Chronic stable angina

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Chronic stable angina

  1. 1. CHRONIC STABLEANGINA GUIDELINES DR. HABIB UR RAHMAN HOD Cardiology,Shifa International Hospital, Islamabad. 1
  2. 2. DEFINITION• STABLE ANGINA: It is a clinical syndrome characterized by: Discomfort in the: chest, jaw, shoulder, back, or arms, typically elicited by exertion or emotional stress and relieved by rest or nitroglycerin.  Less typically in epigastric region. William Heberden first introduced the term ‘angina pectoris’ in 1772 to characterize a syndrome in which there was ‘a sense of strangling and anxiety’ in the chest, especially associated with exercise 2
  3. 3. Risk Factors• Major nonmodifiable • Nonconventional – Age/gender – HS CRP – Family hx – Homocysteine• Major modifiable – Lp(a) – Dyslipidemia – Hypertension – Smoking – DM, insulin resistance – Obesity – Sedentary – Atherogenic diet
  4. 4. Types of angina1. Stable angina.2. Unstable angina
  5. 5. PATHOPHYSIOLOGYThis clinical syndrome is attributable to myocardial ISCHEMIA.• Myocardial ischaemia is caused by an imbalance between myocardial oxygen supply and consumption and coronary flow, which is dependent on the luminal crossectional area of the coronary artery and coronary arteriolar tone.• Both cross-sectional area and arteriolar tone may be dramatically altered by the presence of atherosclerotic plaque within the vessel wall.• Ischaemia-induced sympathetic activation can further increase the severity of ischaemia through a variety of mechanisms including a further increase of myocardial oxygen consumption and coronary 5 vasoconstriction.
  6. 6. PATHOPHYSIOLOGY (CONTD.)• The ischaemic cascade is characterized by a sequence of events, 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.• Ischaemia is followed by reversible contractile dysfunction known as ‘stunning’• Recurrent episodes of ischemia and stunning may lead to a chronic but still reversible form of dysfunction known as ‘hibernation’. 6
  7. 7. • In the majority of patients, the pathological substrate of stable angina is atheromatous, narrowing of the coronary arteries.• Which leads to coronary obstruction.• At Luminal obstruction of 40%  Maximal flow during exercise can usually be maintained.• At luminal obstruction of >50% Coronary ischemia occurs• At Luminal obstruction of >80%  Coronary vascular resistance increases 3 timesIschemic threshold is influenced by other factors including : – The degree of development of collateral circulation – The degree of transmural distribution of myocardial perfusion from the more vulnerable subendocardium to the subepicardium. – coronary vascular tone – platelet aggregation 7
  8. 8. Silent anginaMyocardial ischaemia may also be silent: Lack of pain may be due to: – Ischaemia of insufficient duration and/or severity, – To damage of afferent cardiac nerves, or to – Inhibition of ischemic cardiac pain at spinal or supraspinal level. In patients who exhibit painless ischaemia, shortness of breath, and palpitation may represent anginal equivalents.  Breathlessness may be due to ischaemic left ventricular systolic or diastolic dysfunction or to transient ischamic mitral regurgitation. 8
  9. 9. EPIDEMIOLOGY• The prevalence of angina in community studies increases sharply with age in both sexes 0.1–1%  in women aged 45–54 10–15% in women aged 65–74 2–5% in men aged 45–54 10–20%  in men aged 65According to an estimate 20 000 – 40 000 individuals in most European countries, of the population per million suffer from angina. 9
  10. 10. PROGNOSTIC INDICATORSIn general, the outcome is worse in patients with:• reduced LV function• a greater number of diseased vessels• more proximal locations of coronary stenosis• greater severity of lesions• more severe angina• more extensive ischaemia• greater age 10
  11. 11. Stable Angina Classification• Exertional• Variant or Prinzmetal’s Angina• Anginal Equivalent Syndrome• Syndrome-X• Silent Ischemia• Decubitus angina• Noctural angina
  12. 12. Exertional or classical• It occurs due to increase myocardial oxygen demand during exertion or emotion in a patient of narrow coronary arteries. It relieved by rest and nitroglycerine.• Coronary artery obstructions are not sufficient to result in resting myocardial ischemia. However, when myocardial demand increases, ischemia results.
  13. 13. Variant or Prinzmetal’s Angina• Transient impairment of coronary blood supply by vasospasm or platelet aggregation• Majority of patients have an atherosclerotic plaque• Generalized arterial hypersensitivity• Long term prognosis very good
  14. 14. Prinzmetal’s Angina• Spasm of a large coronary artery• Transmural ischemia• ST-Segment elevation at rest or with exercise• More prolonged than in classical angina.• It occurs more in women under age 50.
  15. 15. Anginal Equivalent Syndrome• Patient’s with exertional dyspnea rather than exertional chest pain• Caused by exercise induced left ventricular dysfunction
  16. 16. Syndrome X• Typical, exertional angina with positive exercise stress test• Anatomically normal coronary arteries• Reduced capacity of vasodilation in microvasculature• Long term prognosis very good• Calcium channel blockers and beta blockers effective
  17. 17. Silent Ischemia• Very common• More episodes of silent than painful ischemia in the same patient• Difficult to diagnose• Holter monitor• Exercise testing
  18. 18. DIAGNOSIS & ASSESSMENT 18
  19. 19. SYMPTOMS Clinical classification of chest pain Typical angina (definite) Meets three of the following characteristics: • Substernal chest discomfort of characteristic quality and duration • Provoked by exertion or emotional stress • Relieved by rest and/or GTNAtypical angina (probable) Meets two of these characteristics Non-cardiac chest pain Meets one or none of the characteristics 19
  20. 20. Classification of angina severity according to the Canadian Cardiovascular SocietyClass Level of symptomsClass- I ‘Ordinary activity does not cause angina’ Angina with strenuous or rapid or prolonged exertion onlyClass - II ‘Slight limitation of ordinary activity’ Angina on walking or climbing stairs rapidly, walking uphill or exertion after meals, in cold weather, when under emotional stress, or only during the first few hours after awakeningClass - III ‘Marked limitation of ordinary physical activity’ Angina on walking one or two blocks on the level or one flight of stairs at a normal pace under normal conditionClass - IV ‘Inability to carry out any physical activity without discomfort’ or ‘angina at rest’ 20
  21. 21. PHYSICAL EXAMINATIONPhysical examination of a patient with (suspected) angina pectoris is important to assess the presence of :• Hypertension• Valvular heart disease• Hypertrophic obstructive cardiomyopathy.Physical examination should include:• Assessment of body-mass index (BMI)• Waist circumference to assist evaluation of the metabolic syndrome• Evidence of non-coronary vascular disease which may be asymptomatic• Other signs of comorbid conditions. However, there are no specific signs in angina pectoris.During or immediately after an episode of myocardial ischaemia:• a third or fourth heart sound may be heard and• mitral insufficiency may also be apparent during ischaemia. Such signs are, however, elusive and non-specific. 21
  22. 22. LABORATORYINVESTIGATIONS 22
  23. 23. Recommendations for laboratory investigation in initial assessment of stable anginaCLASS – I: (In all patients)• Fasting lipid profile, including TC, LDL, HDL, and triglycerides (level of evidence B)• Fasting glucose (level of evidence B)• Full blood count including Hb and white cell count (level of evidence B)• Creatinine (level of evidence C)CLASS – I: (if specifically indicated on the basis of clinical evaluation)• Markers of myocardial damage if evaluation suggests clinical instability or ACS (level of evidence A)• Thyroid function if clinically indicated (level of evidence C) 23
  24. 24. LAB TESTS (Contd...)CLASS – IIa:• Oral glucose tolerance test (level of evidence B)CLASS – IIb:• Hs-C-reactive protein (level of evidence B)• Lipoprotein a, ApoA, and ApoB (level of evidence B)• Homocysteine (level of evidence B)• HbA1c (level of evidence B)• BNP (level of evidence B) 24
  25. 25. Recommendations for blood tests for routinereassessment in patients with chronic stable anginaCLASS IIa:• Fasting lipid profile• Fasting glucoseOn an annual basis (level of evidence C) 25
  26. 26. CHEST X- RAYCLASS – I:• CXR in patients with suspected heart failure (level of evidence C)• CXR in patients with clinical evidence of significant pulmonary disease (level of evidence B)The presence of : • Cardiomegaly • Pulmonary congestion • Atrial enlargement • Cardiac calcifications – has been related to impaired prognosis 26
  27. 27. NON- INVASIVE CARDIAC INVESTIGATIONS 27
  28. 28. ECG Recommendations for resting ECG for initial diagnostic assessment of angina:CLASS – I:• Resting ECG while pain free (level of evidence C)• Resting ECG during episode of pain (if possible) (level of evidence B) Recommendations for resting ECG for routine reassessment in patients with chronic stable angina:CLASS –IIb:• Routine periodic ECG in the absence of clinical change (level of evidence C) 28
  29. 29. ECG• ST segment depression with or without T wave inversion that reverse after ischemia disappears. N.A.N 2009
  30. 30. AMBULATORY ECGRECOMMENDATIONS:CLASS – I:• Angina with suspected arrhythmia (level of evidence B)CLASS – IIa:• Suspected vasospastic angina (level of evidence C) 30
  31. 31. Holter monitor N.A.N 2009
  32. 32. ECG STRESS TESTING• SENSITIVITY = 68%• SPECIFICITY = 77%• Has no diagnostic value in the presence of: o LBBB o PACED RHYTHM o WPW- SYNDROME• FALSE POSITIVE results are seen in: o LVH o ELECTROLYTE IMBALANCE o INTERVENTRICULAR CONDUCTION ABNORMALITY o DIGITALIS USE o ALSO LESS SENSITIVE & SPECIFIC IN WOMEN 32
  33. 33. Interpretation of ETTTEST WOULD BE POSITIVE IF: – Horizontal or down sloping ST – Depression of =/> 1mm (0.1mV) – Chest pain – Occur at low work load or in early stages exercise – Persist for >3 mins in recovery period – Impaired LV function with increased probability of CAD: • Fall in systolic blood pressure • Lack of increase in BP with exercise • Appearance of a systolic murmur of MR • Ventricular Arrhythmias 33
  34. 34. REASON TO TERMINATE ETT• Symptom limitation, e.g. pain, fatigue, dyspnoea, and claudication• Combination of symptoms such as pain with significant ST-changesSafety reasons such as the following:• Marked ST-depression (>2 mm ST-depression can be taken as a relative indication for termination and 4 mm as an absolute indication to stop the test)• ST-elevation 1 mm• Significant arrhythmia• Sustained fall in systolic blood pressure >10 mmHg• Marked hypertension (>250 mmHg systolic or >115 mmHg diastolic)• Achievement of maximum predicted heart rate may also be a reason to terminate the test in patients with excellent exercise tolerance who are not tired and at the discretion of the supervising physician. 34
  35. 35. Stable Angina Exercise Testing• The goal of exercise testing is to induce a controlled, temporary ischemic state during clinical and ECG observation
  36. 36. Exercise Testing Contraindications• MI—impending or acute• Unstable angina• Acute myocarditis/pericarditis• Acute systemic illness• Severe aortic stenosis• Congestive heart failure• Severe hypertension• Uncontrolled cardiac arrhythmias
  37. 37. ECHOCARDIOGRAPHYRECOMMECDATIONS:CLASS – I:1. Patients with abnormal auscultation suggesting valvular heart disease or hypertrophic cardiomyopathy (level of evidence B)2. Patients with suspected heart failure (level of evidence B)3. Patients with prior MI (level of evidence B)4. Patients with LBBB, Q-waves, or other significant pathological changes on ECG, including ECG LVH (level of evidence C) 37
  38. 38. Stable Angina Stress Echo• Ischemia may cause wall motion abnormalities, no rise of fall in LVEF ( left ventricular ejection fraction )• This formula gives one a fraction, e.g., 0.60. Multiply this fraction by 100 gives a % figure, e.g., 60%• Sensitivity/specificity same as nuclear testing
  39. 39. STRESS TESTING IN COMBINATION WITH IMAGING TESTS SENSITIVITY SPECIFICITY % %EXERCISE ECG 68 77EXERCISE ECHO 80–85 84–86EXERCISE MYOCARDIAL 85–90 70–75PERFUSIONDOBUTAMINE STRESS 40–100 62–100ECHOVASODILATOR STRESS 56–92 87–100ECHOVASODILATOR STRESS 83–94 64–90MYOCARDIALPERFUSION 39
  40. 40. CT - SCAN• Detects calcium in coronaries.• Quantifies the extent of calcification.The Agatston score the most commonly used score, is based on the area and density of calcified plaques.SENSITIVITY: 95%SPECIFICITY: 98%NEGATIVE PREDICTIVE VALUE: 93 – 99%RECOMMENDATIONS:CLASS – IIb:Patients with a low pre-test probability of disease, witha non-conclusive exercise ECG or stress imaging test(level of evidence C) 40
  41. 41. INVASIVE CORONARY ANGIOGRAPHYCLASS – I:• Severe stable angina (Class 3 or greater CCS, with a high pre-test probability of disease, particularly if the symptoms are inadequately responding to medical treatment (level of evidence B)• Survivors of cardiac arrest (level of evidence B)• Patients with serious ventricular arrhythmias (level of evidence C)• Patients previously treated by myocardial revascularization (PCI, CABG) who develop early recurrence of moderate or severe angina pectoris (level of evidence C)CLASS – IIb:• Patients with an inconclusive diagnosis on non-invasive testing, or conflicting results from different noninvasive modalities at intermediate to high risk of coronary disease (level of evidence C)• Patients with a high risk of restenosis after PCI if PCI has been performed in a prognostically important site (level of evidence C) 41
  42. 42. Cardiac Catheterization Indications• Suspicion of multi-vessel CAD• Determine if CABG/PTCA feasible• Rule out CAD in patients with persistent/disabling chest pain and equivocal/normal noninvasive testing• percutaneous transluminal coronary angioplasty• coronary artery bypass grafting
  43. 43. RISK STRATIFICATION 43
  44. 44. ANGINA WITH NORMAL CORONARIES: Features of chest pain may suggest:• Non- cardiac chest pain• Atypical angina including vasospastic angina• Cardiac syndrome X Important to differentiate non-cardiac chest pain from other 2 conditions: If angiographic appearances are suggestive of non- obstructing lesions & stress imaging techniques identify an extensive area of ischemia then : Intravascular USG or assessment of coronary flow reserve or fractional flow reserve may be considered to exclude missed obstructive lesions. Intra coronary ACETYLCHOLINE or ERGONOVINE may be administered during coronary arteriography 44
  45. 45. VASOSPASTIC / VARIANT ANGINA• Characterized by typically located pain.• Usually occurs at rest (occasionally with exertion)• Relieved within minutes with Nitrates• Pain is associted with ST elevation• May coexist with typical exertional angina due to fixed coronary lesions.• Vasospasm may occur in response to: – Smoking – Electrolyte disturbance – Cocaine use – Cold stimulation – Autoimmune disease – Hyperventilation – Insulin resistance• Prognosis depends on underlying coronary artery disease.• Ambulatory ST segment monitoring may be helpful.• TREATMENT FOCUSES ON REMOVING THE STIMULUS, Ca CHANNEL BLOCKERS AND Nitrates. 45
  46. 46. Syndrome X It requires the presence of: – Typical exercise induced angina – Positive ETT or STRESS IMAGING – Normal coronary arteries Resting ECHO  LVH & Diastolic dysfunction (CLASS-I , LOE-C) Intracoronary acetylcholine & intracoronary USG , flow reserve or FFR (CLASS- IIb, LOE-C) Survival prognosis is favourable, morbidity is high Treatment should focus on symptom relief Other risk factors of endothelial dysfunction like HTN, Dyslipedemias should be treated appropriately. 46
  47. 47. 47
  48. 48. TREATMENT 48
  49. 49. AIMS OF TREATMENT1. To improve prognosis by preventing myocardial infarction & death o Reduce plaque progression o Stabilize plaque o Prevent thrombosis if endothelial dysfunction or plaque rupture occur2. To minimize or abolish symptoms 49
  50. 50. GENERAL MANAGEMENT• Patients & their close associates should be informed of the nature of angina & the implications of the diagnosis & treatment should be recommended.• Advice should be given for the management of an acute attack i-e to rest briefly at least, from the activity that provoked the angina and the use of sublingual nitrates.• Patient should be informed of the potential S.E of NITRATES & its appropriate use.• Patient should be informed of the need to seek medical advice if angina symptoms persist for > 20 mins after rest & is not relieved after taking Nitrates.• Cigarette smoking should be STRONGLY discouraged.• Patient should be advised to take MEDITERRANEAN diet with vegetables, fruits, fish & poultry being the mainstay.• Alcohol in moderation may be beneficial but excessive consumption is harmful. 50
  51. 51. General management (Cont..)• Fish oils rich in OMEGA-3 are recommended atleast once weekly.• Physical activity within the patient’s limitations should be encouraged.• Concomitant disorders like HTN & D.M should be managed appropriately: – Pts with DM & or Renal disease should be treated with a BP goal of < 130/80 mm of Hg – Multifactorial intervention in diabetic patient may reduce both cardiovascular & diabetic complications.• Anemia & hyperthyroidism, if present, should be corrected. 51
  52. 52. Pharmacological therapy to improve prognosis 52
  53. 53. RECOMMENDATIONSANTITHROMBOTIC DRUGS: – Low dose Asprin (75mg/Day) in all patients without contraindications: • Active GI bleeding • Asprin allergy • Intolerance (CLASS- I, LOE-A ) – Clopidogrel in pts who can not take asprin. (CLASS- IIa, LOE- B) 53
  54. 54.  LIPID LOWERING DRUGS:• STATIN therapy for all patients with CAD. (CLASS – I,LOE-A)• High dose statin therapy in high risk pts with proven CAD. ( CLASS – IIa, LOE- B)• Fibrate therapy in pts with low HDL & high TGs who have DM or METABOLIC syndrome (CLASS– IIb, LOE-B)• Fibrates or Nicotinic Acid as adjunctive therapy to statins in pts with low HDL & high TGs at HIGH RISK. (CLASS – IIb, LOE-C) 54
  55. 55. ACE - INHIBITORS:• Patients with co-incident indications for ACE Inhibition e.g HTN ,HF (CLASS-I, LOE-A)• All patients with Angina & proven CAD. (CLASS-IIa, LOE-B)BETA – BLOCKERS:• Patient post MI or with HF (CLASS–I, LOE-A) 55
  56. 56. PHARMACOLOGICAL AGENTS DRUGS ACTION COMMENTS RECOMMENDA TIONS SHORT ACTING Venodilation, dec. •Sublingual adm. IC NITRATES Diastolic filling, •Situational prophylaxis reduced intra - cardiac pressure, LONG ACTING •Oral/transdermal prep. IC dec. subendocardial NITRATES • Care to maintain a perfusion. nitrate free intervalBETA - BLOCKERS Dec oxygen demand •Less SE with B1 selective IA by dec HR, dec agents contractility, dec BP. •Titrate dose •Proven to red. ferquency of symptoms & improves exercise tolerance. 56
  57. 57. DRUGS ACTION COMMENTS REOMMENDATIONPHARMACOLOGICAL AGENTS (cont...) SCALCIUM channel •Systemic & •Proven to reduce IA BLOCKERS Coronary frequency of vasodilatation by symptoms & inhibition of L-type improve exercise channels tol. •Verapamil & •Efficacy diltiazem red. comparable with myocardial Beta blockers contractility, HR & •Particularly AV cond effective in •Dihydropyridines vasospastic angina are more vasoselective K-CHANNEL •Activates K- Nicorandil has IC OPENER channels shown to dec. •Nitrate like vaso death, MI & dilator effect hopitalizations in one RCT. 57
  58. 58. SINUS NODE Reduces HR directly As effective as Beta IIa BINHIBITORS blockers in reducing symptomsMETABOLIC Increases glucose Limited IIb B AGENTS metabolism haemodynamic effects, Trimetazidine not available in all countries, Ranolazine not yet licensed in Eourope 58
  59. 59. GENERAL RECOMMENDATIONS FOR PHARMACOLOGICAL THERAPY• Anti anginal treatment should be tailored according to the needs of individual patients & should be monitored individually.• Short acting nitrate therapy for immediate relief of acute symptoms.• Different drugs may have additive anti anginal effects• Dosing of 1 drug should be optimized before adding another.• Advisable to switch drug combinations before attempting 3 drugs regimen.• Poor compliance should be considered when drug therapy is unsuccessful.• Patients with symptoms who are poorly controlled on double therapy should be assessed for suitability for revascularization if not already considered. 59
  60. 60. INVASIVE PROCEDURES 60
  61. 61. CABG• Main indications: prognostic & symptomatic• Prognostic benefit mainly due to reduction in cardiac mortality.• Anatomical groups shown to have better outcome: – Significant stenosis of left main stem. – Significant proximal stenosis of 3 major coronary arteries. – Significant stenosis of 2 major coronary arteries including high grade stenosis of LAD artery. – 3 vessel disease with impaired LV function.• Reduces symptoms of angina & ischemia in pts with CAD.• OVERALL OPERATIVE MORTALITY OF 1 – 4% 61
  62. 62. PERCUTANEOUS CORONARY INTERVENTION (PCI)• Single or multivessel PCI can be performed with high likelihood of success using BMS & DES + adjuvent medical therapy. – Risk of death = 0.3 -1 %• Compared with medical therapy: – PCI does not provide survival benefit in stable angina. – PCI is more effective at reducing events that impair quality of life. 62
  63. 63. Revascularization Vs Medical therapy• Initial pharmacological approach to symptom control may be taken in patients NOT at high risk.• Revascularization may be recommended for patients with suitable anatomy who do not respond adequately to medical therapy OR for patients who wish to remain physically active.• Optimal secondary preventive therapy (e.g Antiplatelets & Statins) should be continued in patients after revascularization IRRESPECTIVE of the need of anti-anginal therapy. 63
  64. 64. SELECTION OF PATIENTS FOR REVASCULARIZATIONIt should be based on:• Risk of peri-procedural morbidity & mortality• Likelihood of success ( technical suitability)• Risk of restenosis or graft occlusion• Completeness of revascularization• Diabetic status• Local hospital experience in Cardiac surgery & PCI• Patient’s preference 64
  65. 65. THANK YOU 65

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