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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