What drug class lowers myocardial oxygen demand?

Beta-Blockers Lower Myocardial Oxygen Demand

Beta-blockers are the primary drug class that lowers myocardial oxygen demand through reduction of heart rate, myocardial contractility, and systolic blood pressure. 1

Mechanism of Action

Beta-blockers competitively block beta-1 adrenergic receptors located primarily in the myocardium, producing the following effects that reduce myocardial oxygen consumption (MVO₂): 1

• Decreased heart rate - Reduces the number of cardiac contractions per minute and increases diastolic filling time, improving coronary perfusion 1
• Reduced myocardial contractility - Decreases the force of ventricular contraction, lowering oxygen requirements 1, 2
• Decreased systolic blood pressure - Reduces afterload and the pressure work of the heart 1, 3
• Slowed AV node conduction - Blunts heart rate responses to exertion, pain, and other stimuli 1

The slowing of heart rate has dual benefits: it not only reduces MVO₂ but also increases the duration of diastole and diastolic pressure-time, which are determinants of forward coronary flow and collateral circulation. 1

Clinical Applications in Ischemic Heart Disease

For acute coronary syndromes (ACS), early initiation of oral beta-blockers within 24 hours is recommended in patients without contraindications to reduce risk of reinfarction and ventricular arrhythmias. 1

For stable angina, beta-blockers are first-line anti-ischemic therapy that reduce the frequency of anginal attacks and improve exercise capacity by lowering myocardial oxygen consumption at any given level of exercise. 1, 4

Important Contraindications and Cautions

Beta-blockers should be avoided in the following situations: 1

• Active heart failure or cardiogenic shock (Killip class II-IV)
• Severe bradycardia (heart rate <50 bpm)
• Hypotension (systolic blood pressure <90-100 mmHg)
• Second- or third-degree AV block without a pacemaker
• Marked first-degree AV block (PR interval >0.24 seconds)
• Active bronchospasm or severe asthma
• Evidence of low cardiac output state

The COMMIT trial demonstrated that early aggressive intravenous beta-blockade increased cardiogenic shock risk, particularly in hemodynamically unstable patients, which led to downgrading recommendations for IV administration. 1 Oral administration with gradual uptitration is preferred over intravenous boluses. 1

Alternative Drug Classes

Calcium channel blockers (particularly non-dihydropyridines like verapamil and diltiazem) also lower myocardial oxygen demand through: 1

• Decreased afterload via peripheral arterial vasodilation
• Reduced contractility
• Decreased heart rate (verapamil and diltiazem only)

However, verapamil and diltiazem should be avoided in patients with pulmonary edema or severe LV dysfunction. 1 Rapid-release, short-acting dihydropyridines (like nifedipine capsules) must be avoided in the absence of concomitant beta-blockade due to reflex tachycardia that can increase myocardial oxygen demand. 1, 5

Preferred Beta-Blocker Agents

For patients with ACS and left ventricular systolic dysfunction or heart failure, use one of three evidence-based agents: 1

• Carvedilol (mixed beta/alpha blocker)
• Extended-release metoprolol succinate
• Bisoprolol

Beta-blockers without intrinsic sympathomimetic activity are preferred in the acute setting. 1