What is a demand, non ST-Elevation Myocardial Infarction (non STEMI, MI)?

Understanding Demand, Non-ST-Elevation Myocardial Infarction (NSTEMI)

A demand, non-ST-elevation myocardial infarction (NSTEMI) is a type 2 myocardial infarction caused by an imbalance between myocardial oxygen supply and demand, rather than by atherosclerotic plaque rupture with thrombosis. 1

Pathophysiology

• Type 2 MI occurs when conditions other than primary coronary artery plaque rupture contribute to an imbalance between myocardial oxygen supply and demand, resulting in myocardial injury and necrosis 1
• Common causes include coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachy/brady-arrhythmias, anemia, respiratory failure, hypotension, and hypertension with or without left ventricular hypertrophy 2
• Unlike Type 1 MI (spontaneous MI), which is caused by atherosclerotic plaque disruption with superimposed thrombus formation, Type 2 MI does not involve acute atherothrombosis as the primary mechanism 1
• The myocardial injury in Type 2 MI is detected by elevated cardiac troponin levels with at least one value above the 99th percentile upper reference limit 1

Clinical Presentation

• Patients may present with typical chest pain or with atypical symptoms, especially in women, elderly, diabetics, and critically ill patients 2
• ECG findings in NSTEMI may include:
  • ST-segment depression (≥0.5 mm) in multiple leads 3
  • T-wave inversion (≥2 mm), especially when symmetrical and deep in precordial leads 3
  • Nonspecific ST-segment and T-wave changes 3
  • A completely normal ECG does not exclude NSTEMI 3
• Laboratory findings include elevated cardiac troponin levels with a characteristic rise and/or fall pattern 1

Common Clinical Scenarios

• Severe anemia leading to reduced oxygen supply to the myocardium 4
• Tachyarrhythmias causing increased myocardial oxygen demand 1
• Respiratory failure resulting in hypoxemia 1
• Profound hypotension reducing coronary perfusion 1
• Hypertensive crisis increasing myocardial workload 2
• Critical illness with increased metabolic demands 2

Diagnostic Approach

• Serial cardiac troponin measurements are essential, with measurements at presentation and 3-6 hours after symptom onset 3
• ECG should be performed and interpreted promptly, with serial ECGs if symptoms persist or change 3
• Risk stratification tools like GRACE or TIMI scores should be used regardless of ECG findings 3
• Differentiation between Type 1 and Type 2 MI is crucial for appropriate management 2
• Coronary angiography may show non-obstructive coronary disease or even normal coronary arteries in Type 2 MI 4

Management Considerations

• Treatment should focus on both the underlying cause of the supply-demand mismatch and the myocardial injury 1
• Addressing the precipitating factor (e.g., correcting anemia, controlling arrhythmias, optimizing blood pressure) is essential 1
• Antiplatelet therapy may be appropriate depending on the clinical context, but is not universally indicated as it would be in Type 1 MI 1
• The American College of Cardiology/American Heart Association guidelines emphasize that management strategies for Type 2 MI differ from those for Type 1 MI 1

Clinical Pitfalls and Considerations

• Type 2 MI is often underdiagnosed or misclassified as Type 1 MI, leading to inappropriate management 2
• Patients with Type 2 MI still have significant morbidity and mortality risks that require careful attention 1
• The distinction between myocardial injury and infarction is important - not all elevated troponin levels indicate infarction 1
• Treatment should be individualized based on the underlying cause of the supply-demand mismatch rather than following standard ACS protocols 1

Prognostic Implications

• The prognosis of Type 2 MI depends largely on the severity of the underlying condition causing the supply-demand imbalance 1
• Patients with Type 2 MI often have multiple comorbidities that contribute to worse outcomes 1
• The magnitude of troponin elevation and ECG changes provides important prognostic information 3