Learning Objective
By the end of this section, the learner should be able to:
- Explain the mechanism of action of calcium channel blockers in angina
- Differentiate the role of dihydropyridine and non-dihydropyridine CCBs
- Identify the clinical indications of CCBs in stable and vasospastic angina
Mechanism of Action
Calcium channel blockers (CCBs) act by:
👉 Blocking L-type voltage-gated Ca²⁺ channels
This results in:
- Reduced calcium influx into vascular smooth muscle
- Reduced calcium entry into cardiac myocytes
Which leads to:
- ✔️ Coronary vasodilation
- ✔️ Reduced afterload
- ✔️ Decreased myocardial oxygen demand
Classification and Clinical Effects
| Class | Primary Effect | Clinical Use in Angina |
|---|---|---|
| Dihydropyridines (e.g., Amlodipine, Nifedipine) | Peripheral vasodilation | Especially useful in vasospastic angina |
| Non-Dihydropyridines (e.g., Verapamil, Diltiazem) | ↓ HR and ↓ contractility | Stable angina and rate control |
Role in Vasospastic (Prinzmetal) Angina
Dihydropyridines (“-dipines”) are particularly important because they:
- Cause:
- Direct coronary artery vasodilation
- Help:
- Relieve coronary vasospasm
- Increase myocardial oxygen delivery
✔️ Therefore, they are the drugs of choice in vasospastic angina.
Activity
Clinical Summary
All calcium channel blockers can be used in angina management by:
- Improving coronary blood flow
- Reducing myocardial oxygen demand
- Decreasing systemic vascular resistance
They are especially valuable in:
- ✔️ Patients with contraindications to β-blockers
- ✔️ Vasospastic (Prinzmetal) angina
