Mechanism of Action of Antianginal Drugs_ SlideShare Presentation

Mechanism of Action of Antianginal Drugs: SlideShare Presentation

Slide 1: Introduction to Antianginal Drugs

Definition: Medications used to treat and prevent angina pectoris

Goal: Improve balance between myocardial oxygen supply and demand

Slide 2: Classes of Antianginal Drugs

Nitrates

Beta-blockers

Calcium Channel Blockers

Newer agents (Ranolazine, Ivabradine, Trimetazidine)

Slide 3: Nitrates

Mechanism of Action:

Release nitric oxide (NO) in the body

Venodilation: Reduces preload

Coronary vasodilation: Improves blood flow

Systemic arterial dilation: Reduces afterload

Inhibits platelet aggregation

Examples: Nitroglycerin, Isosorbide dinitrate

Slide 4: Beta-blockers

Mechanism of Action:

Block effects of epinephrine and norepinephrine on beta-adrenergic receptors

Decrease heart rate

Reduce myocardial contractility

Lower blood pressure

Increase diastolic filling time

Examples: Metoprolol, Atenolol, Propranolol

Slide 5: Calcium Channel Blockers (CCBs)

Mechanism of Action:

Inhibit calcium influx into vascular smooth muscle and cardiac myocytes

Coronary and peripheral vasodilation

Decrease myocardial contractility (non-dihydropyridine CCBs)

Reduce heart rate (non-dihydropyridine CCBs)

Examples: Amlodipine, Verapamil

Slide 6: Ranolazine

Mechanism of Action:

Inhibits late sodium current in cardiac myocytes

Reduces intracellular calcium overload

Improves diastolic relaxation and coronary blood flow

Slide 7: Ivabradine

Mechanism of Action:

Selectively inhibits If current in sinoatrial node

Reduces heart rate without affecting contractility or blood pressure

Slide 8: Trimetazidine

Mechanism of Action:

Metabolic modulator

Inhibits fatty acid oxidation

Shifts cardiac metabolism towards glucose oxidation

Improves cardiac efficiency and reduces oxygen demand

Slide 9: Nicorandil

Mechanism of Action:

Dual action: Nitrate-like effect and potassium channel opener

Causes vasodilation through NO release

Hyperpolarizes vascular smooth muscle, leading to vasodilation

Slide 10: Comparison of Antianginal Drug Effects

(Table format)

Drug Class | Heart Rate | Contractility | Preload | Afterload | Coronary Flow

Nitrates | 鈫?| 鈫?| 鈫撯啌 | 鈫?| 鈫?

Beta-blockers | 鈫撯啌 | 鈫?| 鈫?| 鈫?| ?

CCBs | 鈫?(non-DHP) | 鈫?(non-DHP) | ? | 鈫?| 鈫?

Ranolazine | ? | ? | ? | ? | 鈫?

Ivabradine | 鈫撯啌 | ? | ? | ? | ?

Trimetazidine | ? | ? | ? | ? | ?

Slide 11: Clinical Considerations

Combination therapy often used for optimal management

Choice depends on patient's condition, comorbidities, and potential side effects

Antianginal therapy used with lifestyle modifications and risk factor management

Slide 12: Conclusion

Antianginal drugs work through various mechanisms to improve oxygen supply-demand balance

Understanding these mechanisms is crucial for effective patient management

Ongoing research continues to develop new antianginal agents with novel mechanisms of action

This SlideShare presentation provides a concise overview of the mechanisms of action of various antianginal drugs, allowing for easy comparison and understanding of their effects on cardiovascular function.