Diptarco Singha, Durjoy Ghosh & Hrishav Roychowdhury

B.PHARM, 3rd YEAR, 6th SEMESTER

Presented by..

ANGINA PECTORIS & ITS MANAGEMENT

Normal Heart & AnginaAngere= InflammationPectus= ChestAngina Pectoris commonly known as Angina, characterised by chest pain due to imbalance between O2 supply & O2 demand in cardiac muscle or tissue due to the defect or blockage in the coronary artery.

Also known as CAD

O2 Demand

O2Supply

O2 Demand

O2Supply

Normal Condition

But In Angina

Imbalance & Stressed(pressure/discomfort) condition of heartCommonly known left side chest pain.

Types OF Angina

A) Classical Angina/Stable Angina• Atheroma Deposition• Defect in coronary

artery• Excessive

exercise(O2 D )• Stress & tension• Predictable

C) Unstable Angina• Thrombin aggregation• Platelets aggregation• Rapid & severe pain

B)Variant Angina/Vasoplastic Angina• Excessive vasoconstriction • Unpredictable

Pathophysiology of Heart

Most of O2,almost 90% of the body is consumed by heart.

If 100 ml of blood is pumped out in one heart beat

90 ml goes to the body & 10 ml retained by heart through coronary artery.

o Coronary Artery blocks o Blood supply to heart decreases o Heart unable to consume sufficient O2

o O2 demand increases rather than supply

Risk Factors Pathological FactorsHyperlipidaemia Fat accumulation in Coronary artery wall

Stress & Tension

Excessive Exercise

Leads to Hypertension Blood flow through artery & stress to heart leading Angina

Leads to excessive O2 demand

Atheroma deposition on the wall of Coronary artery Blockage of coronary artery

Thrombin or platelets aggregation

Excessive vasoconstriction.

TargetsAntihyperlipidemic should be given. to fat deposition on coronary artery wall.

Antiplatelet & Thrombolytic are given. to thrombin/platelet aggregation.

Calcium channel blockers (CCBs) are given. to vasoconstriction.

Management of Angina Pectoris: FACTORS MECHANISM OF ACTION CLASSIFICATION OF DRUGS

A) Atheroma Stable & predictable Angina

Deposition of fat,LDL on coronary artery wall Blood supply to cardiac muscle

O2 Supply to cardiac muscle

Imbalance between O2D & O2S

chest pain.

β Blockers CO

O2 demand in heart

Imbalance decreases & HR

1) HMG CoA inhibitor Statins, Atravastatins, Simvastatins, Rimvastatins.

2) Organic Nitrates a)Short acting: Glyceryl trinitrate, Nitroprusideb)Long acting: ISDN,ISMN etc

3) β BlockersMetaprolol ( β1 selective)Atenolol ( do ) Esmolol ( do )Propanolol (non selective)

Stable & predictable Angina

long term management

FACTORS MECHANISM OF ACTION CLASSIFICATION OF DRUGS

B)Thrombin/platelet aggregation

Discontinuous platelets aggregation inside the Coronary artery wall

O2 supply towards heart

4) Thrombolytic Steptokinase, Urokinase, Alteplase

5) Antiplatelet Aspirin, Dipysadamol, Ticlopidine β blockers are also given .

6)Vasospasm

Ca+ channel blocks

MLCK MLCK-P

Results in vasodialation

K+ channel opens GC CGMP blocks MLCK-P conversion Vasodialation

6) Calcium channel Blockers (CCBs) Verapamil, Nifedipin, Amlodipin etc

7)K+ channel openers Nicorandil

Contd..

Unstable

Unpredictable

Surgical Management

Angioplasty

Bypass surgery

Conclusion

References: KD Tripathi M.D., Essentials of Medical Pharmacology, 7th

Ed., Jaypee Brothers Medical Publishers (P) Ltd., Antianginal and Other Anti-ischaemic drugs, Page no.: 539-557.

Anne Waugh, Allison Grant, Ross and Wilson Anatomy and Physiology in Health and Illness, 9th Ed., Churchill Livingstone, The cardiovascular System, Disorder of Blood Pressure , Page no.: 124-126.

THANK YOU