1. CHRONIC STABLE
ANGINA GUIDELINES
DR. HABIB UR RAHMAN
HOD Cardiology,
Shifa International Hospital, Islamabad.
1

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. 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. Types of angina
1. Stable angina.
2. Unstable angina

5. PATHOPHYSIOLOGY
This 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. 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 to
be the main mediator of angina (chest pain) through stimulation
of 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. • 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. Silent angina
Myocardial 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. 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 65
According to an estimate 20 000 – 40 000
individuals in most European countries, of the
population per million suffer from angina. 9

10. PROGNOSTIC INDICATORS
In 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. Stable Angina Classification
• Exertional
• Variant or Prinzmetal’s Angina
• Anginal Equivalent Syndrome
• Syndrome-X
• Silent Ischemia
• Decubitus angina
• Noctural angina

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. 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. 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. Anginal Equivalent Syndrome
• Patient’s with exertional dyspnea rather than
exertional chest pain
• Caused by exercise induced left ventricular
dysfunction

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. Silent Ischemia
• Very common
• More episodes of silent than painful ischemia
in the same patient
• Difficult to diagnose
• Holter monitor
• Exercise testing

18. DIAGNOSIS & ASSESSMENT
18

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 GTN
Atypical angina (probable) Meets two of these characteristics
Non-cardiac chest pain Meets one or none of
the characteristics
19

20. Classification of angina severity according to the
Canadian Cardiovascular Society
Class Level of symptoms
Class- I ‘Ordinary activity does not cause angina’
Angina with strenuous or rapid
or prolonged exertion only
Class - 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 awakening
Class - 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 condition
Class - IV ‘Inability to carry out any physical activity
without discomfort’ or ‘angina at rest’
20

21. PHYSICAL EXAMINATION
Physical 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. LABORATORY
INVESTIGATIONS
22

23. Recommendations for laboratory investigation in initial
assessment of stable angina
CLASS – 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. 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. Recommendations for blood tests for routine
reassessment in patients with chronic stable
angina
CLASS IIa:
• Fasting lipid profile
• Fasting glucose
On an annual basis (level of evidence C)
25

26. CHEST X- RAY
CLASS – 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. NON- INVASIVE CARDIAC
INVESTIGATIONS
27

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. ECG
• ST segment depression with or without T
wave inversion that reverse after ischemia
disappears.
N.A.N 2009

30. AMBULATORY ECG
RECOMMENDATIONS:
CLASS – I:
• Angina with suspected arrhythmia (level of
evidence B)
CLASS – IIa:
• Suspected vasospastic angina (level of
evidence C)
30

31. Holter monitor
N.A.N 2009

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. Interpretation of ETT
TEST 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. REASON TO TERMINATE ETT
• Symptom limitation, e.g. pain, fatigue, dyspnoea, and claudication
• Combination of symptoms such as pain with significant ST-changes
Safety 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. Stable Angina
Exercise Testing
• The goal of exercise testing is to induce a
controlled, temporary ischemic state during
clinical and ECG observation

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. ECHOCARDIOGRAPHY
RECOMMECDATIONS:
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. 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. STRESS TESTING IN COMBINATION
WITH IMAGING
TESTS SENSITIVITY SPECIFICITY
% %
EXERCISE ECG 68 77
EXERCISE ECHO 80–85 84–86
EXERCISE MYOCARDIAL 85–90 70–75
PERFUSION
DOBUTAMINE STRESS 40–100 62–100
ECHO
VASODILATOR STRESS 56–92 87–100
ECHO
VASODILATOR STRESS 83–94 64–90
MYOCARDIAL
PERFUSION 39

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, with
a non-conclusive exercise ECG or stress imaging test
(level of evidence C)
40

41. INVASIVE CORONARY ANGIOGRAPHY
CLASS – 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. 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. RISK STRATIFICATION
43

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. 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. 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

48. TREATMENT
48

49. AIMS OF TREATMENT
1. To improve prognosis by preventing
myocardial infarction & death
o Reduce plaque progression
o Stabilize plaque
o Prevent thrombosis if endothelial dysfunction or
plaque rupture occur
2. To minimize or abolish symptoms
49

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. 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. Pharmacological therapy to
improve prognosis
52

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.  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. 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. 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 interval
BETA - 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. DRUGS ACTION COMMENTS REOMMENDATION
PHARMACOLOGICAL AGENTS (cont...) S
CALCIUM 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. SINUS NODE Reduces HR directly As effective as Beta IIa B
INHIBITORS blockers in reducing
symptoms
METABOLIC Increases glucose Limited IIb B
AGENTS metabolism haemodynamic
effects,
Trimetazidine not
available in all
countries,
Ranolazine not yet
licensed in Eourope
58

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. INVASIVE PROCEDURES
60

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. 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. 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. SELECTION OF PATIENTS FOR
REVASCULARIZATION
It 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. THANK YOU
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