Angina pectoris is a clinical syndrome characterized by chest pain or pressure due to insufficient blood flow to the heart muscle. It is usually caused by an imbalance between myocardial oxygen supply and demand. There are different types of angina including stable, unstable, and variant angina. Risk factors include family history, diabetes, hypertension, smoking, and high cholesterol. Diagnosis involves ECG, stress test, and angiography. Treatment focuses on decreasing oxygen demand on the heart and increasing supply by using nitrates, beta blockers, calcium channel blockers, antiplatelet drugs, and statins. Emergency treatment for unstable angina may include thrombolytics. Lifestyle changes and medication aim to prevent future cardiac events associated with untreated

1. Angina Pectoris
and
Antianginal Drug
This Presentation is a evaluating material of
Midterm Examination, belongs to
Cardiovascular Pharmacology Course
Presented By
Muhammad Kamal Hossain
PhD Student
Student ID- 202255221
School of Pharmacy
Jeonbuk National University (JBNU)

2. Topic Contents:
• INTRODUCTION
• ANGINA PECTORIS
• CONSEQUENCES OF ANGINA
• TYPES OF ANGINA
• PATHOPHYSIOLOGY
• RISK FACTORS
• SIGN AND SYMPTOMS
• DIAGNOSIS
• MANAGEMENT AND
TREAMENT
FOR BETTER
UNDERSTANDING
WE HAVE TO
DISCUSS A CASE
STUDY OF ANGINA
PATINET

3. Heart, is a hollow muscular organ that pumps the blood through
the circulatory system by rhythmic contraction and dilation.
INTRODUCTION

4. Coronary Circulation:
The aorta (the main blood supplier to the
body) branches off into two main coronary
blood vessels (also called arteries).
These coronary arteries branch off into
smaller arteries, which supply oxygen-rich
blood to the entire heart muscle.
The cardiac muscle cells depend only on
aerobic respiration for getting energy. So,
they need a continuous supply of
oxygen.
Cardiac muscles have to function
continuously to maintain the
pumping of the heart according to
our needs or oxygen demand.

5. How Myocardial Oxygen Demand equilibrate with Supply of Oxygen?
If Oxygen Demand – Supply Mismatch then what happen?

6. ANGINA PECTORIS
Definition : Angina pectoris is a clinical syndrome usually
characterized by episodes of pain or pressure in the anterior chest .
The cause is usually insufficient coronary blood flow which results in a
decreased oxygen supply to meet an increased myocardial demand for
oxygen in response to physical exertion or emotional stress.

7. The pain related to angina pectoris is temporary, but if left untreated can
make serious heart complications inevitable.
In Angina pectoris lack of proper blood supply to the heart increases the
risk of :
 Severe cardiac chest pain
 Ischemic Heart Disease (IHC)
 Heart Attack
 Stroke
 Heart Failure (HF)
 Arrhythmias (irregular heart rhythms) and
 other Coronary Artery Diseases (CAD)
What happens if we leave Angina untreated?

8. 1. Stable Angina- is a predictable & consistent pain
that occurs when a patient is involved in some kind of
physical activity like exercise. During physical activity, the
heart becomes overactive often leading to pain in the
chest. Stable Angina is also known as chronic angina, as it
follows a regular pattern. Usually it relieved by rest.
2. Unstable Angina- Angina pectoris can occur anytime,
even when a person is resting. Unstable angina is less
common than the stable angina, but can get worse over
time and may lead to a heart attack and need to be
medical emergency. Symptoms occur more frequently,
more severe and longer than stable angina.
3. Variant angina or prinzmetals or vasospastic angina -
pain at rest with reversible ST-segment elevation, caused
by coronary artery vasospasm.
TYPES OF ANGINA PECTORIS

9. OTHER TYPES OF ANGINA PECTORIS
4. Intractable or refractory angina:
Sever incapacitating chest pain lasting as a chronic condition (≥3 months in
duration) characterized by angina in the setting of coronary artery disease (CAD)
5. Angina Decubitus/ Nocturnal Angina :
A pain identical in nature, localization and distribution with angina pectoris of
effort but occurring during the night when the patient is in a recumbent position.
6. Micro vascular Angina:
Microvascular angina is a type of angina that is caused by problems in the smallest
blood vessels of the coronary arteries
7. Silent ischemia:
Objective evidence of ischemia (as ECG changes with a test), but patient report no
symptom.

10. Pathophysiology
Myocardial ischemia can result from:
• A reduction of coronary blood flow caused by fixed &or dynamic epicardial
artery stenosis.
• Abnormal constriction or deficient relaxation of coronary artery.
• Reduce O2-carrying capacity of the blood .
Angina pectoris, a symptom of transient myocardial ischemia occurs when there
is an imbalance between myocardial oxygen supply and demand

11. FIGURE: PLAQUE FORMING CORONARY ARTERY

12. 1. Family history of premature coronary artery disease.
2. Diabetic Mellitus (DM)
3. Systemic HTN.
4. Cigarette smoking.
5. Hypercholesterolemia.
6. Obesity.
7. Dyslipidemia/ Increase levels
- Lipoprotein
- Fibrinogen
- S. Triglycerides
8. Sedentary Lifestyle
RISK FACTORS OF ANGINA:

13. 1. May produce pain vary in severity from
feeling of indigestion to chocking in
retrosternal area , radiate to neck , jaw
shoulders , inner aspects of upper arms.
2. Feeling of weakness or numbness in the
arms , wrists and the hands.
3. Shortness of breath.
4. Pallor, Diaphoresis.
5. Dizziness or lightheadedness.
6. Nausea and vomiting.
SIGN & SYMPTOMS | CLINICAL MANIFESTATIONS
Angina usually causes uncomfortable pressure,
fullness, squeezing or pain in the center of the
chest.
***Many types of chest discomfort — such as
heartburn, lung infection or inflammation — aren't
related to angina

14. COMMON SIGN & SYMPTOMS
The research on gender differences in chronic stable angina suggests that angina
may be experienced differently in women (Wenger, 1997) and that women
report greater functional disability related to angina symptoms (Steingart et al.,
1991; Pinsky et al., 1990).
MEN VS WOMEN
Are there gender differences in angina?

15. • Electrocardiogram (ECG) - records electrical activity of the heart and can detect
when the heart is starved for oxygen.
Diagnostic Tests
Normal ECG Irregular ECG

16. • Stress test - blood pressure readings and an ECG while the patient is increasing
physical activity.
• Chest X-ray - to see structures inside the chest.
• Coronary angiography - dye and special X-rays to show the inside of coronary
arteries (dye is inserted using cardiac catheterization).
• Blood tests - to check levels of fats, cholesterol, sugar, and proteins (homocysteine,
myoglobin, troponin, high-sensitivity C-reactive protein (hs-CRP) and creatine
kinase).
After finding Electrocardiogram
(ECG) report, there are some
Assessment Questions should be
strike on mind to identify angina
pain….

17. Medical management for the patient with
angina pectoris
The main objective is to decrease oxygen demand of myocardium and to
increase oxygen supply. However, the therapeutic goal depends on the types
of angina.
Unstable Angina
Stable Angina
Vasospastic Angina
Increasing myocardial blood flow by dilating coronary arteries
and arterioles ( O2 Delivery)
Decreasing Cardiac Load (preload and afterload: O2 Demand)
Decreasing Heart Rate ( O2 Demand)
Inhibiting platelet aggregation and thrombus formation ( O2
Delivery)
Decreasing Cardiac Load ( O2 Demand)
Vasodilate coronary arteries ( O2 Delivery)
Decreasing vasospasm of coronary vessels ( O2 Delivery)
**Calcium channel blockers are efficacious in >70% of patients

18. Drugs Used to Relieve or Prevent the
Symptoms of Angina
Nitrates Beta Blockers
Calcium
Antagonists
Potassium
Channel
Activators
Antiplatelet
Drugs
Lipid
Lowering
Agents
Short
Acting
Intermediate
Acting
Long
Acting
Beta 1 Blockers
(Cardioselective)
Beta 1 and 2
Blockers
(Nonselective)
Dihydropyridines
Types
Non-
Dihydropyridines
Types
Thromboxane
A- 2
Inhibitor
Short
Acting
Long
Acting
Adenosine
diphosphate
(ADP)
Receptor
Inhibitors
Thrombolytic
Agents
Statins
Fibrates
Hydrophilic
Lipophilic

19. Treatment will depend on:
• The severity of the symptoms
• Severity of the underlying disease, and
• Extent of damage to the heart muscle
If it is only angina, Simple rest and observation, an aspirin, breathing oxygen, and
sublingual nitroglycerin may be all that the patient needs.
• Medication may be administered to reduce anxiety.
• Medication may be administered to lower blood pressure or heart rate.
• Medication may be administered to reduce the risk of having a blood clot or to prevent
further clotting.
• If the chest pain actually represents a heart attack, the patient may be given a fibrinolytic
agent (A powerful clot-buster medication).
• Lifestyle changes recommended :
 Regularly checking cholesterol levels
 Resting and slowing down
 Avoiding large meals
 Learning how to handle or avoid stress
 Eating fruits, vegetables, whole grains, low-fat or no-fat diary products.
Treatment Strategy
IN EMMERGENCY SITUATION

20. Angina pectoris is the medical term for chest
pain or discomfort due to coronary heart
disease. It occurs when the heart muscle
doesn't get as much blood as it needs.
So what should our main concern to treat Angina?

21. Mode of action :
Acts directly on vascular smooth muscle to produce arterial and venous dilatation
Effect during angina:
1.Reduces myocardial oxygen demand (lowers pre-load and after load)
2. Increases myocardial oxygen supply (coronary vasodilatation)
NITRATES

22. 1. Sublingual glyceryl trinitrate (GTN)
2. Buccal glyceryl trinitrate
3. Transdermal glyceryl trinitrate
4. Oral isosorbide dinitrate
5. Oral isosorbide mononitrate
6. Intravenous gtn- for acute myocardial infarction/left
7. Ventricular failure -10 -200 µg /min intravenous infusion,
8. Titrating to clinical response and blood pressure.
Some Nitrate Preparations

23. DURATION OF ACTION OF SOME NITRTATE PREPARATIONS
PEAK ACTION
DURATION OF
ACTION
Sublingual GTN(Tablet 300-500µg
or metered dose aerosol
400µg/spray)
4-8 minutes 10-30 minutes
Buccal GTN (1-5 mg tablet 6 hourly) 4-10 minutes 30-300 minutes
Transdermal. GTN (5-10 daily) 1-3 hours Up to 24 hours
Oral isosorbidedinitrate.(10-20 mg
8 hourly)
45-120 hours 2-6 hours
Oral isosorbide mononitrate
( 20-60 mg once or twice a day)
45-120 hours 6-10 hours

24. - Corrects the imbalance between the flow of oxygen and blood to the heart.
- Vasodilation—widening of the blood vessels.
- Subsiding of chest pain
- Decrease of blood pressure
These effects arise because nitroglycerin is converted to nitric oxide in the body by
mitochondrial aldehyde dehydrogenase, and nitric oxide is a natural vasodilator.
Nitroglycerin
Side effects:
The side effects of nitroglycerin include:
• Lack of sexual desire
• Headache
• Painful urination
• Increased bowel movements.
• Weakness or dizziness.
Headaches are the most prominent side
effect of nitrate therapy.

25. Mode of Action: Lowers myocardial oxygen demand by-
A. Reducing heart rate
B. Reducing blood pressure
C. Reducing myocardial contractility
BETA BLOCKERS
Generations of beta blocker:

26. Why are Cardio selective beta-
blockers preferred?

27. Usual Dose of beta blocker:
Use a once daily cardio-selective preparation.
For example, Atenolol 50-200mg daily, slow release Metoprolol 50-200mg daily, Bisoprolol 5-10
mg daily
The beta-blocker withdrawal syndrome:
Beta blockers should not be withdrawn abruptly (suddenly) because of the possibility of a
rebound effect. Stopping beta-blockers may cause withdrawal symptoms, including:
• Higher blood pressure.
• Chest pain.
• Anxiety.
• Fast heartbeat.
• Heart attack.
How do you prevent beta-blocker withdrawal?
1. In acute withdrawal, reinitiate beta-blockers.
2. Taper regimen: reduce daily dose by 50% per week until at lowest dose.
3. Maintain lowest dose for 1 week prior to discontinuation.

28.  Calcium channel blockers (CCBs) are a class of drugs and natural substances
that disrupt the calcium (Ca2+) conduction of calcium channels.
Calcium Channel Blockers (CCBs)

29. Molecular Mechanism of CCBs:
What is Ultimate outcome?

30.  Dihydropyridine:
• Amlodipine
• Felodipine
• Nicardipine
• Nifedipine
 Non-Dihydropyridine:
Phenylalkylamine
• Verapamil
Benzothiazepine
• Diltiazem
Classes of Ca2+ channel blockers

31. Nifedifine Diltiazem
Verapamil
Nifedipine are the long-term
treatment of hypertension and
angina pectoris.
 Sublingual nifedipine has
previously been used in
hypertensive emergencies.
Serious A/E includes:
①cerebral
ischemia/infarction
②myocardial infarction
③complete heart block
④death
 Verapamil will dilate
blood vessels, which
increases the supply of blood
and oxygen to the heart.
 By relaxing the tone of this
smooth muscle, calcium-
channel blockers dilate the
blood vessels.
 Diltiazem is a potent
vasodilator, increasing
blood flow and variably
decreasing the heart rate
via strong depression of
A-V node conduction.
 Potent vasodilator of
coronary vessels.
 Vasodilator of
peripheral vessels.

32. Mechanism of Action
POTASSIUM CHANNEL ACTIVATORS
Enlisted Drug:
Cromakalim, Pinacidil, and
Nicorandil, are the most
extensively investigated agents
in this class.

33. Nicorandil is the only clinically available potassium channel opener with
antianginal effects, and with comparable efficacy and tolerability to existing
antianginal therapy.
Usual Dose: 10-30 mg 12 hourly
Cautiously Used in:
• Hypovolemic patients
• Patients with pulmonary edema
Side effects:
• Headache
• Flushing
• Dizziness
• Weakness
• May cause a dose dependent increase
in heart rate
• Myalgia
• Angioedema
Nicorandil

34. – ASPIRIN (Thromboxane A 2 Inhibitor by blocking COX-1)
– CLOPIDOGREL (ADP Receptor Antagonist)
ANTIPLATELET DRUGS
NO
PLATELET
AGGREGATION
USED AS
PROPHYLAXIS OF
ANTI-THROMBOTIC

36. Antiplatelet effect by inhibition of
thromboxane A 2 through COX-1
pathway
Usual Dose:
Thrombo-embolic cerebro vascular
accident, ischemic heart disease-
prophylaxis (75mg/day) and acute
treatment (300 mg)
Contraindications:
1. Those under age of 16y-can increase
incidence of Reye's syndrome,
liver/brain damage.
2. Gastro-intestinal ulcers.
3. Bleeding disorders.
4. Gout.
5. Hypersensitivity to any NSAIDs.
6. GFR <10 ml/min.
ASPIRIN
Antiplatelet effect as ADP Receptor
Antagonist.
Usual Dose:
Thrombo-embolic, ischemic heart
disease-prophylaxis (75mg/day)
Use:
• Prophylaxis of anti-thrombotic
events in NSTMI and in STMI -in
combination with aspirin
• Myocardial Infarction
• Ischaemic cerebro vascular accident
• Peripheral arterial disease
Contraindication:
1. Active bleeding.
2. Not recommended with warfarin.
CLOPIDOGREL

37. STREPTOKINASE:
Thrombolytic agent increases plasminogen conversion to plasmin which
increases fibrin breakdown
ALTEPLASE:
Recombinant tissue-type plasminogen activator. Recombinant fibrinolytic
RETEPLASE:
Recombinant plasminogen activator; thrombolytic
THROMBOLYTIC AGENTS

38. STREPTOKINASE
ALTEPLASE
RETEPLASE

39. STREPTOKINASE RETEPLASE
ALTEPLASE
USES:
1. Acute myocardial infarction -1.5
million units intravenous infusion
over 60 min
2. Thromboembolism of arteries
3. Pulmonary embolism
4. Central retinal artery thrombosis
5. Deep vein thrombosis
Other doses-250,000 units
intravenous infusion over 30 min,
then 100,000 units every hour for
upto12-72 hours
Dose: Acute MI (total dose
100mg)-
Regimen depends on time since
onset of pain
0-6hours: 15 mg iv bolus,
followed by 50 mg iv infusion
over 30 minutes and 35 mg iv
infusion over 60 minutes
6-12 hours: 10 mg iv bolus
followed by 50 mg iv infusion
over 60 min, and four further 10
mg iv infusions, each over 30 min
Decrease dose if patient weighs
less than 65 kg.
Uses:
Used only for Myocardial
Infarction
Dose:
10 units as slow
intravenous injection
over 2 minutes, repeat
after 30 min

40. A patients is a 60-year old man, with no previous medical history. During the last month he has
had several attacks of suffocating chest pain, which began during physical labour and
disappeared quickly after he stopped. He has not smoked for four years. His father and
brother died of a heart attack. Apart from occasionally taking some aspirin he has not used
any medication in the past year. Auscultation reveals a murmur over the right carotid artery
and the right femoral artery. Physical examination reveals no other abnormalities. Blood
pressure is 130/85, pulse 78 regular, and body weight is normal.
You are fairly sure of the diagnosis, angina pectoris. Angina pectoris is a common
condition, and you decide to choose a P-drug to help him in the treatment of future
cases. 1. Define the diagnosis
2. Specify the therapeutic objective
3. Make an inventory of effective groups of drugs
4. Choose an effective group according to criteria
5. Choose a P-drug
Steps in choosing a
Personalized drug
(P-drug)
Case Study: Angina Pectoris
Right Drugs For The Right Patient

41. Lets choose a P-drug for this Patient

42. Efficacy Safety Suitability Efficacy Safety Suitability

43. The final decision to select P-drug for above mentioned patient is as follows

44. Prevention is Better Than Cure
Finally If we want to protect our Heart,
we should Remember

45. THANK YOU