The Action of Antianginal Drugs

The Action of Antianginal Drugs

Antianginal drugs work through various mechanisms to alleviate and prevent angina symptoms. Their primary actions are aimed at improving the balance between myocardial oxygen supply and demand. Here's a detailed look at the actions of different classes of antianginal drugs:

Nitrates:

Primary Actions:

Vasodilation: Dilate both venous and arterial vessels.

Preload Reduction: Venous dilation decreases blood return to the heart, reducing preload.

Coronary Artery Dilation: Improves blood flow to the heart muscle.

Afterload Reduction: Arterial dilation decreases systemic vascular resistance.

Physiological Effects:

Decrease myocardial oxygen demand by reducing preload and afterload.

Increase oxygen supply by dilating coronary arteries.

Redistribute coronary blood flow to ischemic areas.

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Beta-Blockers:

Primary Actions:

Heart Rate Reduction: Block beta-1 receptors in the sinoatrial node.

Decrease Myocardial Contractility: Inhibit beta-1 receptors in the myocardium.

Blood Pressure Reduction: Decrease cardiac output and inhibit renin release.

Physiological Effects:

Reduce myocardial oxygen demand by lowering heart rate and contractility.

Increase diastolic filling time, potentially improving coronary perfusion.

Decrease the frequency of angina attacks.

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Calcium Channel Blockers:

Primary Actions:

Vasodilation: Block calcium influx in vascular smooth muscle.

Heart Rate Reduction (non-dihydropyridines): Slow sinoatrial and atrioventricular node conduction.

Decrease Myocardial Contractility (non-dihydropyridines): Reduce calcium influx in cardiac myocytes.

Physiological Effects:

Reduce myocardial oxygen demand through vasodilation and, for some agents, heart rate reduction.

Increase coronary blood flow through coronary artery dilation.

Prevent coronary artery spasm.

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Ranolazine:

Primary Actions:

Inhibit Late Sodium Current: Reduces intracellular sodium and calcium overload in cardiac cells.

Physiological Effects:

Improves diastolic function without affecting heart rate or blood pressure.

Reduces myocardial ischemia and angina symptoms.

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Ivabradine:

Primary Actions:

Selective If Channel Inhibition: Reduces the pacemaker current in the sinoatrial node.

Physiological Effects:

Lowers heart rate without affecting blood pressure or contractility.

Reduces myocardial oxygen demand.

Increases diastolic filling time, potentially improving coronary perfusion.

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Trimetazidine:

Primary Actions:

Metabolic Modulation: Shifts cardiac metabolism from fatty acid to glucose oxidation.

Physiological Effects:

Improves cardiac efficiency without affecting hemodynamics.

Reduces oxygen consumption for a given level of cardiac work.

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Alpha-2 Agonists (e.g., Clonidine):

Primary Actions:

Reduce Sympathetic Outflow: Stimulate central alpha-2 receptors.

Physiological Effects:

Decrease heart rate and blood pressure.

Reduce myocardial oxygen demand.

Common Physiological Effects Across Drug Classes:

Reduction of Myocardial Oxygen Demand:

Achieved through various mechanisms including heart rate reduction, decreased contractility, and reduced preload/afterload.

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Improvement of Myocardial Oxygen Supply:

Primarily through coronary artery dilation and increased diastolic filling time.