The document discusses the management of chronic stable angina. It defines angina and stability, and outlines the typical treatment approach which includes patient education, risk factor modification through lifestyle changes and medical therapy, and consideration of revascularization. The mainstay of treatment is optimal medical therapy focusing on symptom control through anti-anginal medications like beta-blockers, calcium channel blockers, and nitrates, as well as prevention of adverse outcomes with aspirin and other drugs.

1. MANAGEMENT OF
CHRONIC STABLE ANGINA
DR Suman Mitra
CHAIRPERSON- Dr Dipankar
Ghosh Dastidar

2.  Angina pectoris has been coined from the Greek word
“ankhon” and the Latin word “pectus” meaning
‘strangling’ and ‘chest’ respectively.
 Typical angina is defined as substernal chest discomfort
with a characteristic quality and duration that
is(1),provoked by exertion or emotional stress(2) and
relieved by rest or nitroglycerin(3).
 “Stability” usually implies that “there is no substantial
change in symptoms over several weeks(60 days).”
 Also includes the stable and often asymptomatic phases
following an ACS.
SUPPLY
DEMAND
Reversible episodes of demand and
supply mismatch.

3. Gradation of angina as per ccs scale:

4. Ischemia cascade:

5. TREATMENT
BACKBONE
1. PATIENT
EDUCATION
2. RATIONAL
MEDICAL
THERAPY
3.REVASCULA
RISATION
CONSIDERATI
ON
PROPER
FOLLOW UP

6. BASIC BACKBONE TO DIAGNOSIS:
BASICTESTING:
• Biochemical tests- complete hemogram,lipid
profile(including LDL levels),thyroid
profile,LFT,diabetic screening,creatine
kinase(in patients on statins).
• Baseline ECG:
• For future comparisons.
• May help diagnosing vasospasm when taken
at the time of pain.
• Detection of dyanamic ST segment changes.
• Other inherent abnormalities(lbbb,rbbb,lvh)

7. • Resting Echocardiography:
• To asses cardiac structure and function.
• May detect rwma even in presence of normal
LV function which increases likelihood of
CAD.
• May help ruling out AS,HCM as alternative
causes of symptoms.

8. Essential decision making steps:
Pre test
probability
Non invasive
tests in
intermediate
group
Initiation of
OMT and
further risk
stratification
Pre test probability
determination(clinical)
Influenced maximally by
age,gender,nature of
symptoms
Achievement of management
target

9. Essential non invasive modalities:
• Stress ECG:
• Simplest,elementary,most usefull.
• Performs best in a patient where the pre test
probability is around 15-65%.
• Main diagnostic criteria-
“horizontal/downsloping ST-segent
depression>0.1mV,persisting for at least 0.06-
0.08 after qrs completion in one or more leads.”
• Mean sensitivity 68%,mean specificity 77%.(only
valid when the baseline ecg was normal).
• Exercise tsting usually terminated after 85% of
age-predicted maximum heart rate is reached.

10. • Stress Echocardiography
(exercise>pharmacolgical stress)- asseses
changes in myocardial thickening compared
to baseline.
• Overall sensitivity around 85%.
• Myocardial perfusion imaging:
• SPECT & PET.
• Tc99 is the most commonly used tracer.
• PET is qualitywise better while SPECT is more
readily available.

11. Non invasive tests for coronary anatomy:
 Computed tomography
 Calcium scoring
 CCTA
 MRCA

12. INVASIVE PROCEDURE:
 INVASIVE CORONARYANGIOGRAPHY:
Usually rarely required for establishing the diagnosis in patients
of chronic stable angina.
 However,it may be indicated in:
o Patients who cannot undergo stress imaging techniques.
o Patients with typical angina and lvef<50%.
o In special professions like pilots for regulatory issues.
o For revascularization issues after risk stratification by non
invasive means.
o In patients with very high PTP and clinical constellation
suggesting high risk,it can be used as a first line of investigation.

13. SUSPECTED ISCHEMIC HEART DISEASE(or
recent change in the clinical status in a patient
with known IHD)
Ruling out intermediate/high risk UA
Comprehensive clinical assesment of
risk,comorbidities,health
status,cardiac medical associated
conditions
Recent exercise/cardiac imaging study
Contraindications to stress testing
Previous history of
coronary revascularization
resting ecg interpretation
MPI/ECHO without
exercise.
PATIENT ABLETO
EXERCISE
Intermediate/high
likelihood
PHARM
STRESS
MPI/ECHO
PHARM
STRESS
CMR/CC
TA

14. Interpretable baseline ECG
LOW
LIKELIHOOD INTERME
DIATE
INTERME
DIATETO
HIGH
STANDAR
D
EXERCISE
ECG
STANDARD
EXERCISE
ECG
MPI/EC
HO with
E/
PHARM
CMR
IF SUGGESTIVEOF HIGH RISK LESION
MEDICALTHERAPYWITH
REGULAR MONITORING
MEDICALTHERAPY INITIATION
ALONGWITH
REVASCULARIZATION
COUNCELLINGTO IMPROVE
SURVIVAL

15. Known patient of stable IHD
Exercising
ability? Interpretable
resting ecg?
MPI/Echo
with
exercise
Or
Pharm
stress CMR
Standard exercise test
or MPI/Echo with
exercise
Not able to
exercise
Pharm stress
MPI/Echo
Pharm
stress
CMR/CCTA
DOTHETESTS REVEAL EVIDENCE OF HIGH RISK CORONARY LESIONS?
Consider
revascularization to
improve survival
Observe response to
medical therapy
Consider
revascularisation
monit
oring

16. Known case of stable IHD
Irrespective of ability to exercise
LBBB on ECG
MPI/Echo with
exercise
Known stenosis of
unclear significance
Intermediate result
from functional
testing
Pharm
MPI/Echo/CMR/CCTA
CCTA
DOTHE RESULTS SUGGEST ANY HIGH RISK CORONARY LESION?

17. Patient Education:
 Individualistaion of education plans to optimise care and well being.


Education plan
Medical
adherence
Explanation
of medical
managemen
t
Comprehensive review of
therapeutic options
Physical activity
encouragement
Self monitoring
& adversity
awareness

18. Medical
therapy
Risk factor
modification
Prevention of
adverse
outcomes(MI/DEA
TH)
Relief of
symptoms

19. OPTIMAL MEDICALTHERAPY
RISK FACTOR
MODIFICATION
LIPID
MANAGEMENT
BLOOD
PRESSURE
DIABETES
MELLITUS
BODYWEIGHT
PHYSICAL
ACTIVITY
SMOKING
PSYCHOLOGICA
L FACTORS
PREVENTION OF ADVERSE
OUTCOMES
ANTI PLATELATETHERAPY
BETA BLOCKERS
RAAS BLOCKADE
THERAPY
INFLUENZAVACCINATION
SYMPTOM CONTROL
ANTI ISCHEMIC
MEDICATIONS
BETA BLOCKERS
CALCIUM CHANNEL
BLOCKERS
NITROGLYCERIN
RANOLAZINE
IVABRADINE
NICORANDIL
TRIMETAZIDINE

20. Risk factor modification:
 Lipid management: With established
CAD,reduction of LDL cholesterol irrespective of
pretreatment levels, with statins.
 Aggressive management recommended with target
levels<70mg/dl.
 In CKD stage 3/4/5- treat by reno protective statins.
 Aggressive therapy also results in some amount of
plaque regression as shown by IVUS.
 Diabetes management:Target hbA1c levels <
7.(individualised approach).Target blood pressure is
<140/85mm hg.
 An ACEI or ARB should always be included in therapy
considering the reno protective effects.

21. Risk factor modification:
 Hypertension:Target B.P<140/90 mm
hg.(elevated B.P is an independent risk factor for
CAD as well as CVA,heart failure and renal
failure).
 Diet:
saturated fatty acids<10% of total energy intake.
 Trans fatty acids<1%.
<5gms per day.
30-45gms of fibre per day.
200 gms of fruits and vegetable each.
Mediterranian diet closely
resembles this.

22. Risk factor modification:
 Physical exercise: isometric exercises are
contrindicated.
 Aerobic/isotonic exercise with the goal of
achieving a sustained heart rate of about 70-85%
of predicted heart rate atleast 3-4 times a
week.(30 mins per session)
 Definte mortality reduction value in all category
of patients viz prior h/o MI,CABG,PCI or chronic
stable angina.

23. ADVERSE EVENT PREVENTION
 Aspirin (75mg) is the recommended therapy in chronic stable angina
(unless C/I). It reduces death,MI,stroke not only in high risk patients
but also in stable angina patients without previous h/o MI.
 Clopidogrel is used as a second line drug in case of aspirin allergy or
C/I or adverse reactions.
 Dual therapy with aspirin(75mg) and Clopidogrel(75mg) indicated
only in certain high risk patients.
 DAPT- 1 month in BMS implant.
 DAPT-At least 12 months in DES.
 Long duration DAPT only in high risk groups (CHARISMATrial).

24. ADVERSE EVENT PREVENTION…contd
 Beta blockers- At least 3 yrs( if h/o MI or ACS,with
normal left ventricular function.
 To be used in all patients with LV dysfunctin(EF<40%)
With heart failure or prior MI.
(carvedilol,metoprolol,bisoprolol reduce mortality)
 RAAS BLOCKADE- ACEI indicated in all patients with
stable disease having comorbidities in the form of DM,
hypertension,LVEF<40% or CKD(unless contraindicated).

25. Symptom control and relief: anti-anginals
BETA BLOCKERS
CALCIUM CHANNEL BLOCKERS
NITROGLYCERIN
RANOLAZINE
IVABRADINE
NICORANDIL
TRIMETAZIDINE

26. Beta Blockers:
• Reduces rate,contractility,Atrioventricular
conduction,ectopic activity.
• May increase perfusion in ischemic areas by increasing
diastolic time and increasing vascular resistance in non-
ischemic areas.
• Prognostic benefit in patients post MI or heart failure.
• 30% risk reduction of death and adverse CV outcome in
post MI patients.
• Clearly effective in controlling exercise induced
angina,improving exercise capacity and limiting both
symptomatic/asymptomatic episodes.

27. Beta Blockers….contd
• Usually chosen based upon cardioselectivity,lipid
solubility,mode of excreation and dosing frequency.
• Atenolol,metoprolol,nebivolol,bisoprolol most widely
used.(doses?)
• Use metoprolol/carvedilol in renal compromise.
• Avoid combination with non dihydropyridine calcium
channel blockers.

28. Role of nitrates:
 Nitrates act as arterial and veno dialators and
decrease preload,which forms basis of symptomatic
relief in patients.
 Redistribute blood to the ischemic subendocardium.
 Sublingual nitroglycerin (0.3-0.6mg) every 5 mins till
subsidence of pain or maximum dose of 1.2 mg has
been taken within 15 minutes.
 Nitroglycerin spray actually acts even more rapidly.
 Can be used prophylactically.
 Isosorbide dinitrate(5mg sublingual) helps abort an
attack for 1 hour(longer duration protection) but its
onset > nitroglycerin.(owing to hepatic conversion).

29.  Longer acting nitrates act as 2nd line to Beta Blockers in
symptom control.
 Ineffective if used over longer periods(nitrate free interval
warranted).
 Single dose>multiple dosing(Trial proven).
 Single/dual dosing of mononitrates are adequate to provide
good antianginal coverage.
 Tolerance is the main headache.
 Never combine with PDE5 INHIBITORS!

30. CALCIUM CHANNEL BLOCKERS:
 Act by vasodialation and decreasing peripheral vascular resistance.
 Dihydropyridines(greater vascular selectivity) and Non
Dihydropyridines(heart rate lowering agents).
 Metoprolol vsVerapamil similar anti anginal effects.
 Atenolol vsVerapamil fewer new diabetes and anginal attacks
with verapamil.
 Diltiazem has a better safety profile and can be used with equal
effectiveness as verapamil.
 Non dihydropyridines should never be combined with the Beta
Blockers.

31. CALCIUM CHANNEL BLOCKERS….contd
Dihydropyridines
Long acting Nifedepine
•Powerfull vasodialtor
•Few side effects
•ACTIONTrial proved it
to be safe in stable CAD
and it reduces the need
for angiography and CV
interventions.
Amlodepine
•Effective once-a-day anti-
anginal and anti-hypertensive
due to its long half life and
tolerability.
•Amlodepine>atenolol in
reduction of exercise induced
angina.
•In a 24 month trial,in a patient
of CAD with normal blood
pressure,amlodepine reduces
risk of CV events.

32. Symptom control and relief:…(CONTD)
 Ranolazine-usually a 2nd line anti anginal agent that can be combined with Beta
blockers as and when required.(ADD ONTHERAPY in patients of stable angina inadequately
controlled on the 1st line agents).
 Acts by inhibiting late sodium entry selectively into cytosol and hence prevents sodium-
dependent calcium accumulation.
 Has anti-ischemic and metabolic properties,reduces diastolic stiffness,improves diastolic
flow, reduces frequency of anginal attacks(proved in the MERLIN Trial),increases exercise
tolerance, time to ST changes on treadmill tests.
 TERISA study proved the utility of adding this agent to other well established anti anginals
in patients with elevted HbA1c levels.
 Usual dose of 500-2000mg/day(without changes in BP/H.R.
 QT prolongation may be hazardous.

33. Newer agents:
IVABRADINE:
 Heart rate lowering agent acting through selective inhibition
of sinus node pacemaking currents without any effects on BP
or inotropism.(it reduces myocardial o2 demands).
 EMA approved for use in patients inadequately controlled or
intolerant to Beta Blocker therapy.
 Acts best at heart rates>60/min.
 Ivabradine=atenolon=amlodepine(in patients with CAD).
 Adding ivabradine at a dose of 7.5 mg twice daily to atenolol
therapy gave better control of heart rate and angina control.
 The BEAUTIFULTrial on ivabradine proved its efficacy in
reducing composite endpoint of death, MI and
hospitalisation due to MI in patients with angina and heart
rates>70/min.

34.  Nicorandil:
 Can be used both for long term treatment as well
as prevention of angina.
 May be added after Beta Blockers and CCBs.
 Opens ATP-sensitive potassium channels in
vascular smooth muscles and dialates the
epicardial blood vessels.
 In the IONA(impact of nicorandil on angina)study
it significantly reduced adverse CV events.
 Long term use may lead to plaque stabilisation in
patients with chronic stable angina.

35.  Trimetazidine- anti-ischemic metabolic modulator drug.
 Has got non-mechanical anti-ischemic properties.
 No change in heart rate or rate-pressure product at rest or at
peak exercise.
 Usual dose of 35 mg twice daily.
 Contraindicated in parkinsonism and motion disorders.
 Has positive effect on HbA1c and glycemic control.
 Has not been evaluated yet on large scale studies in patients
with SCAD.

36. Persistant symptoms
despite OMT
Consideration of
revascularisation to
improve symptoms
Potential for
revascularisation
After assesing
comorbidities
and patient
preferences
Coronary angiography
“heart team”opinion
Lesions correlated with
evidence of ischemia
CABG/PCI along with
ongoing medications
medical therapy with
carefull monitoring
Depending on
definite factors

37. High risk lesions on non invasive testing
Assesment of
comorbidities and
patient preferences
Potential revasularisation
warranted
Angiography performed
Positive “heart team” opinion
about anatomy /clinical factors
Optimal
revascularisation
procedure
determination
Anatomy
Patient
preferences
Clinical factors
Local resources
Continue ongoing
medical therapy
Continue ongoing
medical therapy

38. Revascularization exploration:
HEARTTEAM
APPROACH
TO IMPROVE
SURVIVAL
HYBRID
CORONARY
REVASCULAR
IZATION
DAPT
COMPLIANCE
TO IMPROVE
SYMPTOMS

39. Revascularization exploration….CONTD
 CLASS 1 Recommendations to improve
prognosis/survival:
 “Heart team” approach for unprotected left
main disease,in diabetics, in multivessel
disease(2/3 vessel disease),comorbidities.
 Left main coronary stenosis>50%
 Proximal LAD stenosis>50%
 2/3 vessel disease with impaired LV
function/heart failure.
 >50% stenosis in single remaining vessel
 Proven large area of ishchemia(>10% of LV).
:

40. WHERE NOT TO DO?
 PCI should not be done in stable patients with
significant(>50% stenosis) of unprotected left main coronary
artery who have unfavourable anatomy for PCI or are good
CABG candidates.
 PCI/CABG not to be done with sole intent to improve survival
in patients with SIHD with:
 1 or more coronary stenosis,not anatomically/functionally
significant(<70% in a non-left main coronary artery
stenosis,FFR>0.8,No/mild ischemia on non invasive testing)
 Involve only left circumflex or right coronary artery or subtend
a small portion of viable myocardium.

41. Revascularization exploration….CONTD
 CLASS 1 Recommendations for improving
symptoms:
 All class 1 Recommendations for survival
improvement,PLUS,
 Any significant stenosis with limiting symptoms
or symptoms not controlled with OMT.
 Multivessel disease(2/3) with features of CHF or
compromised LV is not a CLASS 1
recommendation in symptom improvement.

42. Where not to do?
 In patients who do not meet anatomic(>50% of
left main coronary artery stenosis or >70% of non
left main coronary artery stenosis) or
physiological(eg- FFR criteria) for revasculariztion.
 PCI with stenting(BMS/DES) should not be done
in a patient who is not likely to comply to the
DAPT for the necessary duration depending on
the type of stent employed.

43. OMT
CABGPCI
DILEMMA
PERSONIFIED?????????????
Who
answers??
Trials?

44. OMT vs CABG:
 CABG>OMT(survival advantage) at 3 years in
left main/3 vessel CAD.(Veterans affairs
cooperative study,CASS,European coronary
surgery study).
 CABG>OMT (in terms of less subsequent
MI,need for revascularization,cardiac
death)in a 10yr follow up.(MASS2Trial).
 BARI 2DTrial ( though excluded patients with
left main LAD,Included very small fraction
with prox left main LAD,or with LVEF<50%)
could not show superiority of
OMT+CABG>OMT alone.

45. OMT vs PCI:
 Survival advantage of PCI over OMT could
not be demonstrated.( BARI 2D and
COURAGETrial)- 2 MOST contemporary
trials). (????)
 RCTs failed to show that PCI reduces risk of
death or MI in patients without recentACS!
 TO summarise,PCI compared to OMT,
• Reduces angina incidence
• Dose not improve survival
• May increase short term MI risk
• Doesn’t lower long term MI risk.

46. Potential causes of lack of benefit of
PCI over OMT:
RELATIVELY
BENIGN
PROGNOSIS OF
SIHD
OMT IMPROVES
ENDOTHELIAL
FUNCTION AND
PLAQUE STABILITY
FUTURE CULPRIT
LESIONS ARE
MOSTLY NON
OBSTRUCTIVE
PERIPROCEDURAL
MI WITH PCI
EEFECT OF
COLLATERALS

47. CABG vs PCI :
 SYNTAX(SYNergy between PCI withTAXus
and cardiac surgery) has been a landmark
trial comparing efficacy of CABG with PCI.
 Also led to fomulation of SYNTAX SCORE
which acts as a surrogate marker for extent
of CAD and its complexity.(based on location
of lesion,its complexity and severity).
 SYNTAX SCORE>32 depicts high risk critical
lesion.
 SYNTAX STUDY randomly assigned around
1800 patients to DES PCI vs CABG.

48. CABG vs PCI….contd..
 At 3 years, the rate of
MACE(death,MI,stroke,repeat revascularization)
and repeat revascularization were significantly
higher in the PCI group!
 The rates of death and stroke were similar,but MI
and repeat revascularization were significantly
lower in CABG group.
 In patients with intermediate(22-32) or high(>32)
SYNTAX scores,the MACE was increased in
patients undergoing PCI.
 Outcomes comparable in relatively
uncomplicated CAD whereas
CABG>PCI(EFFICACY) in cases of complex and
diffuse CAD.

49. Follow up of patients:
 At least periodic follow up anually to asses clinical
function,symptoms,surveillance for heart failure and arrythmias.
 Monitoring of cardiac risk factors and ensuring adherence to
recommended lifestyle changes and medical therapy.
 Standard exercise ECG recommended in know patients of stable disease
who have new/worsening symptoms not consistent with UA,and have
modest physical activity,no comorbidity and interpretable ECG.(Go for
exercise nuclear MPI/ECHO if ECG cant be interpreted at baseline).
 Patients with worsening symptoms but incapable of exercise are advised
pharmacological stress imaging with MPI/ECHO or CMR(2nd option).

50. Take Home Message:
 Patient education,knowledge,awareness and rationality on the part
of the physician are essential for management of chronic stable
angina.
 Risk stratification is essential with either non invasive stress testing
or imaging studies to formulate management plan.
 OMT forms a cornerstone of therapy.
 OMT refractory stable angina warrants evaluation by invasive
angiography and formulation of revascularization plans.
 Revascularization procedures have their own set of pros and cons.
 Pragmatic selection of procedure is the key to succsfull treatment
………thank you