Angina is a mismatch between myocardial oxygen supply and demand.

Therapy targets either:

• ↓ Myocardial oxygen demand
• ↑ Myocardial oxygen supply
• Or both

→ Cardiovascular Pharmacology

Oxygen demand is primarily determined by:

• Heart Rate
• Contractility
• Wall Stress (Preload & Afterload)

Wall stress increases with:

• ↑ Blood pressure
• ↑ Ventricular volume

Therefore, angina therapy reduces:

• Heart rate
• Contractility
• Preload
• Afterload

Nitrates

Agents:

• Nitroglycerin
• Isosorbide Dinitrate
• Isosorbide Mononitrate

Mechanism:

• ↑ Nitric oxide
• Venodilation → ↓ preload
• Coronary vasodilation

Primary acute relief agents.

Beta-Blockers

Common agents:

• Metoprolol
• Atenolol
• Propranolol

Mechanism:

• ↓ Heart rate
• ↓ Contractility
• ↓ Myocardial oxygen consumption

First-line in chronic stable angina.

Calcium Channel Blockers

—- Dihydropyridine Calcium Channel Blockers

• Amlodipine

Primarily reduce:

• Afterload

—- Non-Dihydropyridine Calcium Channel Blockers

• Verapamil
• Diltiazem

Reduce:

• Heart rate
• Contractility
• Afterload

Useful when beta-blockers are contraindicated.

Ranolazine

Mechanism:

• Inhibits late sodium current
• Reduces intracellular calcium overload
• Improves myocardial efficiency

Does NOT significantly affect:

• Heart rate
• Blood pressure

Useful as add-on therapy.

Vasospastic (Prinzmetal) Angina:

• Nitrates
• Calcium Channel Blockers

Avoid pure beta-blockers in vasospasm.

Acute Angina:

• Nitroglycerin (sublingual)

Chronic Stable Angina:

• Beta-Blockers first-line
• Add Calcium Channel Blockers or Long-Acting Nitrates
• Consider Ranolazine for refractory symptoms

• Angina = supply-demand mismatch
• Reduce heart rate whenever possible
• Nitrates primarily reduce preload
• Beta-blockers improve mortality post-MI
• Ranolazine improves symptoms without lowering BP
• CCBs preferred in vasospasm

• Hypertension
• Heart Failure
• Dysrhythmias
• Cardiovascular Pharmacology