Chronic Coronary Syndrome refers to stable coronary artery disease and encompasses patients with chronic angina or previous heart attacks. The pathophysiology involves atherosclerotic narrowing of coronary arteries resulting in insufficient blood flow to meet myocardial oxygen demands. Treatment involves lifestyle modifications, risk factor control through medications like statins, and revascularization procedures in addition to medical therapy for selected patients. The goals are to relieve angina, slow disease progression, and prevent further cardiac events.

1. Chronic Coronary
Syndrome DrRichardArmstrongMD
ConsultantCardiologistTUH

2. Introduction
▪ Coronary Artery Disease(CAD) is a pathological process
characterized by atherosclerotic plaque accumulation in the
epicardial arteries, whether obstructive or non-obstructive.
▪ Ischemic Heart Disease(IHD) is a condition in which there is an
inadequate supply of blood and oxygen to a portion of the
myocardium

4. 1772 William Heberden
he described angina as
some account of the
disorder of breast
Later Royal College of Physicians
in London named it as Angina
Pectoris

5. Angina Pectoris
▪Angina pectoris is a symptom
complex caused by transient
myocardial ischemia, which occurs
whenever there is an imbalance
between myocardial oxygen supply
and demand.

6. Natural History of
Chronic Coronary
Syndrome

7. Chronic Coronary Syndrome
▪ The 2019 ESCGuidelines replace the term
“Stable CAD” with Chronic Coronary Syndrome.
▪ This implies that CADis a dynamic process, the
clinical presentation of which can be eitheracute
or chronic

8. Pathophysiology
▪ Narrowing of Coronary arteries
▪ Insufficient blood flow
▪ Myocardial oxygen demands exceed supply
▪ Anaerobic metabolism with lactic acid accumulation
▪ Myocardial nerve fibres irritated
▪ Pain message transmitted to cardiac nerves and upper posterior
nerve root

9. Aetiology
▪ Atheroma(90% cases)
▪ Congenital
▪ Valvular disease
▪ Hypertension
▪ Cardiomyopathy
▪ Vasculitis or Aortitis
▪ Anemia
▪ Thyrotoxicosis

10. History and risk factors
Family history of CAD
Dyslipidemia
Diabetes
Hypertension
Smoking
Other lifestyle factors

11. The characteristics of Angina
Location Chest, near the sternum, but may be felt anywhere from the
epigastrium to the lower jaw or teeth, between the shoulder
blades, or in either arm to the wrist and fingers.
Character The discomfort is often described as pressure, tightness or
heaviness; sometimes strangling, constricting or burning.
Duration The duration of the discomfort is brief less than 10 mins in
the majority of cases, and more commonly just a few
minutes or less and chest pain lasting for seconds isunlikely
to be due to CAD.
Relationship to exertion
and other exacerbating
or relieving factors
Become more severe with increased levels of exertion.

12. Clinical Classification of SuspectedAnginal
Symptoms
Typical Angina
Meets the following three characteristics:
1.Constricting discomfort in the front of the chest or in
the neck, jaw, shoulder or arm.
2.Precipitated by physical exertion
3. Relieved by rest or nitrated within 5mins
Atypical
angina
Meets two of these characteristics.
Non-anginal
chest pain
Meets only one or none of these characteristics

13. Canadian Cardiovascular Society Grading
Grade Description of anginal severity
I Angina only with strenuous
exertion
Presence of angina during strenuous, rapid or prolonged ordinary
activity(walking or climbing the stairs)
II Angina with moderate exertion Slight limitation of ordinary activities when they are performed rapidly,
after meals, in clod , in wind under emotional stress or during the first few
hours after waking up, but also walking uphill, climbing more than one
flight of ordinary stairs at a normal pace, and in normal conditions,
III Angina with mild exertion Having difficulties walking one or two blocks or climbing one flight of stairs,
at normal pace and conditions
IV Angina at rest No exertion needed to trigger angina.

14. Activities precipitating angina
Common
Physical exertion
Cold exposure
Heavy meals
Intense emotion
Uncommon
Vivid dreams (Nocturnal)
Lying flat(Decubitus)

15. Physical Examination
T
oaccess the presenceof-
▪ Hypertension
▪ Valvular Heart Disease
▪ Peripheral Vascular Disease
▪ HOCM
▪ BMI
▪ Waist circumference

16. Investigations(Class I)
Biochemical Test:
▪ FBC
▪ Fasting plasma glucose and HbA1c
▪ Lipid profile
▪ Serum creatinine and eGFR
▪ Serum uric acid test
▪ Thyroid function test

17. Resting ECG
▪ Usually normal
▪ Aresting 12 lead ECGis recommended in all patients with chest pain without
an obvious non-cardiac cause (Class I Level C).
▪ Aresting 12 lead ECGis recommended in all patients during or immediately
after an episode of angina suspected to be indicative of clinical instability of
CAD(Class I LevelC).
▪ Ambulatory ECGmonitoring is recommended in patients with chest painand
suspected arrhythmias(Class I Level C).

18. Chest X-Ray
▪Chest X-ray is recommended for
patients with a typical presentation,
signs and symptoms of HF
,or suspicion
of pulmonary disease(Class I level C).

19. Exercise ECG
▪ Exercise ECGis recommended for the assessment of exercise
tolerance, symptoms, arrhythmias, BPresponse, and event risk in
selected patients(class I level C)–NOTFORDIAGNOSISORFOR
RULINGOUTCORONARYARTERYDISEASE
▪ Exercise ECGis not recommended for diagnostic purpose in
patients with ≥ 0.1 mV St- segment depression on resting ECG
or who are being treated with digitalis(class III level C)

20. Functional non invasive tests
▪ Stress Echocardiography
▪ Single photon emission CT(SPECT)
▪ Positron emission tomography (PET)
▪ Myocardial contrast echocardiography
▪ contrast CMR

21. Anatomical Assessment
Non-invasive – coronary CT
Invasive – coronary angiogram

22. Clinical likelihood
of Obstructive CAD

23. Main diagnostic pathways
in symptomatic patients
with suspected obstructive
CAD

24. Approach for the initial diagnostic management of
patients with angina and suspected coronaryartery
disease

25. Pre-test probability scores

26. Management
▪Lifestyle modification and control of risk
factors
▪Pharmacological management
▪Revascularization

27. Lifestyle recommendations for patients with
chronic coronary syndromes
Smoking cessation Use pharmacological and behavioural strategies to help patients quit smoking. Avoid
passive smoking
Healthy diet Diet high in vegetables, fruit, and wholegrains. Limit saturated fat to ,10% of total intake.
Limit alcohol to ,100 g/wk or 15 g/day
Physical activity 30 -60min moderate physical activity most days, but even irregular activity is beneficial.
Healthy weight Obtain and maintain a healthy weight (<25kg/m2), or reduce weightthrough
recommended energy intake and increased physical activity.
Other Take medications as prescribed. Sexual activity is low risk for stable patients not
symptomatic at low-to-moderate activity levels

28. Recommendations
on lifestyle
management

29. Pharmacological
Management

30. Nitrates:
▪ Nitrates act directly on vascular smooth muscle to producevenous
and arteriolar dilatation.
▪ They help angina by lowering preload and afterload, which reduces
myocardial oxygen demand and by increasing myocardial oxygen
supply through coronary vasodilatation.
▪ No mortality benefit or cannot prevent heart attack.
▪ Short acting nitrates for acute effort angina: Sublingual and spray
nitroglycerin formulations provide immediate relief of effort angina
▪ Long acting nitrates for angina prophylaxis.

31. Beta Blockers
▪ These lower myocardial oxygen demand by
reducing heart rate, BPand myocardial
contractility.
▪ Discontinuation should be tapered and not
abrupt.
▪ The principal side effects of beat blockers are
fatigue, depression, bradycardia, heart block,
bronchospasm, peripheral vasoconstriction,
postural hypotension, impotence and masking of
hypoglycemia symptoms.

32. Calcium Channel Antagonists
▪These drugs lower myocardial oxygen
demand by reducing BPand myocardial
contraction.

33. Potassium Channel Activator
▪Nicorandil(10-30 mg twice daily orally) isa
nitrate derivatives of nicotinamide, with
antianginal effects similar to those of
nitrates or beta blockers.
▪Side effects include nausea, vomiting and
potentially severe oral, intestinal and
mucosal ulcerations

34. If channel antagonists
▪Ivabradine
▪It does not inhibit myocardial contractility
▪ Works specifically on the sinus node
(wont work in AF).

35. Ranolazine
▪Is a selective inhibitor of the late inward
sodium current in coronary artery smooth
muscle cell, with a secondary effect on
calcium flux and vascular tone, reducing
anginal symptoms.
▪Side effects include dizziness,nausea,
constipation, Qt prolongation.
▪375BD is the starter dose, always
uptitrate

36. Trimetazidine
▪ Trimetazidine is an anti-ischemic(anti-anginal)
metabolic agent, which improves myocardial
glucose utilization through inhibition of fatty acid
metabolism, also known as fatty acid oxidation
inhibitor.
▪ It is contraindicated in Parkinson`s disease and
motion disorders, such as tremor(shaking),
muscle rigidity, walking disorders and restlessleg
syndrome.

37. Event Prevention
Recommendations Class level
Aspirin 75-100 mg daily is recommended in patients with a previous MI or
revascularization
I A
Clopidogrel 75 mg daily is recommended as an alternative to aspirin in patients with
aspirin intolerance
I B

38. Anticoagulant Drugs
▪Anticoagulation therapy is
recommended in patients with AFand
CCS for reduction of ischemic stroke
and other ischemic events.

39. ACEinhibitors
▪ACEinhibitors or ARBsare
recommended if a patient has
other conditions (e.g. Heart
failure, Hypertension or diabetes)

40. Statins
Recommendation Class Level
Statins are recommended in all patients withCCS. I A
If a patient`s goal is not achieved with the maximum tolerated dose of statin, combination
with ezetimibe is recommended.
I B
For patients at very high risk who do not achieved their goal on a maximumtolerated dose
of statin and ezetimibe, combination with PCSK9 inhibitor is recommended.
I A

41. Antithrombotic therapy in patients with CCS

42. Suggested stepwise strategy for long term anti-
ischaemic drug therapy in CSS

43. Revascularization
▪ In patients with CCS,optimal medical therapy is key for reducing
symptoms, halting the progression of atherosclerosis and
preventing atherothrombotic events,
▪ Myocardial revascularization plays a central role in the
management of CCSon top of medical treatment, but always as
an adjunct to medical therapy without supplanting it.
▪ Revascularization by PCIor CABGmay effectively relieve angina,
reduce the use of antianginal drugs and improve exercisecapacity
and quality of life compared with a strategy of medical therapy
alone.

44. Thank You