Is demand ischemia considered a type of acute coronary syndrome (ACS)?

Is Demand Ischemia a Type of ACS?

No, demand ischemia (Type 2 MI) is not classified as acute coronary syndrome (ACS), though it can present with similar clinical features including troponin elevation and ECG changes. 1, 2

Key Distinction: ACS vs. Demand Ischemia

The 2014 AHA/ACC guidelines explicitly differentiate these entities based on their underlying pathophysiology:

• ACS (Type 1 MI) is caused by a primary coronary artery process such as spontaneous plaque rupture, ulceration, fissuring, erosion, or dissection with intraluminal thrombus formation—representing an abrupt reduction in coronary blood flow 1

• Demand ischemia (Type 2 MI) results from myocardial oxygen supply-demand mismatch in the absence of a direct coronary artery process, occurring when conditions other than acute plaque disruption create the imbalance 1, 2

The Hallmark of True ACS

The hallmark of ACS is the sudden imbalance between myocardial oxygen consumption and demand that is usually the result of coronary artery obstruction from acute thrombosis. 1 The guidelines state that ACS refers to conditions "usually due to an abrupt reduction in coronary blood flow" from plaque disruption 1

When Supply-Demand Mismatch Occurs Without ACS

The guidelines acknowledge that myocardial oxygen supply-demand imbalance may be caused by "noncoronary causes" including: 1

• Hypotension
• Severe anemia
• Hypertension
• Tachycardia
• Hypertrophic cardiomyopathy
• Severe aortic stenosis
• Sepsis
• Pulmonary embolism
• Severe heart failure

These conditions create demand ischemia but are explicitly listed as separate from the primary ACS pathophysiology. 1

Clinical Implications and Common Pitfalls

Diagnostic Confusion

Demand ischemia can mimic ACS because both conditions may present with: 2

• Elevated cardiac troponin (reflecting myocyte injury even without plaque rupture)
• ECG changes (typically ST-segment depression or T-wave inversions rather than ST elevation)
• Chest discomfort or dyspnea

Critical Management Difference

The key pitfall is assuming all troponin elevation with ischemic symptoms requires immediate catheterization—first identify and treat reversible causes like sepsis, anemia, or hypoxemia. 3, 2

For demand ischemia, management focuses on: 2

• Addressing the underlying cause of increased demand or decreased supply
• Optimizing hemodynamics (controlling heart rate, maintaining adequate blood pressure)
• Treating underlying coronary disease if present as a contributing factor

The Nuance: Demand Ischemia Can Unmask Coronary Disease

Demand ischemia can occur in patients with underlying stable coronary artery disease, where a fixed stenosis becomes flow-limiting during physiologic stress. 1, 2 The guidelines note that "excessive myocardial oxygen demand in the setting of a stable flow-limiting lesion" can cause supply-demand mismatch 1

However, this still differs from ACS because there is no acute plaque rupture or thrombosis—the coronary lesion is stable, and the problem is the superimposed physiologic stressor 2

Algorithmic Approach to Differentiation

When evaluating a patient with troponin elevation and possible ischemia: 3, 2

1. Assess for acute plaque disruption features: Prolonged rest chest pain >20 minutes, dynamic ST-segment changes, hemodynamic instability suggesting cardiogenic shock from acute MI 1

2. Identify potential supply-demand mismatch triggers: Tachycardia >110 bpm, hypotension, severe anemia, hypoxemia, sepsis, hypertensive emergency 3, 2

3. Evaluate the clinical context: Demand ischemia typically occurs in the setting of an obvious physiologic stressor with resolution when the stressor is corrected 2

4. Consider troponin kinetics: Both can show rising/falling patterns, but demand ischemia troponin elevations often correlate temporally with the precipitating stressor 2