This document discusses angina pectoris, a heart condition marked by chest pain due to reduced oxygen to the heart. It is caused by decreased blood flow in the coronary arteries, usually due to plaque buildup (atherosclerosis). There are three main types of angina - stable angina which occurs predictably with exertion, unstable angina with pain at rest, and variant angina caused by coronary artery spasm. Diagnosis involves stress tests, ECGs, and angiography. Treatment includes nitrates, beta blockers, calcium channel blockers, and other drugs to relieve symptoms and reduce oxygen demand on the heart. Combination therapy is often used for better management of angina.

1. Presented by:
Mr. Shaikh Akhil
M.Pharm
Asst. Prof. Dept. of Pharmacology,
BCCO Pharmacy, Naigaon,
S.R.T.M. University, Nanded

4. ANGINA PECTORIS
 A Chronic disease of CVS
 Occurs with Interminent
chest pain spread along the
Chest, Shoulders and Arms.

5. Angina- Characterstics sudden severe pressing chest pain
Radiating- neack jaw back arm ( left)
Different from CAD- Angina pectoris, acute syndrome,
arrythmia,short breath
Caused by- decreased O2 in coronary blood flow spasm of ventricle &
muscle
Obstruction of blood vessels by- atheroma
Increase Demand of O2 decrease the supply of O2 ----angina
Angina pectoris: a heart condition marked by paroxysms of chest pain
due to reduced oxygen to the heart
• Angina pectoris, or angina, as it is commonly referred to, and
coronary artery disease or arteriosclerosis are closely related.
• Angina occurs in people who have some form of blockage in the
coronary arteries. In other words, it occurs in people with coronary
heart disease.

6. ANGINA-CORONARY OCCLUSION
CORONARY OCCLUSION

7. Types Of Angina Pectoris
1. Stable Angina
2. Unstable Angina
3. Variant Angina (Prinzmetal’s Angina)

8. STABLE ANGINA
 Predictable
 Occurs on exercise, emotion or eating.
 Caused by increase demand of the heart and by a fixed
narrowing of coronary vessels, almost always by
atheroma.
 Coronary obstruction is ‘fixed’
 Blood flow fails to increase during increased demand
despite the local factors mediated ‘vasodilation’ and so
ischeamic pain is felt.

9.  So, the diastolic pressure increases and this causes a
endocrinal ‘crunch’ and thus causing Ischeamatic pain
in this region.
 Thus, a form of acutely developing and rapidly
reversible left ventricular failure results which is
relieved by taking rest and reducing the myocardial
workload.

10. UNSTABLE ANGINA
 This is characterized by Pain that occurs with less
excertion , cumulating pain at rest.
 The pathology is similar to that involved in Myocardial
Infraction, namely platelet-fibrin thrombus associated
with a ruptured atheromatous
plaque, but without complete
occulation of the vessels.
 The risk of infraction is
subtanial, and the main aim
of therapy is to reduce this.

11. VARIANT ANGINA (PRINZMETAL’S ANGINA)
 Uncommon
 Occurs at rest generally during sleep
 Caused by Large Coronary Artery Spasm
 Usually associated with atheromatous
disease
 Abnormally reactive and
hypertrophied segments
in the Coronary Artery
 Drugs aimed at preventing
& relieving Coronary Spasm.

12. DIAGNOSIS
1. STRESS (EXERCISE) TEST.
2. ECG (ELECTROCARDIOGRAPHY)
3. CHEST X-RAY
4. CARDIAC ANGIOGRAPHY
5. BLOOD TEST (BIO-MARKERS)

13. 1. EXERCISE TEST/STRESS TEST
 Used to measure heart’s response to exercise
 Patient asked to walk on a treadmill while the
physician takes the ECG
 So any changes in heart function can be determined
 Alternatively the patient recieves an injection of a
radioisotope (generally Thallium) which makes the
heart visible to a special-linked camera
 90% accurate
 But doesn’t identify the exactly where and how the
coronary arteries are blocked.

14. 2. ELECTROCARDIOGRAM (ECG)
 Measures electrical activity of the heart
 Provides info about the changes or damages to the
heart muscle
 Doesn’t detect the narrowing of the coronary arteries
 During an Anginal attack the ECG may show
1. S-T phase depression.
2. T- phase inversion and/or
3. Ventricular arrythmia
 ECG- more abnormal with Unstable Angina where
the elevation in S-T segment is found.

15. Anti Anginal Drugs
1. Nitrate-
• short acting- Glyceryl trinitrate, isosorbide dinitrate
• Long acting- Isosorbide dinitrate, isosorbide mononitrate
1. Beta blocker- propranolol, metoprolol, atenolol
2. Calcium channel locker- verapamil, diltiazem,
amlodipine
3. Potassium channel opener- nicorandil
4. NA+ channel blocker- Ranolazine

17. NITRATES
Nitrate-
• short acting- Glyceryl trinitrate, isosorbide dinitrate
• Long acting- Isosorbide dinitrate, isosorbide mononitrate
Nitrates- Nitrate are the vasodilator
1. Nitrates are converted to nitric oxide in the presence of
by-gulutathion-s-transferase & aldehyde reductase
2. Nitric oxide activate the vascular guanylyl cyclase
3. Guanylyl cyclase is increase the synthesis of cAMP( cyclic
guanosine monophosphate)
4. cGMP cause the dephosphorylation of protein kinase
5. This prevent interaction of action with myosin
6. They also decrease free cytosolic calcium
7. The smooth muscle relexation

18. Mechanism

19.  Side effects
Headache, Increased mortality, Recurrence of Myocardial
Infraction, Dizziness, Flushing, Rapid heart beat,
Restlessness, Dry mouth, Skin rash, Nausea
PK- nitrates are lipid soluble well absorbed frum buccal
mucous, intestine, skin
Ingested orally
First pass metabolism in liver, half life is longere
• Interaction-
Sildenafil is interact with nitrates cause dangerous- severe
hypotension ( reduce the body oxygen leavel which can
hearts & brain damage

20. MARKETED FORMULATIONS
 GTN Sorbitrate (PIRAMAL)
 Vasovin (TORRENT)
 ISMO retard (PIRAMAL)
 Angicor (NOVARTIS)
Nitroglyceride
Isosorbide-5-
monophosphate

21. K + channel opener
 Nicorandil
 open ATP sensitive K+ channel
 hyperpolaraziation
 Relaxation vascular smooth muscle
 se Preload se Afterload se Workload
 Increase coronary dilation
 Decrease angina
 Side effects- flushing, dizziness, palpitation, weakness,
headache, nausea, vomiting

22. CALCIUM CHANNEL ANTAGONISTS
 types:-
1. Dihydropyridine (amlodipine, nifedipine,
nicardipine)
2. Non-Dihydropyridine
1. Phenylalkylamine (verapamil, gallopamil)
2. Benzodiazapenes (diltiazem)
3. Non-selective (bepridil, mibefradil)

23. MECHANISM OF ACTION

24. MARKETED PREPARATIONS
 Calaptin (PIRAMAL)
 Vasopten (TORRENT)
 Coriem XL (RANBAXY)
 Dicard (INTAS)
 Amtas (INTAS)
 Cadeut (PFIZER)
Verapamil
Diltiazem
Amplodipine

25. Beta blocker - propranolol, metoprolol, atenolol
 Beta blocker inhibit the activation of heart by blocking
Beta 1 receptor
 They reduce of work by the heart rate, contraction,
cardiac output, blood pressure
 The reduce demand of O2 during exercise & rest
 All the blocker are non selective at high dose &
decrease beta 2 receptor
 In classical angina beta blocker + Nitrates is a better
response
 Contraindication in asthma, diabetes, brady cardia

26. -ADRENOCEPTOR
ANTAGONOSTS
 Important in prophylaxis of angina and treating
unstable angina
 Decrease O2 consumption by the heart
 Effects on coronary vessels-not important
 Avoided in variant angina
 As they increase the chances of spasm
 Eg:-
 Atenolol
 Propranolol

27. MECHANISM OF ACTION

28. MARKETED PREPARATIONS
 Betacard ( TORRENT)
 Aten (ZYDUS CADILA)
 Betacap (SUN PHARMA)
 Cardilax (INTAS)

29. COMBINATION THERAPY
1. Nitrates + -blockers :- in stable angina
2. Ca++ channel blockers + -blockers :-in stable
angina when the treatment with nitrates and -
blockers has failed.
3. Ca++ channel blockers + Nitrates :- in unstable
angina
4. All 3 together:- when the combinations of 2 drugs
has failed, where:-
1. Nitrates:- decrease Preload
2. Ca++ channel Blockers:- decrease Afterload
3. -blockers:- decrease heart rate and myocardial
contractions

30. THANK YOU!!!!