Prof' A' Jnosi M'D', D'Sc

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Stable angina pectoris - optimal
medical management silent ischaemia

• Prof. A. Jánosi M.D., D.Sc
• FACC, FESC
• Med. Habil. Semmelweis Univ.Budapest

Budapest
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Heberdens anginaSome account of a disorder of
the breast Royal College Of Physicians London,
1767 Julius

• They who are afflicted with it, are seized
• while they are walking (more especially if it
• be up hill, and soon after eating) with a
• painful and most disagreeable sensation in
• the breastbut the moment they stand still,
• all this uneasiness vanishes.
• ..the pain is situated in the upper part,
  sometimes
• in the middle, sometimes in the bottom of the os
• sterni
• ..it not improperly be called angina pectoris

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Supply Demand
Coronary flow Oxygen capacity
Heart rate
Contractility Wall tension
RR syst
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Myocardial ischaemia
Supply Demand
Ischemic heart disease
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Ischemic heart disease
Stable angina pectoris
Conduction disturbances
Acut coronary syndrome
Sudden death
Congestive heart failure
ST elevation YES
ST elevationNO
Non ST elevation myocardial infarction
Myocardial infarction (non Q)
Myocardial infarction (Q)
Unstable angina
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Patological changes
Stable plaque
RCA
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Prognosis
N3031
Positive coronary angiography
3,9,,
2,3
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Clinical assessment

• Angina is a clinical syndrome
• characterized by discomfort in the chest, jaw,
  shoulder, back or arm.
• It is tipically provoked or aggraveted by
  exertion or emotinal stress.
• It is relieved by rest or nitroglycerin
• Typical angina
• Atypical angina
• Extracardial chest pain

CCS I-IV
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Provocative factors

• Cardiac factors
• Tachyarrhythmia
• Bradyarrhythmia
• HOCM
• Aortic valve disease

• Extracardial factors
• Anaemia
• Hypertension
• Fever
• Hyperthyreosis
• Hypoxaemia

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Algorithm for the initial evaluation of patients
with clinical symptoms of angina I.
Clinical Evaluation History and
physical ECG Laboratory tests
Suspected pulmonary disease
ACS management algorithm
CXR
Unstable syndrome
Assesment of Ischaemia Exercise ECG or
Pharmacological stress imaging or Exercise stress
imaging
Reassure. Refer for investigation and/or
management of alternative diagnosis if appropriate
Suspected heart failure, prior MI, abnormal ECG
or clinical examination, hypertension or DM
Re-assess likehood of ischaemia as cause of
symptoms
Echocardiography (or MRI) to assess structural or
functional abnormalities
No evidence for cardiac cause of symptoms
Evaluate prognosis on basis of clinical
evaluation and non-invasive tests
If diagnosis of CAD is secure, but assesment of
ventricular function not already performed for
Class I indications then assess ventricular
function at this stage
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Algorithm for the initial evaluation of patients
with clinical symptoms of angina II.
Low risk Annual CV mortality lt1 per year
High risk Annual CV mortality gt2 per year
Intermediate risk Annual CV mortality 1-2 per
year
Medical therapy
Medical therapy Coronary arteriography Depending
on level of symptoms and clinical judgement
Medical therapy AND Coronary arteriography for
more complete risk stratification and
assessment of need for revascularisation
Coronary arteriography if not already performed
High risk coronary anatomy known to benefit from
revascularization?
NO
Evaluate response to medical therapy
YES
If symptomatic control unsatisfactory, consider
suitability for revascularization (PCI or CABG)
Revascularize
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Recommendation for evaluation of pts presenting
with chest pain

• Provement of myocardial ischemia
• Exclusion of extracardial causes
• Risk stratification
• Treatment strategy
• Evaluation of treatment effectiveness

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ExT (ECG)
Einthoven ECG 1901

• MASTER two step test 1935

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Indications of exercise test

• Evaluation of pts with chest pain (pretest
  probability of CAD between 10-90)
• Evaluation of pts with stress provoked symptoms
• Prognostic evaluation of pts with known CAD
• Evaluation of antiischemic therapy (drugs and/or
  revascularization procedure

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Non invasive diagnostic tests
Exercise perfusion scintigraphy Exercise
echocardiography CT angiography MRI
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Summary of recommendations for routine
non-invasive investigations in evaluation of
stable angina I.
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Summary of recommendations for routine
non-invasive investigations in evaluation of
stable angina II.
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Summary of recommendations for routine
non-invasive investigations in evaluation of
stable angina III.
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Summary of recommendations for routine
non-invasive investigations in evaluation of
stable angina IV.
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Summary of recommendations for routine
non-invasive investigations in evaluation of
stable angina V.
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Summary of recommendations for routine
non-invasive investigations in evaluation of
stable angina VI.
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Treatment stable angina pectoris

• A Aspirin and antianginal therapy
• B Beta blocker and Blood pressure
• C Cigarette smoking and cholesterol
• D Diet and diabetes
• E Education and Exercise

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Optimal treatment of stable angina pectoris

• Treatment which can improve symptoms
• nitrate
• calcium antagonist
• Beta blockers
• Metabolic drugs
• If channel inhibitors

• Treatment which prolongs life
• Smokimg cessation
• aspirin
• statins
• Beta blockers ( in postinfarct pts)

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Pharmacological agents to reduce symptoms and
ischaemia I. (Recommendations relate to
monotherapy, for relief of symptoms, and
ischaemia.)
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Pharmacological agents to reduce symptoms and
ischaemia II. (Recommendations relate to
monotherapy, for relief of symptoms, and
ischaemia.)
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Algorythm for medical management of stable angina
Stable angina for medical management
Level of evidence
Immediate short term relief
Prognosis Symptoms
B
Short acting sulingual or buccal nitrate, prn
A B A B/C A/B A A
B A A/B B/C
Aspirin 75-150 mg od
Contraindication (e.g. aspirin allergic)
Clopidogrel 75 mg od
Treatment aimed at improving prognosis
Statin /- Titrate dose ? to get target
cholesterol
Interchange statins, or ezetimibe with lower dose
statin, or replace with alternative lipid
lowering agent
Intolerant or contraindication
ACE-inhibitor in proven CVD
Beta-blocker post-MI Beta-blocker-no prior MI
Treatment aimed at relief of symptoms
Intolerant (e.g. fatigue) or contraindication
Symptoms not controlled after dose optimisation
Calcium antagonist or long acting nitrate or K
channel opener or If inhibitor
Intolerant
Add calcium antagonist or long-acting nitrate
Symptoms not controlled after dose optimisation
Either substitute alternative subclass of calcium
antagonist, or long acting nitrate
Symptoms not controlled after dose optimisation
Combination of nitrate and calcium antagonist or
K channel opener
Consider suitability for revascularization
Symptoms not controlled on 2 drugs after dose
optimatisation
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Special drugs for treatment of angina pectoris
Metabolic agent If chanel inhibitors
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Glucose
Fatty Acids
Glycolysis
Glycolysis
ADP
Trimetazidin decreases fatty acid oxidation and
inreases the glucose oxidation which enegatically
better situation. Trimetazidine has antianginal
effect .
ATP
ß-Oxidation Spiral
Pyruvate
Fatty Acid Oxidation
Lactate
Glucose Oxidation
Pyruvate Dehydrogenase
Acetyl CoA
Acetyl CoA
O2
H2O
Electron Transport Chain
Ischemia
Contractile Function Basal Metabolism
ADP
ATP
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Regulation of sinus node automatism
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Procoralans selective If inhibition
Closed
Open
Blockade
Extracellular
Intracellular
Na
K
Ivabradine
Decreases heart rate
Bucchi A, et al. J Gen Physiol. 20021201-15.
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The Fab Four
Beta-blocker Statin
Antiplatelet ACE-inhibitor
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Silent ischaemia
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Ischaemic cascade
Angina pectoris
ExT
MRI
ECG
ECHO
Wall motion abnormality
Relaxation disturbance
SPECT
Metabolic abnormality
Perfusion abnormality
NYUGALOM
T E R H E L É S
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Ischaemic cascade
Angina pectoris
ExT
MRI
ECG
ECHO
Wall motion abnormality
Can be asymptomatic
Relaxation disturbance
SPECT
Metabolic abnormality
Perfusion abnormality
NYUGALOM
T E R H E L É S
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Type of silent ischemia according to Cohn
Type I totally asymtomatic patients with severe
obstructive CAD. These pts do not experinece
angina pectoris at any time Type II silent
ischemia in pts after documented myocardial
infarction Type III this form of ischemia occurs
in pts chronic stable AP, UAP and Prinzmetal AP
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Type III silent myocardial ischemia
This is the much more frequent form of silent
ischaemia. The patient sometime has angina
pectoris and severel times has silent ischemic
episods without symptoms
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Type III silent ischemia
Angina pectoris silent ischemic episodsTOTAL
ISCHEMIC BURDEN
TIB has prognostic significance
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Mechanism of silent ischaemia

• Autonomic neuropathy
• Increased release of endorphins
• Anti-inflammatory cytokines

?
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How to detect silent ischemia?
Ambulatory ECG/ Holter monitoring Silent
ischemic episodes are four times more frequent
than symptomatic one
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Management of silent ischemia
Drugs that are effective in the treatment of
symptomatic ischemic episodes are effective in
prevention of asymptomatic episodes as well.
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How we guide the therapy?
Ischaemia guided or angina guided therapy ????
In the ACIP trial no difference was found in the
outcomes