonexertionalsymptoms due to vasospasm may also occur inpatients with minimal or no angiographically evident coronarydisease, and typical exertional angina and dyspnoeamay also occur in patients with vasospasm but entirelynormal coronary arteries. This indicates some overlap withpatients suffering from Syndrome X (Figure 6). 314 The prevalenceof vasospastic angina is difficult to assess, not leastbecause of its overlap with typical angina and Syndrome X.Vasospasm may occur in response to smoking, electrolytedisturbances (potassium, magnesium), cocaine use, coldstimulation, autoimmune diseases, hyperventilation orinsulin resistance. There is also an ethnic pre-disposition,with a higher prevalence in Japanese populations.Pathogenesis. The mechanisms leading to vasospastic anginaare not entirely clear, but hyperreactivity of smooth musclecells of the involved coronary segment 315 mayplayarole,and endothelial dysfunction may also be involved. 316,317 Thecauses of smooth muscle cell hyperreactivity are unknown,but several possible contributing factors have beensuggested, including increased cellular rho-kinase activity, 318abnormalities in ATP-sensitive potassium channels, 319 andmembrane Na þ -H þ countertransport. 320 Other contributingfactors may be imbalances in the autonomic nervoussystem, 321,322 enhanced intracoronary concentrations ofvasoconstricting substances, such as endothelin, 323 andhormonal changes, such as post-oopherectomy. 324,325Natural history and prognosis. The prognosis of vasospasticangina depends on the extent of underlying CAD. Deathand MI are not frequent in patients without angiographicallysignificant obstructive disease, but do occur. 326 Coronarydeath in the population with non-obstructive lesions hasbeen reported as 0.5% per annum, 327,328 but those withspasm superimposed on stenotic lesions do significantlyless well. 327,329–332Diagnosis of vasospastic anginaElectrocardiography. The ECG during vasospasm is classicallydescribed as showing ST-elevation. 312 In others, ST-depressioncan be documented, 333 whereas others may show noST-segment shift at all. 334,335 However, as attacks tend toresolve quickly, 12-lead ECG documentation tends to be difficult.Repeated 24 h ECG monitoring may be able to captureST-segment shifts associated with anginal symptoms inthese patients. 336Coronary arteriography. Although the demonstration ofST-elevation at the time of angina and a normal coronaryarteriogram make the diagnosis of variant angina highlylikely, there is often uncertainty about the diagnosis inless well-documented or clinically less straight forwardcases. Moreover, there is no unanimously accepted definitionof what constitutes coronary vasospasm.Spontaneous spasm during coronary arteriography is onlyoccasionally observed in patients with symptoms suggestiveof vasospastic angina. Hence, provocation tests are commonlyused to demonstrate the presence of coronary vasospasm.337 Hyperventilation and the cold pressor test haveonly a rather limited sensitivity for the detection ofcoronary spasm. 338 Thus, acetylcholine injections into thecoronary artery 339 are used in most centres today, but intracoronaryergonovine provocation gives similar results. 340,341Acetylcholine is injected in incremental doses of 10, 25, 50and 100 mg separated by 5 min intervals. Intravenous ergonovinemay also be used but may be associated with morediffuse spasm, which is not desirable.Coronary spasm may be focal or diffuse. 335 Lumenreductions between 75 and 99% when compared with thediameter following nitroglycerin injection are defined asspasm in the literature, 342,343 whereas lumen reductions,30% are commonly seen in non-spastic coronary segments344 and may represent the ‘physiological’ constrictorresponse to acetylcholine provocation. 342Acetylcholine or ergonovine provocation of coronaryspasm is a safe test, 341,345 if the agent is infused selectivelyinto each of the three major coronary arteries. Non-invasiveintravenous ergonovine provocative testing has also beendescribed with the addition of echocardiographic or perfusionscintigraphy to electrocardiographic monitoringincreasing the sensitivity and specificity of these
ESC <strong>Guidelines</strong> 25tests. 346,347 However, invasive documentation of vasospasmremains the gold standard against which diagnostic testsare evaluated, and as fatal complications due to prolongedspasm involving multiple vessels may occur with intravenousinjection of ergonovine, 348 the intracoronary route is preferred.Provocative testing without coronary arteriographyor provocative testing in patients with high-gradeobstructive lesions on coronary arteriography are notrecommended.Recommendations for diagnostic tests in suspectedvasospastic anginaClass I(1) ECG during angina if possible (level of evidence B)(2) Coronary arteriography in patients with characteristicepisodic chest pain and ST-segment changes thatresolve with nitrates and/or calcium antagonists todetermine the extent of underlying coronary disease(level of evidence B)Class IIa(1) Intracoronary provocative testing to identify coronaryspasm in patients with normal findings or nonobstructivelesions on coronary arteriography and theclinical picture of coronary spasm (level of evidence B)(2) Ambulatory ST-segment monitoring to identifyST-deviation (level of evidence C)TreatmentAims of treatmentTo improve prognosis by preventing MI and death. Efforts toprevent MI and death in coronary disease focus primarily onreducing the incidence of acute thrombotic events and thedevelopment of ventricular dysfunction. These aims areachieved by lifestyle or pharmacological interventionswhich (i) reduce plaque progession, (ii) stabilize plaque,by reducing inflammation and preserving endothelial function,and finally (iii) by preventing thrombosis if endothelialdysfunction or plaque rupture occur. In certain circumstances,such as in patients with severe lesions in coronaryarteries supplying a large area of jeopardized myocardium,revascularization offers additional opportunities toimprove prognosis by improving existing perfusion or providingalternative routes of perfusion.To minimize or abolish symptoms. Lifestyle changes, drugs,and revascularization all have a role to play in minimizing oreradicating symptoms of angina, although not necessarily allin the same patient.General managementPatients and their close associates should be informed of thenature of angina pectoris, and the implications of the diagnosisand the treatments that may be recommended. Thepatient can be reassured that, in most cases, both the symptomsof angina and prognosis can be improved with propermanagement. Comprehensive risk stratification should beconducted as outlined above, and particular attentionshould be paid to the elements of lifestyle that could havecontributed to the condition and which may influence prognosis,including physical activity, smoking, and dietaryhabits. The recommendations of the Third Joint EuropeanSocieties’ Task Force 250 on Cardiovascular DiseasePrevention in Clinical Practice should be followed.Treatment of the acute attackPatients should be advised to rest, at least briefly, from theactivity which provoked the angina and advised regardingthe use of sublingual nitrate for acute relief of symptoms.It is also useful to warn the patient of the need to protectagainst potential hypotension by sitting on the firstnumber of occasions when taking sublingual nitrate andalso other possible side-effects, particularly headache. Theuse of prophylactic nitrate to prevent predictable episodesof angina in response to exertion can be encouraged.Patients should be informed of the need to seek medicaladvice if angina persists for .10–20 min after resting and/or is not relieved by sublingual nitrate.All preventive measures, pharmacological and nonpharmacological,described in this document apply similarlyto men and women, 349 even if there is less documentation ofhealth benefits among female compared with male patientswith stable angina pectoris and the clinical presentation ofthe disease may differ between genders. Risk factors, clinicalpresentation, and the level of risk for serious cardiovascularcomplications should determine the need forpreventive and therapeutic interventions, rather than thegender of the patient. Recommendations concerninghormone replacement therapy have changed and are commentedupon subsequently.SmokingCigarette smoking should be strongly discouraged, as thereis abundant evidence that it is the most important reversiblerisk factor in the genesis of coronary disease in manypatients. 350,351 Cessation of smoking greatly improves bothsymptoms and prognosis. Patients often require specialhelp in abandoning their addiction, and nicotine replacementtherapy has proved effective and safe in helpingpatients with CAD to quit smoking. 352–355Diet and alcoholDietary interventions are effective in the prevention ofevents in patients with established CAD, when properlyimplemented. 1 Certain food types are to be encouragedsuch as fruit, vegetables, cereal, and grain products as wellas skimmed dairy products, fish, and lean meat, many ofwhich are major components of the Mediterranean diet.Patients should thus be encouraged to adopt a ‘Mediterranean’diet, with vegetables, fruit, fish, and poultry beingthe mainstays. The intensity of change needed in the dietmay be guided by the total and LDL cholesterol levels andother lipid abnormalities. 356 Those who are overweightshould be put on a weight reducing diet.Alcohol in moderation may be beneficial, 357 but excessiveconsumption is harmful, especially in patients with hypertensionor heart failure. It has been difficult to developpublic health recommendations on safe limits of alcoholuse, but moderate alcohol consumption should not bediscouraged. 1,358–360Omega-3 fatty acidsFish oils rich in omega-3 fatty acids (n-3 polyunsaturatedfatty acids) are useful in the reduction of hypertriglyceridaemia,and in the GISSI-Prevenzione trial, supplementation
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Guidelines on the Management of Stable Angina Pectoris ... - Cardio

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